Differential diagnosis and treatment of Devergie's disease

Ringworm (microsporia) is a disease manifested as a fungal infection of the skin, nail plates and hair follicles. The pathogen is a mold fungus of the genus Microsporum. Its colonies form in keratinized substrates. Microsporia remains a relatively common disease - dermatologists identify 60-75 cases for every hundred thousand Moscow residents. The pathology has a pronounced seasonality. The peak incidence occurs at the end of summer and beginning of autumn - the period of breeding of offspring in cats and other animals.

Routes of infection

The causative agent of microsporia enters the body when a healthy person comes into contact with a carrier of the disease. An alternative way is to interact with objects covered with fungal spores. Ringworm is most often detected in children aged 5-10 years; in boys, microsporia is diagnosed five times more often than in girls. The pathology almost does not affect adults due to the presence of organic acids in their hair structure, which suppress the growth of fungal mycelium.

The reasons for the development of ringworm are microtraumas of the skin and its dryness. Spores get into cracks, scratches or open calluses. Healthy skin becomes an insurmountable barrier to fungus. The pathogen does not survive contact with personal hygiene products - thorough hand washing after contact with spore carriers eliminates the possibility of infection.

The risk group includes people who regularly come into contact with the ground and wild animals. The active growth of the fungus is facilitated by disturbances in the functioning of the sebaceous glands due to changes in the chemical composition of their secretions. Microsporum spores can remain viable for three months when left in open ground.

Differential diagnosis and treatment of Devergie's disease

Devergie's lichen pilaris (syn.: Devergie's disease; pityriasis rubra pilaris; lichen ruber acuminatus) is a heterogeneous chronic inflammatory skin disease, which is divided into both hereditary forms, transmitted autosomal dominantly, and sporadic, acquired ones. Although the name and description are generally believed to be by Alphonse Devergie, the first case was reported in 1828 by Claudius Tarral. He noted isolated scaly rashes, penetrated in the center by hair, upon palpation of which a very dense roughness was felt on the surface of the skin [1–6].

Devergie's disease (DD) is a rare disease accounting for 0.03% of all skin diseases. The etiology and pathogenesis of dermatosis are still not fully understood; the opinions of modern authors differ. The theory of hereditary predisposition plays a dominant role, although there are other theories [3, 5]. An immunomorphological study of cells in the inflammatory infiltrate in patients with BD was characterized by an increased number of cells with the expression of markers involved in the development of the inflammatory immune response through the mechanism of delayed-type hypersensitivity. This allows us to classify the disease as a chronic dermatoses characterized by hyperproliferation of keratinocytes mediated by T cells [7]. According to K.N. Suvorova et al. (1996), the onset of the disease can be observed in all age periods from 5 to 72 years. The course of the disease is chronic, sometimes for decades, with no seasonality noted [8].

In 1980, Griffiths described 5 clinical forms of the disease, which doctors used for quite a long time:

1. Classic adult type of the disease.
2. Atypical adult type.
3. Classic juvenile type.
4. Limited juvenile type.
5. Atypical juvenile type.

However, in modern dermatology it is generally accepted that the classic adult type and the classic juvenile types of the disease have identical clinical manifestations and differ only in the age of the patients. For this reason, the current classification of BD includes three clinical forms:

1. Classic type.
2. Limited juvenile type.
3. Type associated with HIV infection [6].

Diagnosis of BD, especially in the initial stage, is difficult, since the clinical picture of the disease develops slowly. The pathological process is represented by a rash consisting of follicular papules with perifollicular erythema surrounding the hair shaft. The papules have a conical shape with characteristic horny spines - “Beignet cones”. This form of nodules forms the pathognomonic symptom of “grater” - a sensation of a rough surface upon palpation (Fig. 1). Localization of follicular hyperkeratosis on the dorsal surface of the I–II phalanges of the fingers is found in the literature under the name “Besnier’s symptom.” Typical for BD is the brick-red or yellowish-red color of the rash. The disease can begin either acutely or gradually. Typically, the rash appears on the upper half of the body in the form of erythematous spots or a single plaque and spreads downwards (Fig. 2) [1–5, 9]. This dermatosis debuts with erythemosquamous lesions on the face and pityriasiform peeling of the scalp, which are accompanied by itching of varying intensity, which can mimic seborrheic dermatitis. Over time, the clinical picture changes; as a result of the fusion of erythemosquamous plaques, the process spreads and gradually takes on the character of diffuse erythroderma, then a typical symptom is the presence of islands of healthy skin against the background of erythroderma (Fig. 3). The presence of islands of healthy skin is of great clinical importance for the diagnosis of BD, sometimes being one of the most important differential signs. This symptom is the presence of small areas of healthy-looking, coin-shaped skin with a diameter of about 1 cm, scattered on an erythrodermic background on any part of the skin. Peeling is heterogeneous: the scales on the upper half of the body are small, on the lower half they are often large-plate. A clinical symptom such as follicular hyperkeratosis on the dorsal surface of the phalanges of the fingers (Besnier's sign) is observed in 50% of cases. Simultaneously with the onset of the disease or later, palmoplantar hyperkeratosis appears, which occurs in 80% of cases with this type of disease [4, 5, 8, 9].

