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Verrucous papules definition: Papule – an overview | ScienceDirect Topics

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Describing a Rash – CanadiEM

When describing a rash there are many characteristics to make note of, including its primary morphology, secondary morphology, demarcation, colour, configuration, and distribution. The focus or this article will be on primary morphology.

Reasoning through the first blush

Within primary morphology you can stratify a lesion based on whether it is flat or elevated. If the lesion is flat, then it will be either a macule or patch.  A macule is a flat lesion smaller than 1 cm and a patch is a flat lesion larger than 1 cm.

Elevated lesions are either solid or fluid-filled. Solid lesions can be described as either a papule, plaque, nodule, or wheal. A raised solid lesion is a papule when it is less than 1 cm and a plaque when it is a confluence of papules greater than 1 cm. A nodule is a solid lesion with a deeper cutaneous involvement. A wheal is essentially a papule or plaque that is characteristically evanescent. It is often white at the core with an erythematous base. A fluid-filled lesion would be a vesicle, bulla, or pustule. A vesicle is less than 1cm while a bulla is greater than 1cm. A pustule is similar to a vesicle where it is usually less than 1 cm but instead of simple fluid, it is filled with pus.

It is always important to examine the rash in the context of a detailed history and physical examination. However, by determining a rash’s primary characteristics, you can narrow your differential diagnoses. Here are some common examples of dermatological findings and their associated primary morphology.

  • Freckles (macule)
  • Seborrheic keratosis (papule)
  • Psoriasis (plaque)
  • Lipoma (nodule)
  • Mosquito bites (wheal)
  • Herpes rash (vesicles)
  • Large burn blisters (bullae)
  • Folliculitis (pustule)
It’s not always so easy

There are also less common examples that you do not want to miss. If you see red macules or red/purple plaques that do not blanch, you start to think about petechia or purpura. In a sicker patient, you would worry about thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), meningococcemia, and other life threatening illnesses. If you see a vesiculobullous rash that is very localized, you may be concerned about necrotizing fasciitis.  If you see a diffuse pustular rash and the patient has recently started a medication, you may consider acute generalized exanthematous pustulosis (AGEP). Other life threatening rashes such as Staphylococcal scalded skin syndrome (SSSS), toxic epidermal necrolysis (TENS), and Stevens-Johnson syndrome (SJS) may have bullous lesions however can present with a variety of primary morphologies.1–4

This post was copyedited and uploaded by Josiah Butt

References

1.

Soutor C, Hordinsky M. Clinical Dermatology. McGraw Hill Professional; 2013.

4.

Murphy-Lavoie H, Leigh LeGros T. Emergent Diagnosis of the Unknown Rash: An Algorithmic Approach. Emergency Medicine. 2010;42(3):6-16.

Reviewing with the Staff

Determination of the primary morphology of a cutaneous lesion is critical in making a diagnosis. Correctly utilizing these specific terms will allow one to quickly access electronic resources and get to relevant content. Understanding the terminology is also important for communication in the medical record and for consultation.
As highlighted in the introduction, further description of secondary lesions (e.g. scale, ulceration), configuration, color, demarcation, and distribution will further assist in narrowing the diagnosis. The specific size is helpful as well; 1mm papules have a different differential diagnosis than 1cm papules.
I would like to highlight two tips for those learning to diagnose and describe skin lesions.
As you learn the more specific dermatologic terminology, do not be afraid to use regular English when uncertain. A flesh coloured verrucous papule in the lateral nail fold is the same as a warty raised bump next to the nail. Plain English is better than using a specific term incorrectly.
Another common pitfall is seeing only the lesion the patient has brought to your attention. A full exam is often beneficial. Take for example a rash on the hand.
• Changes in the scalp or nails may help make the diagnosis of psoriasis.
• Associated tinea pedis may suggest tinea manuum “two feet one hand syndrome”.
• Oral vesicles will help make the diagnosis of hand foot and mouth disease.
• Facial rash may clue you in to the diagnosis of gottron’s papules in dermatomyositis.

With this in mind, for any new patient with a skin concern, my practice is to have my medical assistants have the patient wear a gown.

Michael Cosimini, MD

University of Southern California / Children’s Hospital Los Angeles, Assistant Professor of Clinical Pediatrics, Keck School of Medicine

(Visited 57,310 times, 90 visits today)

Mike Xue is an incoming PGY-1 in Family Medicine at Queen’s University, Oshawa Lakeridge site. He completed medical school at McMaster University. His clinical interests include dermatology, preventative medicine, and acute care.

Dr. Michael Cosimini is a Paediatrician at the University of Southern California, Children’s Hospital Los Angeles. He is an Assistant Professor of Clinical Paediatrics, at the Keck School of Medicine.

Recognizing Neoplastic Skin Lesions: A Photo Guide

LEWIS C. ROSE, M.B., B.S.(LOND), University of Texas Health Science Center, San Antonio, Texas

Am Fam Physician. 1998 Sep 15;58(4):873-884.

 
Patient information: See related handout on skin cancer, written by the author of this article.

Malignant lesions of the skin are common. Patients who develop squamous cell carcinoma and malignant melanoma often have recognizable precursor conditions. A few skin lesions resemble malignancies. Lesions that are growing, spreading or pigmented, or those that occur on exposed areas of skin are of particular concern. Knowing the similarities and differences between these lesions allows the primary physician to make a diagnosis in most cases by simple inspection and palpation. When in doubt, it is appropriate to perform an excisional biopsy of small lesions or punch biopsy of larger lesions. Removal of premalignant lesions will reduce the occurrence of malignant disease. Almost all skin cancers can be cured by early excision or destruction. For these reasons, physicians should be aware of the risk factors for skin cancer, educate patients about risk reduction and include skin inspection for premalignant and malignant lesions as a part of routine health maintenance examinations.

Primary neoplastic disease of the skin is common. Early recognition of such lesions is important because complete excision will cure almost all cases of skin cancer if performed in the early stages. A presumptive diagnosis can often be made by considering the patient’s risk factors, the history of the lesion and its location, appearance and texture. The definitive diagnosis is made by histologic examination of biopsy specimens.

Factors that Contribute to Skin Cancer

Most primary skin neoplasms occur in skin that is exposed to adverse conditions. Ultraviolet light from sunlight is most often a contributing factor. Desert sunlight is particularly dangerous, but water and snow both reflect a high proportion of the ultraviolet light from the sky, increasing the risk for sailors, beach lovers and winter-sports enthusiasts. In farmers and ranchers, the skin of the face, neck and arms is also at high risk.

Exposure to immunosuppressive drugs or ionizing radiation is a less common cause.1 Use of organic arsenics and tars predisposes to skin cancer. A history of malignant melanoma in a first-degree relative or the presence of numerous melanotic nevi, which may be familial or sporadic, greatly increases the risk of developing malignant melanoma.2–4 Persons with fair or freckled skin that does not tan are at increased risk. Dark hair and skin provide some protection from skin cancer. Family physicians should educate their patients about these risks and encourage them to protect their skin.

Skin lesions come to the attention of the physician in three ways: (1) the patient may be aware of the lesion and consult the physician about it; (2) the physician may notice the lesion when examining the patient for some other reason; or (3) the physician inspects the entire skin surface for lesions as part of a pre-employment or health maintenance examination. A complete skin examination is important particularly in high-risk patients because, at the stage when they are curable, skin cancers are painless and often inconspicuous. The top of the head, the face, the neck, the shoulders and the extensor surfaces of the arms are particularly important, but the areola, the vulva and the foreskin are also areas of high risk. In black patients, the palms of the hands, soles of the feet and periungual areas are particularly vulnerable. A detailed description and measurement of all suspicious skin lesions should be documented in the patient’s medical record.

Basal Cell Carcinoma

Comprising 60 percent of primary skin cancers, the basal cell carcinoma is a slow-growing lesion that invades tissue but rarely metastasizes. Most metastatic basal cell carcinomas arise from large tumors.5 Basal cell carcinomas that have recurred after excision may be at greater risk of metastasis.6 Basal cell carcinoma is common on the face and on other exposed skin surfaces but may occur anywhere (Figure 1). The common form first appears as a small round or oval area of skin thickening. Usually there is no itching, pain or change in skin color. The area very slowly extends circumferentially, creating a slightly raised edge, which may have a shiny, pearly or slightly translucent appearance (Figure 2).


FIGURE 1.

Small basal cell carcinoma.

View/Print Figure

FIGURE 2.

Basal cell carcinoma with the characteristic shiny appearance.


FIGURE 2.

Basal cell carcinoma with the characteristic shiny appearance.

As the lesion continues to grow, the central area becomes atrophic, leaving a hollow that is covered by thin skin, often with visible vessels, which eventually ulcerates (Figure 3). The growing edges become more irregular, and the shape becomes uneven. The base is also invasive and gradually erodes the underlying tissue, making it difficult to excise the lesion completely.


FIGURE 3.

Ulcerating basal cell carcinoma.

Less common forms include a superficial basal cell carcinoma that resembles a patch of dermatitis, a pigmented basal cell carcinoma that resembles a nodular malignant melanoma and an aggressive-growth basal cell carcinoma. Aggressive-growth basal cell carcinoma is an infiltrating sclerosing lesion that may appear similar to a scar with a firm or hard base. In patients younger than 35 years, basal cell carcinoma tends to adopt the more aggressive forms.7

No premalignant conditions precede basal cell carcinoma. Basal cell carcinoma and lesions of similar appearance are compared in Table 1.

View/Print Table

TABLE 1

Features of Basal Cell Carcinoma and Lesions of Similar Appearance
Lesion Location Surface Color Outline Other features

Basal cell carcinoma

Most common on face, but can occur anywhere

Raised, pearly, firm

Normal skin color

Round at first, irregular later

May ulcerate

Superficial basal cell carcinoma

Any location

Roughened

Skin-colored or pink

Round or irregular

Resembles dermatitis

Pigmented basal cell carcinoma

Most commonly occurs on the face

Nodule

Growing area is dark brown or black

Becomes irregular as growth progresses

Looks like a nodular malignant melanoma

Infiltrating basal cell carcinoma

Any location

Smooth

Skin-colored

Various

Looks like a firm scar that grows aggressively

Tricoepithelioma

Any location

Raised, pearly

Normal skin color

Round

Does not become malignant

Keloid after

Site of previous injury

Raised, rounded, smooth

Usually pink, may be skin-colored

Varies, often linear

Often large, but no growth one year

Molluscum contagiosum

Face and hands of children, areas of sexual contact

Raised, rounded central hollow

Skin-colored

Round

Usually multiple, in clusters or scattered; contagious

Soft, fleshy

Dermatofibroma

Often occurs on limbs, rarely on face

Flat or slightly raised, edge not thickened or pearly

Skin-colored, firm under the surface but not on the surface

Usually round or oval

Usually >5 mm diameter when first noticed

TABLE 1

Features of Basal Cell Carcinoma and Lesions of Similar Appearance
Lesion Location Surface Color Outline Other features

Basal cell carcinoma

Most common on face, but can occur anywhere

Raised, pearly, firm

Normal skin color

Round at first, irregular later

May ulcerate

Superficial basal cell carcinoma

Any location

Roughened

Skin-colored or pink

Round or irregular

Resembles dermatitis

Pigmented basal cell carcinoma

Most commonly occurs on the face

Nodule

Growing area is dark brown or black

Becomes irregular as growth progresses

Looks like a nodular malignant melanoma

Infiltrating basal cell carcinoma

Any location

Smooth

Skin-colored

Various

Looks like a firm scar that grows aggressively

Tricoepithelioma

Any location

Raised, pearly

Normal skin color

Round

Does not become malignant

Keloid after

Site of previous injury

Raised, rounded, smooth

Usually pink, may be skin-colored

Varies, often linear

Often large, but no growth one year

Molluscum contagiosum

Face and hands of children, areas of sexual contact

Raised, rounded central hollow

Skin-colored

Round

Usually multiple, in clusters or scattered; contagious

Soft, fleshy

Dermatofibroma

Often occurs on limbs, rarely on face

Flat or slightly raised, edge not thickened or pearly

Skin-colored, firm under the surface but not on the surface

Usually round or oval

Usually >5 mm diameter when first noticed

Squamous Cell Carcinoma

Squamous cell carcinoma comprises 20 percent of all cases of skin cancer. It typically occurs on areas of the skin that have been exposed to sunlight for many years. It may also appear in areas that have been subjected to ionizing irradiation or in other locations in patients who have undergone treatment with immunosuppressive drugs1 or have been exposed to organic trivalent arsenic compounds or tars. Squamous cell carcinoma of the lip may be related to pipe smoking, as well as to sunlight exposure.

Human papillomavirus infection may be a precursor of keratoacanthoma and periungual, genital and other squamous cell carcinomas, especially in immunosuppressed patients.8 The affected area develops a slight redness, scaling, fissuring and an uneven surface. Superficial dilated vessels may be visible. The lesion often appears very dry and may bleed when stretched or abraded. It spreads laterally from the edges and may heap up irregularly. New lesions often appear near old ones. Clusters of lesions may occur as fleshy masses (Figure 4). The centers may become atrophic and develop raw patches or frank ulceration (Figure 5).


FIGURE 4.

Squamous cell carcinoma showing clusters of lesions.


FIGURE 5.

Ulcerating squamous cell carcinoma of the lip.

Two other skin lesions are considered part of the squamous cell carcinoma spectrum. The first type, keratoacanthoma, is closely related to squamous cell carcinoma. Like squamous cell carcinoma, it appears on skin damaged by sunlight or chemicals. It often occurs at the site of trauma, especially in immunosuppressed patients. It is sometimes associated with human papillomavirus infection. Keratoacanthoma appears as a skin-colored or pink smooth lesion, which becomes dome-shaped during a period of very rapid growth. When mature, it is volcano-shaped, with protruding masses of keratin resembling lava. Classic keratoacanthoma is not malignant and regresses spontaneously, but atypical lesions may actually be squamous cell carcinoma.7 Many dermatopathologists include keratoacanthoma in the spectrum of squamous cell carcinoma9 (Figure 6).


FIGURE 6.

Keratoacanthoma with typical volcano appearance.

The second type is verrucous carcinoma, a variant of squamous cell carcinoma that features an irregular warty surface (Figure 7).


FIGURE 7.

Irregular warty surface of verrucous carcinoma.

While metastasis of common sunlight-induced squamous cell carcinoma is unusual, lesions more likely to metastasize are lesions of the lip or ear, lesions that recur after previous therapy, lesions at the site of a burn and those that are more deeply invasive. Squamous cell carcinoma of the skin may be metastatic from other locations (Figure 8).

A variety of skin lesions are considered precursors of squamous cell carcinoma. Actinic keratosis appears very similar to the less severe lesions of squamous cell carcinoma. It is always found on skin that has received heavy exposure to sunlight.9,10 Actinic keratosis should be sought during routine inspection of the skin, especially in fair-skinned patients who have been exposed to sunlight frequently. Regular reexamination of affected skin and treatment of any areas showing growth or change can prevent neoplastic transformation or provide early treatment of malignancy11 (Figure 9).


FIGURE 8.

Metastatic squamous cell carcinoma.


FIGURE 9.

Actinic keratosis.

Epidermodysplasia verruciformis is an uncommon autosomal recessive disorder that predisposes patients to the development of squamous cell carcinoma (Figure 10). Actinic cheilitis is a condition that is similar to actinic keratitis but occurs on the vermilion of the lips.


FIGURE 10.

Epidermodysplasia verruciformis of the hand.

Bowen’s disease is squamous cell carcinoma in situ that resembles a plaque of psoriasis. When Bowen’s disease occurs on the penis, it is called erythroplasia of Queyrat (Figure 11). Leukoplakia of the mouth or genital area may be premalignant (Figure 12).


