What is atrophic pityriasis versicolor. How does it differ from typical pityriasis versicolor. What are the unique features of this case involving a patient with Sjögren’s syndrome. How is atrophic pityriasis versicolor diagnosed and treated.

Understanding Pityriasis Versicolor: A Common Fungal Skin Infection

Pityriasis versicolor is a widespread chronic-relapsing mycosis caused by the Malassezia species, a lipophilic yeast that normally exists as part of the skin’s microbiome. Under certain conditions, this yeast can overgrow and become pathogenic, leading to characteristic skin lesions. The infection typically presents as brownish-red, macular, oval or round lesions that may coalesce. These lesions often have a fine, bran-like scale that can be revealed by gently scraping the skin.

What factors contribute to the development of pityriasis versicolor? Several conditions can promote the overgrowth of Malassezia, including:

• Hormonal changes
• Increased sebum production
• Excessive sweating (hyperhidrosis)
• Immunosuppression (congenital or acquired)
• Endocrine disorders

Where does pityriasis versicolor typically occur? The most common sites include:

• Upper trunk
• Back
• Chest
• Shoulders
• Upper arms

In rare cases, the infection may spread to the groin area and thighs.

Atrophic Pityriasis Versicolor: A Rare Variant

While typical pityriasis versicolor is well-documented, its atrophic variant is a rare occurrence. This form of the infection is characterized by skin atrophy accompanying the typical lesions. The term “atrophying pityriasis versicolor” was coined by Crowson and Magro to describe this unique presentation.

How does atrophic pityriasis versicolor differ from the typical form? The key distinguishing feature is the presence of skin atrophy within the affected areas. This atrophy gives the lesions a depressed appearance and can be appreciated through palpation.

What causes the atrophy in this variant? The exact etiology remains unknown, but two main hypotheses have been proposed:

1. Long-term use of topical steroids
2. Delayed-type hypersensitivity reaction to epicutaneous antigens derived from fungal components

It’s important to note that while atrophic pityriasis versicolor is benign, it needs to be distinguished from other more severe skin conditions that can cause cutaneous atrophy.

A Unique Case: Atrophic Pityriasis Versicolor in a Patient with Sjögren’s Syndrome

This case report presents a 42-year-old woman with an extensive presentation of atrophic pityriasis versicolor. What makes this case particularly interesting is the patient’s underlying condition of Sjögren’s syndrome, an autoimmune disorder that primarily affects the exocrine glands.

What were the key features of this patient’s presentation?

• Hundreds of faintly erythematous, scaly, roundish patches
• Lesion diameter ranging from 0.5 to 1 cm
• Distribution across the back (from shoulders to lumbar area) and both sides of the neck
• Depressed appearance of patches with palpable atrophy
• Asymptomatic nature of the lesions
• Gradual onset over a two-month period

Patient History and Comorbidities

The patient’s medical history provided important context for this case:

• 20-year history of Sjögren’s syndrome with severe musculoskeletal involvement (polyarticular arthritis)
• Long-term systemic corticosteroid use for Sjögren’s syndrome management
• Concomitant Hashimoto’s thyroiditis treated with levothyroxine
• No reported use of topical steroids

Diagnostic Approach for Atrophic Pityriasis Versicolor

How is atrophic pityriasis versicolor diagnosed? The diagnosis typically involves a combination of clinical observation and laboratory confirmation. In this case, the following steps were taken:

1. Clinical examination: The characteristic appearance of the lesions, including their distribution and atrophic nature, raised suspicion of atrophic pityriasis versicolor.
2. Mycological examination: Scales from the lesions were collected for further analysis.
3. Microscopic observation: The scales were soaked in 15% potassium hydroxide (KOH) and examined under a microscope.

What does the microscopic examination reveal in cases of pityriasis versicolor? The hallmark finding is the presence of both hyphae and spores, creating what is often described as a “spaghetti and meatball” appearance. This distinctive pattern is considered diagnostic for pityriasis versicolor.

The Role of Sjögren’s Syndrome in This Case

The presence of Sjögren’s syndrome in this patient adds an intriguing layer to the case. How might Sjögren’s syndrome have influenced the development of atrophic pityriasis versicolor?