The nail plates are often affected, have a yellowish color, are streaked with longitudinal or transverse grooves, and subungual hyperkeratosis is often pronounced. In some cases, there is deformation of the nail plates of the feet and hands, up to onychogryphosis.

Clinical diagnosis of the disease is based on characteristic signs:

• ostifollicular papules, forming the “grater” symptom;
• perifollicular erythema, with a tendency to merge;
• the presence of “islands of healthy skin” against the background of erythroderma;
• brick-red color of the skin;
• palmoplantar hyperkeratosis;
• nail changes;
• Besnier's sign.

However, quite often rashes with BD resemble psoriasiform elements, and the presence of diffuse erythroderma makes the dermatosis similar to psoriasis and toxicoderma. Psoriasis and BD share not only the similarity of clinical manifestations, but also the mechanisms of development of the inflammatory process. The results of a histological and immunomorphological study conducted by O. R. Katunina (2005) indicate a common pathogenetic pathway for the development of the inflammatory process in the skin in psoriasis and BD. In both cases, activation of antigen-presenting cells occurs, hyperproliferation of keratinocytes, which, acquiring the features of immunocytes, contribute to the maintenance of the pathological process [7].

Diagnostics

We conducted clinical observations of 23 patients with Devergie's lichen pilaris. The clinical diagnosis of each subject was confirmed by histological examination of a skin biopsy. 15 (65.2%) patients were initially diagnosed with psoriasis, 6 (26%) patients were treated for toxicoderma, and only 2 (8.8%) of them were allegedly diagnosed with Devergie pilaris. Due to such a large number of diagnostic errors, we analyzed the main differential diagnostic features of BD.

First of all, our attention was drawn to the good health of all patients with BD, which persists even with diffuse damage to the skin, in contrast to patients with toxicoderma or psoriatic erythroderma, in whom complaints of prodromal phenomena, low-grade fever and weakness prevail. Subjective sensations of patients with BD are mainly focused on changes in the skin, a feeling of tightness and dryness, which contradicts the observations of foreign authors who indicate that approximately 20% of patients experience itching or burning [6]. In the differential diagnosis of BD, one should pay attention to the pathognomonic symptom of “islands of healthy skin.” This sign was recorded in all observed patients. The symptom is easy to distinguish from areas of healthy skin in psoriatic erythroderma, if we keep in mind that the characteristic islands of healthy skin in psoriatic erythroderma do not exceed 1.5 cm in diameter, have clear rounded boundaries and are located against the background of diffuse erythroderma. When establishing a diagnosis of BD, it should be remembered that this is ostiofollicular dermatosis and the primary element is a papule penetrated in the center by hair. However, we must not forget about the follicular form of psoriasis, when in a patient with psoriasis we can also observe pink ostiofollicular papules, riddled with hair in the center. In this case, it can be quite difficult to distinguish these diseases if you do not pay attention to typical psoriatic plaques in characteristic locations: the scalp, extensor surfaces of the extremities. Dynamic observation of the patient will allow you to establish the correct diagnosis. In psoriasis, papules always tend to grow peripherally and coalesce due to infiltration of the dermis, in contrast to BD, in which diffuse erythroderma is formed due to the erythemosquamous process. The absence of infiltration and lichenification, abundant large-plate peeling, characteristic of psoriasis, once again speaks in favor of the diagnosis of BD.

The next very important symptom of BD is the characteristic color of the skin - brick red or carrot, described by numerous authors [3–10]. We noted that 7 patients (30.4%) had a carrot-colored skin tone, and the rest had a brick-red color (n = 16; 69.6%). However, palmoplantar hyperkeratosis, which developed in 19 (82.6%) of the patients we observed, in all cases gave a yellowish-carrot coloration to the skin.

Although damage to the nail plates among the examined patients was diagnosed only in 18 (78.2%) patients, I would like to note that the severity of this symptom most likely depends on the duration of the disease, since the growth rate of the nail plate is much slower than the development of the pathological process. This assumption was confirmed by our observations: in patients with damage to the nail plate, the duration of the disease ranged from 4 to 10 months. Changes in the nail plate were characterized by subungual hyperkeratosis, color changes, and longitudinal and transverse striations. However, onycholysis, characteristic of psoriasis, was not observed in any patient.