FIGURE 11.

Erythroplasia of Queyrat (Bowen’s disease of the penis).


FIGURE 12.

Leukoplakia of the genital area.

Human papillomavirus includes several strains that are associated with squamous cell carcinoma, especially in the genital areas.12  The virus may not be a precursor of squamous cell carcinoma but does increase the patient’s risk for developing squamous cell carcinoma. In Table 2, squamous cell carcinoma and its variants are compared with other lesions of similar appearance (Figures 13 through 16).

View/Print Table

TABLE 2

Features of Squamous Cell Carcinoma and Lesions of Similar Appearance
Lesion Location Surface Color Outline Other features

Squamous cell carcinoma

Areas exposed to sunlight, radiation or arsenicals

Rough, irregular, sometimes scaly, sometimes has visible vessels, sometimes warty or with fleshy masses

Skin-colored at first, sometimes reddened later

Vague

New lesions may appear near old ones

Does not clear with corticosteroid therapy

Keratoacanthoma (a variant of squamous cell carcinoma)

Exposed areas, especially face and hands

Smooth dome, becoming volcano-shaped

Skin-colored or slightly reddened

Well-defined

Goes through aperiod of very rapid growth, often regresses

Eczema and atopic dermatitis (Figure 13)

Atopic dermatitis behind ears, on flexure areas

Reddened, slightly scaly, sometimes with vesicles

Dry at first, fissured, may weep

Indefinite

Common in atopic persons and those exposed to irritants

Contact dermatitis (Figure 14)

Wherever skin comes in contact with an irritant

Reddened, slightly scaly, sometimes with vesicles

Dry at first, fissured, may weep

Circumscribed

Dermatitis clears with corticosteroid therapy

Psoriasis (Figure 15)

Elbows, knees, scalp, sacral cleft, nails

Scaly with underlying reddened base

White dry scales, smooth pink or red wherescales are removed; may bleed

Well-demarcated; round, irregular or confluent

Often widespread, sometimes itchy; varies with season

Seborrheic dermatitis (Figure 16)

Scalp, forehead, nasolabial fold, midline trunk

Raised, with scales

Yellow or brown

Well-demarcated

Some lesions can be easily removed

TABLE 2

Features of Squamous Cell Carcinoma and Lesions of Similar Appearance
Lesion Location Surface Color Outline Other features

Squamous cell carcinoma

Areas exposed to sunlight, radiation or arsenicals

Rough, irregular, sometimes scaly, sometimes has visible vessels, sometimes warty or with fleshy masses

Skin-colored at first, sometimes reddened later

Vague

New lesions may appear near old ones

Does not clear with corticosteroid therapy

Keratoacanthoma (a variant of squamous cell carcinoma)

Exposed areas, especially face and hands

Smooth dome, becoming volcano-shaped

Skin-colored or slightly reddened

Well-defined

Goes through aperiod of very rapid growth, often regresses

Eczema and atopic dermatitis (Figure 13)

Atopic dermatitis behind ears, on flexure areas

Reddened, slightly scaly, sometimes with vesicles

Dry at first, fissured, may weep

Indefinite

Common in atopic persons and those exposed to irritants

Contact dermatitis (Figure 14)

Wherever skin comes in contact with an irritant

Reddened, slightly scaly, sometimes with vesicles

Dry at first, fissured, may weep

Circumscribed

Dermatitis clears with corticosteroid therapy

Psoriasis (Figure 15)

Elbows, knees, scalp, sacral cleft, nails

Scaly with underlying reddened base

White dry scales, smooth pink or red wherescales are removed; may bleed

Well-demarcated; round, irregular or confluent

Often widespread, sometimes itchy; varies with season

Seborrheic dermatitis (Figure 16)

Scalp, forehead, nasolabial fold, midline trunk

Raised, with scales

Yellow or brown

Well-demarcated

Some lesions can be easily removed


FIGURE 13.

Eczema dermatitis.


FIGURE 14.

Contact dermatitis.


FIGURE 15.

Psoriasis.


FIGURE 16.

Seborrheic dermatitis.

Malignant Melanoma

Although it comprises only 1 percent of skin cancers, malignant melanoma accounts for over 60 percent of skin cancer deaths.13 It metastasizes to remote sites early, and its metastases are characteristically unresponsive to treatment. Like the other skin cancers, malignant melanoma is more common on skin that has undergone excessive exposure to sunlight, but it can occur anywhere. Four types of malignant melanoma are identified.

The lesions of superficial spreading melanoma are dark brown or black. In the initial phase they have a slowly spreading irregular outline. Some areas may be a lighter shade. Vertical growth occurs later, penetrating into the dermis and causing some parts of the lesion to become raised. This is the most common kind of melanoma (Figure 17).


FIGURE 17.

Superficially spreading malignant melanoma.

Nodular melanoma grows vertically from the start and is more likely to mestastasize early. It has little or no lateral extension, appearing as a shiny black dome.

Lentigo maligna melanoma occurs in a pre-existing lentigo maligna. The appearance of one or more nodules signals the change to an invasive lesion (Figure 18).

View/Print Figure

FIGURE 18.

Lentigo maligna. Note the multiple nodules signaling invasiveness of the lesion.


FIGURE 18.

Lentigo maligna. Note the multiple nodules signaling invasiveness of the lesion.

Acral lentiginous melanoma occurs on the palms of the hands, the soles of the feet, under the nails and on mucosal surfaces. It is uncommon, comprising only 5 percent of melanomas in pale-skinned persons. Dark-skinned persons rarely get melanomas, but if they do, the lesions are likely to be acral melanomas (Figure 19).


FIGURE 19.

Acral lentiginous melanoma.

Since not all malignant melanomas are visibly pigmented, physicians should be suspicious of any lesion that is growing or that bleeds on minor trauma. If the diagnosis is in doubt, it is better to take one or more adequate full skin thickness biopsies for histologic examination.

Certain skin lesions are considered precursors of malignant melanoma. Blue nevi occasionally become the site of melanocytic malignant change. Suspicious features, such as location on the scalp of men in their forties, growth, bleeding on minor trauma and the occurrence of dark satellite lesions around the nevus, may signal this change. All blue nevi should be carefully monitored or excised (Figure 20).


FIGURE 20.

Blue nevi.

Lentigo maligna (melanotic freckle of Hutchison) occurs on the face or other sun-exposed skin of older, fair-skinned persons. It is a brown macule with some color variation, spreading slowly and unevenly at the edges. Dark invasive lesions with irregular borders may grow from it (Figure 18). Congenital nevomelanocytic nevi are brown patches of skin that are present at birth or develop in infancy. They usually have an irregular surface, and they may be slightly raised and exhibit coarse hair. Lesions that are more than 20 cm across are more likely to undergo neoplastic change into malignant melanoma, often when the child is between three and five years of age.

The presence of 10 or more dysplastic nevi confers a 12-fold risk of developing malignant melanoma.2 Dysplastic nevi may appear de novo or may develop from common melanocytic nevi.3 They occur in 5 percent of the general white population, but in 30 to 50 percent of those with sporadic (nonfamilial) primary melanoma and in almost all patients with familial cutaneous melanoma.4

In Table 3, the common varieties of malignant melanoma are compared with lesions of similar appearance (Figures 21 through 23).

View/Print Table

TABLE 3

Features of Four Forms of Malignant Melanoma and Lesions of Similar Appearance
Lesion Location Surface Color Outline Other features

Superficially spreading malignant melanoma

Most common on sun-exposed skin, but can occur anywhere

Smooth; vertical growth occurs later

Dark brown or black, may be variegated

Becomes more irregular as it grows

May have a pink or reddish halo

Nodular melanoma

Most common on sun-exposed skin, but can occur anywhere

Nodular form

Dark brown or black, may be variegated

May be regular or irregular

Grows aggressively, invades early

Lentigo maligna melanoma

In a pre-existing lentigo maligna, usually facial

Nodular against a smooth background

Dark or black on pale brown background

Irregular

Acral lentiginous melanoma

Nailbeds, palms of the hands, soles of the feet, mucosal areas

Smooth

Dark brown or black

Irregular

Occurs in both black and white persons

Common melanocytic nevi (Figure 21)

Widely scattered

Smooth, flat or uniformly elevated

Uniform light or dark brown

Regular, round or oval, rarely >10 mm diameter

Less common in black persons

Lentigo (freckles)

Mainly on sun-exposed surfaces

Smooth, flat brown or tan

Uniform light

Round, oval or polyhedric

Darken with sun exposure, lighten in winter

Blue nevi (Figure 20)

Most commonly occur on hands or feet; may occur anywhere

Papules or nodules

Blue, blue-gray, or blue-black

Round or oval, usually <10 mm diameter

Firm on palpation

Pigmented basal cell carcinoma (Figure 23)

Most common on the face

Nodule

Growing area is dark brown or black

Becomes irregular as growth progresses

TABLE 3

Features of Four Forms of Malignant Melanoma and Lesions of Similar Appearance
Lesion Location Surface Color Outline Other features

Superficially spreading malignant melanoma

Most common on sun-exposed skin, but can occur anywhere

Smooth; vertical growth occurs later

Dark brown or black, may be variegated

Becomes more irregular as it grows

May have a pink or reddish halo

Nodular melanoma

Most common on sun-exposed skin, but can occur anywhere

Nodular form

Dark brown or black, may be variegated

May be regular or irregular

Grows aggressively, invades early

Lentigo maligna melanoma

In a pre-existing lentigo maligna, usually facial

Nodular against a smooth background

Dark or black on pale brown background

Irregular

Acral lentiginous melanoma

Nailbeds, palms of the hands, soles of the feet, mucosal areas

Smooth

Dark brown or black

Irregular

Occurs in both black and white persons

Common melanocytic nevi (Figure 21)

Widely scattered

Smooth, flat or uniformly elevated

Uniform light or dark brown

Regular, round or oval, rarely >10 mm diameter

Less common in black persons

Lentigo (freckles)

Mainly on sun-exposed surfaces

Smooth, flat brown or tan

Uniform light

Round, oval or polyhedric

Darken with sun exposure, lighten in winter

Blue nevi (Figure 20)

Most commonly occur on hands or feet; may occur anywhere

Papules or nodules

Blue, blue-gray, or blue-black

Round or oval, usually <10 mm diameter

Firm on palpation

Pigmented basal cell carcinoma (Figure 23)

Most common on the face

Nodule

Growing area is dark brown or black

Becomes irregular as growth progresses


FIGURE 21.

Common melanocytic nevi.


FIGURE 22.

Malignant melanoma.


FIGURE 23.

Pigmented basal cell carcinoma.

Other Primary Malignancies of the Skin

Kaposi’s sarcoma appears as intensely red, nonblanching, slightly raised or nodular lesions of the skin and mucous membranes. Usually there are many lesions of various sizes. It occurs more frequently in patients with acquired immunodeficiency syndrome (Figure 24).


FIGURE 24.

Kaposi’s sarcoma.

Sebaceous carcinoma has a nonspecific appearance similar to that of a squamous cell carcinoma of the skin, with nodularity, telangiectasias and hair loss (Figure 25).


FIGURE 25.

Sebaceous carcinoma at the outer angle of the left eye.

Malignant eccrine spiradenoma is a slowly growing, deeply invasive sclerotic plaque that occurs on the face of older women. It is often painful (Figure 26).


FIGURE 26.

Malignant eccrine spiradenoma.

Syringoid sweat duct carcinoma is a rare malignant condition that occurs on the face or scalp of elderly patients, causing local hair loss. The surface may be warty and secrete fluid (Figure 27).

View/Print Figure

FIGURE 27.

Syringoid sweat duct carcinoma. Note the characteristic warty appearance.


FIGURE 27.

Syringoid sweat duct carcinoma. Note the characteristic warty appearance.

Paget’s disease of the nipple appears to be an unresponsive eczema of the areola but actually is a carcinoma in the ducts of the breast that grows outward to involve the skin.

Pigmented lesions that appear suspicious can be evaluated by using the “ABCD” rules: asymmetry, border irregularity, color variation and diameter 6 mm or greater.14,15 Two other suspicious signs are more rapid growth than other lesions and the presence of a narrow pink halo around the lesion.

Squamous cell carcinoma may be treated by excision, cryotherapy or topical chemotherapy; it should be diagnosed by full skin thickness punch biopsies. For basal cell carcinoma and other skin malignancies, it is better to remove the lesion completely whenever possible, with lateral and deep margins of several millimeters of healthy tissue. If any of the ABCD signs are found in a new pigmented lesion or in a melanocytic nevus that was previously uniformly colored, smooth, flat, round or oval (Figure 28), an excisional biopsy should be performed. All suspicious lesions should be excised down to a connective tissue base with a 2- to 3-mm lateral margin.15


FIGURE 28.

Dysplastic nevi cascade.

If a cosmetically acceptable result would be difficult to obtain after excisional biopsy, full skin thickness punch biopsy of several areas may be performed, including the margins and any raised areas. If a biopsy shows dysplasia, the whole lesion should be removed with 5-mm margins using plastic surgical techniques, and the site should be monitored for recurrence. Malignant melanoma also requires excision with a margin of at least 5 mm, and many dermatologists recommend a 2-cm margin. All other pigmented lesions that occur in these patients should be observed for change at least annually. Serial photographs may be valuable.16

Final Comment

Physicians should assist patients in reducing factors that increase the risk for developing skin cancer. A complete skin examination for premalignant and malignant lesions should be performed during periodic health evaluations and when other opportunities occur. By doing so, the vigilant physician can intervene and reduce the morbidity and mortality of malignant skin disease. Excisional biopsy with an adequate margin is recommended whenever possible. For a large lesion, multiple punch biopsies of selected areas, including the growing edge, is an acceptable method for reaching a diagnosis. In these cases the definitive excision will require plastic surgical techniques. Mohs’ micrographic surgery is a technique in which the histology of each layer of tissue is determined before removing the next layer. This technique permits complete excision without excessively large margins.17,18

Clinician’s Update on the Benign, Premalignant, and Malignant Skin Tumours of the Vulva: The Dermatologist’s View

Correct and rapid diagnosis of skin tumours often requires biopsy and histopathological examination to differentiate benign lesions such as seborrhoeic keratoses or melanocytic naevi from premalignant and malignant lesions such as malignant melanoma. Particularly, to the untrained eye, any benign skin tumour—pigmented or nonpigmented—is easily mistaken for a malignant lesion. Qualified clinical evaluation is paramount in order to reduce the frequency of unwarranted skin biopsies. Herein, the most common benign, premalignant, and malignant vulvar skin tumours are reviewed.

1. Introduction

A variety of vulvar tumours are seen in daily clinical practice and the vast majority are benign. However, correct and rapid diagnosis often requires biopsy and histopathological examination in order to differentiate benign lesions such as seborrhoeic keratoses or melanocytic naevi from premalignant and malignant lesions such as malignant melanoma. Herein, we review the most common benign, premalignant, and malignant vulvar skin tumours.

2. Benign Tumours
2.1. Vulvar Squamous Papillomatosis

Multiple squamous papillae of the vulva are a benign normal variant of the vestibule in young women often mistaken for disseminated genital warts. Wart remedies such as podophyllotoxin and imiquimod, cryotherapy, and laser surgery may have been applied without benefit. The condition is asymptomatic and previous reports of vulvar squamous papillomatosis as a cause of concomitant pruritus and vulvodynia/vestibulodynia have not been substantiated [1, 2]. The clinical presentation is multiple prominent teardrop and rod-shaped papillae in the inner aspects of the labia (Figure 1). Histopathology shows prominent fibrovascular cores covered by mature squamous epithelium. Active treatment is not indicated.