• Immune dysregulation: Sjögren’s syndrome is an autoimmune condition that could potentially alter the skin’s immune response to Malassezia.
• Systemic corticosteroid use: Long-term corticosteroid therapy, often used in Sjögren’s syndrome management, can lead to immunosuppression and skin atrophy.
• Altered skin microenvironment: The exocrine gland dysfunction in Sjögren’s syndrome might create favorable conditions for Malassezia overgrowth.

While a direct causal relationship cannot be established, these factors may have contributed to the development and unique presentation of atrophic pityriasis versicolor in this patient.

Treatment Approaches for Atrophic Pityriasis Versicolor

How is atrophic pityriasis versicolor treated? The approach is generally similar to that of typical pityriasis versicolor, with some considerations for the atrophic component:

• Topical antifungal agents: These form the mainstay of treatment and can include azoles (e.g., ketoconazole, clotrimazole) or allylamine derivatives (e.g., terbinafine).
• Systemic antifungals: In extensive or recalcitrant cases, oral antifungal medications may be considered.
• Addressing underlying factors: Managing any predisposing conditions or medications that may contribute to fungal overgrowth or skin atrophy.
• Skin care: Gentle skin care practices to support the healing of atrophic areas.

In this particular case, the patient’s condition responded well to topical antifungal treatment, resulting in complete resolution of the lesions.

Implications and Considerations for Clinical Practice

What lessons can clinicians draw from this case of atrophic pityriasis versicolor in a patient with Sjögren’s syndrome?

• Heightened awareness: Clinicians should be alert to the possibility of atrophic pityriasis versicolor, especially in patients with underlying autoimmune conditions or those on long-term immunosuppressive therapy.
• Differential diagnosis: The atrophic variant of pityriasis versicolor should be considered in the differential diagnosis of conditions presenting with cutaneous atrophy.
• Diagnostic confirmation: While clinical presentation may be suggestive, microscopic examination remains crucial for definitive diagnosis.
• Holistic management: Treatment should address not only the fungal infection but also any underlying conditions or medications that may predispose to its development.
• Follow-up care: Given the chronic-relapsing nature of pityriasis versicolor, patients should be educated about potential recurrence and preventive measures.

Future Research Directions in Atrophic Pityriasis Versicolor

This case highlights several areas where further research could enhance our understanding of atrophic pityriasis versicolor:

• Pathogenesis: What are the precise mechanisms leading to skin atrophy in this variant of pityriasis versicolor?
• Host factors: How do underlying conditions like autoimmune diseases influence the development and presentation of atrophic pityriasis versicolor?
• Malassezia strains: Are certain Malassezia species or strains more likely to cause the atrophic variant?
• Treatment optimization: What are the most effective treatment regimens for atrophic pityriasis versicolor, especially in patients with complex medical histories?
• Long-term outcomes: Does the atrophic variant have different recurrence rates or long-term skin effects compared to typical pityriasis versicolor?

By addressing these questions, researchers and clinicians can work towards improved diagnosis, management, and prevention strategies for atrophic pityriasis versicolor.

Case Report: Atrophic pityriasis versicolor occurring in a patient with Sjögren’s syndrome

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BMJ Case Rep. 2017; 2017: bcr2016218108.

Published online 2017 Jan 18. doi: 10.1136/bcr-2016-218108

Case Report

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Pityriasis versicolor is one of the most frequent epidermal mycotic infections in the world, but its atrophic variant is rarely described. The aetiology of the atrophy is still unknown, and two main hypotheses have been formulated, one suggesting a correlation with long-term use of topical steroids and the other a delayed type hypersensitivity to epicutaneous antigens derived from components of the fungus. Atrophic pityriasis versicolor is a benign disease, but needs to be distinguished from other more severe skin diseases manifesting with cutaneous atrophy. The diagnosis can be easily confirmed by direct microscopic observation of the scales soaked in 15% potassium hydroxide, which reveals the typical ‘spaghetti and meatball’ appearance, or by a skin biopsy in doubtful cases. Here, we describe a case of extensive atrophic pityriasis versicolor occurring in a woman affected by Sjögren’s syndrome which completely resolved after topical antifungal treatment.