As mentioned above, in the majority of patients with BD we observed (n = 21; 91.2%), the correct diagnosis was not initially established. Patients received hyposensitizing and antihistamine drugs, and more than half of them (n = 15; 65.2%) received long-acting steroids, but despite intensive therapy, no positive dynamics in treatment were noted. This fact once again confirms that BD is resistant to conventional therapy. Summarizing the above, we can identify the main differential diagnostic features that allow us to distinguish lichen pilaris from psoriasis:

• the good general condition of patients with BD is maintained even with diffuse damage to the skin, in contrast to psoriasis;
• a characteristic feature is the presence of islands of healthy skin;
• the primary element is the ostiofollicular papule;
• brick-red or carrot-colored skin;
• absence of infiltration, lichenification and abundant large-plate peeling characteristic of psoriasis;
• onycholysis, characteristic of psoriasis, is observed very rarely;
• palmoplantar hyperkeratosis without infiltration, giving a yellowish-carrot tint to the skin;
• torpidity to hyposensitizing, antihistamine and hormonal therapy.

Treatment

Currently, drugs that affect keratinization processes are retinoids. For the first time in 1930, Moore synthesized retinol from carotenoids and began to study its effect on the body. Today it has been proven that vitamin A is involved in the regulation and proliferation of many types of cells from the moment of embryonic development and throughout life. The most effective among all synthetic retinoids in the treatment of BD is Neotigazon at a dose of 0.5–0.7 mg/kg/day [4–6, 10].

Neotigazone (acitretin 10 mg, 25 mg) has pronounced lipophilicity and easily penetrates tissues. It should be borne in mind that due to individual differences in the absorption and rate of metabolism of acitretin, the dose must be selected individually. The initial daily dose is 25 or 30 mg per day for 2–4 weeks. It is better to take capsules once a day in the evening with meals or with milk. As a rule, the therapeutic effect is achieved with a daily dose of 30 mg. In some cases, it may be necessary to increase the dose to a maximum of 75 mg/day. However, one should not count on a rapid clinical effect from the therapy in the treatment of BD, especially in adults. Our opinion coincides with the opinion of foreign authors who believe that symptomatic improvement in BD occurs within 1 month, but significant improvement and, perhaps, resolution of the process is possible within 4–6 months, and according to some data, the average duration of therapy is about 4 years [6]. Our observations of patients with BD established an average duration of therapy of 9 months (Fig. 4).

Given the possibility of developing severe side effects, during long-term treatment the possible risk should be carefully weighed against the expected therapeutic effect. Contraindications to the use of Neotigazon include hypersensitivity to the drug (acitretin or excipients) or to other retinoids; severe liver and kidney failure; severe chronic hyperlipidemia, chronic alcoholism; cholelithiasis, chronic pancreatitis; diseases of the central nervous system, accompanied by increased intracranial pressure. A. A. Kubanova et al. (2005) indicate contraindications to the prescription of retinoids if there is a history of epithelioma (including familial), squamous cell or basal cell carcinoma [10]. Neotigazon has a strong teratogenic effect. The risk of having a child with developmental defects is especially high if Neotigazon is taken before or during pregnancy, regardless of the dose and duration of therapy. The literature indicates various time intervals between the end of taking retinoids and pregnancy necessary to eliminate the risk of a teratogenic effect. According to various authors, this period ranges from 6 months to 2 years [10].

The lipophilic properties of the drug suggest that it passes into breast milk in significant quantities. For this reason, Neotigazon should not be prescribed to nursing mothers. Adverse reactions are observed in most patients taking Neotigazon; they usually disappear after reducing the dose or discontinuing the drug. It should be noted that at the beginning of treatment there is an increase in the symptoms of the disease. Our analysis of Neotigazon therapy for patients with BD showed that the most common side effects are: dry lips (n = 23; 100%), cheilitis and cracks in the corners of the mouth (n = 23; 100%); dryness and flaking of the skin (n = 23; 100%); dry mucous membranes (n = 23; 100%); hair loss (n = 12; 52%); feeling of thirst and dry mouth (n = 5; 21.7%); intolerance to contact lenses is less common (n = 3; 13%); conjunctivitis (n = 2; 8.6%), stomatitis (n = 2; 8.6%), nosebleeds (n = 1; 4.3%), rhinitis (n = 1; 4.3%); disturbance of taste (n = 1; 4.3%). These side effects are usually reversible and disappear after discontinuation of Neotigazon. If severe headaches, nausea, vomiting and visual disturbances occur, the drug should be immediately discontinued and the patient referred to a neurologist. The physician is required to monitor liver function before starting treatment with Neotigazon, every 1-2 weeks during the first month after starting treatment, and then every 3 months while taking a maintenance dose. During treatment with large doses of Neotigazon, a reversible increase in the level of triglycerides and serum cholesterol is possible, especially in patients at high risk (with lipid metabolism disorders, diabetes mellitus, obesity, alcoholism). If liver function does not return to normal, the drug must be discontinued. In this case, it is recommended to continue monitoring liver function for another 3 months.

