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Syphilis hair loss pictures: What Is Syphilis in Women? Pictures, Symptoms, Treatment & Signs


Syphilitic Alopecia: Case Reports and Trichoscopic Findings – FullText – Skin Appendage Disorders 2017, Vol. 3, No. 4


There has been a resurgence of syphilis in the last decade. Although alopecia is not a common manifestation of the disease, the “moth-eaten” pattern is considered patognomonic. However, diffuse hair loss, termed essential alopecia, sometimes can be the only sign of syphilis infection and mimic other conditions, such as alopecia areata and telogen effluvium. We describe three patients with syphilis in whom the pattern of alopecia was not typical. Although clinical, histopathological, and trichoscopic examinations may share some similar findings with other hair diseases, the inclusion of syphilis in the differential diagnosis of hair loss causes is fundamental to a correct screening and diagnosis.

© 2017 S. Karger AG, Basel

Established Facts

• Syphilis can cause patchy or diffuse nonscarring hair loss.

• Alopecia can be the sole manifestation of the disease.

Novel Insights

• This is the first time zigzag hairs are described in the setting of syphilitic alopecia.

• Trichoscopy may help distinguish syphilitic alopecia from other causes of hair loss, especially in the absence of clinical lesions.


Syphilis has become widespread worldwide with resurgence of new cases in the last decade. Alopecia is an uncommon clinical manifestation of secondary syphilis, ranging from 2.9 to 7% [1]. Two basic patterns of syphilitic alopecia (SA) have been described in the literature, symptomatic and essential. The first type presents with either a patchy or diffuse scalp alopecia associated with typical skin lesions of secondary syphilis. The “moth-eaten” pattern is the most common type of scalp alopecia and is considered to be a patognomonic manifestation of secondary syphilis [1,2,3]. Essential alopecia is extremely rare and presents as a unique clinical presentation of the disease. However, it appears as a nonscarring hair loss which can occasionally affect hair-bearing areas other than the scalp [1,2] and mimic telogen effluvium and alopecia areata [3,4]. Even though the clinical aspects of SA are well described, the trichoscopic findings are not commonly reported in the literature [5,6]. We describe three cases of SA and their corresponding trichoscopic findings.

Case Reports

Case 1

A 51-year-old Caucasian man presented with a 3-month history of scalp hair shedding. The patient had been treated with topical steroids and 5% minoxidil lotion with no improvement. Physical examination revealed diffuse nonscarring scalp alopecia mainly over the parietal, vertex, and occipital areas, associated with eyebrow and extremity hair loss. No patches of alopecia elsewhere or other skin lesions were noted. Scalp hair was thin and had a rough texture. Pull test was positive for telogen and anagen dystrophic hairs. Trichoscopy showed decreased hair density, yellow dots, broken hairs, and zigzag hairs (Fig. 1). Blood tests were within normal limits. Serological screening for syphilis showed increased titers for the Venereal Disease Research Laboratory (VDRL) test (1:8), and fluorescent treponemal antibody absorption was also positive. Histological examination from the affected parietal area showed decreased hair density, irregular hair shafts, and normal terminal/velus ratio (9:1) with moderate periinfundibular inflammatory lymphocytic infiltrate and hypoplastic sebaceous glands. Direct immunofluorescence demonstrated homogeneous, continuous, and mild deposition of IgG in the follicular basal membrane zone, C3 on the follicular epithelium, and IgG and C3 on the epidermal keratinocyte nuclei. Liquor analysis excluded neurolues. Immunohistochemistry with Treponema pallidum staining was negative in the hair shafts. After the use of erythromycin 500 mg b.i.d. for 30 days, the patient presented with complete hair regrowth. VDRL was negative after 6 months and dermoscopy did not show any specific findings after the therapy (Fig. 2).

Fig. 1

Syphilitic alopecia. Decreased hair density, yellow dots (circles), broken hairs (arrows), and zigzag hairs (stars).

Fig. 2

Note complete hair regrowth after treatment.

Case 2

A 32-year-old Caucasian man presented with diffuse scalp hair loss associated with irregular alopecia areata-like patches, and palmoplantar lesions. Trichoscopy showed hair shaft variability and broken hairs of different length, but no yellow dots or exclamation mark hairs (Fig. 3). The patient had complete regrowth after treatment with penicillin.

Fig. 3

Hair shaft variability and broken hairs (arrows) of different length, but no yellow dots or exclamation mark hairs.

Case 3

A 41-year-old African-American man was referred with patchy scalp alopecia of 2-week duration resembling alopecia areata. A maculopapular rash involving the trunk and oral lesions could also be noted. Broken hairs were seen on trichoscopy. None of the patients complained of scalp itching or trichodynia.


The precise pathogenesis for SA still has to be ascertained. However, the immune response to T. pallidum, or its presence, could be related to the loss of terminal hairs, hair follicle cycle arrest, and hair bend resulting in empty follicles and broken hairs. Diffuse SA can mimic alopecia areata on both clinical and histopathological examinations [3,4]; however, noninflammatory biopsies can be misdiagnosed as telogen effluvium [7]. Although zigzag hairs can often be seen in patients with tinea capitis [8], it is not patognomonic of a fungal infection. Trichotillomania and systemic lupus must also be ruled out. In our cases, although clinical lesions were not diagnostic, serological tests led to the correct diagnosis and complete hair regrowth was achieved after antibiotic therapy. Clinical, histopathological, and trichoscopic evaluations may help distinguish SA from other causes of hair loss, especially when typical skin lesions of syphilis are absent.

Statement of Ethics

The authors state that all subjects have given their informed consent for the pictures and the study has been approved by the ethics committee of the University of São Paulo.

Disclosure Statement

The authors declare no conflict of interest and no funding sources for this paper.


  1. Vafaie J, Weinberg JM, Smith B, et al: Alopecia in association with sexually transmitted disease: a review. Cutis 2005;76:361-366.

  2. Cuozzo DW, Benson PM, Sperling LC, et al: Essential syphilitic alopecia revisited. J Am Acad Dermatol 1995;32:840-843.

  3. Bi MY, Cohen PR, Robinson FW, et al: Alopecia syphilitica – report of patient with secondary syphilis presenting as moth-eaten alopecia and a review of its common mimickers. Dermatol Online J 2009;15:6.

  4. Lee JW, Jang WS, Yoo KH, et al: Diffuse pattern essential syphilitic alopecia: an unusual form of secondary syphilis. Int J Dermatol 2012;51:1006-1007.

  5. Ye Y, Zhang X, Zhao Y, Gong Y, Yang J, Li H, Zhang X: The clinical and trichoscopic features of syphilitic alopecia. J Dermatol Case Rep 2014;8:78-80.

  6. Piraccini BM, Broccoli A, Starace M, Jasper V, D’Antuono A, Dika A, Patrizi A: Hair and scalp manifestations in secondary syphilis: epidemiology, clinical features and trichoscopy. Dermatology 2015;231:171-176.

  7. Sperling LC, Cowper SE, Knopp EA: An Atlas of Hair Pathology with Clinical Correlations. Second edition. United Kingdom, Informa, 2012.

  8. Elghblawi E: Idiosyncratic findings in trichoscopy of tinea capitis: comma, zigzag hairs, corkscrew, and morse code-like hair. Int J Trichology 2016;8:180-183.

Author Contacts

Isabella Doche, MD, PhD

Rua Cubatao 86 cj 1302 Vila Mariana

São Paulo, SP 01321001 (Brazil)

E-Mail [email protected] com

Article / Publication Details

First-Page Preview

Received: May 05, 2017
Accepted: May 08, 2017
Published online: June 17, 2017

Issue release date: November 2017

Number of Print Pages: 3

Number of Figures: 3

Number of Tables: 0

ISSN: 2296-9195 (Print)
eISSN: 2296-9160 (Online)

For additional information: https://www.karger.com/SAD

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a sign of secondary syphilis

CMAJ. 2013 Jan 8; 185(1): 61.

From the Department of Dermatology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China

Copyright © 1995-2013, Canadian Medical Association

A 39-year-old man presented with a three-month history of progressive hair loss on his scalp. Five months earlier, he had a generalized rash that lasted for three weeks. He reported having sexual intercourse without condoms with multiple female partners, but he had no history of genital ulceration. Examination revealed multiple patches of nonscarring alopecia, giving the scalp hair a “moth-eaten” appearance (). His skin and mucosa appeared normal. The results of a rapid plasma reagin test were positive (titre 1:64) and Treponema pallidum agglutination was positive, supporting a diagnosis of syphilitic alopecia. He was given benzathine penicillin G via intramuscular injection. Five weeks later, hair regrowth began.

A 39-year-old man with noncicatricial patchy alopecia over the scalp, giving it a moth-eaten appearance.

Syphilis is still “the great mimicker.” Although other concurrent clinical features of secondary syphilis (e.g., roseola syphilitica, mucous patches, condylomata lata, and ophthalmologic and auditory findings) may facilitate diagnosis,1 alopecia can be the only presenting feature of syphilis.2 Syphilitic alopecia can mimic alopecia areata both clinically and histopathologically;1,2 however, “exclamation point” hairs, a diagnostic clinical feature of alopecia areata, have not been described in syphilis. Tinea capitis can be noninflammatory and resemble moth-eaten syphilitic alopecia, but laboratory testing of scrapings should indicate the presence of fungus. Trichotillomania can also present with an appearance similar to moth-eaten alopecia, but this would be confirmed by history and findings of a biopsy. 1,2

The frequency of hair loss in secondary syphilis ranges from 2.9% to 7%.1 The precise pathogenesis is unknown. The hair loss can be moth-eaten, diffuse or both. The “moth-eaten” pattern is the most common type and is considered to be a pathognomonic manifestation of secondary syphilis.13 The alopecia, which is nonscarring, can occasionally affect hair-bearing areas other than the scalp.1,3 The biopsy sample can be noninflammatory or show changes indistinguishable from alopecia areata.2T. pallidum is usually not seen with silver staining. The alopecia usually resolves within three months of appropriate treatment for syphilis.1


This article has been peer reviewed.

Competing interests: None declared.


1. Vafaie J, Weinberg JM, Smith B, et al.
Alopecia in association with sexually transmitted disease: a review. Cutis
2005;76:361–6 [PubMed] [Google Scholar]2. Bi MY, Cohen PR, Robinson FW, et al.
Alopecia syphilitica-report of a patient with secondary syphilis presenting as moth-eaten alopecia and a review of its common mimickers. Dermatol Online J
2009;15:6. [PubMed] [Google Scholar]3. Cuozzo DW, Benson PM, Sperling LC, et al.
Essential syphilitic alopecia revisited. J Am Acad Dermatol
1995;32:840–3 [PubMed] [Google Scholar]

Syphilis Hair Loss – Know Its Causes And Treatments

Hair loss is a very common concern and most of us face this at some point in our lives. While a few strands of hair falling out each day, is normal but anything beyond 100 strands a day and apparent signs of hair loss from specific areas of scalp, is a cause of concern. When hair loss is caused due to infections or health condition it becomes even more serious. One such condition is syphilis, caused by Treponema pallidum, it is a bacterial infection of the skin where hair loss can be a potential side effect. The mechanism and the relation between syphilis and hair loss is explained below along with possible treatment options.