2.2. Seborrhoeic Keratosis

A seborrhoeic keratosis is a common benign keratinocyte neoplasm that in elderly women may be located in the vulvar area. The tumour is brown-black (but may be skin coloured in its early developmental stages), sharply delineated, smooth or verrucous, oval or round with a greasy texture, located on the keratinised skin in the vulvar area (Figure 2). Intensely pigmented lesions may mimic and be mistaken for a malignant melanoma [3]. Histopathology is characterised by a papillomatous acanthotic epithelium consisting of basal cells with small regular nuclei. There is hyperkeratosis with formation of pseudohorn cysts and melanin pigmentation may be prominent. Dermoscopy may be used in trained hands to differentiate highly pigmented seborrhoeic keratoses from malignant melanoma [3]. Therapy is curettage or cryosurgery with liquid nitrogen.

2.3. Epidermoid Cyst

Epidermoid cysts (atheromas) are 5–10 mm, smooth, dome-shaped, yellow-white lesions located on labia majora and around the clitoris in middle-aged and elderly women (Figure 3). Ruptured lesions may drain a thick greasy material. Giant vulvar epidermoid cysts may be encountered including lesions that may result in pseudoclitomegaly [4, 5]. Epidermoid cysts are unilocular, lined with flattened squamous epithelium containing laminated keratin. Secondary infection may result in a painful inflammatory reaction with rupture of the cyst wall. Small lesions may be removed by electrocautery or laser surgery, but larger lesions should be excised in toto.

2.4. Sebaceous Cyst

Sebaceous cysts are caused by blocking of the duct of the multiple sebaceous glands of the hair-bearing surface of the vulva. Sebaceous retention cysts are usually asymptomatic small dome-shaped lesions with a translucent or yellowish colour that may contain a greasy yellow-white material (Figure 4) [6]. Occasionally, a lesion may present as a 2-3 cm large polypoid tumour of the vulva [7]. Women with steatocystoma multiplex, an autosomal inherited disease, have multiple sebaceous cysts in the axillae and femoral fold as well [8]. Histopathology is characterised by a thin-walled intraepidermal cyst lined with cells forming stratified nonkeratinised squamous epithelium. An inflammatory reaction may be seen if the cyst ruptures with the formation of a foreign body reaction (lipoid granuloma). Therapy is excision or in the case of inflammation intralesional triamcinolone may induce involution.

2.5. Bartholin Gland Cyst

Bartholin’s glands located bilaterally at the posterior introitus drain through ducts that empty into the vestibule at the 4 and 8 o’clock positions and moisten the vulvar area. If the duct is obstructed, it may result in a unilateral painless small cystic swelling and palpable mass in the posterior commissure [9, 10]. Small cysts may be asymptomatic but larger cysts may cause discomfort when walking or sitting or during intercourse. The cyst is lined by columnar squamous or flattened epithelium and acini are present within the cyst wall. A small cyst may resolve spontaneously, whereas larger cysts may be treated with either catheterisation or marsupialisation. In recurrent cases, excision of Bartholin’s gland is the best option.

2.6. Mucinous Cyst

Multiple mucinous glands of urogenital sinus origin are present during the development of the vulva. Small cysts may arise as a result of obstruction of the neck of these glands resulting in mucinous cysts located in the vulvar vestibule [11, 12]. A larger vulvar mucinous cyst is often a Bartholin’s gland cyst when reviewed histopathologically after excision [13]. The cysts are lined with columnar epithelium. Therapy is usually not indicated as the cysts are asymptomatic.

2.7. Mesonephric Cyst

Mesonephric cysts, also termed Gardner’s duct cysts, are located on the lateral aspects of the vulva and develop from mesonephric remnants [14]. The epithelial lining of the cyst is usually cuboidal. Therapy is rarely indicated, but larger cysts may be excised.

2.8. Milia

Milia are minute superficial epidermoid cysts lined with epidermis and filled with keratin that are thought to result from pilosebaceous or eccrine sweat duct plugging. Milia may be primary or secondary, the latter resulting from injury to the skin. Mila are 1-2 mm, white, domed-shaped papules usually located at the cheeks and eyelids of adults, but milia may also affect the vulvar area [15, 16]. Due to cosmetic reasons, lesions may be removed with electrodissection or expression of the keratin contents after incision.

2.9. Haemangioma

Infantile capillary and cavernous haemangiomas are common lesions in newborns and may arise at any cutaneous site including the vulvar area. The lesion is a flat erythematous plaque that over months progresses to a nodular vascular tumour (Figure 5). Haemangiomas are rare in adult women, but large cavernous vulvar lesions have been described, including lesion causing clitomegaly [17, 18]. The diagnosis is clinical in infantile haemangiomas but biopsy and histopathology may be needed in adults with a vascular lesion to exclude endometriosis [19]. Infantile haemangiomas usually involute spontaneously over years, whereas this is not the case in adults with vulvar haemangiomas. Therapy in infantile haemangiomas is rarely indicated, but in children with giant lesions or lesions interfering with urination/defecation or in case of a painful ulcerating lesion, therapy with oral propranolol should be considered [20]. In adults with large haemangiomas, excision may be the treatment of choice. In rare instances, infantile haemangiomas may be associated with internal malformations.

2.10. Pyogenic Granuloma

A pyogenic granuloma is common benign vascular proliferation of the skin and mucous membranes that occasionally is located in the vulvar area [21, 22]. Minor trauma may cause excessive local production of angiogenic factors, which are suggested to be a pathogenic factor. Children and pregnant women are predisposed to developing pyogenic granulomas. A solitary sessile or pedunculated erythematous lesion that easily bleeds after minor trauma is the rule, but multiple exophytic vulvar lesions have been described [23]. Treatment is curettage in combination with electrocautery, CO2, or dye laser therapy.

2.11. Angiokeratoma

Angiokeratomas are vascular tumours consisting of numerous ectatic blood vessels in the superficial dermis. Angiokeratomas are seen in middle-aged and older women presenting with multiple asymptomatic erythematous or purple papules in the vulvar area (Figure 6) [24, 25]. Histopathology is characterised by ectatic vascular channels superficially in the papillary dermis surrounded by elongated dermal papillae. Angiokeratomas usually require no therapy, but treatment with electrocautery or pulsed dye laser may be effective [26].

2.12. Lymphangioma

Primary lymphangiomas or lymphangiomata circumscripta are rare, usually congenital lymphatic malformations diagnosed during infancy, whereas secondary or acquired lymphangiomas arise in adulthood as sequelae to surgery, radiotherapy, or other traumatising events. A vulvar lesion is characterised by frog egg-like confluent grouped thin-walled vesicles filled with serosanguineous fluid (Figure 7) [27]. Histopathologically, the lesions consist of dilated lymphatic channels with a flat endothelium. Therapy is difficult as recurrences are common irrespective of the treatment modality, which is why a conservative approach should be considered. Management options include surgical excision, laser, or sclerotherapy [27].

2.13. Syringoma

A syringoma is a common tumour of eccrine sweat glands usually located on the lower eyelids, neck, chest, axillae, and genital area, including the vulva [28]. They emerge in early adult life with multiple small (1–3 mm), firm, skin-coloured or brownish papules bilaterally to the vulva (Figure 8). Vulvar lesions are usually asymptomatic but pruritus may be prominent in a subgroup of women. Pruritus may be aggravated by pregnancy [29]. Histopathology shows small strands of cells and ducts in a fibrous stroma within the dermis. The ducts are lined by two layers of cuboidal cells. Therapy should be restricted to women with intense pruritus and CO2 laser may be effective [30].

2.14. Schwannoma

Schwannomas or neuromas are benign encapsulated nerve sheath neoplasms that occasionally may be located in the vulvar area in adults [31]. The clinical presentation is a solitary nodular lesion. Histopathology shows neoplastic proliferation of Schwann cells. Surgical excision is the treatment of choice.

2.15. Leiomyoma

A leiomyoma is a rare benign neoplasm in adults derived from labial muscle presenting as a solitary flesh-coloured or reddish-brown, occasionally painful, nodule. The lesions range in size from a few mm to 1 cm [32]. Histopathology shows abundant smooth muscle fibres forming a solid tumour with intervening collagen. Malignant transformation to leiomyosarcoma is rare [32]. Therapy is excision.

2.16. Lipoma

Lipomas are common soft tissue tumours that can be located anywhere on the body, including the vulvar area [33]. Vulvar lipomas may also be seen in children [34]. The clinical presentation is a soft, painless, slowly growing vulvar nodule. Histopathology is characterised by a circumscribed tumour composed of mature adipocytes. Therapy is excision.

2.17. Hidradenoma Papilliferum

Hidradenoma papilliferum is an uncommon benign cutaneous adnexal tumour arising from apocrine sweat glands with predilection to the vulvar area in middle-aged women [35, 36]. It usually presents as a firm, well-circumscribed, skin-coloured, or erythematous cystic nodule measuring 1-2 cm in size, occasionally larger [36]. Histopathology reveals a tumour with tubular and papillary proliferation and cystic dilated spaces lined with columnar cells in the surface layer and cuboidal epithelium in the basal layer and usually with an outer layer of myoepithelial cells. Malignant transformation has been described in chronic cases [36]. Therapy is excision.

2.18. Endometriosis

The vulva is an uncommon site for endometriosis; however, the diagnosis should be considered in women with a persistent tender erythematous-bluish nodule usually located at the labia majora [37, 38]. It is associated with dyspareunia and increase of the lesion during menstruation. Histopathology shows endometrial stroma and glands with variable amounts of fibrosis and haemosiderosis. Therapy is excision.

2.19. Melanosis

Vulvar melanosis or vulvar lentiginosis, also referred to as lentigo simplex, is the most common pigmented lesion in adult women, representing approximately 70% of all pigmented vulvar lesions [39, 40]. The aetiology is unknown. Vulvar melanosis presents as single or multiple small (1–5 mm) dark-brown to black macules or patches on the mucosal surfaces (Figure 9). Histopathology shows increased melanin and a normal or slightly increased number of melanocytes in the basal layer of the epidermis and increased pigmentation within macrophages (melanophages) in the papillary dermis [41]. Vulvar melanosis follows a benign course and the risk of malignant melanoma is not increased. Regular follow-up may be considered in selected patients with disseminated lesions or in women with vulva melanosis in advanced age [42]. Therapy is not indicated.

2.20. Melanocytic Naevi

Vulvar melanocytic naevi are seen in approximately 2% of adult premenopausal women and account for 23% of all pigmented lesions in this area [39, 40]. A similar number of children have vulvar melanocytic naevi [43]. A subgroup of younger women have “atypical melanocytic naevi of the genital type” (AMNGT) representing 5% of vulvar naevi [44]. These patients may have a personal or family history of dysplastic naevi or malignant melanoma [45]. Most vulvar naevi are pink to dark black-brown macules or flat-topped papules with well-demarcated borders, with uniform pigmentation, and with a diameter of less than 10 mm located on the labia majora, labia minora, and the clitoral hood (Figure 10). Blue macular naevi are occasionally seen. AMNGT may have darker pigmentation, irregular borders, and larger size. In trained hands, dermoscopy may assist in the diagnosis of vulvar naevi and AMNGT presenting with a predominant globular or homogeneous pigmentation pattern [46]. Histopathology shows groups of benign naevi cells in the basal epidermis, dermis, or both. Vulvar naevi have very low malignant potential as most (98%) of the malignant vulvar melanomas occur de novo [47]. Similarly, AMNGT have been found to possess low malignant potential [45, 48]. Therapy with excision is only indicated if malignancy is suspected.

3. Premalignant Tumours
3.1. Vulvar Intraepithelial Neoplasia

Vulvar intraepithelial neoplasia (VIN) is a high-grade intraepithelial precursor of invasive squamous cell carcinoma. Two different types of VIN have been defined: the common human papilloma virus (HPV) related type and the differentiated non-HPV-related type, the latter being associated with vulvar dermatoses, especially lichen sclerosus [49]. HPV-related VIN is the predominant clinical lesion (95%) with the highest frequency among younger women aged 20–35 years whereas the differentiated type of VIN (2–5%) most commonly occurs in elderly women [50]. The main HPV types involved in the pathogenesis of VIN are HPV 16, HPV 18, and HPV 33 [51]. In approximately 50% of women, VIN is asymptomatic. When symptomatic, the main complaints are pruritus, pain, and dyspareunia. The clinical findings are variable including unique or multiple flat, raised or eroded, white, erythematous or pigmented papules or plaques (Figures 11, 12, and 13). The differentiated type of VIN is usually unifocal, whereas the HPV type of VIN has a higher tendency to be multifocal and disseminated in the vulvar area.



The diagnosis should be confirmed by histopathology showing moderate to severe intraepithelial dysplasia; in the differentiated type of VIN, there are concomitant signs of lichen sclerosus or lichen simplex. Therapies of HPV-related VIN include surgical excision, CO2-laser ablation, photodynamic therapy, or topical treatment with imiquimod, 5-fluorouracil, or cidofovir [50, 52–54]. Surgical excision should be the first choice in women with the differentiated type of VIN due to the increased risk of malignant transformation. Irrespective of the treatment, the risk of recurrence is significant and long-term follow-up is mandatory. Similarly, women with vulvar VIN should be examined for concomitant cervical, vaginal, and intra-anal dysplasia often found in women with HPV-related VIN. The risk of malignant transformation of HPV-related VIN is lower (2.7% in younger women and 8.5% in elderly women) than for the differentiated type of VIN (33%) [55]. In general, immunosuppressed women have a higher risk of malignant transformation of VIN to invasive squamous cell carcinoma. On the other hand, spontaneous regression of VIN does occur in immune competent women.

HPV-related VIN due to HPV 16 and HPV 18 may be prevented by vaccination with the 4- or 2-valent vaccines [56]. A newly introduced 9-valent vaccine may also protect from VIN caused not only by HPV 16 and HPV 18, but also by HPV 31, HPV 33, HPV 45, HPV 52, and HPV 58 [57]. In addition, regular clinical examination of women with lichen sclerosus is recommended in order to recognise possible VIN in this high-risk group [58].

4. Malignant Tumours
4.1. Squamous Cell Carcinoma

Approximately 95% of malignant tumours of the vulva are squamous cell carcinoma (SCC), however only representing 5–10% of all gynaecological cancers [52]. Chronic vulvar HPV infection with one or more of the oncogenic HPV types is involved in half of the cases of SCC, whereas lichen sclerosus and to a lesser degree other chronic dermatoses, such as lichen planus, are predisposing factors in the non-HPV-related cases. Smoking may be an additional factor in HPV associated vulvar SCC. In the subset of women with the verrucous variant of SCC, the nononcogenic HPV types 6 and 11 may be a significant aetiological factor [59]. The incidence of both types of SCC (HPV and non-HPV associated) increases with age with a mean age at presentation of around 70 years, but HPV associated SCC may be seen in younger women and non-HPV associated SCC occasionally in younger women who have had lichen sclerosus since early childhood [55, 60, 61]. Vulvar SCC may appear as either an ulcerated endophytic lesion or a nodular exophytic tumour, most often located on labia majora or minora (Figure 14). Initial symptoms of pruritus, pain, and dyspareunia may be misdiagnosed as eczema and fungal infection and many women have been prescribed various topical therapies delaying correct diagnosis. The majority of vulvar SCC is solitary and only 10% is multifocal. At the time of diagnosis, approximately 20–30% has spread to regional lymph nodes [62]. The diagnosis is confirmed by histopathology showing irregular strands and cords of atypical squamous cells within the stroma. In the most common subtype, islands of keratinisation are present. Other histopathological subtypes include nonkeratinising SCC, basaloid carcinoma, warty carcinoma, verrucous carcinoma, SCC with tumour giant cells, and keratoacanthoma-like carcinoma.