Pityriasis versicolor is a widespread chronic-relapsing mycosis caused by the Malassezia species, a lipophilic yeast that, under normal conditions, is part of the physiological flora of the skin surface. Many factors may favour proliferation of the yeast and its transition into a pathogen: hormonal changes, increases in sebum secretions, hyperidrosis, congenital/acquired immunodepression and endocrine disorders.¹² Predilection sites for pityriasis versicolor are the upper trunk, back, chest, shoulders and upper arms. In rare cases, the groins and thighs are involved. The disease typically starts with brownish-red, macular, oval and round, coalescing, flat, non-pruritic lesions of various sizes, in which discrete bran-like scaling may be evoked by tangential scraping.³ The lesions of pityriasis versicolor can be rarely accompanied by skin atrophy and in order to describe this variant, Crowson and Magro coined the term ‘atrophying pityriasis versicolor’.⁴ To the best of our knowledge, <20 cases have been reported since then. We report a case of atrophic pityriasis versicolor occurring in a woman affected by Sjögren’s syndrome with a review of the literature.

A 42-year-old woman presented with hundreds of faintly erythematous scaly roundish asymptomatic patches varying in diameter from 0.5 to 1 cm, diffuse all over the back from the shoulders to the lumbar area and on both sides of the neck (A, B). The patches presented a depressed appearance and a slight atrophy could be appreciated by palpation. The first patches appeared 2 months before on the neck and gradually increased in number.

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Erythematous roundish patches varying in diameter from 0.5 to 1 cm on the back of a 42-year-old woman (A). Close-up view of the patient’s skin under tangential lighting shows mild scaling and atrophy (B).

The patient had been affected by Sjögren’s syndrome with a severe musculoskeletal involvement (polyarticular arthritis) for 20 years requiring systemic corticosteroids since the beginning of the disease. She also was affected by Hashimoto’s thyroiditis treated with levothyroxine. She denied the use of topical steroids. When the patient was referred to us, mycological examination of the lesions was performed to verify the clinical hypothesis of atrophic pityriasis versicolor.

For direct microscopic observation, the scales were soaked in 15% potassium hydroxide (KOH) and microscopic evaluation revealed both hyphae and spores creating the ‘spaghetti and meatball’ appearance (), consequently the diagnosis of tinea versicolor was confirmed.

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Microscopic examination of scales soaked in 10–15% potassium hydroxide (KOH). Hyphae are visible and grown into strands within clumps of keratinocytes. Thick-walled spores occur in grapelike clumps. Individual spores and short stubby hyphae float in the clear areas between clumps of keratinocytes. This combination is commonly referred to as ‘spaghetti and meatballs’.

The patient was treated with daily application of topical ketoconazole 2% cream over a 6-week period. After this period, the skin lesions and the atrophy completely resolved ().

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Complete resolution of both scaly patches and atrophy after topical therapy with ketoconazole.

There was no recurrence of the disease after 3 months of follow-up.

De Graciansky and Mery reported the first case of pityriasis versicolor associated with skin atrophy in 1971.⁵ Since then, this finding has been rarely described.^46–9 The mechanism of cutaneous atrophy in atrophic pityriasis versicolor is not well understood. So far, two hypotheses have been proposed to explain skin atrophy. The first hypothesis suggests a pathogenetic role of long-term use of topical steroids in the patients affected.^10–12 The authors suggested that atrophy induced by topical steroids, entirely confined to the pityriasis versicolor lesions, was due to the reduction in cutaneous barrier functions at sites of infection. The structural properties of the outer two-thirds of the horny layer are altered in pityriasis versicolor,¹³ and this may be responsible for the increased penetration of topical steroid and consequent atrophic dermal changes through the inhibition of collagen synthesis and reduction of the mitotic activity of keratinocytes. Therefore, the atrophy might have occurred only in the pityriasis versicolor lesions, although topical steroids were applied to the whole body of the affected patients.⁶ In our patient we cannot exclude a role of the systemic treatment with corticosteroids. Crowson and Magro conducted clinical and histological studies in 12 patients with atrophic pityriasis versicolor, but only one of these had been treated with topical steroids for a long time before diagnosis.⁴ The second hypothesis, suggested by these authors, is that the atrophy seen clinically and histologically in all of their patients may reflect a delayed type hypersensitivity to epicutaneous antigens derived from components of the pityriasis versicolor throughout the release by T helper lymphocytes of cytokines such as interleukin-1β and tumour necrosis factor α. These mediators could be responsible for the epidermal atrophy by provoking the apoptosis and impaired proliferation of keratinocytes and/or stimulating the histiocytes to release elastase that leads to elastolysis perturbing the collagen metabolism.