In patients with diabetes, retinoids may improve or worsen glucose tolerance, so blood glucose levels should be checked more frequently than usual early in treatment.

Due to the risk of developing hypervitaminosis A, concomitant use of vitamin A and other retinoids should be avoided. Since both Neotigazon and tetracyclines can cause increased intracranial pressure, their simultaneous use is contraindicated. With the combined use of methotrexate and Neotigazon, there is a risk of developing hepatitis, so the use of these two drugs simultaneously is also contraindicated.

To reduce the toxic effect of Neotigazon on the body, adjuvant therapy is prescribed: hepatoprotectors, lipotropic agents and gastric enzymes, B vitamins, nicotinic and pantothenic acids. To reduce the risk of hyperlipidemia, foods rich in fat should be avoided during treatment.

According to various authors, alternative treatment methods may include Prednisolone (15–20 mg/day), Diprospan (2.0 IM once every 10 days No. 3) and cytostatics: Prospidin (50–100 mg IM daily per course 2.0–3.0 g) or Methotrexate (15 mg IM once every 7 days) [6, 11].

External treatment while taking retinoids is not of fundamental importance, but it significantly improves the general condition of the patient and increases his quality of life. Both classic ointments and creams and modern dry skin care products from various manufacturers are used. To eliminate massive horny deposits, ointments with 2–5% salicylic acid, 10% urea, and 1–20% malic acid are prescribed.

In addition, physical therapy is used to treat patients with BD. Basically, various baths are used: sulfide baths lasting 6–10 minutes every other day, 12–15 baths per course; positive radon baths for 10–20 minutes every other day; At home, it is possible to use starch baths: 300–500 g of potato starch are diluted in 2–5 liters of cold water and then poured into a bath at a temperature of 36–37 ° C, the duration of the procedure is 15–20 minutes every other day, the course is 15–20 procedures. In children, the duration of the procedure should not exceed 15 minutes; the course is 8–12 baths.

The question of the advisability of using ultraviolet irradiation (UVR) in such patients has not yet been resolved; the opinions of modern authors are contradictory and require further study [6, 12]. According to our observations, in all examined patients, ultraviolet radiation or insolation provoked an exacerbation of the process.

Thanks to the achievements of domestic and foreign science, in recent years there have been significant shifts in the understanding of the clinical and genetic polymorphism of hereditary skin pathology, knowledge in the field of pathomorphology and immunomorphology has significantly advanced, which has expanded the possibilities of accurate diagnosis of BD. The use of synthetic retinoids has made it possible to increase the effectiveness of therapy for this category of patients. However, treatment of BD is long-term and is always accompanied by the development of a number of side effects, which leads to limited possibilities for prescribing the drug to elderly people and patients with a complicated medical history.

Literature

1. Berenbein B. A., Studnitsin A. A. et al. Differential diagnosis of skin diseases. M.: Medicine, 1989. 672 p.
2. Elkin V.D., Mitryukovsky L.S. Selected dermatology. Rare dermatoses and dermatological syndromes. Handbook of diagnosis and treatment of dermatoses. Perm, 2000. 699 p.
3. Mordovtsev V.N. Hereditary diseases and malformations of the skin. M.: Nauka, 2004. 174 p.
4. Kalamkaryan A. A., Kubanova A. A., Akimov V. G., Arifov S. S. Devergie pilaris versicolor // Bulletin of Dermatology and Venereology. 1990, no. 6. pp. 20–23.
5. Kubanova A. A., Akimov V. G. Differential diagnosis and treatment of skin diseases: Atlas-reference book. M.: Medical Information Agency LLC, 2009. 304 p.
6. European guidelines for the treatment of dermatological diseases / Ed. A. D. Katsambasa, T. M. Lotti. M.: MEDpress-inform, 2008. 736 p.
7. Katunina O. R. Comparative immunomorphological characteristics of inflammatory infiltrate cells involved in a delayed-type hypersensitivity reaction in patients with psoriasis and Devergie's disease. Author's abstract. diss. Ph.D. honey. Sci. M., 2005. 20 p.
8. Suvorova K. N., Kuklin V. T., Rukovishnikova V. M. Pediatric dermatovenerology. Kazan, 1996. 441 p.
9. Kubanova A. A., Arifov S. S. Features of the clinical course of pityriasis ruber pilaris Devergi // Bulletin of Dermatology and Venereology. 1990, no. 7. pp. 59–61.
10. Rational pharmacotherapy of skin diseases and sexually transmitted infections: Hand. for practicing doctors, ed. Kubanova A.A., Kisina V.I.M.: Litera, 2005. 882 p.
11. Holliday AC, Megan NM, Berlingeri-Ramos A. Methotrexate: Role of Treatment in Skin Disease. // Skin Therapy Letter. 2013;18 (3).
12. Osorio F., Magina S. Phototherapy and Photopheresis // Expert Rev Dermatol. 2011;6(6):613–623.