Can Syphilis Cause Hair Loss?

Yes, syphilis can cause hair loss just like other reasons such as genetics, hormonal imbalance, stress, unhealthy diet. Syphilis is essentially a sexually transmitted disease that results in the formation of lesions and rashes by affecting the skin’s mucous membrane. Hair loss does not occur in the primary stage of the disease. However, secondary syphilis hair loss is reported in many cases and has about 2% to 7% incidence rate. Hair loss in the secondary stage of the disease can be due to the lesions forming on the head. Apart from the rashes being extremely itchy, they also damage the hair follicles and impair the regular hair growth cycle. Scratching and the damage caused to the follicles, leads to hair loss. Another hair loss scenario commonly seen, is in the absence of any syphilis rashes on the head.   Hair loss occurs in the form of patches or as general hair thinning.

Also Read:

Does PRP Treatment Work For Hair Regrowth?

Types Of Syphilitic Alopecia (Hair Loss)

Depending on the occurrence of hair loss in the presence or absence of characteristic symptoms of syphilis, syphilitic alopecia is divided into two types –

I – Symptomatic Syphilitic Alopecia – When the hair loss is due to the formation of skin lesions on the scalp, it is called symptomatic syphilitic alopecia.

II – Essential Syphilitic Alopecia – When skin lesions are absent on the scalp but secondary syphilis hair loss is seen, it is called essential syphilitic alopecia. This is further divided in three categories –a) Moth-eaten alopecia b) General thinning of hair c) Moth-eaten alopecia accompanied with general thinning of hairMoth-eaten alopecia occurs in the form of patchy hair loss. It not just affects the scalp but also other areas of the body such as eyebrows, beard, and pubic area.

Also Read:

How to Cure Male Pattern Baldness?

Effects Of Syphilis On The Hair Follicles

Syphilis can affect the hair follicles and damage them in two ways – either by forming rashes on the scalp or by generally affecting the hair growth cycle and pushing more hair into the telogen (resting) and catagen (shedding) phase. Some other effects of syphilis on the hair follicles are –

• Causes loss of hair shaft

• Interferes with the hair growth cycle

• Causes inflammation (in symptomatic syphilitic alopecia)

• Plugs or clogs the hair follicles

• Accumulates lymph cells near the affected hair follicles

• Telogenization

• Clumping of melanin close to follicles

• Formation of sheaths around anagen hair roots

• Dystrophic hair roots

• Increase in catagen hair follicles with decrease in anagen (growing phase) hair follicles

All of these effects may or may not be present at the same time but are characteristic to the various types of syphilitic alopecia. Some of these effects resemble alopecia areata. Hence, a proper diagnosis is needed to distinguish between these two types of hair loss.

Also Read:

What Are The Main Causes Of Hair Loss In Men & Women

Will Hair Lost Due To Syphilis Grow Back?

Yes, as syphilis hair loss is not permanent. In many cases, the hair loss slowly reverts to its original growth rate when appropriate treatment is being taken for the bacterial infection. Once the infection is cleared from the body, the hair starts to grow again and there can be an increase in hair density and volume. However, in some cases, the hair follicles are damaged beyond repair and cannot be rejuvenated to their healthy state.

What are the Treatments For Syphilis Hair Loss?

Apart from taking the prescribed antibiotics for getting rid of the syphilis bacteria from the body, additional treatments that specifically target the hair follicles can be taken to ensure that the syphilis hair loss becomes reversible.

Platelet Rich Plasma (PRP) therapy is being widely used across India to treat different types of hair thinning and hair loss. This treatment can also be used for syphilis hair loss. Once the infection has cleared from the body, blood is drawn from the arm and subjected to centrigufal to separate the platelets from the plasma. These platelets are then injected back into the affected areas of the scalp after being activated with necessary ingredients. The motive behind injecting platelets is that these cells found in the blood are rich in essential growth factors. Supplying these directly to the hair follicles will repair the damaged follicles and enhance hair growth.

Before And After Results

Also Read:

PRP Vs. Other Treatments For Hair Fall – Which Is Better?

Depending on the hair loss you have experienced, the dermatologist will recommend the number of sessions required for desired results. This procedure poses no adverse effects and has no downtime at all. In addition to PRP therapy, topical lotions or gels such as minoxidil and finasteride may also be prescribed to you by the dermatologist. These are the only USFDA approved hair fall control topical medicines which are readily available over the counter.

Research and incidence reports state that syphilis causes hair loss. An efficient diagnosis is essential to identify the underlying cause of the hair loss, so that the best course of treatment can be administered to treat both the bacterial infection and the aesthetic hair loss from scalp. Antibiotics in conjunction with dermatologically approved treatments make syphilis hair loss curable.

Stages of Syphilis | Michigan Medicine

Topic Overview

Syphilis is described in terms of its four stages: primary, secondary, latent (hidden), and tertiary (late).

Primary stage

During the primary stage, a sore ( chancre) that is usually painless develops at the site where the bacteria entered the body. This commonly occurs within 3 weeks of exposure but can range from 10 to 90 days. A person is highly contagious during the primary stage.

  • In men, a chancre often appears in the genital area, usually (but not always) on the penis. These sores are often painless.
  • In women, chancres can develop on the outer genitals or on the inner part of the vagina. A chancre may go unnoticed if it occurs inside the vagina or at the opening to the uterus (cervix), because the sores are usually painless and are not easily visible.
  • Swelling of the lymph nodes may occur near the area of the chancre.
  • A chancre may also occur in an area of the body other than the genitals.
  • The chancre lasts for 3 to 6 weeks, heals without treatment, and may leave a thin scar. But even though the chancre has healed, syphilis is still present and a person can still pass the infection to others.

Secondary stage

Secondary syphilis is characterized by a rash that appears from 2 to 8 weeks after the chancre develops and sometimes before it heals. Other symptoms may also occur, which means that the infection has spread throughout the body. A person is highly contagious during the secondary stage.

A rash often develops over the body and commonly includes the palms of the hands and the soles of the feet.

  • The rash usually consists of a reddish brown, small, solid, flat or raised skin sore or sores that are less than 2 cm (0.8 in.) across. The rash may look like other more common skin problems.
  • Small, open sores may be present on mucous membranes. The sores may contain pus, or moist sores that look like warts may be present (condyloma lata).
  • In dark-skinned people the sores may be a lighter color than the surrounding skin.

The skin rash usually heals without scarring within 2 months. After healing, skin discoloration may develop. But even though the skin rash has healed, syphilis is still present and a person can still pass the infection to others.

When syphilis has spread throughout the body, the person may have:

  • A fever of usually less than 101°F (38°C).
  • A sore throat.
  • A vague feeling of weakness or discomfort throughout the body.
  • Weight loss.
  • Patchy hair loss, especially in the eyebrows, eyelashes, and scalp hair.
  • Swelling of the lymph nodes.
  • Nervous system symptoms of secondary syphilis, which can include neck stiffness, headaches, irritability, paralysis, unequal reflexes, and irregular pupils.

Latent (hidden) stage

If untreated, an infected person will progress to the latent (hidden) stage of syphilis. After the secondary-stage rash goes away, the person will not have any symptoms for a time (latent period). The latent period may be as brief as 1 year or range from 5 to 20 years.

Often during this stage an accurate diagnosis can only be made through blood testing, the person’s history, or the birth of a child with congenital syphilis.

A person is contagious during the early part of the latent stage and may be contagious during the latent period when no symptoms are present.

Relapses of secondary syphilis

About 20 to 30 out of 100 people with syphilis have a relapse of the secondary stage of syphilis during the latent stage.footnote 1 A relapse means the person had passed through the second stage, had no symptoms, then began to experience secondary-stage symptoms again. Relapses can occur several times.

When relapses no longer occur, a person is not contagious through contact. But a woman in the latent stage of syphilis may still pass the disease to her developing baby and may have a miscarriage, a stillbirth, or give birth to a baby infected with congenital syphilis.

Tertiary (late) stage

This is the most destructive stage of syphilis. If untreated, the tertiary stage may begin as early as 1 year after infection or at any time during a person’s lifetime. A person may never experience this stage of the illness.

The symptoms of tertiary (late) syphilis depend on the complications that occur. Complications of this stage include:

  • Gummata, which are large sores inside the body or on the skin.
  • Cardiovascular syphilis, which affects the heart and blood vessels.
  • Neurosyphilis, which affects the nervous system.

Moth-eaten essential syphilitic alopecia | QJM: An International Journal of Medicine

A 35-year-old man in good general health presented with a 5-month history of progressive patchy hair loss of the scalp. He had been diagnosed with alopecia areata 4 months earlier and treated with minoxidil without improvement. The hair loss had gradually spread over the whole scalp. He denied any recent sexual activity, and he had no history of genital or mouth ulceration. Physical examination revealed diffuse non-scarring, ‘moth-eaten’ patches of alopecia of the whole scalp (Figure 1). These patches of alopecia were free from other cutaneous lesions. His skin and mucosa appeared normal, as were his eyebrows and axillary and pubic hair. Serological screening for syphilis showed increased titers for rapid plasma reagin test (1:64), and Treponema pallidum agglutination assay was positive, supporting a diagnosis of secondary syphilis. He was treated with intramuscular injections of benzathine penicillin (2.4 million units) weekly for 4 weeks. Ten weeks later, the patient’s hair loss resolved, and there is no evidence of recurrence.

Figure 1.

Patches of hair loss on the whole scalp.

Figure 1.

Patches of hair loss on the whole scalp.

Alopecia syphilitica is an uncommon manifestation of secondary syphilis, occurring in only 4–12.5% of these individuals.1 It is non-inflammatory and non-cicatricial hair loss that can present in a diffuse pattern, a classic patchy moth-eaten pattern or a combination of both.2 Of these, moth-eaten alopecia occurred most frequently and most characteristic of alopecia syphilitica.1,3 The common mimickers of moth-eaten alopecia syphilitica include alopecia areata, tinea capitis and trichotillomania.

There are two types of syphilis-associated alopecia: ‘symptomatic syphilitic alopecia’ with other lesions of secondary syphilis and ‘essential syphilitic alopecia’ free from any other cutaneous manifestations. 2 Essential syphilitic alopecia is extremely rare.4 Moth-eaten alopecia as the only cutaneous symptom of secondary syphilis as in our patient has rarely been described.