Before therapy, the vulvar SCC should be staged according to the TNM system with extent of the carcinoma (T), whether the carcinoma has spread to lymph nodes (N) and whether it has spread to distant sites (M) [63]. In stage 1A with an invasion depth of less than 1 mm and size of less than 2 cm, the risk of nodal involvement is negligible. In stage 1B, stage II, and stage III, the risk of lymph node metastases increases to 10%, 25%, and 65%, respectively [63]. Early stage vulvar SCC should be excised with macroscopic tumour-free margins of 1 cm. Nodal staging is recommended in selected patients and if the tumour depth exceeds 1 mm with initial sentinel lymph node dissection and only radical inguinofemoral lymph node dissection if signs of metastases have been identified. MR- and PET-CT scans also add significant benefit in the staging of the tumour.

Local advanced disease with vaginal, urethral, or anal involvement can be treated with surgery combined with radiation therapy. The 5-year survival in women with radically excised local disease is 90%, but in case of metastases to regional lymph nodes survival decreases to 50% [62]. In nodal-negative patients with advanced local disease and recurrent disease, a 5-year survival rate of over 40% has been achieved [64].

4.2. Basal Cell Carcinoma

Basal cell carcinoma (BCC) is a common malignant tumour in elderly women usually located in UV exposed areas, but occasionally lesions occur in the vulvar area where it constitutes 2-3% of all vulvar cancers [65, 66]. HPV is not an aetiological factor in BCC [67]. The slowly growing tumour arises on labia majora with a nodular ulcerating lesion with rolled margins. The diagnosis is confirmed by histopathology usually showing irregular nests of basaloid cells with sparse cytoplasm and hyperchromatic nuclei within the dermis. Palisading of the most peripheral cells within the nest is common. However, the histopathological picture may deviate in the superficial and sclerosing types of BCC. Histopathologically, BCC should be differentiated from the HPV-related basaloid type of SCC. Therapy is excision with free margins. Recurrence is commonly seen if the margins initially were not sufficiently wide [65, 66]. Metastases do not occur.

4.3. Malignant Melanoma

Vulvar melanoma accounts for approximately 10% of all vulvar malignancies only exceeded by SCC [68]. An epidemiological study showed that 2.6% of all melanomas occurred in the vulvar region most commonly in older women [47]. Vulvar melanoma on the mucosal surface resembles the acral lentiginous type of melanoma rather than the cutaneous type of melanoma and ultraviolet radiation is not a significant factor in the pathogenesis. A vulvar melanoma is characterised by an asymmetrical black macule, papule, or nodule often with an irregular border and with a diameter larger than 7 mm located on the mucosal surface most frequently on the labia majora, labia minora, or the clitoral hood [47, 69]. Vulvar amelanotic melanoma is an erythematous lesion without the typical characteristics of melanoma which may imitate a pyogenic granuloma [70]. Dermoscopy may facilitate early identification of a melanoma suspect lesion with irregular dots and globules, multiple colours (black, blue, brown, pink, gray, and white), a blue-white veil, and atypical vessels [71]. The diagnosis is based on histopathology showing atypical melanocytes within the epidermis and dermis. The cells are arranged in confluent nests and sheets and contain varying amounts of melanin, and mitotic figures are usually abundant. The thickness of the lesion and the depth of invasion, ulceration, and lymph node involvement are important negative prognostic indicators. Therapy is wide excision or vulvectomy. In tumours thicker than 1 mm, sentinel node examination is recommended. Recently, immune therapy with monotherapy or combination therapy with one or more of the following drugs, ipilimumab, pembrolizumab, nivolumab, vemurafenib, dabrafenib, and trametinib, may be considered in women with disseminated melanoma. Due to late diagnosis, the prognosis of vulvar melanoma is poor with estimated 5-year survival ranging from 27 to 60% [72].

4.4. Vulvar Paget’s Disease

Although the vulva is the commonest site of extramammary Paget’s disease, it only comprises 1-2% of vulvar malignancies [73]. Vulvar Paget’s disease is a neoplastic condition representing an in situ intraepithelial adenocarcinoma derived from the intraepidermal component of apocrine sweat ducts in the majority of patients (75%) and in only 16% with concomitant dermal invasion [74]. In approximately 9%, vulvar Paget’s disease is a manifestation of an underlying adenocarcinoma of dermal apocrine glands [74]. Finally, the lesion may also occasionally be due to epidermotropism from a more distant rectal, urogenital, or adenocarcinoma arising from elsewhere [75]. Vulvar Paget’s disease affects elderly Caucasian women with a mean age of 65 years who over months develop a sharply demarcated pruritic or painful erythematous eczematoid plaque most often located at the labia majora and more rarely labia minora, introitus, and vagina (Figure 15). The size of the lesion varies from a few cm to an average of 6–12 cm [75]. Occasionally, the lesion may extend to the inguinal folds and the perianal region. A delay of the diagnosis is common and many have received corticosteroids and antifungals for months before a biopsy reveals vulvar Paget’s disease. The diagnosis is based on histopathology demonstrating hyperplastic epidermis containing large cells with abundant pale-staining cytoplasm and large pleomorphic nuclei. The atypical cells contain mucin and express carcinoembryonic antigen. Surgical excision remains the mainstay of therapy despite the high risk of recurrence, probably because the visible borders do not correspond to the extent of histopathological involvement, which is why Mohs micrographic surgery is preferable [76]. In women with localised disease, a variety of other treatment modalities have been successful including topical imiquimod, 5-fluorouracil, laser surgery, and radio- and photodynamic therapy [75]. Combination of surgery with nonsurgical treatment may be used in selected cases [75]. Chemotherapy regimens have been used in women with metastatic Paget’s disease [75].

4.5. Other Malignant Tumours

A variety of rare malignant tumours may arise in the vulvar area, many with a common clinical picture of a growing nodular lesion, which include sarcomas (epitheloid sarcoma, leiomyosarcoma, rhabdomyosarcoma, myxoid sarcoma, liposarcoma, dermatofibrosarcoma protuberans, and hemangiosarcoma) [77–81], adenocarcinomas (mucinous adenocarcinoma, eccrine hidradenocarcinoma) [82, 83], Merkel cell carcinoma [84], lymphomas, and metastases [85]. These vulvar malignant tumours may imitate benign lesions, but since many have metastatic potential rapid diagnosis is essential and biopsy and histopathologic examination of all vulvar lesions are of paramount importance. Therapy is primarily surgical with wide excision and groin lymphadenectomy in women with lymph node metastases after sentinel node technology [86].

Conflicts of Interest

The authors declare that they have no conflicts of interest.

(PDF) Verrucous plaque on the face: What is your diagnosis?

Routine H & E staining showed pseudo-epitheliomatous hyperplasia of the epidermis and a

predominantly neutrophilic infiltration in the dermis with focal areas of microabscess formation.

Many golden-brown thick-walled round structures were seen representing sclerotic bodies.

Discussion

Our patient was a middle-aged man who presented to us with an asymptomatic slowly growing

verrucous plaque. Our initial diagnosis included cutaneous tuberculosis and atypical mycobacterial

infection. However, histopathology study demonstrated the presence of a huge number of classical

copper penny bodies or muriform bodies and a predominantly neutrophilic dermal infiltrate confirmed

the diagnosis of chromoblastomycosis. We started the patient on itraconazole 200 mg daily and

planned for regular follow-up. Unfortunately, the patient was lost to follow up in the very first month

of the commencement of therapy.

Chromoblastomycosis is a chronic fungal infection of the skin and subcutaneous tissue. Five species

of dermatophyte fungi, Fonsecaea pedrosoi, Fonsecaea compactum, Cladosporium carrionii,

Phialophora verrucosum and Phialophora dermatitidis, are the main causative agents of this disease

[1]. It is primarily a disease of tropical or subtropical regions like Africa, the West Indies, South

America, and India, mainly in persons working outdoors in agricultural occupations; it is thus reported

most commonly in men. The infection usually results from trauma such as a puncture from a wood

splinter [2].

Carrion described five types of lesions in a case of chromoblastomycosis-nodules, tumors, plaques,

warty lesions, and scarring lesions [3]. The disease spreads in the adjacent skin with characteristic

satellite lesions surrounding the primary source. Metastatic spread to other organs is reported in a

minority of cases [4].

Chromoblastomycosis usually occurs on the hands, feet, and legs. In the present case, the primary

involvement of the face was unusual. Pradhan et al. found that involvement of extremities accounts

for more than 90 percent of the cases of chromoblastomycosis [5]. There are very few reported cases

of involvement of the face [6]. Other unusual sites mentioned in the literature are the nasal ala, ear,

penile shaft, vulva, tracheolaryngeal region, tonsil, ileocecal region, and pleural cavity [7].

The diagnosis of chromoblastomycosis is based on KOH examination, identification of organism in

histological sections, and culture of the organism that reveals slowly growing green to black colonies.

The microscopic appearance of the conidia formation identifies the species [8].

Treatment of chromoblastomycosis is difficult and not well established. Small lesions can be treated

by simple surgical excision with large margins followed by systemic treatment with an oral antifungal

drug to avoid dissemination. Usually, itraconazole (200-400 mg/day orally for 6 months) is the

treatment of choice, with an 80-90 percent rate of success [9]. Clinical and biologic cure has been

reported in mild to moderate disease after a mean duration of therapy of 7.2 months with itraconazole

alone [10]. A combination of fortnightly liquid nitrogen cryotherapy and pulsed monthly itraconazole

(200 mg twice daily for 7 days per month) is more cost-effective and shortens the duration of therapy

compared with the use of itraconazole or cryotherapy alone [11]. The combinations of itraconazole

with 5 fluocytosine or amphotericin B were found synergistic for F. pedrosoi by an in vitro

susceptibility study [12]. Terbinafine, fluconazole, ketoconazole, and thiabendazole have been used

with a reasonable amount of success. Intravenous amphotericin B (up to 1 mg/kg daily) is

recommended in extensive cases [9]. Voriconazole and posaconazole efficacy is being tested [13].

Topical heat [14], cryotherapy [15], and CO2-laser ablation [16] also have been described as treatment

options.

Dermatological Descriptive Terms; information. Patient

See also separate Dermatological History and Examination article.

The need for terminology

Dermatologists can sound erudite when they use the abundance of descriptive terms at their disposal. These terms are often simply describing the rash in Latin. Sometimes the words are of Greek derivation such as ichthyosis (meaning scales like a fish). Latin or Greek terminology may be used but the two should not be mixed.

The skin is affected by a vast number of insults and diseases, including genetic and metabolic abnormalities as well as infections and yet there is a limited number of ways in which it can respond. History and examination involve making an assessment of the condition, including describing it. Simply understanding dermatological terminology will facilitate diagnosis.

Basic terminology

  • A lesion is any single area of altered skin. It may be solitary or multiple.
  • A rash is a widespread eruption of lesions (greater than 20 lesions).
  • Dermatosis simply means skin disease.
  • Dermatitis means inflammation of the skin. It is not a final diagnosis.

Structure of skin

The skin has three layers called epidermis, dermis and deep subcutaneous tissue with a basement membrane between the epidermis and the dermis.

Epidermis

The epidermis has an outer layer of cells called keratinocytes, which produce keratin. The epidermis also contains pigment cells called melanocytes, which produce melanin, Langerhans’ cells, which are part of the immune system, and Merkel’s cells, which have a sensory function.

  • The basal layer is the columnar cells at the base of the epidermis from which new cells are continuously produced. Melanocytes are normally scattered through this layer.
  • Squamous cells are produced as the keratinocytes mature and move upwards towards the surface of the skin. They become flat in shape, or squamous and are also called spinous or prickle cells. Langherhans’ cells are found in this layer.
  • The granular layer contains flattened cells filled with dark granules containing keratohyaline protein.
  • The horny layer is stacks of dead cells without nuclei and they make up the dry or keratinised stratum corneum. The top layer of cells loosens and falls off.
  • Desmosomes are the structures that produce adherence of keratinocytes and they bind them together.

Epidermal appendages
These include:

  • Eccrine glands, which produce sweat.
  • Apocrine glands, which are scent glands found in armpits and groins.
  • Pilosebaceous structures containing hair and sebaceous glands.
  • Nails.

Dermis

The dermis is composed of connective tissue that supports the epidermis, providing nutrients and protection. The papillary dermis is the upper portion beneath the epidermis and the lower portion is the reticular dermis.

  • Collagen is protein fibres arranged in bundles to give strength to the skin.
  • Elastin is a protein that allows the skin to stretch.
  • Ground substance is gel containing hyaluronic acid and other polysaccharides.
  • Fibroblasts produce collagen, elastin and ground substance.
  • The dermis also contains sensory and autonomic nerves, blood vessels as arteries, arterioles, capillaries, venules and veins, and an extensive network of lymphatics.
  • Erector pili muscles are attached to hair follicles.
  • There may be a cellular infiltration of immune cells around blood vessels in infection, allergy and trauma.

Subcutaneous tissue

This is also called subcutis and is composed of adipose cells or lipocytes. These are surrounded by connective tissue, blood vessels and nerves.

Distribution of lesions

This is important, as the distribution of lesions is often characteristic and hence of diagnostic importance:

  • Acral means affecting the distal portions of limbs (hand, foot) and head (ears, nose).
  • Blaschko’s lines means that lesions follow a segmental pattern described by Blaschko and this is thought to suggest somatic mosaicism.
  • Dermatomal means corresponding with nerve root distribution, as with shingles.
  • Flexural means occurring in the flexor surfaces, such as the antecubital fossa and back of the knee, whilst extensor is occurring on the extensor surfaces, such as over the tip of the elbow and usually just below the patella.
  • Herpetiform means grouped umbilicated vesicles, as seen in herpes simplex and herpes zoster infections.
  • Morbilliform means that the patient has a rash that looks like measles.
  • Seborrhoeic refers to the areas generally affected by seborrhoeic dermatitis, with a tendency to oily skin or seborrhoea. They include the scalp, behind the ears, eyebrows, nasolabial folds, sternum, natal cleft and interscapular region.
  • Truncal means affecting the trunk and (rarely) the limbs.

Shape of lesions

  • Annular lesions are grouped in a circle.
  • A gyrate rash appears to be whirling in a circle.
  • A linear lesion, also known as striate, is like a line and often occurs from trauma such as scratching.
  • Nummular or discoid means round or coin-shaped lesions.
  • Target lesions, also known as iris lesions, have concentric rings like an archery target.

Colour

  • Erythroderma is a skin condition in which the whole body or nearly the whole body is affected. It is red all over.
  • Erythema is red skin due to increased blood supply and it will blanch on pressure.
  • Purpura is bleeding into the skin. This may be as petechiae (small red, purple or brown spots) or ecchymoses (bruises). Purpura does not blanch with pressure. Diascopy, is the ‘glass test’ that is publicised for meningococcal septicaemia.
  • In carotenaemia, excessive circulating beta-carotene results in yellow-to-orange skin colouration. It is most pronounced on palms and soles and, unlike jaundice, it does not affect the cornea.
  • Hyperpigmentation may be caused by excess of melanin or haemosiderin deposits which result in skin colour that is darker than normal. Hypopigmentation is loss of normal melanin and results in skin colour which is paler than normal but not completely white.
  • In leukoderma, also known as achromia, the skin is white.
  • Infarcts are black areas of necrotic tissue due to ischaemia.