Atrophic pityriasis versicolor needs to be distinguished from other more severe skin diseases manifesting with cutaneous atrophy such as anetoderma, atrophoderma of Pasini and Pierini, mid-dermal elastolysis, confetti like macular atrophy, morphea, parapsoriasis and mycosis fungoides. Differential diagnoses especially with anetoderma, a rare elastolytic disorder characterised by circumscribed areas of flaccid skin due to the loss of elastic tissue in the superficial dermis, may be difficult because the clinical manifestations are very similar; however, anetoderma is associated with histological evidence of dermal loss and elastic tissue loss.¹⁴ Primary anetoderma (PA) is frequently observed in patients with autoimmune diseases, especially with antiphospholipid antibodies with or without antiphospholipid syndrome and in patients with systemic lupus erythematosus.¹⁵ Moreover, there are isolated reports of PA and autoimmune diseases like primary hypothyroidism, Graves’ disease, Addison’s disease, Sjögren’s syndrome, alopecia areata, vitiligo and multiple sclerosis. ¹⁶ The evolution towards conspicuous atrophy, the irreversibility of skin lesions and the lack of therapeutic success are also typical of primary anetoderma. In our patient, the atrophic areas showed a complete regression after antimycotic therapy, so the diagnosis of anetoderma was definitively excluded. On the basis of typical clinical findings as the concurrent presence of scales and a positive KOH test; however, a differential diagnosis can be made in case of unclear presentation. Extensive biopsies and histological examinations might not be required in cases that are clinically and microscopically unequivocal.⁹ However, in doubtful cases, biopsy provides histological confirmation of the presence of the yeast in the horny layer and it may document reduction in number and fragmentation of elastic fibres, especially in long-standing forms.¹⁴ In this condition, following treatment of Malassezia the atrophy usually resolves,⁷ therefore some authors suggest the term of ‘pseudoatrophy’ to indicate its reversible character. ⁸¹²

Moon et al⁸ performed skin biopsies on the lesions before and after treatment and on perilesional normal skin of an affected man to investigate more accurately the mechanism of skin atrophy, and on the basis of their histopathological findings they suggested that atrophy observed in atrophic pityriasis versicolor may be more likely associated with alterations in dermis rather than epidermal changes. These dermal alterations seem to be related to defect of elastic fibres but not to changes or loss of collagen. As a matter of fact, focal fragmented or decreased elastic fibres were found only on lesional skin before treatment compared with the other two specimens.

Learning points

• Pityriasis versicolor is a widespread epidermal mycotic infection, but this atrophic variant is rarely described in the literature.

• Atrophic pityriasis versicolor is a benign disease, but needs to be distinguished from other more severe skin diseases showing cutaneous atrophy.

• The diagnosis is based on the typical clinical findings and the positive potassium hydroxide test, but histological examination might be required in case of unclear presentation.

Twitter: Follow Elena Marinello @[email protected]

Contributors: EM made substantial contribution to acquisition of clinical data and drafting the manuscript. SP made substantial contribution to interpretation of clinical data. MA made substantial contribution to acquisition of clinical data and drafting the manuscript.

Competing interests: None declared.

Patient consent: Obtained.

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

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Articles from BMJ Case Reports are provided here courtesy of BMJ Publishing Group

Tinea versicolor: Overview – InformedHealth.org

Created: December 17, 2014; Last Update: August 29, 2019; Next update: 2022.

Introduction

Tinea versicolor, also referred to as pityriasis versicolor, is a skin condition characterized by patches of lighter or darker skin. It is caused by a type of yeast (fungus) that is found on most people’s skin. It is generally not harmful and it isn’t contagious.

Topical treatments (applied directly to the affected area), such as special creams or shampoos, are usually effective.

Symptoms

In tinea versicolor, small round or oval patches of skin appear at first, and later merge into larger patches with irregular shapes. They are especially common on the back, chest, neck and/or arms. They may occur on the face as well, particularly in children.

The patches may be yellow or brownish, or sometimes red or pink. They are usually lighter or darker than the surrounding healthy skin. Because these patches hardly change color in the sun, they are more noticeable if you have a suntan. The affected areas of skin may also be somewhat scaly. They rarely itch. If they do, then they only itch a little.