Syphilitic alopecia can closely resemble alopecia areata both clinically and histopathologically. The characteristic histologic features of alopecia syphilitica are follicular plugging; a sparse, perivascular and perifollicular lymphocytic infiltrate; and telogenization and follicle-oriented melanin clumping.3 Lee and Hsu5 reported that alopecia areata can be differentiated from alopecia syphilitica by the presence of peribulbal eosinophils. In our patient, positive serologic tests for syphilis and response to benzathine penicillin support the diagnosis of syphilitic alopecia.

Conflict of interest: None declared.


1,  ,  ,  . 

Alopecia in association with sexually transmitted disease: a review



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Syphilis | DermNet NZ

Author: Vanessa Ngan, Staff Writer, 2003. Updated by Dr Daniela Vanousova, Dermatologist, Czech Republic, July 2015, and by Dr Susan Bray, Sexual Health Physician, Hamilton, New Zealand, March 2018. DermNet NZ Editor in Chief: Adjunct A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Gus Mitchell, January 2020.

What is syphilis?

Syphilis is a sexually transmitted infection caused by the spirochete Treponema pallidum. Syphilis can cause many signs and symptoms similar to other diseases, including human immunodeficiency virus (HIV), and thus is nicknamed ‘the great imitator’.

Syphilis has symptomatic and asymptomatic stages. If left untreated, syphilis can have significant consequences to the infected individual (long-term neurological and cardiac disease), in pregnancy (stillbirth and congenital infection), and to public health (spread in the population).


Who gets syphilis?

Syphilis is transmitted sexually from person to person, either by direct contact with syphilitic ulcers or by infected blood through microtrauma during sexual intercourse. Syphilis ulcers occur most commonly on the genitals and on the anal area, but can also occur on the lips or mouth. Hence, sex in any form — vaginal, anal, or oral — is the main way of passing syphilis from one individual to another. Syphilis also transmits vertically (infected mother to fetus) during pregnancy. Another potential route of transmission is needle sharing (eg, intravenous drug use).

Reported cases of syphilis increased in New Zealand and worldwide over the last decade, particularly among men who have sex with men (MSM). Most recently, a resurgence is being seen in the heterosexual population. This is a particular concern as untreated syphilis in pregnancy can have serious health implications for the mother, the pregnancy, and the unborn child.

What are the clinical features of syphilis?

Once infected with syphilis, an incubation period of 10–90 days (average 21 days) ensues before signs become apparent. Untreated syphilis passes through distinct clinical (symptomatic) stages as well as latent (asymptomatic) stages. During latency, diagnosis can only be made by serology. During the clinical stages, signs and symptoms of syphilis differ according to the stage — primary, secondary, or tertiary — as described below.

Primary syphilis

Primary syphilis is characterised by chancre(s) at the point of entry of the T. pallidum spirochete. T. pallidum uses its spiral shape to twist into the skin. A painless ulcer results.

  • Typically, a solitary, small firm red painless papule on the genital area quickly becomes a painless ulcer with a well-defined margin and an indurated base.
  • Multiple chancres occur in 30% of cases.
  • The initial ulcerated chancre may go unnoticed, particularly if hidden inside the vagina, cervix, mouth, or on the anal region.
  • Non-tender lymphadenopathy might occur in the region of ulceration (eg, inguinal lymphadenopathy in ulcers on the genitals and cervical lymphadenopathy with an oral ulcer.
  • The ulcer usually heals without treatment within a few weeks.

Syphilis: primary chancre

Secondary syphilis

Secondary syphilis is a generalised infection. Secondary syphilis is characterised by rash and systemic symptoms, during which the patient is very infectious. If the patient is untreated, these symptoms will eventually resolve over a number of weeks, but they can recur.

  • Untreated, 25% of patients develop secondary syphilis within three months (average six weeks) after the initial chancre.
  • Syphilis is a multisystem infection and the patient is very infectious during this stage.
  • Systemic symptoms may include fever, headache, malaise, myalgia, arthralgia, and lymphadenopathy.
  • Other affected organs can include liver, kidneys, central nervous system (cranial nerve palsies, meningitis), joints, and eyes (resulting in visual impairment).

Cutaneous features of secondary syphilis

  • A non-itchy rash is present in 90% of patients with secondary syphilis
  • The rash might be subtle or might appear as rough, red or reddish-brown papules or plaques
  • The rash occurs typically on the trunk and frequently affects palms and soles
  • Rarely, the rash presents as a cluster of erythematous papules around a central scaly plaque, resembling a flower; this floral morphology is described as ‘corymbose’ syphilis
  • Patchy hair loss (alopecia) can occur
  • Mucosal surfaces — such as inside the mouth, throat, genital area, vagina, and anus — can become raw and red (mucous patches)
  • Greyish-white, moist plaques called condyloma lata occur in the groin, inner thighs, armpits, umbilicus, or under the breasts 

Rash of secondary syphilis on trunk and limbs

Secondary syphilis involving flexures and mucosa

See more images of syphilis.

Latent syphilis

Between the secondary and tertiary clinical stages of syphilis, many years of latency ensue. The latent years are subdivided into early and late. During latency, the patient is asymptomatic with no signs on clinical examination. Therefore, continued syphilis infection will only be found by positive treponemal antibody tests. 

Early latent syphilis (first two years)

The patient is very infectious.

  • Syphilis infection can pass to sexual partners.
  • Syphilis infection can pass from a pregnant woman to her fetus.

Late latent syphilis (after two years)

Transmission of syphilis occurs only specific circumstances.

  • The patient is non-infectious to sexual partners.
  • Syphilis infection can still pass from a pregnant woman to her fetus.

Tertiary syphilis

Tertiary syphilis develops decades after the initial infection.

  • Late signs and symptoms can develop 20–40 years after initial infection in up to one-third of untreated cases.
  • The untreated infection can lead to endarteritis, and complications include gumma, cardiovascular, and neurological disease.A gumma is a solitary granulomatous lesion with central necrosis. Gummas typically occur on the skin or bone but can be found anywhere:
    • Skin gummas can be painless
    • Gummas in long bones cause a deep, boring pain that is worse at night.
  • Cardiovascular disease is a rare complication. The aorta is the most likely organ affected and becomes dilated, resulting in aortic aneurysm and aortic valve regurgitation.
  • Neurosyphilis can present as meningovascular disease (endarteritis leading to ischaemic stroke), as general paresis (neuronal loss in the cortex leading to progressive dementia), and as tabes dorsalis (wasting away of the spinal cord).

Tertiary syphilis

Congenital syphilis

Untreated maternal syphilis can lead to miscarriage, stillbirth, or congenital infection. Many infants with congenital syphilis will be asymptomatic at birth. Congenital syphilis is divided into early and late stages.

Early congenital syphilis (during the first two years of life)

In the first few weeks of life, the effects to the infant resemble secondary syphilis with a multi-organ infection.

  • Maculopapular rash, vesiculobullous lesions, mucous patches, condyloma lata, rhinitis (inflamed mucous membrane in the nose causing snuffles).
  • Other affected organs include the bones (osteochondritis), kidney (glomerulonephritis), liver (hepatosplenomegaly), and lymph nodes (lymphadenopathy).
  • Neurological, ocular, and haematological involvement also can occur.

Congenital syphilis

Late congenital syphilis (after two years of age)

Late congenital syphilis presents similar to the tertiary gummatous syphilis in adult infection with chronic, persisting inflammation.

  • This chronic infection often affects the eyes (interstitial keratitis), ears (deafness), bones, joints, and central nervous system.
  • Characteristic signs include Hutchinson incisors, mulberry molars, typical facial appearance (frontal bossing, saddle nose), bowed sabre shins, and swollen knees (Clutton joints).

What is the differential diagnosis of syphilis?

The differential diagnosis for syphilis depends on which of its many possible clinical features are present.

The differential diagnosis for ulcers of primary syphilis

  • Genital ulcers: genital herpes, trauma, cancer; and less commonly, tuberculosis, and chancroid
  • Anal ulcers: genital herpes, anal fissure, bacterial infections, trauma, and inflammatory bowel disease
  • Mouth ulcers: herpes simplex (cold sore), aphthous ulcers, and trauma.

The differential diagnosis for rash of secondary syphilis

How is syphilis diagnosed?

The diagnosis of syphilis is made from clinical history and physical examination, supported by laboratory and serological testing.

Syphilis can be diagnosed by demonstrating T. pallidum spirochetes in samples from infected lesions or lymph nodes. Spirochaetes can be identified by dark-field microscopy or by treponemal polymerase chain reaction (PCR) testing. These tests are not always readily available to the diagnosing clinician.

Skin biopsy might or might not show characteristic histopathological features. [See Syphilis pathology]

Serological testing to detect antibodies produced from treponemal infection is the most common test used to diagnose infection. Serological testing cannot distinguish between different types of treponemal infection (yaws, pinta, syphilis) or the duration of infection. Reactive treponemal tests will remain positive lifelong, regardless of treatment or disease activity.

The treponemal antibody tests can be divided into non-specific or specific tests. Which test is used depends on what is available at the local laboratory. The non-specific tests include:

  • Venereal disease research laboratory (VDRL)
  • Rapid plasma reagin (RPR).

The specific tests include:

  • Enzyme immunoassay (EIA)
  • Treponema pallidum haemagglutination (TPHA)
  • Treponema pallidum particle agglutination assay (TPPA).

The sample is screened with a primary test (commonly EIA or TPHA) that detects IgG and IgM and confirmed with a different treponemal test. For example, a positive EIA screen is confirmed with a positive TPHA.

After confirmation, the sample is evaluated for the serological activity of the infection by the RPR/VDRL test.

  • RPR/VDRL titre > 16 indicates active disease.
  • RPR/VDRL titre < 16 does not exclude active infection but is more consistent with late latent infection or with treated infection.

The patient’s history is therefore important for interpretation. RPR/VDRL titre is also used to monitor the effectiveness of treatment.

After high-risk sexual encounters, repeat screening is advised at both six and 12 weeks post-exposure, as initial serological tests can be negative in primary syphilis. Serological tests are always positive in secondary syphilis but beware of the possibility of the prozone effect, which can lead to a false negative. The prozone effect occurs when high antibody titre interferes with the formation of the antibody-antigen lattice, which is needed to see a positive flocculation test.

False-positive serological tests occur, particularly in autoimmune disease, injecting drug use, pregnancy, and older age, but it is important to obtain a detailed history, test the sexual partner, and follow up with repeat testing, in order to ensure that the suspected false-positive result is truly false.

Other tests that might be required particularly if neurological signs and symptoms include computed tomography (CT), magnetic resonance imaging (MRI), and cerebrospinal fluid (CSF) exam.

A full sexual health screen should be carried out, including — most importantly — HIV testing.

What is the treatment for syphilis?

Penicillin by injection is still the mainstay of treatment for all stages of syphilis.

  • Infectious syphilis (primary, secondary, early-latent) requires a stat dose of benzathine or procaine penicillin.
  • Non-infectious syphilis (late latent) and neurosyphilis require longer courses of benzathine or procaine penicillin.