Discrete lesions

  • A macule is an area of colour change less than 1 to 1.5 cm in diameter. The surface is smooth.
  • A papule is a small palpable lesion. The usual definition is that they are less than 0.5 cm in diameter, although some authors allow up to 1.5 cm. They are raised above the skin surface, and may be solitary or multiple. Papules may be:
    • Acuminate (means pointed).
    • Dome-shaped or hemispherical.
    • Filiform or thread-like.
    • Flat-topped.
    • Oval or round.
    • Pedunculated (have a stalk).
    • Sessile (have no stalk).
    • Umbilicated (have a central depression).
    • Verrucous (like warts).
  • A patch is a large area of colour change (bigger than a macule) with a smooth surface.
  • A nodule is an enlargement of a papule in three dimensions (height, width and length). It is a solid lesion.
  • A cyst is a papule or nodule that contains fluid and so is fluctuant although it may be tense.
  • A plaque is a palpable flat lesion greater than 0.5 cm in diameter. Most plaques are elevated but a plaque can also be a thickened area without being visibly raised above the skin surface. They may have well-defined or ill-defined borders. Plaques may be:
    • Annular – ring-shaped.
    • Arcuate – like a half-moon.
    • Polygonal – have varied non-geometrical shapes.
    • Polymorphic – being of varied shape.
    • Serpiginous – in the shape of a snake or serpent.
    • Poikilodermatous – have a variegated appearance, usually mixed pallor, telangiectasia and pigmentation.
  • Vesicles are small fluid-filled blisters less than 0.5 cm in diameter. They may be single or multiple.
  • A pustule is a purulent vesicle. It is filled with neutrophils and may be white or yellow. Not all pustules are infected.
  • A bulla is a large fluid-filled blister. It may be a single compartment or multiloculated.
  • An abscess is a localised collection of pus.
  • A wheal is an oedematous papule or plaque caused by swelling in the dermis. Wheals often indicate urticaria.

Epidermal changes

Scaling or hyperkeratosis is an increase in the dead cells on the surface of the skin called the stratum corneum. Descriptive terms for scale include:

  • Desquamation – skin coming off in scales.
  • Psoriasiform – large white or silver flakes, as in psoriasis.
  • Pityriasiform – a branny powdery scale.
  • Lichenoid – when scale is tightly adherent to the surface of the skin.
  • Keratotic – horny scale with plenty of keratin.
  • Exfoliation – peeling off of skin.
  • Maceration – moist peeling skin.
  • Verrucous – resembling a wart.

Secondary changes

  • Lichenification is caused by chronic rubbing, which results in palpably thickened skin with increased skin markings and lichenoid scale. It occurs in chronic atopic eczema and lichen simplex.
  • Crust occurs when plasma exudes through an eroded epidermis. It is rough on the surface and is yellow or brown in colour. Bloody crust appears red, purple or black.
  • Dystrophy refers to degeneration or abnormal formation of the skin. It is often used to refer to nail diseases.
  • An excoriation is a scratch mark. It may be linear or a picked scratch called prurigo.
  • An ulcer is full-thickness loss of epidermis or epithelium. It may be covered with a dark-coloured crust called an eschar.
  • Erosion is caused by loss of the surface of a skin lesion. It is a shallow moist or crusted lesion. These terms are not confined to the skin but may be used to differentiate gastric erosions and ulcers.
  • A fissure is a thin crack within the epidermis or epithelium and is due to excessive dryness.
  • Fungating describes a large, usually malignant tumour, which is erupting like a mushroom or fungus.
  • Granulation tissue is a mass of new capillaries and fibrous tissue in a healing wound.
  • A granuloma is a histological term referring to chronic inflammation in which there are several types of inflammatory cells including giant cells. Granulomas form in response to foreign bodies, certain infections including tuberculosis and leprosy, and with inflammatory skin diseases including granuloma annulare, granuloma faciale and sarcoidosis.
  • In hypertrophy, some component of the skin such as a scar is enlarged or has grown excessively. The opposite is atrophy or thinned skin.

Nails

  • Onychodystrophy is any abnormality of nails.
  • Nails may show pitting, including thimble pitting, as in psoriasis when they have numerous tiny indentations like a thimble.
  • Onychomadesis is loosening and shedding of nails.
  • Onychogryphosis is an abnormal condition of the nails characterised by marked hypertrophy and increased curvature.
  • Onychoschizia is a condition of the nails marked by lamination in two or more layers and by scaling away in thin flakes.
  • Koilonychia is spoon nails and is a feature of iron deficiency.
  • Clubbing involves increased curvature in both directions. It may be congenital or indicate other diseases.
  • Subungual means under the nails.
  • Pterygium is a forward growth of the cuticle over the nail. It is also a triangular fleshy mass of thickened conjunctiva at the inner side of the eyeball, covering part of the cornea, and causing a disturbance of vision.

Mucocutaneous membranes

It is important in dermatology to examine the mucocutaneous areas of the body, particularly the mouth and lips. Most oral involvement in the mucocutaneous diseases is associated with an immunological component to the disease. When an eruption is on a mucous membrane, it is called an enanthem. Examples include:

  • Strawberry tongue (eg, with scarlet fever and with Kawasaki’s disease).
  • Leukoplakia – a thick, whitish-colour patch that forms on the inside of the cheeks, gums or tongue.
  • Gingivitis – a form of periodontal disease that affects the gums.

Miscellaneous terms

  • In Köbner’s phenomenon, lesions arise in an area of trauma. This is typical of psoriasis and lichen planus.
  • Dermatographism (dermatographia) is the ability to write on skin. It occurs with urticaria. If a firm instrument, like an orange stick, is used to make lines or letters on the skin then, shortly afterwards, the wheal will form and the pattern of marks will be very obvious.
  • In Nikolsky’s sign, the skin of a bulla is lightly rubbed and it separates, showing failure of the adhesive process.
  • Telangiectasia is prominent cutaneous blood vessels, the size of tiny red hairs.
  • Exanthem is another term for a rash.
  • Excoriation is an area of the skin covered by a crust, or scab, usually caused by scratching.

Epilepsy Due to Incontinentia Pigmenti

What is Incontinentia pigmenti?

Incontinentia pigmenti (IP) is one of the genetic diseases collectively known as neurocutaneous disorders. These neurocutaneous disorders cause characteristic patterns of discolored skin and invariably involve other systems like brain, eyes, nails, and hair.

IP is caused by genetic alteration of the IKBKG gene. Genetic transmission is such that it occurs primarily in females and on occasion in males. Male fetuses generally do not survive.

Symptoms include characteristic skin discolorations that appear within the first few weeks of life. Neurological abnormalities include seizures, slow development, mental retardation, and stroke. Other key features include visual problems, dental, and nail anomalies.

How is IP inherited?

IP is a rare disorder and until 2010 only 1,200 cases have been reported. IP is due to a mutation in IKBKG gene that is located on the X chromosome. It is inherited in an X-linked dominant manner.  This means that it is inherited maternally and affected woman have a 50% chance of transmitting the mutant IKBKG at conception. Spontaneous mutation of the IKBKG gene also occurs. IP is embryonic lethal in most of the male pregnancies.

How it is diagnosed?

Diagnosis of IP should be suspected in individuals with characteristic clinical finding, family history, and genetic testing. The clinical characteristics include major and minor criteria.

Major criteria (skin findings that evolve from infancy to adulthood)

  • Stage 1: Vesicular Stage – marked redness with linear vesicles (blisters), bullae, and pustules seen in linear distribution (1 week to 24 months of life). Figure-1.
  • Stage 2: Verrucous lesions – wart like papules and thick skin patches that respect Blaschko’s line (normal swirling pattern on skin) (seen between 1 week to 24 months of life).
  • Stage 3: Hyperpigmented Stage – swirling or whirling macular patches of hyperpigmentation (age 4 months to 16 years). Figure-2
  • Stage 4: Hypopigmented Stage – patchy areas of hypopigmentation (light color), usually arranged in streaks or whorls (present by early adulthood).

Figure-1. IP in an affected female
Stage 1: blistering

Figure-2. IP in an affected female
Stage 3: rash

Figures courtesy of GeneReviews® [Internet].Pagon RA, Adam MP, Ardinger HH, et al., editors. Seattle (WA): University of Washington, Seattle; 1993-2015.

Minor criteria

  • Teeth: partial or complete absence of teeth, small teeth, and abnormally shaped teeth
  • Hair: lusterless, wiry, and coarse hair, alopecia
  • Nails: mild ridging or pitting
  • Eyes:  retinal detachment
  • Family history: consistent with X-linked inheritance or history of multiple miscarriages
  • Other suggested minor criteria: CNS, palate, and breast anomalies

The diagnosis of IP is established with identification of pathogenic IKBKG gene.

What are clinical findings?

  1. Skin: as described in the diagnosis criteria.
  2. Central nervous system: seizures, strokes, intellectual disability, and CNS structural abnormalities have been reported in approximately 30% of the individuals with IP.
    • Epilepsy: patients with IP whose nervous system is effected by the disease have a high incidence of epilepsy. It has been reported that almost 77% of these IP patient had seizures.  Seizures in IP can range from few episodes to lifetime chronic epilepsy.  Focal clonic type seizures are most frequently observed in patients with IP. There are reports of patients presenting with severe form of infantile epilepsy called infantile spasms or West syndrome. Others have reported cases where epilepsy was severe in infancy, moderate during early childhood and later resolved.
    • EEG: IP has no typical signature electroencephalogram (EEG) changes. Often the EEG shows presence of an underlying neuronal injury caused by brain vasculopathy (inflammation of brain blood vessels). These changes on EEG would be seen as either localized spikes/sharp waves or focal delta slowing. Localized spikes/sharp waves would indicate presence of an underlying brain cortex that has been injured and can be a potential source for a seizure onset. Similarly focal delta slowing is indicative of underlying neuronal dysfunction.
    • Intellect: the majority of patients with IP, both male and female, are intellectually normal. 25 to 35% of male patients known to have IP were found to have intellectual disability.
    • Brain anomalies: in general, neurological problems in patients with IP appear to be associated with underlying brain vasculopathy. This leads to blood vessel occlusion, transient ischemic attacks, and stroke.
  3. Eye findings: patients with IP have a high susceptibility (20 to 70%) for eye abnormalities. Vasculopathy at an early age can lead to increase in growth of retinal blood vessels with resultant retinal detachment or hemorrhage. Additional non-retinal presentations include cataract, strabismus, optic atrophy, and nystagmus. Regular and frequent eye examination by an ophthalmologist is recommended until the patient is 3 years old.
  4. Teeth: the abnormalities include small teeth (microdontia), too few teeth (hypodontia), and abnormal shaped teeth.
  5. Hair: alopecia can be seen on the scalp as well as on the body. Hair may also be lusterless and coarse.

How is the condition treated?

It is mostly limited to treatment of symptoms:

  • Routine management of blisters and skin infections.  
  • Laser surgery of retina to prevent retinal detachment.
  • Neurological assessment for seizures, spasticity, and acute focal deficits.
  • Brain MRI for structural neurological abnormalities.
  • Dental care by pedodontist.
  • Developmental programs and special education as needed for developmental delay.
  • Surveillance and eye examination: monthly until age 4 months; then every 3 months from age 4 months to 1 year; followed by every 6 months from age 1 to three years; and annually after age 3 years.

What is the life expectancy of someone with IP?

For a person without major complications during neonatal or infancy period, life expectancy is considered normal.

90,000 Skin cancer

Skin cancer is a malignant tumor of skin cells. In most cases, it develops as a result of exposure of the skin to ultraviolet radiation.

In the early stages, skin cancer is asymptomatic. The success of treatment depends on the type of cancer and its stage. With timely diagnosis, the disease is usually curable.

Symptoms

Initially, skin cancer is usually asymptomatic.Often a papule forms on the body – a reddened eminence on the skin.

Cancer develops primarily in areas exposed to sunlight – the face, lips, ears, scalp, neck, chest, arms and legs. However, in some cases, tumors form in areas that are rarely exposed to the sun: on the palms, under the nails, between the fingers, on the genitals.

The disease affects the skin of all shades, including dark ones. Symptoms of a skin cancer depend on the type of skin cancer.

  • Basal cell carcinoma usually affects areas of the skin that are exposed to the sun – the face, ears and scalp. Most often, a light papule is formed first, which rapidly increases; after a few months or years, excessive local expansion of small vessels becomes noticeable. The lesions then crust over and sometimes bleed. Basal cell carcinoma can manifest as:
    • Small dense, almost opaque nodules of light color;
    • crusted papules or nodules,
    • flat scar-like plaques,
    • red papules or plaques.
  • Squamous cell carcinoma most often affects areas of the skin exposed to the sun: face, lips, ears and hands. At first, it may appear as a red papule or plaque with a scaly surface, a nodule, or a warty surface. Then ulceration develops, the tumor affects the tissue. Squamous cell carcinoma can look like:
    • dense red nodules;
    • 90,017 papules or plaques with a scaly surface;

    • non-healing skin lesion.
  • Melanoma can develop on any part of the skin and mucous membranes. In men, it most often appears on the torso, head, neck, in women – on the legs. Also, in men and women, melanoma sometimes occurs on areas of the skin that are not exposed to the sun. It can affect the skin of all shades. In people with dark skin, melanoma is most often found on the palms and soles of the feet, under the nails, or on the nails themselves.
  • Squamous cell carcinoma most often affects areas of the skin exposed to the sun: face, lips, ears and hands.At first, it may appear as a red papule or plaque with a scaly surface, a nodule, or a warty surface. Then ulceration develops, the tumor affects the tissue. Squamous cell carcinoma may look like:
  • Melanoma manifests itself as:
    • Flat brown irregular spots measuring 2-6 cm in diameter, covered with black dots scattered over the surface;
    • plaques with raised brown margins producing red, white, black and blue spots or protruding bluish-black nodules;
    • papules or plaques varying in color from pearly to gray and black;
    • moles that change color, size, bleeding moles, touching which causes pain;
    • Dark areas on the palms, fingers or toes, on the mucous membranes of the mouth, nose, vagina or anus.
  • Kaposi’s sarcoma appears as red or purple spots on the surface of the skin and mucous membranes.

General information about the disease

Skin cancer is a malignant tumor of skin cells.

The skin is the outer cover of the human body. It performs a receptor function, participates in metabolism, carries out thermoregulation; protects the body from mechanical and chemical effects, ultraviolet radiation, penetration of foreign substances, infections and microbes, loss and ingress of liquids.

In skin cancer, normal skin cells are transformed into cancerous cells. In a healthy body, skin cells, appearing in the required amount, die off at a certain time, giving way to new ones. Unlike normal cells, cancer cells begin to grow uncontrollably without dying off at the right time. Their clusters form a tumor. They can spread beyond the primary focus – metastasize to adjacent tissues, lymph nodes, and other organs.

Skin cancer can be caused by ultraviolet radiation exposed to sunlight or tanning beds.There are also additional risk factors.

Skin cancer begins in the epidermis – the upper layer of the skin, which is a thin layer that protects the deeper layers of the skin. The epidermis is constantly renewing itself.

The main types of skin cancer are defined according to the type of cells affected by the cancer.

  • Basal cell carcinoma involves the degeneration of basal cells that produce new cells into cancerous ones. This type occurs in about 80% of skin cancers.Metastasis is extremely rare, but the tumor itself can grow into the surrounding tissue. As a rule, this type is successfully treatable if detected in the early stages. It recurs in 5% of cases.
  • Squamous cell carcinoma involves the transformation of protective epidermal keratinocytes into cancerous cells and accounts for 16% of skin cancers. It rarely metastasizes with skin lesions, much more often with mucosal lesions. When detected early, squamous cell carcinoma responds well to treatment.
  • Melanoma. In this case, melanocytes located in pigmented areas are affected: on the skin, mucous membranes, eyes. Melanocytes produce melanin (the pigment that gives the skin its normal color) and is located in the lower part of the epidermis. When a person is frequently exposed to sunlight, melanocytes actively produce melanin to protect the deeper layers of the skin. As a result, the skin tans and takes on a darker shade. This type accounts for 4% of skin cancers.The risk of melanoma metastasis depends on the depth of penetration and the extent of the process. The tumor can spread quickly; the success of treatment depends on the timeliness of its detection.
  • Kaposi’s sarcoma is rare, most often in people with weakened immune systems – in AIDS patients, organ transplant recipients and taking immunosuppressive medications. It affects blood vessels and is an aggressive form of cancer, often metastasizing to nearby tissues and lymph nodes.