Tinea versicolor on the upper body

Causes

Tinea versicolor is caused by a type of yeast (fungus) that is found on most people’s skin. It’s not clear exactly why the fungus grows and causes visible patches in some people but not in others.

It’s important to know that tinea versicolor has nothing to do with poor hygiene, and it’s not contagious.

Risk factors

Various factors can increase your chances of developing tinea versicolor. These include

• a warm and humid climate,

• sweating a lot (for instance in people who generally sweat more or who do a lot of sports) and

• the use of oils or cosmetics that may clog the skin pores.

Genes probably play an important role too.

People who have a weakened immune system are generally more susceptible to infections, so they are also more likely to develop tinea versicolor. The immune system may be weakened by things like certain types of cancer or medication that suppresses the immune system – for instance, following an organ transplant.

Prevalence

Tinea versicolor is a common skin condition. In countries with a more moderate climate it affects about 1% of the population, and in some tropical countries it affects about 40%. It is just as common in men as it is in women. Most people first get it at a young age.

Diagnosis

Doctors can often recognize tinea versicolor just by looking at the typical groups of light or dark patches on the upper body and/or arms. To rule out other possible skin conditions, your doctor might use a strip of clear adhesive tape to take a sample of the scaly skin and look at it under a microscope. This is usually enough to determine whether it is tinea versicolor.

Treatment

Tinea versicolor may improve a little in cool or dry weather, but it usually doesn’t go away on its own. There are a number of effective treatments. These mainly include creams, lotions and shampoos that contain antifungals (substances that kill the fungus or inhibit its growth). The creams and lotions are applied to the affected areas of skin. The shampoo is used too, so that the fungus doesn’t spread back to the skin from the scalp and hair. Depending on the exact product used, it needs to be left on for anywhere from a few minutes to several hours. The creams and lotions are often put on in the evening and then rinsed off in the shower the next morning.

But even when treatment works, it can take up to several weeks or months for the skin patches to disappear. Treatment with tablets is only rarely needed.

Sometimes tinea versicolor comes back again after successful treatment. If this keeps happening, doctors may recommend using a special shampoo on your skin and hair every two to four weeks to prevent it from returning again. The shampoo contains an active ingredient like selenium sulfide or ketoconazole. There are also oral medications (tablets) that can be taken every four weeks to prevent tinea versicolor from returning. Doing either of these things can greatly reduce the risk of it coming back.

Sources

• Choi FD, Juhasz ML, Atanaskova Mesinkovska N. Topical ketoconazole: a systematic review of current dermatological applications and future developments. J Dermatolog Treat 2019 [Epub ahead of print]: 1-12.

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• IQWiG health information is written with the aim of helping
  people understand the advantages and disadvantages of the main treatment options and health
  care services.

  Because IQWiG is a German institute, some of the information provided here is specific to the
  German health care system. The suitability of any of the described options in an individual
  case can be determined by talking to a doctor. We do not offer individual consultations.

  Our information is based on the results of good-quality studies. It is written by a
  team of
  health care professionals, scientists and editors, and reviewed by external experts. You can
  find a detailed description of how our health information is produced and updated in
  our methods.

Lichen planus – KVD No. 2

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• Lichen planus

Lichen planus (LP) is a chronic inflammatory disease of the skin and mucous membranes, rarely affecting nails and hair, characterized by a polymorphism of rashes, among which typical elements are papules, accompanied by itching.

Etiology and epidemiology

The etiology of the disease is unknown. LP is considered as an autoimmune disease, in which the expression of an antigen that has not yet been identified by keratinocytes of the basal layer leads to the activation of T-lymphocyte migration into the skin with the formation of an immune response and an inflammatory reaction.

LP is most common in people aged 30 to 60 years.

Classification

There is no generally accepted classification of KPL.

The most common forms of skin lesions in LP are:

1. Typical.

2. Hypertrophic, or verrucous.

3. Atrophic.

4. Pigmented.

5. Bubble.

6. Erosive and ulcerative.

7. Follicular.

There are 6 forms of lesions of the oral mucosa and the red border of the lips in LP.