Other antibiotics are less reliable than penicillin, but tetracyclines or cephalosporins can be used in patients who are allergic to penicillin. [See Cutaneous adverse reactions to antibiotics] A pregnant woman who is allergic to penicillin should first be desensitised and then treated with penicillin anyway.

Treatment failures can occur at any stage of the infection, so close follow-up is important, with repeated serology tests for one to two years.

All sexual activity should be refrained from until all syphilis sores or lesions are completely healed and treatment is completed.

Partner notification and management are extremely important to prevent reinfection and to prevent spread in the community. Guidelines are available to guide the clinician on how far back to trace with each stage.

Can syphilis be prevented?

There is no vaccine for syphilis.

Syphilis can be acquired repeatedly; antibodies and treatment do not protect against a new infection.

If you think you are infected, stop all sexual contact and see your doctor or sexual health clinic. Notify all sexual contacts immediately so they can be checked for infection and treated appropriately.

Other measures to prevent the spread of syphilis include:

  • Limiting the number of sex partners
  • Using condoms
  • Regular blood tests, if sexual behaviour is high-risk.

What is the outcome of syphilis?

Early treatment of syphilis has a very good outcome and prevents later complications. Delay of treatment until advanced stages can leave irreversible consequences for example, neurological or problems with vision.

RACGP – Female pattern hair loss


Female pattern hair loss (FPHL) is a commonly encountered clinical presentation in primary care. Patterned hair loss in women is characterised by diffuse hair thinning and often becomes an ongoing cause of psychosocial distress.


The aim of this article is to present a practical approach for the clinical assessment of female hair loss and to review the up-to-date treatment modalities.

Approximately 49% of women will be affected by hair loss throughout their lives, with female pattern hair loss (FPHL) being the most common cause of female alopecia.1 The incidence steadily increases with age in all ethnicities, and the age-adjusted prevalence among adult Australian women of European descent is >32%.1–4 This translates to 800,000 women who suffer from moderate-to-severe FPHL.4 Alopecia is associated with significant psychological distress and reduced quality of life. In one survey, 40% of women experienced marital problems and 64% had career difficulties that they ascribed to their hair loss.5 Alopecia can also be the first symptom of underlying systemic illness within the primary care setting.1,6

FPHL is a non-scarring alopecia characterised by progressive transformation of thick, pigmented terminal hair into short, thin, non-pigmented villous hair. This undesired process is known as hair follicle miniaturisation.1,3,5,6 The trigger for miniaturisation remains unclear but is postulated to be a combination of genetic predisposition, androgen influence and other not yet elucidated factors. Androgens exert their effect on hair via circulating levels of testosterone, which is produced in females by the ovaries and adrenal glands. The free testosterone either binds to intracellular androgen receptors in the hair bulb, causing follicular miniaturisation, or is metabolised by enzyme 5-alpha reductase into dihydrotestosterone (DHT). DHT and testosterone both bind to the same androgen receptors, but DHT does so with more affinity, leading to increased miniaturisation.3,5,6

Female pattern hair loss and general health

As alopecia is highly visible, a patient may note hair loss as the first symptom of a host of underlying or contributing medical and psychiatric conditions. All causes of hyperandrogenism, such as ovarian or adrenal tumours, polycystic ovarian syndrome and adrenal hyperplasia, can induce rapid hair loss in women. The diagnosis of FPHL is associated with underlying hypertension in women aged £35 years and coronary artery disease in women aged £50 years.7 One study found that patterned hair loss was an independent predictor of mortality from diabetes mellitus and heart disease in both females and males.7–9 Screening for metabolic cardiovascular risk factors is useful in patients presenting with patterned hair loss.3,10

Risk factors

The risk factors for FPHL include increasing age, family history, smoking, elevated fasting glucose levels and ultraviolet light exposure of >16 hours/week.8

Psychological morbidity

FPHL is less well understood and accepted by society than alopecia in males. This generates feelings of greater confusion and distress for female patients. A study showed that 52% of women were very-to-extremely upset by their hair loss, compared with 28% of men.1 In another questionnaire, 70% of surveyed women with hair loss had a negative body image and poorer self-esteem, with poorer sleep, feelings of guilt and restriction of social activities.3 Clinicians should also screen for maladaptive coping mechanisms such as compulsive fixing of one’s hair and underlying psychiatric trichotillomania.1,10,11


The diagnosis of FPHL is made on clinical grounds.4,5


Classically, the pattern of alopecia begins with hair density reduction on the mid‑frontal hairline. The anterior part width then widens, resulting in prominent thinning in a Christmas tree pattern (Figure 1) .

Figure 1. Female pattern hair loss with Christmas tree pattern

Generalised and rapid shedding with global hair thinning is unusual and points to other causes such as hyperadrenalism, medication exposure, major stressors or change in hair care practices.1,3,6,10,11 Hair loss over the temporal region is uncommon in FPHL, compared with male pattern alopecia. If temporal thinning was the first symptom, telogen effluvium, frontal fibrosing alopecia, tractional alopecia and hypothyroidism should be considered.6 Symptoms of scalp pruritus, burning and pain point to another diagnosis (Table 1).6


Table 1. Key features in history taking and examination for detection of underlying systemic illnesses1,6,10

Underlying systemic diseases that may present with alopecia

  • Virilising tumours

  • Polycystic ovarian syndrome

  • Hyperandrogenism +/– associated metabolic syndrome

  • Thyroid dysfunction

  • Systemic lupus erythematosus (SLE)

  • Dermatomyositis

  • Iron deficiency +/– anaemia

  • Caloric restriction: anorexia/bulimia

  • Psychiatric disorder: trichotillomania

  • Medication/toxin exposure or ingestion

  • Infection: syphilis

Red flags on history taking for underlying systemic illnesses

  • Generalised and rapid hair shedding

  • Lateral eyebrow hair loss/thinning

  • Menstrual irregularity, fertility difficulty

  • Severe acne

  • Marked hirsutism

  • Associated cutaneous eruption

  • New photosensitivity

  • Severe fatigue

  • Weight changes: gain or loss

  • Fevers or chills

  • Joint and muscle aches

  • Severe psychological stressors

Examination findings suggestive of underlying disorders

  • SLE: isolated parietal alopecia, scarring alopecia (violaceous papules, follicular erythema), associated cutaneous malar rash, arthralgia

  • Thyroid dysfunction: temporal region alopecia, lateral eyebrow hair-loss

  • Trichotillomania: broken hair shafts of variable length, diffuse and patchy hair loss

  • Endocrinopathy: acanthosis nigricans, hirsutism, truncal acne (especially nodulocystic), high body mass index

  • Nutritional deficiency: conjunctival pallor, glossitis, muscle wasting

After diagnosing FPHL, concurrent medical illnesses that exacerbate alopecia should be ruled out to improve overall outcome. These include iron deficiency, infection, thyroid dysfunction and nutritional deficiencies.3,11 Occupational history and exposure to, or ingestion of, toxic chemicals should be elicited.10

Gynaecological history

A detailed gynaecological history is necessary to rule out hyperandrogenism, polycystic ovarian syndrome or a virilising tumour as underlying diagnoses. History should include age of menarche; menstrual cycle details; whether menopause has occured and, if so, at which age; use of hormonal contraception; fertility concerns and any previous gynaecological surgery.1,3,5 A discussion of pregnancy plans is necessary as some treatments are teratogenic.1

Family history

Fifty-four per cent of patients have a first-degree male relative of age >30 years with alopecia, and 21% have a first‑degree female relative aged >30 years with FPHL. An Australian gene-wide study of Caucasian women suggested that aromatase gene CYP19A1 may contribute to FPHL.3


General observations for body habitus, acne, hirsutism and acanthosis nigricans should be made. Focused examination should identify the calibre of the hairs and the location of the affected areas. Findings consistent with FPHL include:

  • loss of terminal hair in the mid-frontal scalp

  • normal hair density in occiput regions and preserved frontal hairline1,6

  • miniaturised hairs: hair of various lengths and diameters in thinning areas3,6

  • widening of central part with diffuse reduction in hair density in a Christmas tree pattern1,11

  • normal-appearing scalp

  • negative hair pull test: hold a bundle of 60 hairs close to the scalp between the thumb, index and middle finger. The test is positive when more than three hairs can be pulled away.12

Non-classic symptoms and signs that suggest other types of alopecia are outlined in Tables 1 and 2.

Table 2. History and examination findings of common non-scarring and scarring alopecia disorders6,10,11

Non-scarring alopecia (common)

Typical history

Examination findings

Hair pull

Female/male pattern hair loss


Age: puberty or older

Onset: gradual

Commonly positive family history

No marked shedding

Hair thinning, wider midline part of the crown, no bare patches, occipital region spared

Negative (usually)


Telogen effluvium


Age: adults

Onset: abrupt – triggered by iron deficiency, thyroid dysfunction, general anaesthesia, childbirth and medications

Prominent shedding

Global hair thinning – evenly distributed throughout scalp

No bare patches

Positive (if worse on frontal than occipital)

Alopecia areata


Age: ≤20 years

Onset: abrupt

Personal or family autoimmune history


Prominent shedding

Well-defined bald patches –

can be isolated or multifocal

Rarely with diffuse hair thinning

(5% can have complete alopecia)


Tinea capitis



Age: children

Onset: gradual/abrupt

Animal contact history (pets, zoos)

Prominent shedding

Bare patches of scalp

Any area of scalp can be affected, isolated or multifocal – can have inflammation and scales

Positive (can have broken hairs)




Age: children/adolescents

Onset: gradual/abrupt

Sensation of tension that is only relieved by pulling hair

History of other psychiatric disorders

Minimal shedding

Fronto-temporal hair or frontal parietal areas affected

Irregularly shaped patches of reduced hair density with irregular borders


Other common non-scarring alopecia differentials:

Hypothyroidism, nutritional deficiencies, traction alopecia, anagen effluvium, infections (syphilis)

Scarring alopecia

Typical history

Examination findings

Hair pull

Lichen planopilaris


Age: adults

Onset: gradual

Scalp itch and burning

50% of patients also have lichen planus

Variable shedding

Bare patches and/or diffuse thinning

Begins in parietal scalp

Perifollicular erythema and scales


Chronic cutaneous lupus erythematosus (discoid lupus)


Age: young adults

Onset: gradual/acute

Scalp itch and pain

More prevalent in Caucasian women

Associated systemic lupus erythematosus 10%

Variable shedding

Parietal area with bare patches

Scaly papules, erythematous and violaceous discolouration of scales, follicular plugging and telangiectasia




Folliculitis decalvans


Age: young and middle-aged adults

Onset: gradual

Scalp pain and itch

Common in men

Variable shedding

Begins at the vertex with bald patches

Follicular papules, pustules and crusting


Other differentials for scarring alopecia:

Dermatomyositis, dissecting cellulitis, central centrifugal cicatricial alopecia

Laboratory investigations

Laboratory testing should be considered in patients with diffuse alopecia, signs of androgen excess and early-onset FPHL. Recommended tests and rationale are outlined in Table 3. Note that testing of androgen levels needs to occur during the follicular phase, between the fourth and seventh days of the menstrual cycle, and oral contraceptives should be discontinued eight weeks prior to the test.1,3


Table 3. Laboratory tests in hair loss evaluation1,3,10,11

Patient characteristics

Underlying disorder


Menstrual irregularity, dysmenorrhea, severe acne and marked hirsutism

(Endocrine screen)


Ovarian hyperandrogenism

Adrenal hyperandrogenism

Androgen index test

Prolactin level

Dehydroepiandrosterone sulfate (DHEA-S) and 17-hydroprogesterone (17-OH)

Obesity, hirsutism, menstrual irregularity, severe acne and confirmed female pattern hair loss

Associated metabolic syndrome

Fasting blood sugar level

Fasting lipid profile

Blood pressure monitoring

Marked temporal region thinning and lateral eyebrow loss

Thyroid dysfunction related hair loss

Thyroid function test, thyroid antibodies


Systemic lupus erythematosus, autoimmune disorders

Erythrocyte sedimentation rate, rheumatoid factor, autoantibody tests

Rapid and diffuse hair shedding in a sexually active individual

Alopecia syphilitica

Non-treponemal and treponemal antigen testing


Tinea capitis

Scalp fungal scrapings for culture and microscopy

Rapid and diffuse hair shedding, low body mass index

Nutritional deficiency

Iron studies and full blood count


Key points of counselling and non-pharmacological treatment options are outlined in Figure 2. Pharmacological management is categorised into androgen-independent (non–androgen dependent) and androgen-dependent options.

Figure 2. Summary of counselling points and treatment options1,2,10,15

Non–androgen dependent treatments

Minoxidil is a piperidinopyrimidine derivative and a vasodilator that is used orally for hypertension. When applied topically, minoxidil is effective in arresting hair loss and producing some degree of regrowth.2

Topical minoxidil is the first-line therapy for FPHL, with Food and Drug Administration approval since 1992. It has been shown to stop hair loss and induce mild-to-moderate regrowth in 60% of women.2,13 It is available as a solution or foam in 2% and 5% concentrations, which show a 14% and 18% increase respectively in non-vellus hair after 48 weeks.2 Topical minoxidil has a well-established safety profile; local irritation and temple hypertrichosis are the main side effects.2,14 Treatment needs to be continued indefinitely. If treatment is stopped, clinical regression occurs within six months. The degree of alopecia will return to the level that would have occurred if there were no treatment.2

Oral minoxidil 0.25 mg daily in combination with spironolactone 25 mg was shown to be effective in reducing hair loss severity and hair shedding score at six months and 12 months in an Australian prospective study with 100 women with mild-to-moderate FPHL. Spironolactone was added to reduce the risk of fluid retention and augment treatment response.2 Side effects in the study were seen in eight patients: two had postural hypotension that was controlled with 50 mg sodium chloride; six patients had hypertrichosis that was managed with waxing. Two patients terminated oral minoxidil because of urticaria. There were no reports of hyperkalaemia or laboratory function abnormality.2

Androgen-dependent treatments

Androgen receptor blockers target androgen conversion and subsequent binding onto hair follicle target receptors in alopecia. Spironolactone and cyproterone acetate are most commonly prescribed as they have been shown to produce regrowth in 44% of patients.4

Spironolactone is an aldosterone antagonist and is used as a potassium-sparing diuretic. In alopecia, it acts by reducing the levels of total testosterone and completely blocking androgen receptor activity in target tissues. It is approved in Australia for the treatment of female hirsutism. It has been used off-label for FPHL with a treatment regimen of 50–200 mg daily for at least six months and shown to arrest progression in 90% of women and improve hair density in 30%.2 Common side effects are lethargy and menorrhagia, which improve after three months. This is a pregnancy category D medication.5,14

Cyproterone acetate directly blocks androgen receptor activity and decreases testosterone levels by suppressing luteinising hormone and follicle stimulating hormone release. Effective dosages are 100 mg daily in postmenopausal women, and 50 mg for 10 days in premenopausal women for three months.4 In one study of 80 patients, cyproterone produced similar results to 200 mg daily of spironolactone.5 This is a pregnancy category X medication as it may cause feminisation of the male fetus.14 Side effects include weight gain, breast tenderness and decreased libido.5

5-Alpha reductase inhibitors

Although 5-alpha reductase inhibitors have revolutionised the treatment of male pattern alopecia, their use in FPHL is limited because of lack of efficacy and the teratogenic potential (pregnancy category X).5 A finasteride dose of 1 mg daily was no better than placebo in treating FPHL in postmenopausal women and was only mildly efficacious in premenopausal women who had associated hyperandrogenism.14,15


FPHL is a common, non-scarring alopecia that affects women of all ages and carries significant psychological morbidity. It may be the first presenting complaint of hyperandrogenism, thyroid dysfunction or chronic deficient diet. A detailed history with appropriate laboratory testing to screen for associated cardiovascular disease, hypertension and metabolic syndrome is indicated. Sufficient time should be dedicated to discussing psychological adaptation, treatment options and realistic treatment goals. The introduction of low-dose oral minoxidil is the key recent advancement in the management of this challenging condition.

Competing interests: None.

Provenance and peer review: Not commissioned, externally peer reviewed.

90,000 Alopecia as an important symptom of syphilis in a patient

Alopecia is an atypical manifestation of syphilis, mimicking other common forms of hair loss, but is an alarming symptom for a patient who may have had no other signs of illness. Inadequate assessment of cosmetic defects can increase the duration of the disease and lead to a delay in appropriate treatment.

As an example, take the medical history of a 42-year-old patient (HIV-negative) with 2 months of progressive general thinning of hairs and small non-scarring lesions of alopecia in the parieto-occipital scalp. The patient received sertraline therapy for a newly diagnosed bipolar disorder and expressed concern that the drug was causing hair loss. An accurate history and examination of the patient revealed pale pink spots on the skin of the trunk and extremities, as well as bilateral psoriasis-like palmar-plantar hyperkeratosis, suggesting secondary syphilis, additionally confirmed serologically.Specific antibiotic therapy cured all skin manifestations, as well as mood disorders, which made it possible to completely abandon psychotropic drugs.

Clinical experience and careful patient evaluation are the keys to identifying the minimum signs of a serious systemic disease such as syphilis. Doctors should pay more attention to cosmetic defects in order to timely identify and begin treatment of this pathology, especially among patients who are not at risk.

Atzori L. et al. Alopecia as unique clue to syphilis in a patient. G Ital Dermatol Venereol. 2017 Oct; 152 (5): 520-523. doi: 10.23736 / S0392-0488.17.04911-2.

Medicna newspaper “Zdorovya Ukrainy 21 storichchya” No. 2 (447), since 2019 p.




Could the light emitted from smartphone screens and selfies cause premature aging and wrinkles?

The widespread use of light-emitting diodes (LED), smartphones, tablets, laptops and desktops has led to a significant increase in the human eye’s exposure to shortwave visible light.Recent studies show that exposure of human skin cells to light emitted by electronic devices, even for as little as 1 hour, can induce the formation of reactive oxygen species (ROS), apoptosis and necrosis. …



The effectiveness and possible mechanisms of action of botulinum toxin in the treatment of oily skin

Most of the therapeutic approaches used to treat oily skin have varying degrees of efficacy and include topical therapies (eg photodynamic therapy and lasers).However, some of these methods can lead to serious side effects. The widespread use of botulinum toxin type A (BoNT-A) in the treatment of oily skin raises serious concerns; in addition, relevant reports have accumulated to assess the effectiveness of BoNT-A and study the mechanisms of its action ….

90,000 types, symptoms, treatment / Articles

Alopecia (from Latin alopecia) is a process of complete or partial hair loss.

There are types of alopecia, among which:

  • focal (hair loss in separate areas),
  • diffuse,
  • androgenic,
  • seborrheic,
  • cicatricial.

The causes of alopecia can vary by type of condition. In addition to physiological disruptions in the work of the human body, a polluted environment and nervous stress can contribute to baldness.

Alopecia can occur as a result of effects on the hair: due to frequent blow-drying, regular hair coloring, unsuccessful perm, poor-quality hair cosmetics. Therefore, types of alopecia occur in more people, and the average age of those suffering from the disease is critically decreasing.

Non-Surgical Hair Replacement – The Expert’s Choice

They are looking for the most rational way out of the current situation, but there is no clear solution to the problem.The disease occurs in men, women, congenital alopecia in children occurs. Experts who do not consider surgery to be a panacea are considering the hair system (a method of non-surgical hair replacement) as a solution to the problem.


androgenic alopecia

We recommend that you look at a photo of alopecia to make sure that the hair system is a rational solution.Some people with the disease prefer wigs: these products can be considered a suitable option for complete alopecia.

A hair system can be used for masking, regardless of the type of baldness, be it androgenetic, scarring, diffuse, total, subtotal alopecia or areata alopecia. The only contraindication for using the method is serious diseases of the scalp.

  • The use of the replacement system is safe because the method is non-surgical and provides a cosmetic (visual) effect of the presence of hair.
  • When using it, no interference with the human body occurs, therefore the method is suitable for any age.
  • Non-surgical replacement provides a positive psychological effect, which is achieved due to the cosmetic effect of the presence of hair.
  • A person returns a feeling of health, calmness, feels confident in any situation.

Let us consider in detail the frequently occurring types of the disease, signs of alopecia of each type.

Alopecia totala

It is a generalized form of alopecia areata, which leads to hair loss all over the head, sometimes on other parts of the body. With total baldness, the entire scalp is affected; with universal – all body hair falls out.

Alopecia totalis can occur in both children and adults. The first sign of a malignant course of the disease is a sharp loss of hair on the head and face (the hair of the eyebrows and beard, eyelashes disappear).Within a couple of months, the hair on the scalp will fall out completely.

Alopecia areata (focal)

In this disease, hair falls out in certain areas of the head. At the same time, on the bald parts of the head, the skin looks smooth and non-inflamed, devoid of hair, or the hair is severely thinned, in the form of a fluff that changes color. Alopecia of this type occurs in adolescents, women, men and children (regardless of age).

Trichologists say that the main causes of this type of baldness are diseases of the nervous system, immune disorders, infections and heredity.

Diffuse or telogen alopecia

The first symptom of this alopecia is hair thinning on the scalp. In recent years, the number of people who develop the disease has increased. This is not only male alopecia, it often occurs in women during pregnancy (due to hormonal changes in the body).It can occur after the use of hormonal contraceptives, strict diets that are harmful to health.

But the hair is restored on its own when hormones are normalized, a healthy, balanced diet. Therefore, the question of whether it is possible to cure alopecia in this case disappears by itself! And in order to support a weakened body, doctors recommend drinking vitamins with macro- and microelements.