Stages of skin cancer:

  • local cancer – at this stage, the tumor affects only the skin;
  • metastatic cancer – the tumor spreads outside the skin, affecting nearby tissues, lymph nodes, internal organs, bones and other tissues.

Who is at risk?

  • People with fair skin. Cancer can occur on skin of any shade, but light-skinned people are more likely to get sick – they have less melanin, which protects the skin from the harmful effects of ultraviolet radiation.Indicators of low melanin levels are also light or red hair, light eyes, and a large number of freckles.
  • Persons prone to sunburn.
  • People who are overexposed to the sun, spending a lot of time in the sun or in a tanning bed.
  • Living in warm sunny climates, especially in the mountains.
  • People who have a large number of normal or abnormal moles on their skin. Abnormal moles are large bulging moles that can vary in size and shape.If you change the shape, size, color of a mole, you must urgently consult a doctor.
  • Persons with precancerous skin lesions (for example, with keratosis – keratinization, thickening of skin areas). Precancerous growths are usually hard, scaly patches of skin that are brown, red, or pink in color. Most often they appear on the face, hands, forearms of people with fair skin.
  • Persons with a hereditary predisposition to the development of skin cancer.
  • Skin cancer survivors.Even with successful treatment, there is a risk of getting sick again.
  • People with weakened immune systems: HIV / AIDS patients, recent organ transplants, patients with leukemia.
  • Elderly people. The risk of getting sick increases with age.

Diagnostics

First of all, a thorough examination of suspicious skin areas is carried out, then a biopsy. When the diagnosis of skin cancer is confirmed, its stage is determined, diagnostic measures are taken to identify metastases.

  • Biopsy – taking cells from a suspicious area of ​​skin for subsequent examination under a microscope to determine the type of cancer.
  • Computed tomography (CT) and magnetic resonance imaging (MRI) can detect metastases.
  • Densitometry (bone scan) is used to measure bone density and detect cancer.

Treatment

Features of treatment of skin cancer depend on the characteristics of the lesion, its stage, type, condition of the patient.

  • Cryodestruction (freezing). Pre-cancerous lesions and early skin cancers can be removed by freezing with liquid nitrogen.
  • Surgical removal of cancerous tissue and surrounding small areas of healthy skin.
  • Laser therapy. The use of a laser destroys neoplasms with little damage to the surrounding tissue, with minimal bleeding and swelling. It is used to treat superficial types of skin cancer.
  • Radiation therapy. Radiation aimed at destroying cancer cells. It is used when it is impossible to carry out the operation.
  • Chemotherapy. Drugs are used to kill cancer cells. For the treatment of skin cancer, there are special creams and lotions that contain anti-cancer agents.
  • Photodynamic therapy. The use of special preparations – photosensitizers – and light exposure.
  • Biological therapy.Stimulates the immune system to kill cancer cells.

Prevention

  • Avoid the sun in the middle of the day, between 11:00 and 15:00. Clouds provide little or no protection from harmful UV radiation.
  • Use of sunscreen all year round. Creams and lotions may not protect against all harmful UV rays, but they can still reduce the risk of skin cancer. The higher the sun protection factor (SPF), the better the skin is protected.It is necessary to apply the cream not only to the face, but also to the lips, the tips of the ears and all areas of the body exposed to the sun.
  • Tanning salons should be discontinued.

Conduct self-examinations of the skin of the face, neck, ears, head, torso, arms, legs, genitals. You also need to check all available freckles, moles. If you find abnormal areas or changes, see your doctor right away.

90,000 warts, molluscs, condylomas, keratomas, papillomas, nevi.

Moles and other skin neoplasms: warts, molluscs, condylomas, keratomas, papillomas, nevi.

Moles and other skin neoplasms: warts, molluscs, condylomas, keratomas, papillomas, nevi.

Nevi (mole, nevoid tumor, birthmark, English nevus, Spanish lunar, Italian neo, segno, voglia, German muttermal, naevus, French.envie, tache de vin, lat. naevus – birthmark) – genetically determined skin formations, divided into 2 main groups:

  1. Limited focal dysplasia – a malformation of peripheral sensory nerves, differs from the surrounding skin in color and type of surface;
  2. Benign focal proliferation of melanin-forming cells in the skin that occurs in the first years of life (nevoid tumor).

Nevi are skin neoplasms.

Skin neoplasm (blastoma, tumor) – excessive pathological proliferation of dermal tissue, their pathological proliferation, not coordinated with the functions of organs and systems and continuing after the cessation of the action of etiological factors. Skin neoplasms vary:

  • by origin: congenital, acquired, malformations or tumors,
  • downstream: benign, malignant, precancerous;
  • by etiology: genetically determined, viral, actinic, post-traumatic.

The initial stage of nevus development is the proliferation of melanocytes (borderline activity). Further development of the nevus is determined by their differentiation.

Forms of nevi: pigmented (melanocytic or non-cellular, lentigo, “Mongolian spot”, blue, dysplastic, etc.), warty, vascular, skin appendages (hair follicles, sebaceous glands, apocrine and eccrine glands), systematized (linear, extensive) … They can be found at the time of birth – congenital, or appear during life – acquired.According to etiology, type of clinical course and transformation into melanoma, nevi are divided into 4 groups:

  1. Nevi of epidermal melanocytic origin:
  • Main types: borderline (intraepidermal) nevus, mixed (complex) nevus, intradermal (intradermal) nevus.
  • Special types: spindle cell or epithelioid nevus, balloon-forming cell nevus, halonevus.
  • Nevi of dermal melanocytic origin: Mongolian spot, Ota nevus, Ito nevus, simple and cellular blue nevi.
  • Nevi of mixed dermal and epidermal origin: combined nevus, congenital nevus.
  • Precursor nevi of melanoma: congenital, dysplastic.
  • Nevi can be pigmented, warty, vascular, skin appendages. Clinical types of melanocytic nevi: flat, nodular, papillomatous, polyposis, pilous, verrucous, keratotic, etc. Melanocytic nevi – dysplastic, congenital, blue nevus, Ota’s nevus, giant pigmented nevus, Dubreus melanosis.Moles often resemble other formations – papillomas, keratomas, warts. These are viral formations that spread through the skin by contact. They need to be removed. Only a specialist can diagnose and choose the right treatment tactics.

    You can live your whole life with most nevi, but at the same time, they should not be injured, rubbed, irritated, or exposed to sunlight. Sunbathing should only be before 10 am and after 5 pm.Better to spend from 12 to 17 o’clock in the shade, when the scorching radiation is especially strong. Prolonged sun exposure is dangerous, especially for those with many nevi. Ultraviolet radiation is a well-known melanoma provocateur. Moreover, it is pointless to cover moles with a towel or a Panama hat, to cover them with a plaster – melanoma does not sleep even under such cover. If you want to sunbathe, remove the nevi first. It is necessary to strictly dose the exposure of children to the sun. Every sunburn at a tender age multiplies the risk of developing melanoma in adulthood.American scientists believe that solarium radiation is more dangerous than natural solar radiation. Sunbathing in a solarium is contraindicated for any neoplasms on the skin. Permanent microtrauma is very dangerous, therefore moles localized at places of friction (back, mammary glands, in the area of ​​shoulder straps, elastic bands, on the face) are worthy of the greatest attention. A mole is harmless for the time being. She is a kind of atomic bomb that can “explode” at any moment and be reborn into melanoma. Melanoma is the most malignant human tumor, in 95% of cases it arises from nevi, most often from congenital and dysplastic, rarely can appear on smooth skin spontaneously.When they say “removed a mole – died of cancer,” it means that there was no longer a mole, but melanoma. You should pay attention to any change in the mole – its color, size, shape, surface (the disappearance of the skin pattern or ulceration), the appearance of itching, soreness, bleeding, the appearance of satellites (small black dots around the mole). These signs indicate the activation of pigment formation and its transformation into melanoma. When they appear, you need to urgently consult a specialist.

    In order to prevent the degeneration into cancer, regular monitoring of moles is necessary, it is recommended to exclude any injury and massage. Timely removal of a mole is the most reliable prevention of melanoma. But the decision “to remove or not to remove the mole” can only be a dermato-oncologist. There are nevi that are removed for medical reasons, others for cosmetic reasons, and there are those that cannot be touched. In no case should you independently act on moles with various solutions, ointments, moxibustion, tie them with threads, and also remove them at home, in beauty salons, clinics and in other non-specialized medical institutions.It is also impossible, first to take a piece of the mole for a biopsy, and then after some time to remove it. The nevus is removed only by specialists oncologists or dermato-oncologists (specialists in both dermatology and oncology) by the method of resection or electroresection with the simultaneous taking of the entire removed formation for histological examination. When removing moles with a laser, it is not possible to take the material for histology, which does not guarantee the further safety of the patient’s life. It is a misconception that a laser does not leave scars.Leaves, and scars after laser exposure cannot be removed.

    Removal of moles on open parts of the body, especially on the face, should be aesthetic, requiring special skill and skill from a specialist, and here everything depends not so much on the apparatus, but mainly on the skills, hands and knowledge of the doctor.

    At the Center for Curative Cosmetology of the SOCVD, dermatovenerology-cosmetologists with a specialization in dermato-oncology can expertly advise on any skin neoplasm, select and carry out the correct treatment tactics.Removal of all neoplasms is carried out with obligatory histological examination. At the same time, medical methods with a high cosmetic effect are used.

    90,000 Publications in the media

    Lichen planus (Wilson’s lichen, true lichen) – chronic itchy dermatosis of unknown etiology, characterized by the appearance of flat red polygonal papules with a smooth shiny surface and slight depression in the center.Frequency. 450: 100,000. The predominant age is 30-60 years.

    Risk factors • Diseases of the teeth, poor condition of dentures contribute to the development of lichen planus on the oral mucosa • Exposure to drugs (gold preparations, aminosalicylic acid, tetracyclines) and chemicals (paraphenylenediamine compounds – reagents for color photographic and film films) • SLE • Emotional stress.

    Clinical picture
    Skin lesions •• Itching, often severe •• Flat, with a shiny surface, polygonal brownish-cyanotic papules 1–10 mm in diameter.The rashes can coalesce, forming shagreen-shaped plaques covered with tightly seated scales. On the surface of some papules, a peculiar reticular pattern is noticeable – Wickema’s mesh, caused by uneven thickening of the granular layer of the epidermis (pathognomonic sign) •• Localization – the rash is usually located on the flexor surface of the forearms, the anterior surface of the legs, external genitalia; less often – on the dorsum of the feet, in the groin and sacral regions. There have been cases of generalization of dermatosis with the development of secondary erythroderma (erythematous form) •• An isomorphic reaction at the sites of scratching is characteristic (Koebner’s phenomenon) •• Depending on the clinical picture, the following forms are distinguished ••• Pigmented – flat papules are barely noticeable against the background of diffuse melasma ••• Erythematous – large itchy edematous erythematous spots and papules, difficult to distinguish until the intensity of erythema decreases; accompanied by general intoxication ••• Vesicular (bullous) – blisters form against the background of papular rashes ••• Hypertrophic (warty) – large purple papules, often covered with horny layers, usually located on the anterior surface of the legs ••• Hyperkeratotic (horny) – on surfaces of papules – pronounced hyperkeratosis, localized on the legs ••• Coral-shaped – papules up to 1 cm in diameter in the form of reddish-cyanotic beads alternate with areas of hyperpigmentation; located usually in the abdomen and neck ••• Atrophic – at the site of papules skin atrophy occurs ••• Dull (flattened) – large hemispherical, smooth, dense, low-pruritic papules are located on the legs, lower back and buttocks •• Depending on the location of the elements • •• Scattered single rashes ••• Linear rashes (lichen planus linear) – papules are located linearly, sometimes along a nerve or along scratches ••• Ring-shaped rashes (lichen planus annular) – papules are located in rings, growing eccentrically, are usually located on the trunk and mucous membranes.
    Lesions of mucous membranes – in 40-60% of patients with skin lesions. In 20%, only the mucous membranes are affected. This condition is often considered as precancerous (the development of carcinoma is possible) •• The rash is painful, especially with ulceration •• Papular, often ring-shaped rashes of a whitish-pearlescent color in the form of a mesh, lace pattern, usually on the mucous membrane of the cheeks, less often on the tongue, gums, the palate, on the red border of the lips – a continuous scaly band •• Depending on the clinical picture ••• The cystic (bullous) form develops quite often ••• Erosive-ulcerative form with multiple erosions on the mucous membrane of the mouth and lips – the most severe form, can combined with diabetes mellitus and essential arterial hypertension (Grinshpan – Vilapol syndrome).
    Damage to hair and nails •• Hairy part of the head ••• Deprive of flat hair – rash of small papules around the mouths of the follicles on the scalp ••• Skin atrophy and destruction of hair follicles, as a result of which persistent total alopecia may develop •• Nails – the formation of proximal-distal grooves and partial or complete destruction of the nail bed. The big toes are most commonly affected.

    Research methods • Wickham’s mesh is better visible after local application of inorganic oils • Skin biopsy – inflammation with hyperkeratosis, thickening of the granular layer, uneven acanthosis, vacuolization of cells of the basal layer, hyaline bodies under the epidermis, heavy lymphocytic layers of derologic dermis for examination • exclusion of syphilis.

    Differential diagnosis • Secondary papular syphilis • Psoriasis • Atopic dermatitis • Leukoplakia (localized on the mucous membrane) • Squamous and basal cell carcinoma of the skin • SLE • Exudative erythema multiforme • Exposure to drugs • Rash.

    TREATMENT
    Management tactics • Dispensary observation, especially of patients with hypertrophic lichen planus, periodic examination of the skin • Timely detection and treatment of somatic diseases, functional changes in the nervous system, oral cavity sanitation, rational dental prosthetics (dental crowns should be of the same metal) • PUVA-therapy, heliocadmium laser therapy, inductothermy of the lumbar region (especially for generalized or refractory lesions).PUVA-therapy is carried out periodically for 1-2 years • UAC, liver function tests, determination of the ANAT titer is carried out every six months • Anti-relapse therapy – repeated courses of vitamins, spa treatment • Due to the possibility of malignancy of ulcerative erosive forms on the mucous membranes regular monitoring by an oncologist is necessary.

    General recommendations • Regime with prolonged sleep, rational employment with the elimination of irritating skin production factors • Correction of reactions to stress • In case of lichen planus of the oral mucosa, exclusion of hot, spicy, spicy and rough foods.

    Drug therapy • For all forms of the disease •• Sedatives •• Penicillin preparations •• Vitamins (nicotinic acid, thiamine, pyridoxine, retinol) •• Histoglobulin 2 ml 2 r / week SC, per course – 8– 10 injections • For skin lesions •• Topically – HA ointments (for example, triamcinolone 0.1%) •• Antihistamines (for example, diphenhydramine 25 mg every 6 hours) – to reduce itching • For mucosal lesions •• Retinol topically , tigazone 30–75 mg / day by mouth (contraindicated in pregnancy) •• HA inside • In erosive-ulcerative and bullous forms – combined treatment •• HA (for example, prednisone 20-25 mg every other day for 2-4 weeks) •• Chloroquine 0.25 g 1-2 r / day for 4-6 weeks •• Xanthinol nicotinate 150 mg 3 r / day •• Erosion of the oral mucosa is smeared with a paste with solcoseryl.

    Complications • Malignant transformation of long-existing hypertrophic, ulcerative-erosive lesions on the mucous membranes (1% of cases) • Alopecia • Destruction of nails.