1. Typical.

2. Hyperkeratotic.

3. Exudative-hyperemic.

4. Erosive and ulcerative.

5. Bullous.

6. Atypical.

Clinical picture

Skin lesion in a typical form of lichen planus is characterized by flat papules 2–5 mm in diameter, with polygonal outlines, with an impression in the center, pinkish-red color with a characteristic purple or lilac tint, waxy sheen, more distinct at the side lighting. Characteristic signs of lichen planus are a tendency to a grouped arrangement of rashes with the formation of rings, garlands, lines. In most cases, the rash is located symmetrically on the flexor surfaces of the limbs, trunk, genitals, and quite often on the oral mucosa. Subjectively, patients are concerned about itching.

Diagnosis

In most cases, the diagnosis of LP is based on clinical findings. To clarify the diagnosis, a histological examination of skin biopsies from the most characteristic lesions is carried out.

Differential diagnosis

Differential diagnosis of LP is carried out with secondary syphilis, atopic dermatitis, pityriasis versicolor pilaris, Darier’s disease, psoriasis.

Treatment

The choice of treatment for LP depends on the severity and localization of clinical manifestations, the form and duration of the disease, and information about the effectiveness of previous therapy. During the period of exacerbation of the disease, patients are recommended a sparing regimen with limitation of physical and psycho-emotional stress. In the food regimen, salty, smoked, fried foods should be limited. In patients with lesions of the oral mucosa, it is necessary to exclude irritating and coarse food.

In the presence of limited rashes, treatment begins with the appointment of topical glucocorticosteroid drugs of medium and high potency. According to experts, antimalarial drugs can be used in the treatment of patients with lichen planus, which are used as systemic therapy and can be prescribed along with corticosteroid drugs.

Non-pharmacological treatment

1. Narrow-band medium-wavelength phototherapy with a wavelength of 311 nm (C-D) is prescribed for minor infiltration of lesions 3-4 times a week for 6-12 weeks.

2. Patients with more severe infiltration in the lesions are indicated for PUVA therapy with oral or topical application of a photosensitizer.

Prevention

There are no methods of prevention

Differential diagnosis of psoriasis and lichen planus

July 15, 2020

Differential diagnosis of psoriasis and lichen planus plays an important role in dermatology. These two diseases have common features, but there are also many differences. Today we will talk about the most basic ones.

What you need to know about psoriasis

Psoriasis is lichen. Despite the fact that in the minds of many, lichen is associated exclusively with something contagious, psoriasis has a second name “scaly lichen”, although it does not pose a threat to others. The disease often recurs, reduces the quality of life. It is impossible to completely get rid of psoriasis, but unpleasant symptoms can be removed with the help of ointment and lifestyle correction.

The number of patients with psoriasis is increasing every year. Lichen squamous has several typical symptoms:

• raised, pink, scaly patches;
• these spots have white scales;
• psoriatic plaques tend to coalesce;
• itching of varying intensity – from a slight tingling to the desire to scratch the skin until it bleeds;
• white exfoliating spots on nails;
• dryness and peeling.

Most often, psoriasis appears on the elbows, knees, head and groin. It can occur for the first time at any age, it is not uncommon for the first symptoms to be observed in puberty and at the age of 20 to 30 years. Scientists believe that the main cause of psoriasis is an autoimmune process, when one’s own immune system attacks skin cells and causes chronic inflammation.

How to recognize lichen planus

The fact that a person has this particular type of lichen can be indicated by flat papules of red or purple color. At the very beginning of the disease, the papules are very small, they reach no more than 2-4 mm in size, while their surface slightly shines in mixed light. Most often, rashes appear on the flexion areas of the arms and legs, on the trunk, genitals, including mucous membranes, and also in the mouth. As with psoriasis, the patient unbearably wants to comb the affected areas.

It is believed that LP is also caused by autoimmune factors, like psoriasis. The trigger for the appearance of rashes can be a variety of factors, such as hepatitis C or the use of certain drugs.

How to understand whether lichen or psoriasis is in front of us

To summarize all of the above, we can distinguish several similar features of the two diseases:

• autoimmune nature;
• rash in the form of papules;
• itching;
• red papules;
• the folds of the arms and legs are often affected.

The question arises, how to distinguish psoriasis from lichen. Diseases have several differences:

• psoriatic plaques are flaky, scales can be seen on the surface, and with lichen planus, the surface of the papules is smooth;
• psoriasis does not occur on mucous membranes, but LP often affects the oral cavity and mucous surfaces of the genitals;
• plaques of psoriasis are larger than those that form with lichen;
• If lichen planus affects the scalp, scarring alopecia may occur.