Androgenic alopecia

This type of disease is more common in men.There are many reasons, but the main one is hormonal disorders in the body. This species got its name because of its origin. Female hormones called estrogens are responsible for the growth of hair on the head, while male hormones – androgens – stimulate the growth of hair on the face (mustache, beard) and on the body.

Androgens, which have a strong effect on the parietal and frontal regions, reduce the effect of estrogens, so the hair follicles (hair root) begin to gradually “die off”, the growth of healthy hair stops.

Hormonal disorders can be hereditary in men. Other causes can be infection, stress, trauma. In women, as in men, the cause can be hormonal disruption: during menopause, when there is a global hormonal change in the body. Treatment of alopecia can be prescribed only after establishing the causes of the disease.

Cicatricial alopecia

Occurs with the secondary destruction of hair follicles due to reasons: skin scarring, inflammation, etc.e. Root Causes:

  • developmental defects,
  • hereditary disorders (for example, pigment incontinence, skin aplasia, etc.),
  • traumatic effects that violate the skin (radiation dermatitis, burns),
  • 90,029 destruction of follicles due to infectious diseases (syphilis, tuberculosis).

Methods of treatment include the obligatory intake of vitamins that increase the tone of the body, as well as autohemotherapy.It has been proven that cicatricial alopecia is irreversible, but you can stop the development of the disease, the main thing is to be careful to immediately seek help when the first signs appear!

Seborrheic alopecia

The disease occurs as a complication of seborrhea, is diffuse in nature. Hair thinning occurs over the entire surface of the head. Primary causes: impaired sebum secretion, peeling of the skin, increased greasy hair and other symptoms of seborrhea.In this case, the main thing is to take timely measures, because the occurrence of seborrheic alopecia depends on the success of the fight against seborrhea.

If you are concerned about baldness, contact a trichologist or other specialist in this field to determine the type of alopecia and choose the appropriate treatment. Do not throw this problem into a distant box!

In order to feel healthy and confident when baldness occurs, without experiencing psychological inconvenience, we offer a baldness masking method – a hair system that is selected and attached to the bald part of the scalp.Your hair will look natural and invisible, and you can forget about the problem forever!

I, hairdressers and trichologists answer your questions in consultation

Anticonvulsant and hair loss – Question to a dermatologist

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Varieties (stages) of syphilis / Venereologist Panarin

Syphilis (photo): Varieties (stages) of syphilis / Venereologist Panarin

Primary syphilis

the main symptom of which is the appearance of chancre
(syphilitic ulcer or erosion) with the most frequent localization on
penis or genitals in women


Second stage of syphilis –

secondary syphilis

a characteristic symptom of which is a syphilitic rash on the skin
torso (e.g. roseola)


Secondary syphilis,
rashes on palms


Secondary syphilis
eruptions on the soles


Secondary syphilis
focal hair loss


Secondary syphilis, wide
(condylomas) on the vulva


Note. There are many
other external signs
syphilis that can detect
dermatovenerologist at a clinical examination.

Syphilis: Question-Answer

presented on the site should not be used for independent
diagnostics and treatment, and also cannot serve as a substitute for face-to-face consultation
attending physician



2009–2010 O.V.




90,000 The skin is the mirror of the body. About the pimple problem in an interview with dermatovenerologist Andrey Garmonov

What should Pasha do if Masha walks with Sasha, and Pasha walks in a helmet? This question was answered by TIA dermatovenerologist Andrey Garmonov .Specialist of the Tver Regional Center named after Avaeva told everything about acne, rashes, irritations and other unpleasant phenomena on the skin, shared dermatological horror stories.

First year of life and first acne

The skin of a newborn baby is very thin, sensitive, in the first months of life it will have to adapt to new conditions, after the baby has been in the mother for a long time. In the meantime, any irritant can lead to redness, rashes, peeling and other minor troubles that cause discomfort to the baby.

Andrey Garmonov named the main causes of rashes in babies under one year old:

1. Power supply
If the baby is breastfed, it feeds only on the mother’s breast milk, one of the causes of the rash is a violation of the mother’s diet. Moreover, the child at this stage does not need much. Any chocolates or oranges Mom eats can cause problems. If the child is an artificial person, that is, he eats a mixture, then the mixture is chosen incorrectly.She should be selected individually with a pediatrician, taking into account the characteristics of your baby’s health.
Often, the baby’s skin reacts negatively to the introduction of complementary foods. There is also no rush here, but you need to consult a pediatrician and dermatologist. (TIA told earlier about nutrition in the first year of life and the peculiarities of introducing complementary foods. Interview with pediatrician Olga Ustinova)

2. Contact dermatitis – redness, rashes in places of contact with an irritant. We changed the washing powder, the bath cleaner, bought new soap, baby cream, any cosmetic product for bathing – the baby’s skin can negatively perceive these changes.That is, if the mother is sure that she has not eaten anything new, then you need to remember whether she changed the means for caring for the baby. Particular attention should be paid to diapers. The inscription on the pack “hypoallergenic” does not guarantee that they will be so for the butt of your little one.

3. Rashes can be an allergic reaction to the appearance in the body of such parasites as: lamblia, toxocara, roundworm. These protozoa enter the child’s body through the mouth, very often pets become carriers.
By the nature of the rash, the mother’s stories about the child, the doctor can assume what exactly caused the rash. The diagnosis will be clarified by blood tests, feces for dysbiosis and coprogram.

In older children (from one year to 10-12 years), the causes of rashes are generally the same as in babies. Only, if we are talking about food, then chips, numerous sweets, and soda are already to blame. Often at this age, warts often appear on the skin of children. Hand warts are usually caused by a malfunction in the immune system.On the sole, warts appear most often at the site of microtraumas. In any case, it is worth contacting a dermatologist. Most likely, the doctor will offer to remove warts with liquid nitrogen and pay more attention to the health of the child as a whole, prescribe drugs to strengthen the immune system.

Microsporia (in common people “ringworm”) is a fungal disease that affects the skin, hair and very rarely nails. The main source of the disease is cats, less often dogs. The disease is extremely contagious, it is enough to stroke a sick animal for the fungus to move to the human body.Microsporia mainly affects children, adults – less often. On the child’s skin, spots of a pale pink color appear with a diameter of 2-3 cm, with a red corolla, in the center the spot is peeling. If the fungus affects not only the skin, but also the hair, it will not be easy to cure microsporia, it will take more than one month. Having noticed the symptoms of this disease, parents should immediately contact a pediatrician and a dermatologist.

Why “Masha walks with Sasha, and Pasha walks in a helmet.” Two Causes of Teenage Acne

1.Improper hygiene. During puberty (and in modern children it starts earlier than in children 20 years ago), from about 11 years old, more attention should be paid to hygiene. The sebaceous glands of the skin begin to work much more intensively than before, and therefore it is imperative to wash your face with water and baby soap in the morning and in the evening.

2. The second reason is a change in hormonal levels. In no case should you prescribe treatment yourself, armed with advertising.Most of the advertised creams and lotions only exacerbate the problem, rather than cure it. To prescribe adequate treatment, the doctor will offer to donate blood for hormones – “hormonal mirror”, check the level of sex hormones and the thyroid gland, you will also need to pass a clinical and biochemical blood test, do an ultrasound of the abdominal organs, take culture for flora and antibiotic sensitivity. If the cause of acne in a teenager is a hormonal disorder, then a pediatric gynecologist or a pediatric urologist will take care of the treatment, depending on the sex of the child.

If hair falls out, the spine may be ill. Adult dermatological problems

Patients go to a dermatologist not only when the skin is covered with acne, but also when problems with nails and hair arise.
If the hair grows in bunches, the problem needs to be looked deeper. Andrey Garmonov named the main causes of baldness:

1. Stress. They primarily affect the condition of our hair
2.Hormonal Disorders.
3. Metabolic disorders
4. Changes in the cervical spine.

The last reason may seem strange to someone, but in fact it often leads to hair loss. Due to osteochondrosis, the blood supply to the scalp worsens, that is, the nutrition of the hair follicles is impaired.

Hormonal disruptions are also the main cause of dandruff. Another reason for dandruff is uncleanliness: you need to wash your hair at least every other day, and preferably every day.Moreover, you should not treat the appearance of dandruff as an insignificant problem. This is especially true for men.

If a man suddenly develops dandruff, the level of the male hormone testosterone has most likely dropped. The scalp was the first to respond to this change. So that other more serious male problems do not appear next, you should consult a doctor.

Nails break and exfoliate mainly due to the abuse of cosmetic varnishes. The nails should be allowed to rest.Once every 2-3 months, nails should be left without varnish for 10-14 days so that they breathe. If you abuse varnishes, shellacs, build-ups, then a fungus can develop under all this artificial coating, and it is very difficult to cure it, sometimes nail fungus is treated for years.

Problems with acne and other various rashes on the face and body are not only in babies and adolescents. In adulthood, in women, low-quality cosmetics are added to such reasons as hormonal disorders and food allergies.Because of lipsticks, inflammation of the lips often occurs, because of mascara and shadows – inflammation of the eyelids. In this case, you need to temporarily abandon cosmetics altogether, consult a doctor when the inflammation has passed, change the unsuccessful lipstick, mascaras, shadows.

Once again about food

Beautiful skin and a healthy complexion are impossible without proper nutrition. Less flour and sweets, more fruits, vegetables, complex carbohydrates, protein, dairy products. You need to drink at least 2 liters of water daily.It is better to completely abandon strong alcohol, it destroys the liver, intoxication occurs in the body, the skin suffers, including, the face becomes sallow.

Pregnancy and acne

An interesting situation for most women is accompanied by hard-hitting problems. Many women complain about the return on their face of “adolescence, transitional age.” It happens that small warts appear on the face and neck of a pregnant woman. The fact is that pregnancy, although a physiological state, is still a serious stress for a woman’s body, all forces in these 9 months are aimed at bearing a child, while a woman’s own immunity is weakening.In addition, significant hormonal changes take place during this period.

In most cases, there is only one advice for pregnant women – to be patient. Six months – a year after giving birth, the problem will be resolved by itself, everything will return to normal. If you don’t come, a gynecologist and a dermatologist will help you.


Moles should be watched. If a mole changes color, size, shape, then you should definitely consult a doctor. Most likely, a specialist will offer you to remove it.Particular attention should be paid to moles that are located on frequently injured areas of the body. For example, a mole is on the back, and a woman regularly bumps her bra clasps. It is also better to remove such a mole. You don’t just need to remove all moles and birthmarks in a row.

Horror stories from a dermatologist: some acne is a sign of syphilis and AIDS

If HIV is not treated, then at the AIDS stage the body will be covered with multiple rashes, ulcers, and tumor formations will appear.Andrey Garmonov told a case from his practice. Many years have passed, but he still remembers this girl, although Andrei Garmonov had a lot of different cases for more than two decades of work as a dermatologist, to put it mildly.