    Prognosis • The disease is benign, but long-term, especially erosive and ulcerative forms • An individual therapeutic approach to the patient, taking into account pathogenetic factors, contributes to positive treatment results • Possibly spontaneous resolution within a few weeks • There is a tendency to relapse, especially against the background of emotional stress …A recurrent course is observed in 20% of cases, mainly in generalized forms.
    Prevention. Exclusion of chemical factors and drugs that provoke lichenoid reactions, thorough sanitation of the oral cavity, reduction of stress.

    MKB-10 • L43 Lish red flat

    Clinical and morphological features of the pigment form of lichen planus

    In recent years, lichen planus (LP) has been the subject of study and discussion of specialists in various specialties (dermatologists, hematologists, therapists, surgeons, oncologists, transplantologists) [1-4], since typical rashes for it can be observed in autoimmune, paraneoplastic diseases, drug intoxication, and also be one of the manifestations of the graft rejection reaction [1, 5, 6].

    In general, LP is an inflammatory skin disease caused by the cytopathogenic action of T-lymphocytes, which is realized at the level of the dermo-epidermal junction and mucous membranes, and belongs to the group of papular dermatoses, in the clinical picture of which epidermal-dermal papules are a typical symptom [7, 8 ]. However, along with typical manifestations in some cases, this disease may also have other morphological elements: spots (erythematous, pigmented), blisters, as well as atypical secondary signs in the form of erosive-ulcerative, verrucous and atrophic changes in the skin and mucous membranes [3].

    In this regard, two forms are distinguished in the KPL classification. For a typical (classic) polygonal papules are characteristic. Atypical variants are hypertrophic (warty, verrucous), atrophic, pemphigoid, follicular (pointed), pigmented, annular, hyperkeratotic (vegetative), psoriasiform, erythematous, coral, flattened. Separately, there are clinical forms of LP of the mucous membrane and the red border of the lips: typical, hyperkeratotic, exudative-hyperemic, erosive-ulcerative, bullous, atypical [2-4, 9, 10].The listed forms of lesions of the oral mucosa in LP can pass one into the other and be combined with typical polygonal lichenoid papules on the skin [6].

    Various clinical forms of dermatosis reflect the features and severity of inflammatory, trophic and regenerative processes caused by delayed-type hypersensitivity, in terms of its protective and pathological role [1].

    Currently, the average incidence of LP is about 1% of all skin diseases [8, 11], and the incidence of LP among other dermatoses varies from 0.72 to 1.5% [3, 9-12].

    According to a number of researchers [3, 6, 8], the pigmented form of LP is especially common in the countries of the East, where it accounts for 20-30% of all cases of LP (6.2% – among people who chew tobacco), while in Western Europe and America – only 0.3-1.5%.

    One of the rarest forms of LP is the pigment form, which was first described in 1918 by J. Fabri and D. Pirila. The frequency of its occurrence is 0.9-1.0% of the usual forms of LP and 2.5-3.0% of the atypical ones [3, 4, 8, 10, 12].

    The pigmentary form of the disease is characterized by the primary appearance of foci of brownish-brown pigmentation, in the zone of which typical lichenoid papules may later appear. The process is widespread with predominant localization on the skin of the neck, chest, buttocks, back and extensor surfaces of the limbs [3, 12].

    A clinical feature of the pigmented variety of LP is the presence of pronounced pigmentation, which precedes the formation of lichenoid papules [3].L.N. Mashkillayson [6] gives the definition of J. Gougerot, given to this form of LP, – “invisible lichen”, or “lichen without lichen” (lichen sine lichen), which is characterized, first of all, by skin pigmentation with typical papular lesions of LP that are invisible to the eye. … This definition aptly reflects the clinical features of this form. Often, pigmentation in the form of spots merging into extensive lesions is so intense that it is clinically impossible to detect typical lichenoid elements [13].

    According to the literature [3], the pigmented form of LP is more common in patients with long-term hepatopathies and pancreatitis.

    We also met a description of a case of an achromic type of LP with depigmentation foci on open skin areas [10].

    The pigmented form of LP must be differentiated primarily from toxic melasma. Differential diagnostic criteria in this case are the localization of lesions in toxic melasma in open areas of the skin, the long-term existence of lesions with a tendency to exacerbate under the influence of ultraviolet radiation, anamnestic data indicating the effect on the patient’s body of oil refinery products, coal, shale (benzene, autol, toluene, engine oil, etc.). Kaposi’s sarcoma is distinguished from pigmented LP by the slow development of pigmented nodes on the extremities, the absence of diffuse lesions on the trunk and hips, characteristic of the pigmented form of LP.

    When the foci of Kaposi’s sarcoma are localized on the oral mucosa, the latter look like single brownish nodules that do not merge with each other and do not form openwork linear whitish figures characteristic of LP [3, 14].

    In the literature [15], a rare case is described when a Latin American woman with a clinical diagnosis of “acral lentiginous melanoma”, according to the results of a biopsy, revealed a typical lichenoid reaction of tissues with a pronounced deposition of pigment without cellular signs of melanoma, which makes it possible to carry out differential diagnosis of a rare pigmented form of LP, in including melanoma.

    We present our clinical observation.

    Patient B., 59 years old, a resident of Moldova. She considers herself sick for 3 years, when, after suffering stress, she first noted the appearance of rashes on the skin of the groin folds, which then spread to the skin of the armpits, trunk, upper and lower extremities, accompanied by moderate itching. For a long time she was treated symptomatically, without effect.

    In connection with the progression of the disease and difficulties in verifying the diagnosis, she turned to the MOCVD, where she was consulted and then hospitalized in the department of dermatovenerology and dermato-oncology of the MONIKI them.M.F. Vladimirsky for examination, diagnosis and treatment.

    Heredity is not burdened, does not note occupational hazards, does not have bad habits.

    Upon admission, the general condition of the patient is satisfactory. In the lungs, breathing is vesicular, the borders of the heart are within normal limits. Heart sounds are clear, rhythmic, pulse 75 beats per minute, satisfactory tension and filling. Blood pressure 130/80 mm Hg. The tongue is bright red, coated with a whitish bloom at the root.The abdomen is soft, painless, the liver is at the edge of the costal arch, the spleen is not palpable. On the part of the urinary system, no pathology was revealed. The neuropsychic status was unremarkable.

    Local status. The pathological process on the skin is of a widespread subacute inflammatory nature. It is represented by spots from brownish-brown to purple color, rounded, with clear outlines, 0.3-1.0 cm in diameter. Some elements merge in places into large foci up to 3-4 cm in size (Fig.one). Figure 1. Patient B .: pigmented form of LP, axillary region.

    In the center of most elements, areas of atrophy are formed (symptom of Pospelov’s “tissue paper”) (Fig. 2). Figure 2. Patient B .: pigmented form of LP, groin area. On the skin of the dorsum of both wrists, there are single polygonal papules 0.2-5.0 mm in diameter, with a livid shade, a smooth, shiny surface, a small umbilical depression in the center, where a positive symptom of “Wickham mesh” is noted.Peeling is insignificant, clearly expressed at the border of the central and peripheral zones. The rashes are located symmetrically on the skin in the armpits, under the mammary glands, inguinal folds, the back of the wrists. Visible mucous membranes are pale pink in color. Nails, hair are not changed. There are no deformities of bones, joints, pressure and tapping are painless.

    Laboratory data: bladder cancer, HBS, HIV – negative.

    Complete blood count: hemoglobin – 140 g / l, erythrocytes – 5.010 12 / l, hematocrit – 0.41 1/1, platelets – 205.010 9 / l, leukocytes – 4.6 × 10 9 / L, lymphocytes rel.(device) – 26.10%, lymphocytes abs. (device) – 1.1 · 10 9 / L, granulocytes rel. (device) – 68.1%, granulocytes abs. (device) – 3.3 × 10 9 / L, monocytes rel. (device) – 5.80%, monocytes abs. (device) – 0.2 · 10 9 / l, the erythrocyte sedimentation rate according to Westergren is 10 mm / h. General analysis of urine: relative density – 1.025; protein, glucose are absent, leukocytes are absent, erythrocytes are absent. Biochemical blood test: direct bilirubin – 2.2 μmol / L, total bilirubin – 13.9 μmol / L, indirect bilirubin – 11.7 μmol / L, total cholesterol – 6.2 mmol / L, total protein – 72 g / L, albumin – 42 g / L, glucose – 5.6 mmol / L, alanine aminotransferase – 48 U / L, aspartate aminotransferase – 41 U / L, alkaline phosphatase – 113 U / L. Blood coagulogram: Activated partial thromboplastin time (IL) – 26.00 s, prothrombin activity according to Quick (IL) – 101.00%, international normalized ratio (IL) – 0.97, thrombin time (IL) – 3, 76 g / l.

    Conclusion of histological examination of pathological focus (Fig. 3): Figure 3. Histological picture. Orthohyperkeratosis, vacuolization of cells of the basal layer. Severe atrophy of the epidermis, mild lymphohistiocytic perivascular infiltrates in the upper dermis, accumulations of melanophages.Staining with hematoxylin and eosin (× 200). epidermis with insignificant orthohyperkeratosis, vacuolization of cells of the basal layer is thinned in places. In the upper dermis, there is a strip-like lymphohistiocytic infiltrate, accumulations of melanophages and colloidal bodies. The histological changes correspond to the element of the pigmented form of the LP.

    Diagnosis: LP, pigmented form.

    Treatment was prescribed.

    General complex therapy: loratadine (1 tablet in the morning), 1% suprastin solution (2.0 ml intramuscularly at night), photopheresis No. 3.

    External therapy: sinaflan ointment (2 times a day on the affected skin).

    During the treatment, positive dynamics was observed (flattening and smoothing of plaques), subjectively, there was a decrease in itching.

    The described clinical case demonstrates a rare pigmented form of LP, which developed in a patient with Fitzpatrick skin phototype 4. Our observation demonstrates the clinical features of this form of LP, which present difficulties for diagnosis and choice of therapy.According to the literature, this form of dermatosis is often combined with liver disease. However, in the case described by us during the examination of the patient, this assumption was not confirmed. A reliable diagnosis is based on the analysis of anamnestic and clinical data, as well as the results of histological examination.

    Oral cavity concept, features of structure, function and processes 1


    Chapter 1. Oral cavity – concept,

    Features of structure, function and processes

    1

    There are several cavities in the human body – formations bounded by bone and soft tissue structures that have a free volume filled (partially or completely) with gases or liquids.These include the abdominal cavity, which lines the inner surface of the abdomen, contains a special liquid and gas environment, the pleural cavity, which is similar in structure and content; the cavity of the outer and inner ear, the cavity of the osseous-articular spaces, the cavity of the bladder and renal pelvis, the cavity of the nose, pharynx and mouth, the cavity of the neural spaces, etc.

    A feature of all these cavities is the presence of a free space, unoccupied by biological tissue, usually containing a certain biological fluid.

    The main purpose of all cavities is to provide specific mobility of organs, to create reliable isolation of some organs from others, to create a gradual connection and, at the same time, to isolate the external from the internal environment, to provide the most biological conditions for the functioning of internal and external organs of the body.

    The purpose of this section is to describe the features of the structure, composition, function and conditions that ensure the processes occurring in the oral cavity and organs included in it: teeth, lips, tongue, gums, surfaces of the cheeks, hard and soft palate, papillae and numerous glands of external secretion, etc. …

    The oral cavity is the space bounded in front by the lips and teeth, from the side by the surface of the cheeks, from the back by the glossopharyngeal rings, from below by the tongue and the hyoid space. The oral cavity communicates through the oral opening and nose – with the external environment, through the pharynx and esophagus – with the lungs, ear cavity, stomach and esophagus. Thus, the oral cavity is a unique formation for the human body, which simultaneously borders on the external and internal environment of the body, which can, through physiological and physiologically expedient movements, limit or completely isolate itself from the external environment, from the environment of the nose, pharynx and the digestive system.That is, this is a formation that is simultaneously widely communicated both with the external environment and with the internal environments of the body, while with the help of physiological mechanisms and adaptations it is able to restrict itself from both the external and internal environment of the human body.

    One of the main features of the oral cavity is its constant connection and communication with the external environment. In this respect, it has an analogy only with the naso-ear-pharyngeal space, the anus. However, these last two cavities are intended for communication with the external environment either episodically (anus), or in order to gradually adapt the external environment, its main element – air for the conditions of its consumption by the human body – for moisturizing, warming, and purification.

    Chapter 1

    In this respect, the communication of the oral cavity with the external environment has completely different functions, goals and objectives. The main function of communicating the oral cavity with the external environment is to receive and prepare food and liquid for the internal environment, and also partially for the intake of air into the body. The oral cavity is designed for biting, moving, softening, chewing, soaking, initial enzymatic digestion and subsequent ingestion of food.Since any food, like the air environment, is an infected environment, it is natural that the oral cavity is an environment in which microflora of various types, composition and quantities are constantly located. The microflora of the oral cavity has several mechanisms of adaptation in the mouth, mechanisms of existence, reproduction and life in the oral cavity. Conventionally, the microflora in the oral cavity can be divided into a number of types.

    The main one is various types of saprophytes, which have adapted to the conditions of the oral cavity, are in physiological equilibrium, survive in it and do not seem to do any harm to individual tissue formations of the oral cavity.

    The second group – microflora, in transit bypassing the oral cavity, accidentally falling into it. Sometimes it can be pathogenic. In this case, it can contribute to infection and invasion and have an adverse effect on the macroorganism or its individual organs and systems and be the cause of their main infection (the so-called oral route of infection).

    The third group – opportunistic microorganisms that infect the oral cavity, live and multiply in it, finding a niche for infection, reproduction and residence.These are various types of fungi, cocci, bacilli, specific microflora. They are constantly in the oral cavity without causing any negative effects. However, if the body is weakened, a decrease in protective properties is observed, these types of microorganisms can acquire a pathogenic property and cause the development of various pathological processes in the oral cavity.

    Finally, there is a fourth group of microorganisms. This is mostly un-

    10

    Hot spirited microbes that survive well in the oral cavity, eg Str.mutis. These types of microorganisms, under the influence of sugar consumption, have learned to colonize the oral cavity in the form of dental plaque, soft dental plaque, which have adapted to an autonomous existence in the oral cavity, which is practically not dependent on the macroorganism. They store food for future use, in the form of glycogen-like compounds, which allows them to safely survive the periods between human meals. Dental plaque can only be removed mechanically, which makes the fight against it, using a large arsenal of various means for oral hygiene, a very important and pathogenetically justified method of preventing dental caries and parodont diseases.In the plaque, the microflora lives autonomously, which allows it to exist and multiply regardless of the state of the macroorganism. Therefore, in the supra- and subgingival plaque, both saprophytic and pathogenic microflora can survive for a long time. At the same time, the effect on the macroorganism, even very active, cannot disrupt the autonomous life of the plaque microorganisms, they can persist there indefinitely and the plaque at the same time performs the function of a kind of microflora depot.

    Thus, the microflora of the oral cavity is specific, unlike the flora of other cavities, both in composition, quantity, and function.It is necessary to clearly understand that without microflora in the oral cavity normal functioning of its organs is impossible and any attempts to remove it are not only useless, but harmful, since they can lead to dys-bacteriosis. Therefore, microbial maintenance of the oral cavity cannot be considered as a pathogenetic method of combating major dental diseases. However, this does not mean that antimicrobial effects on the oral cavity organs are not needed. No, they are necessary in cases where they are of a specific pathogenetic purposeful nature.