Yulia was about 28 years old, she was, as they say, a complete drug addict who did not give a damn about herself. Her parents and doctors fought for her life. She contracted HIV through a shared needle, but did not take any drugs to fight the virus. As a result, a tumor the size of a large grapefruit grew in the genital area, and her whole body was covered with ulcers.The tumor has grown into the pelvic organs. The sight was terrible, there was no way to save her life. She died of blood poisoning.

Another rather unpleasant disease is syphilis. On average, after 14 days, with a typical course of the disease after infection with syphilis, a chancre will appear at the site of the introduction of pale treponema, in other words, a red dense spot about 1 cm in diameter with a shiny surface will grow on the genitals. This chancre tells the person what unprotected sex led to a week ago.If you do not immediately consult a doctor, do not start treating syphilis, then after a while the whole body will be covered with a rash, hair will begin to fall out, then irreversible consequences will begin – the disease affects all organs and systems: the central nervous system, bones, internal organs.

Warts on the body and genitals are a sign of the human papillomavirus (HPV).

In the mouth, on the genitals, around the anus, papillary formations appear, they can grow and outwardly resemble “cauliflower”.HPV is sexually transmitted, an infected person may not even suspect that he is sick, since the disease may not manifest itself for a long time. You can find out about the disease only by donating blood for this virus or by scraping the mucous membranes and skin. The disease can be treated with antiviral drugs, but it is not always possible to cure it completely.

The virus can permanently settle in the human body, in this case it is important to be examined regularly and monitor the concentration of the virus.HPV is especially dangerous for women as it causes cervical cancer.

Summing up what was said, dermatovenerologist Andrei Garmonov noticed that skin, hair and nails are inherited,
If you inherited from your parents lush hair, perfect skin and nails, then their owner will really need to try to spoil this inheritance. But if you are less fortunate, then there is nothing left to do but take care of yourself every day, follow all the advice and recommendations of doctors, and regularly visit dermatologists.

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Role of Malassezia spp. during atopic dermatitis. Dermatologist

Malassezia spp. is a genus of lipophilic yeast and is the most common fungus for healthy skin. Despite its role as synanthropus on healthy human skin, Malassezia spp. attributed pathogenic role

in the development of atopic dermatitis (AD).The mechanisms by which Malassezia spp. possibly contributes to the pathogenesis of blood pressure, not fully disclosed. The most recent discoveries of the pathogenic role of Malassezia spp. Are reviewed here. with blood pressure. For example, Malassezia spp. produces a variety of immunogenic proteins that induce the production of specific IgE antibodies and possibly induce the release of pro-inflammatory cytokines. In addition, Malassezia spp. induces autoactivation of T cells, which cross-react to fungal proteins and their human counterparts. These mechanisms promote skin inflammation in AD and thus influence the course of this disease.Finally, we discuss the possible benefits of treating Malassezia spp. in patients with blood pressure.


Allergic dermatitis (AD) is a frequent chronic recurrent inflammatory skin disease. It is characterized by highly itchy skin eczema and is often associated with allergic rhinoconjunctivitis and allergic asthma. The prevalence of AD in industrialized countries has tripled over the past 30 years, covering 15% -30% of children and up to 10% of the adult population. Despite its frequency and impact on the health of the population, its pathogenesis is not fully understood.As you know, it is genetically determined, and some factors contribute to development. For example, the skin of patients with AD is characterized by impaired skin barrier function with increased transepidermal water loss, increased surface pH, decreased hydration of the stratum corneum, and decreased expression of dense connective components. Secondly, the immune system of the skin in patients with AD changes compared to healthy individuals. For example, patients with AD have increased levels of cytokines, interleukin (IL-) 4, IL-10 and IL-13 in the skin as compared to healthy ones.These cytokines decrease the production of the antimicrobial peptides LL-37, human beta-defensin (hBD) -2 and hBD-3 keratinocytes, which are important components of the skin’s innate immune system against microorganisms. It can be assumed that dysfunction of the skin barrier and changes in the immune system may play a role and contribute to the colonization and growth of microorganisms on the skin of patients with AD. In recent years, blood pressure research also draws attention to a possible pathogenetic correlation between eczema and the synanthropic skin fungus Malassezia spp.because AD patients are often sensitized to Malassezia spp. And in patients with AD, antifungal therapy may be effective. This has led to the publication of many studies on the possible role of Malassezia spp / in the development and course of AD. Here we look at the biology of Malassezia in human skin and the current state of research on the role of Malassezia spp. in the development of blood pressure.

Malassezia spp .. As part of the flora of normal and atopic skin

The skin is an ecosystem and harbors a diverse and locally specific microbial environment called the skin microbiome.Phylogenetic profiling of the skin microbiome showed that fungi are part of the normal skin flora in all parts of the body and make up 1% -22% of the phylogenetic composition of the skin microbiome. The fungal flora of healthy skin practically exclusively includes Malassezia spp. And hence Malassezia spp. is the main eukaryotic member of the microbial flora of the skin .. Malassezia spp. is a genus of lipophilic yeast. Most species within this genus lack fatty acid synthesis genes and therefore depend on exogenous sources of fatty acids to meet nutritional needs.M. pachydermatis, obtained from dogs and other animals, is the only known species of Malassezia that grows in the absence of exogenous lipids. Their need for exogenous lipids explains Malassezia’s tendency to settle on seborrheic-affected areas of the scalp and neck.

The taxonomy of Malassezia spp .. has been controversial since it was identified as an element of the human skin flora in the mid-19th century. The taxonomy was defined in its current form in 1996, based on morphology, ultrastructure, physiology, and molecular biology.Malassezia spp. belongs to the type Basidiomycota and currently includes 14 species that have been isolated on the skin of humans and animals. Two of these species, M. globosa and M. restricta, predominate on human skin and are found on the face and almost all areas of the body. Several studies have examined the epidemiology of Malassezia spp .. in healthy and diseased skin by cultural and molecular methods such as PCR. The studies yielded varying results, presumably due to methodological discrepancies between studies; for example, sampling sites were different between these studies.Sequencing the next generation revealed that the fungal microbiome of the skin is extremely specific to each site of the body.

Therefore, comparing the prevalence of Malassezia spp. Between different body sites sampled in different studies gives unreliable results. In addition, various culture media have been used in epidemiological studies to identify Malassezia species and have been shown to promote the growth of a particular Malassezia species.Thus, the use of only one or a few types of culture medium does not necessarily indicate the full range of Malassezia species present in the sample. Despite these methodological considerations, epidemiological studies indicate geographic variability in the distribution of individual Malassezia species, presumably due to climatic factors. For example, M. sympodialis in studies from Canada, Russia and Sweden is the most common species, while in Japan M.furfur was the most common. Importantly, studies comparing healthy and AD patients found no difference in the incidence of Malassezia spp. Skin colonization. between both groups.

Sensitization to Malassezia spp. may correlate with the severity of atopic dermatitis.

Malassezia spp. as part of the flora, it regularly interacts with the skin’s immune system. Therefore, Malassezia spp.-specific IgG and IgM antibodies can be detected in healthy individuals. However, healthy people are generally not sensitized to Malassezia spp.While a high proportion of AD patients are sensitized to this yeast. This has been demonstrated using patch tests, skin puncture tests, or the presence of Malassezia spp.-specific IgE antibodies. For example, 30% -80% of adult AD patients test positive for subcutaneous injection with Malassezia spp. Extract. Unfortunately, the standardized test with Malassezia spp. Extract. not yet widely available, making it difficult to compare results from different studies. In contrast, reactions to Malassezia spp.β-specific IgE sera can be performed using a standardized kit based on M. sympodialis (ATCC strain 42132).

Recently, with a new kit containing several varieties of Malassezia (ImmunoCAP® m227), the sensitivity slightly increased compared to the test of one species, according to our experience. With these commercial kits, Malassezia spp.-specific IgEs have been detected in 5% -27% of children and 29% -65% of adults with AD, which is in line with injection tests.Indicators of sensitization to Malassezia spp. especially higher in patients with atopic dermatitis of the scalp and neck. Thus, some authors believe that Malassezia spp .. plays a pathogenetic role, in particular, in this type of blood pressure.

The reason for the high incidence of sensitization to Malassezia spp in AD patients compared to healthy subjects is still unclear, but is associated with a combination of skin barrier dysfunction, genetic background, and environmental factors. Several recent studies have looked for a possible correlation between the severity of blood pressure and IgE-mediated sensitization to Malassezia spp.132 children and 67 adults with blood pressure were analyzed and a significant correlation was found between the severity of blood pressure and sensitization to Malassezia spp. in adults, but not in children. These results substantiated previously obtained data in 61 adult AD patients from Japan. Low incidence of Malassezia spp. – sensitization in children compared with adults and the lack of correlation between the severity of blood pressure and Malassezia spp.-specific IgE in children, possibly due to poor conditions for the growth of Malassezia spp. in children compared to adults.Sebum lipid content, which is a prerequisite for skin colonization by Malassezia spp. low in children, but increases during puberty and continues until 50 years of age. Accordingly, sensitization to Malassezia spp .. occurs preferentially in adulthood, while sensitization to food allergens and aeroallergens often occurs in childhood. To date, 13 allergens from two species of Malassezia – M. furfur and M. sympodialis – are listed on the official allergen list.Test tube tests confirmed that Malassezia spp. releases more allergens in a less acidic environment at pH 6.0, which is observed in atopic skin, than in a more acidic environment at pH 5.5 of healthy skin. However, despite frequent sensitization to Malassezia spp. In adult patients, it remains unclear whether IgE production plays a pathogenetic role in the development of AD, or rather serves as a marker for its severity.

Malassezia spp. interacts with the skin’s immune system.

Interaction between Malassezia spp.and the immune system of the skin allegedly promotes skin inflammation in patients with AD. For example, the allergen Malassezia SPP. – Mala s 13 is a fungal thioredoxin that is very similar to its human homologue. CD4 + T cells that react to fungal thioredoxins from Malassezia spp. completely cross-reactive to the human enzyme. Therefore, in addition to recognizing the fungal enzyme, these T cells cross-react with the human enzyme, which may contribute to the inflammation of the skin in Hell.A similar induction of autoreactive T cells has been observed for various allergens of Malassezia spp. Mala s 11 is a manganese-dependent superoxide dismutase with a high degree of identity to the corresponding human enzyme. Like Mala s 13, Mala s 11 activates T cells, which then react against the human homologue and maintain skin inflammation. These findings were supported by a strong correlation between the severity of blood pressure and sensitization to Mala s 11. A protein from M. globosa, MGL_1304, has recently been identified in the sweat of FL patients and is a potential allergen that may contribute to inflammation…. Sensitization to this protein also positively correlates with the severity of blood pressure.

Previous studies have shown that Malassezia spp cells interact with various types of human skin and cells of the immune system. This induces a pro-inflammatory immune response in the skin by cells of the immune system, which can maintain skin inflammation in AD. It is still unclear how this interaction occurs between Malassezia spp. and a host cell, but a hypothesis has been put forward about two possible modes of interaction.First, disruption of the skin barrier facilitates physical collision between Malassezia spp / and epidermal and dermal cells such as keratinocytes, Langerhans cells, dermal dendritic cells, natural killer cells and fibroblasts. A second possible mechanism is mediated by immunogenic proteins from Malassezia spp. These proteins can be released in nanobubbles and these proteins, which may be present in these vesicles, have been shown to cause increased release of TNF-alpha, IL-6, IL-8, IL-10 and IL-12p70 from dendritic cells and mast cells.Other proteins such as MGL_1304 cause mast cell degranulation and the release of IL-4 by basophils.

Some authors have suggested that Toll-like receptors (TLRs) mediate communication between Malassezia spp or their immunogenic proteins and human cells. TLRs are members of a large family of recognition receptors that play a key role in the innate immune system as they recognize molecules that pathogens normally share. It is known that especially TLR2 recognizes yeast components such as Malassezia spp.Several recent studies have substantiated the relevance of TLRs for the immune response of human cells against Malassezia spp. For example, Malassezia spp. induces the expression of TLR2 and TLR4 on human keratinocytes, which mediate increased production of the antimicrobial peptide beta-defensin 2 and CXLC8 chemokines. Others attribute a pro-inflammatory response to dendritic cells against Malassezia spp. through TLR-mediated mechanisms.

Interaction between Malassezia spp. and by human cells causes the release of cytokines.For example, various Malassezia species activate the NLRP3 inflammasome in dendritic cells of the skin and induce the production of IL-1, IL-4, IL-5, IL-13, and IL-18. In addition, the mast cells of AD patients release an increased amount of IL-6 in response to interaction with M. sympodialis. This cytokine is released from human cells and in response to Malassezia spp, which contributes to the development of inflammation.

Therapeutic approaches with Imidazole at blood pressure

The most effective therapy for patients with AD includes excellent skin care to repair the damaged skin barrier, anti-inflammatory treatment, often with topical steroids or calcineurin inhibitors, and the identification and elimination of triggers.The value of antifungal therapy has been debated for many years. Azole imidazole are the most common class of antifungal drugs prescribed for patients with AD. In vitro, imidazole azole is effective against Malassezia spp], but susceptibility testing for M. pachydermatis, the species most commonly obtained from dogs, showed that strains isolated from AD dogs were less susceptible to azole imidazole than strains isolated from healthy dogs. The relevance of this find to Malassezia isolated from humans remains to be seen.

In daily clinical practice, topical application of ketoconazole to the face of patients with blood pressure of the scalp and neck often improves eczema, presumably due to a partial combination with seborrheic dermatitis in some cases. However, a placebo-controlled study with miconazole-hydrocortisone cream and ketoconazole shampoo for scalp and neck BP showed no difference using hydrocortisone alone. The effect on blood pressure alone compared to topical steroids or calcineurin inhibitors and topical antifungals has not yet been studied.The benefit of systemic antifungal therapy for patients with AD has been evaluated in several randomized, placebo-controlled clinical trials. Thirty-six BP patients receiving ketoconazole were compared with 39 BP patients receiving placebo. The severity of blood pressure was significantly reduced in the ketoconazole group, but did not improve in the placebo group. In another study, a total of 53 patients were treated with either two different doses of itraconazole or placebo. The improvement in blood pressure severity was significantly higher with itraconazole than with placebo.These beneficial effects of antifungal drugs were not confirmed in another study comparing 15 AD patients treated with ketoconazole with 14 patients receiving placebo. Notably, both groups received steroids. Despite the severity of blood pressure, the condition improved in both groups, this improvement did not correlate with ketoconazole, but rather with steroids. The mixed results from these clinical trials can be attributed to sample bias. It can be assumed that antifungal therapy is more effective in one subgroup of patients with AD than in another, for example, patients with eczema of the scalp and neck.More recently published studies were of lower quality, for example, they were retrospective observations and did not have a standardized scoring system for assessing the severity of AD. Such trials are not suitable to finally make a positive decision in favor of antifungal therapy. Thus, randomized placebo-controlled trials are needed to evaluate the benefits of antifungal therapy in AD. These studies should be designed to identify the subgroup of patients with AD that appears to benefit from antifungal therapy and to determine the optimal treatment regimen.

It is interesting to note that azole imidazole such as ketoconazole or itraconazole have anti-inflammatory properties. These drugs have been shown to inhibit the production of IL-4 and IL-5 by T cells, which can reduce skin inflammation and therefore ameliorate the condition during antifungal therapy.

Other therapeutic approaches for patients with AD, in particular against Malassezia spp. maybe photodynamic therapy. M. furfur was cultured in the presence of a cationic photosensitizer.Irradiation with a 670 nm diode laser significantly reduces the viability of M. furfur, depending on the duration of the irradiation and the dose. However, the relevance of these results in clinical practice has yet to be proven.


Thus, there is no doubt that Malassezia spp. plays a role in the pathogenesis of blood pressure. This yeast can interact with the skin’s immune system, facilitated by impaired skin barrier function, atopy and sensitization to Malassezia spp.correlates with the activity of blood pressure. In addition, antifungal therapy is beneficial in some patients. However, the pathogenetic mechanism and the interaction between Malassezia and AD are still partially unclear and require further research.

Glatz M., Bosshard P., Hoetzenecker W., Schmid-Grendelmeier P .. The Role of Malassezia spp. in Atopic Dermatitis.

Role of Malassezia spp. during atopic dermatitis

Glatz M, Beauchard F, Getzenecker W, Schmidt-Grendelmeier P, University of Zurich

This material was taken from the dermatology site.ru

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Dermatovenereology and cosmetology center, dermatologist in Tashkent
Republican specialized scientific and practical medical center for dermatovenerology and cosmetology of Uzbekistan

Gynecologist in Ulyanovsk, obstetrician-gynecologist, paid admission

According to the most current standards in gynecology, every woman is recommended to undergo a full gynecological examination once a year.The gold standard of such a survey, according to obstetricians-gynecologists of Ulyanovsk Medgard, are:

  • initial appointment and examination by an obstetrician-gynecologist
  • colposcopy
  • gynecological ultrasound
  • smears for the purity of flora and oncocytology
  • repeated doctor’s appointment

Ultrasound has long and firmly entered the field of diagnostics of women’s reproductive health.According to the experience of gynecologists of the Medgard-Ulyanovsk clinic, ultrasound of the pelvic organs is very popular among the patients of the clinic.

It is a safe, non-invasive and most accurate way to assess the condition of female organs. It is used by women both during pregnancy and during the planning period, and to control ovulation when planning conception. The advantage of ultrasound over other types of research is in showing the patient’s organs in dynamics, thus, it is easier for the doctor conducting the ultrasound examination to diagnose abnormalities and establish a diagnosis.

Contraindications to ultrasound

Oddly enough, there are also contraindications to the safest diagnostic method, but they are associated not with the risk of harm to the patient’s health, but with low diagnostic feasibility. For example, on the wrong day of the cycle, with a full bowel, etc.

Indications for gynecological ultrasound

There are many indications for ultrasound of female genital organs, except for the purpose of an annual examination. Gynecologist Medgarda will issue a referral or independently conduct a study in the event of:

  • monthly female cycle failures
  • too abundant or too scanty periods
  • pain in the lower abdomen
  • bleeding outside of menstruation
  • abnormal discharge, suspicious odor
  • suspected neoplasms in the fallopian tubes, ovaries and cervix (cysts, endometrial hyperplasia, tumors)
  • to determine pregnancy
  • and etc.

Preparation for ultrasound examination

For ultrasound with a transabdominal (external sensor), transvaginal (internal sensor) and transrectal (for patients who are not yet sexually active), preparation for the study is different.

General requirements for preparation for ultrasound

exclusion of high-carbohydrate food in 2-3 days (gases in the intestines make it difficult to examine the internal organs).

bowel movement (sometimes patients are additionally prescribed simethicone preparations)

When prescribing a transabdominal ultrasound for an effective examination, the patient should fill the bladder well (drink a liter of any liquid, preferably still water) 15-20 minutes before the procedure.

On the contrary, before examination with a vaginal probe, the bladder must be emptied for a good result.

On a dual transducer examination, the patient will be asked to present with a full bladder and, prior to examination with an internal transducer, to empty it.

How is gynecological ultrasound performed in the Medgard clinic

Gynecological ultrasound examination is performed in the first week after the end of menstruation.It is then that the doctor will receive a more effective image. From 7 to 10 days of the cycle, a study is prescribed to detect cysts, fibroids in the uterus and other abnormalities.
Endometriosis is determined in the last days of the cycle, before the onset of menarche. To control ovulation, patients planning to conceive are using an ultrasound scan with a vaginal sensor on days 5, 9 and 14 to 17 of the cycle.

The duration of the procedure is 10-15 minutes, depending on the purpose of the study, the number of sensors used and the organs examined.Sometimes, in difficult-to-diagnose cases, the patient will be examined with both an abdominal sensor and a vaginal one. On the sensors and on the surface of the abdomen, the doctor will apply a special water-soluble gel of various viscosities, which increases the degree of transmission of the sound wave through the patient’s tissues. The picture formed by the sound signal goes to the monitor of the ultrasound machine, where the doctor decrypts it.

Ultrasound during pregnancy

During pregnancy, expectant mothers undergo ultrasound screenings three times – as determined by the medical standards in force in the territory of the Russian Federation.The study is prescribed in each trimester: at 13-14 weeks from the onset of pregnancy, then from 18 to 21 weeks and in the 3rd trimester – extended screening with Doppler control of blood flow.

Ultrasound of the first trimester, in combination with laboratory tests, predicts the likelihood of a patient getting into a group of increased risk of genetic pathologies. In the next study, doctors examine the fetus and placenta for medical problems, and the parents, if desired, will tell the gender of the unborn child.Three-dimensional ultrasound on special equipment in the third trimester shows the compliance of fetal development with medical standards, and future parents will be able to see even the baby’s face.

Pay attention! Pregnant patients are examined with a transabdominal probe only.

Description of the results of gynecological ultrasound

Based on the data obtained thanks to the ultrasound waves, the examining physician describes the image and issues an examination protocol.It includes the size and position of organs, echogenicity, the presence of formations, tissue proliferation, other deviations from the norm or their absence.

The results of diagnostics in Medgard, depending on the equipment on which the ultrasound was performed, are provided to patients either in the form of printed images or in the form of a recording of the research process on a CD-ROM. In the department of ultrasound diagnostics of Medgard, modern ultrasound scanners are installed.

The patient receives the ultrasound examination protocol in a printed form.Also, the results of the research in the form of a description are available in the user’s personal account on our website.