    Other important functions of the oral cavity include providing conditions for chewing food, preparing a food lump, participating in the process of digestion and swallowing food. Such conditions are created in it primarily due to the constant presence of oral fluid in the mouth. Its main sources are

    Oral cavity – concept, features of structure, function and processes

    mi is the secret of three pairs of large salivary glands – parotid, submandibular and sublingual, which constantly function to provide moisture to both the organs of the oral cavity, teeth, mucous membrane, and the food entering it.Due to its high viscosity, viscosity, adsorption, the mixed secret reliably moisturizes the oral cavity and also impregnates the food mass. Without such impregnation, it is impossible to moisten and crush food, to lick it and overcome its friction in the mouth. Only after reaching the grinding and soaking process with the help of saliva can the food be prepared to be swallowed and swallowed.

    In addition to the large salivary glands, ducts of a significant number of small salivary glands exit into the oral cavity, which are located in large numbers in the areas of CO, to a lesser extent washed by saliva.Therefore, the role of small salivary glands in moisturizing the mucous membrane is very great. The secretion of all glands is constant, but it goes at different rates, which increases sharply when stimulated, especially in connection with food intake. There is always a residual amount (1-3 ml) of free secretion in the oral cavity, which is the norm. In total, the glandular apparatus located in the tissues of the mouth secretes up to 1.5-2 liters of its secretion during the day.

    At the same time, it is necessary to know that about 25 % of of all people suffer from decreased secretion of the salivary glands (dry mouth syndrome), which brings serious suffering to such patients.A dry mouth leads to disruption, difficulty and pain in moving food in the mouth, to difficulties in the formation of a food lump. Such patients cannot take food without drinking it with water, they are prone to various inflammatory diseases of the oral mucosa. It is likely that the “dry mouth syndrome” is associated with the epochal process of jaw reduction, a decrease in free anatomical space for the salivary glands, a violation of their reduction, innervation, and blood supply. The establishment and treatment of such a syndrome plays an important role in both the pathogenesis and treatment of diseases of the oral mucosa.In the clinic, there are sometimes cases of prolonged and pronounced hypofunction of the glandular apparatus, this condition leads to a disease that is called xero

    miya. His clinic, the mechanism of development, several decades ago, was described in detail by the domestic teacher F.A. Zverzh-Khovsky (1915).

    The third source of fluid in the oral cavity is the sweating of fluid from the gingival sulcus (“gingival fluid”). It is a liquid very rich in cell forms and enzymes, the volume of which is small.On the one hand, it also plays a certain role in the formation of the composition and volume of saliva, on the other hand, it has a significant effect on the state and nature of the protective mechanisms of the marginal periodontium.

    In addition to the salivary glands, in some individuals, an accumulation of sebaceous glands is sometimes observed. A favorite place for their localization is the transitional CO of the lips, cheeks, along the line of closing of the teeth. Their excessive development in the epithelial integuments of the mucous membrane and skin is described under the name seborrhea.

    A number of chemical and physical processes play a huge role in the oral cavity.Of the chemical processes, first of all, I would like to mention the digestive function of the oral cavity. It is mainly due to the high activity of salivary amylase, which acts on starch-like constituents of food, breaking them down into dextrose up to maltose. This stage of digestion is very important and should always be considered by dentists and internists. In mixed saliva there are many other digestive enzymes – protease, peptidase, glycosidase, maltase, etc., but they are all of microbial or cellular origin, low concentration and do not play any significant role in digestion (table.1), but on the other hand, fluctuations in the content of individual enzymes and their inhibitors are very significant for the development of individual dental diseases.

    The saliva contains the hormone parotin, which is produced by the parotid salivary glands and is involved in the regulation of Ca metabolism. It contains in a high concentration the factor of the coagulation and anti-coagulation systems of the blood, a number of factors affecting the processes of regeneration, the metabolic processes of the liver, the function of the stomach, etc.

    There are a number of factors in saliva (most of which have biologically active properties) – lysozyme, im-


    11

    Chapter 1

    Table 1.

    Characteristics of the composition and properties of saliva cariogenic (CD) and persons subject to caries (CD)


    No.

    Indicators

    Quantitative characteristic

    M + t, n, R

    Limits of individual fluctuations, variability of the indicator (CV,%)

    CR

    KP

    CR

    KP

    1

    2

    3

    4

    5

    6

    1

    Secretion ml / min

    0.40 ± 0.02 82

    0.31 + 0.02 91 001

    0.7 – 0.87 40.0 + 3.1

    0.08 – 0.80

    45.2 + 3.4%


    2

    pH

    7.25 + 0.024 328

    7.6 +0.026 358 001

    5.40 – 7.95 6.07 ± 0.24%

    5.0-7.85 5.16.94 + 0.24%

    3

    Sediment ml / 100 ml

    Mineral components


    6.76 + 0.38 30

    10.14 + 0.52 35 001

    4.0-12.50 30.8 + 4.0%

    4.53 -1750 30.4 + 3.6%

    4

    Calcium

    g / l

    0.459 + 0.0011 356


    0.486 + 0.0007 367 .05

    0.60 – 0.1230 43.6 + 1.6

    0.14 – 0.0965 28.8 + 1.1%

    5

    Phosphorus

    g / l


    0.1929 0.0076 177

    0.1677 0.0056 169.01

    0.86 – 0.640 52.9 + 2.8%

    0.82 – 0.473

    43.2 ± 2.3%


    6

    Ca / P Biopolymers, their components

    0.257 0.007

    0.285 0.010 .05

    0.044 – 0.544

    0.044-0.712

    7

    Protein g / l

    1.636 ± 0.101 46> 0

    1.676 + 0.138 48 .05

    0.230-3.280 42.0 ± 4.4%

    0.542-4.830 57.2 ± 5.8%

    8

    Fractions (quantity)

    14.9 0.6

    12.6 0.3 .01

    9-20

    9-16

    9

    Hexoses

    g / l


    0.127 ± 0.014 20> 0

    0.150 + 0.36 20 .05

    0.22 – 0.246 47.3 ± 7.8%

    0.64 – 0.647 104.0 ± 16.4%

    10

    Fructose mg / l

    8.5 + 0.8

    20> 0

    9.2 + 0.8 18 .05


    2.4-16.1 43.5 ± 6.9%

    5.5-17.5 35.9 ± 6.0%

    11

    Neutramic acid, g / l

    0.200 + 0.0017 20> 0

    0.220 + 0.0018 20 .05

    0.85 – 0.0368 38.0 ± 6.0%

    0.69 – 0.0368

    37.2 + 5.9%


    12

    Uronic acids

    g / l

    0.231 +0.0021

    20

    > 0


    0.238 + 0.0021 20 .05

    0.48 – 0.0386 39.4 + 6.2%

    0.103 + 0.0343

    39.1 ± 6.2%


    13

    Hexosamines g / l

    0.150 ± 0.020 15

    > C

    0.157 ± 0.020 15 .05


    0.27-0.316

    55.5 ± 10.1%


    0.84 – 0.346 50.2 ± 9.2%

    14

    Oxyproline

    g / l

    0.233 ± 0.0016 39


    0.186 + 0.0013 65 .05

    0.44 – 0.0489 44.6 ± 5.0%

    0 – 0.0489 56.2 ± 4.9%

    15

    Acid phosphatase nmol / min in 1 ml

    0.271 ± 0.016 111> C

    0.292 ± 0.014 116 .05

    0.83-0.936 62.0 ± 4.2%

    0.56-0.856

    53.7 ± 3.6%

    12

    Oral cavity – concept, features of structure, function and processes

    Table 1. (continued)


    1

    2

    3

    4

    5

    6

    16

    HPT nmol / minv 1ml

    2.58 ± 0.32 162

    3.60 ± 0.38 101 .05

    0-21 80 159.4 + 8 8%

    0-19.50 106.9 ± 7.5%

    17

    gsht

    nmol / min in 1 ml


    3.68 + 0.25 87

    4.92 + 0.40 74.01

    0-11.20 62.0 + 4.7%

    0-16.70 70.5 + 5.8%

    18

    Amylase μmol / min in 1 ml

    2.70 + 0.13 158

    2.26 ± 0.12 171 .05

    0.22-8.63 60.8 ± 3.4%

    0 – 8.45 70.0 ± 3.8%

    19

    Aldolase μmol / min in 1ml

    0.255 + 0.011

    21

    0.351-0.030 23.01


    0.168-0.358 19.7 + 3.0%

    0.175-0.710 39.3 ± 5.8%

    20

    Lactate dehydrogenase isozymes: LDH-1

    2.5 ± 0.5% 23> 0

    3.7 ± 0.7% 3.8 34 .05

    0 – 9.50% 98.0 ± 14.4%

    0 – 16.5% 106.0 ± 12.8%

    LDG-P

    17.7 ± 1.2% 27> 0

    18.1 + 1.0% 34.05

    6.9 – 30.7% 33.6 + 4.6

    10.3-33.7% 31.0 ± 3.8%

    LDG-Sh

    39.0 ± 1.6% 27> 0

    36.5+ 1.7% 34.05

    22.5 – 54.5 34.6 ± 4.7%

    10.4 – 39.8% 27.0 ± 3.3%

    LDH-IV

    41.2 ± 2.6% 27> 0

    41.5 + 2.6% 34 .05

    13.1 – 66.8% 32.5 + 4.4%

    21.4-63.1% 36.0+ 4.4%

    ldg-v

    0 27> 0

    Footprints 34.05

    0

    0 – 5.8%

    21

    Alkaline phosphatase nmol / min in 1 ml

    Low molecular weight organic compounds


    0.70 + 0.03 100> 0

    0.65 + 0.004 111 .05

    0.11-0.181

    45.2 ± 3.0%


    0.18-0.245 69.2 + 4.7%

    22

    a – amine nitrogen g / l

    0.811 ± 0.038 197

    > 0

    0.769 ± 0.034 182 .05


    0.174-3.074 65.1 ± 3.3%

    0.42 – 2.497 59.2 ± 3.1%

    23

    Lactic acid

    g / l

    0.330 ± 0.0036 28> 0


    0.455 ± 0.0082 28 .05

    0 – 0.0750 56.4 ± 7.5%

    0.60-0.1780 93.8 ± 12.5%

    24

    Pyruvic acid, g / l

    0.0090 + 0.0008> 0

    0.0109 ± 0.0012 .05

    0.37-0.0165 0.38 35.2 ± 5.9%

    0.39-0.0215 44.0 ± 7.3%

    13

    0> 0> 0> 0> 0> 0> 0> 0>

    Dostarykyzben bulisu:

    Bowenoid papulosis: causes, symptoms and treatment

    Bowenoid papulosis is a sexually transmitted disease caused by the papilloma virus.The disease manifests itself in the form of erythematous spots, plaques or papules. The disease affects the skin of the genitals, perineum and perianal region, and also affects the thighs.

    This disease is considered a precancerous stage of the skin. Diagnostic studies are based on the clinic, PCR determination of the papilloma virus and serological reaction to syphilis, and various histological studies are also carried out. Treatment of bowenoid papulosis involves general antiviral therapy with further removal of elements on the skin using a laser.An excision procedure or electrocoagulation is also possible.

    The disease can be described as a form of Bowen’s disease. However, over the years of research, a link was found between the disease and the human papillomavirus. Bowenoid papulosis is characteristic of both sexes, more often the age of which is from 17 to 40 years. In their long-term practice, venereologists have also identified the appearance of bowenoid papulosis in children, including newborns, whose mothers suffered from this ailment.

    Today, we can say for sure that bowenoid papulosis is a rare disease, but in recent years there has been a tendency to an increase in the number of patients.The latter is explained by the increased level of promiscuous sexual intercourse.

    Prevention of bowenoid papulosis

    Preventive measures to prevent bowenoid papulosis are nothing more than adherence to the principles of STI prevention. Such principles include proper sexual behavior, the use of contraceptives during sex.


    Causes of bowenoid papulosis

    The main etiological factor of bowenoid papulosis is the human papillomavirus, which causes the appearance of warts, papillomas and condylomas.Many scientists point to a close relationship between bowenoid papulosis and various types of HPV (16, 18, 31 and 33). Many studies confirm the presence of other types of HPV in people with bowenoid papulosis.

    It is possible to become infected with bowenoid papulosis, as well as other sexually transmitted diseases (syphilis, gonorrhea, ureaplasmosis) – through sexual contact. As for the incubation period, it ranges from 2 months.


    Bowenoid papulosis symptoms

    A rash of bowenoid papulosis is red spots, papules of a pigmented or lichenoid nature, which are more like leukoplakia, which manifests itself in the form of plaques.Elements can be single or multiple in nature, and their size can reach 3 cm. Such elements are not accompanied by any sensations of a subjective nature, only sometimes patients talk about itching. In case of inflammation, soreness may appear.

    Themselves pigmented papules with bowenoid papulosis are characterized by red and brown color, papules can also be pink, yellow or purple. The consistency of such papules is doughy with a smooth surface and occasionally warty.If we talk about lichenoid papules, then they are local-type thickenings that form on the skin with a coarser pattern. Most often, these papules are flesh-colored and have a rough surface. Sometimes they are covered with serous crusts.

    Interestingly, individual papules can coalesce and form whole plaques. Plaques of a leukoplakia-like nature are usually milky or gray in color, their edges are clearly delimited from healthy skin.

    The most characteristic location of the elements of this disease among men is the penis, while in women – the clitoris or labia.It happens that the elements are localized in the groin, as well as on the thighs or in the perineal region. It happens to meet elements near the anus, as well as on the mucous membranes (in the mouth and throat). Usually, pigmented papules are located on the shaft of the penis, while lichenoid is inherent in the head of the penis.

    When bowenoid papulosis appears in patients, warts and genital warts are also noted. If we talk about women, then they may have a combination of cervical dysplasia and bowenoid papulosis.

    This disease is very long-lasting in its course, but not accompanied by the progression of the painful condition and periods of sudden remissions. In rare cases, self-healing occurs. But nevertheless, carriers of bowenoid papulosis should be careful and not be negligent about the disease, it is not as harmless as it might seem. The disease is therefore referred to as precancerous, since the likelihood of modification of its elements in the tumor is very high. Typically, such elements transform into squamous cell skin cancer (genital skin cancer), penile cancer, vulvar cancer, or Bowen’s disease.People with bowenoid papulosis should be constantly registered at the dispensary with a dermatologist and venereologist, and also regularly undergo all the necessary examinations.

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    Diagnosis of bowenoid papulosis

    Identification of the elements of bowenoid papulosis is possible both on examination by a gynecologist and by a urologist or andrologist.If detected, the specialist sends the patient to a venereologist, who must confirm or deny the diagnosis based on the clinic, the results of PCR diagnostics, as well as histology and cytology studies using the material of the affected skin.

    If we talk about PCR studies, then their purpose is to detect the papilloma virus. This diagnosis is carried out by taking a scraping, blood or smear of the patient. Such samples are taken from the skin of the genitals.In order to exclude the nature of syphilis on the skin elements, a study is carried out for pale treponema. Serological diagnostics are also carried out in parallel.

    Carrying out a cytological examination of a scraping (or smear) taken from the surface of the elements of this disease involves the detection or refutation of the presence of coylocytosis, that is, a large accumulation of epithelial cells with their inherent light edges near the nuclei (or cells with double nuclei).

    It should be said that the histological picture of the disease often indicates cancer in situ.This is followed by atypical mitosis or keratinocyte proliferation. Also characteristic is the presence of polymorphic atypical cells that have hyperchromic nuclei and are scattered over all skin surfaces, whereas in the case of Bowen’s disease, such cells are located in groups and compactly.

    Differential diagnosis should be carried out with syphilis, psoriasis, genital warts, lichen planus, warts and Bowen’s disease.


    Treatment of bowenoid papulosis

    Bowenoid papulosis treatment is prescribed in order to avoid possible malignant complications.For this, cryodestruction, removal of elements with a laser, electrocoagulation, excision of elements are carried out. They also apply cytostatics directly to the affected areas of the dermis or inject the skin with interferon. If we talk about local treatment, then it is expressed in the intake of antiviral therapy.