A. A. Kubanov*, Doctor of Medical Sciences, Professor Yu. A. Gallyamova**, 1, Doctor of Medical Sciences, Professor

* FSBI SNTsDK MH RF, Moscow ** GBOU DPO RMAPO MH RF, Moscow

1 Contact information

Abstract. Diagnostics of Devergie pityriasis rubra pilaris criteria and approaches to treatment are presented in the article. Application of synthetical retinoids allows increasing effectiveness of therapy of such patients. But treatment of Devergie disease requires long time and is followed by development of several side effects that cause limitations for prescription of medicine to elderly people and to patients with compromised history.

Symptoms of pathology

Symptoms of ringworm appear 4-6 weeks after the patient becomes infected. A red spot appears on a smooth area of ​​skin of a child or adult. It rises above the surface and has smooth boundaries. Over time, the size of the lesion increases. The surface becomes covered with nodules, blisters and scabs. The spots develop into rings that can intersect or merge with each other. The diameter of skin formations ranges from 5 to 30 millimeters.

Signs of ringworm include an acute inflammatory reaction. It often develops in children and girls. The lesions begin to peel off intensively. Patients suffering from dermatitis do not immediately identify symptoms of microsporia. Areas of active fungal growth may appear as inflammatory skin lesions.

A common manifestation of ringworm in a child is damage to the scalp. This symptom affects patients aged 5-12 years. Older children experience changes in the chemical composition of sebum. Its elements become dangerous for the microsporia pathogen.

The suppurative type of ringworm is characterized by the appearance of soft nodules on the patient’s skin. The nodes are dotted with numerous abscesses. When they are compressed, purulent contents are released.

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Reasons for development

The main causes of ringworm are contact with the pathogen:

1. A child aged 4–11 years whose sweat reaction is predominantly alkaline.
2. A child or adult with reduced immunity, the presence of scratches, scabs, microtraumas that can become infected.

Most often the carrier is an animal, less often a person. Infection also occurs through objects or personal belongings on which infected hairs, hairs or skin scales remain. Infection is possible through undisinfected hairdressing tools, through soil on which the causative agent of the disease can persist for up to 3 months, during processing of hay. According to statistics, up to 70–80% of cases of the disease occur as a result of contact with stray young cats and kittens.

Diagnostic measures

Diagnosis and treatment of ringworm are carried out by a dermatologist. The doctor examines the patient and identifies typical manifestations of microsporia. Examination of skin scrapings under a microscope reveals fungal mycelium and changes in the structure of hair and skin. Differential diagnosis makes it possible to exclude trichophytosis from the patient’s history, which has similar manifestations upon microscopy of the patient’s biomaterials.

Microflora culture appears to be a more informative diagnostic technique. Laboratory staff determine the type and genus of fungi. Based on the laboratory report, the dermatologist selects drugs that will cure the patient.

Luminescent examination makes it possible to identify pathological lesions on the skin of the patient and those living with him. This diagnostic method is based on the green glow of the fungal mycelium under the influence of a gas-discharge light source.

Diagnostics

It is not difficult to make a primary diagnosis if you know what ringworm looks like. To clarify the diagnosis use:

• analysis of clinical data;
• results of luminescent analysis;
• microscopic studies;
• sowing material.

In some cases, the source of infection is difficult to determine, since the incubation period ranges from 2 to 45 days. Symptoms may appear on the head, neck, arms, legs, including the palms, soles of the feet, groin areas and folds. Fungal infection causes itching, discomfort in the area of ​​inflammation, and creates psychological discomfort.

Treatment

The combination of drugs prescribed to the patient depends on the severity of damage to the skin, nail plates and hair follicles. Antifungal therapy may be local or general. In the first case, a child or adult needs to use creams and ointments that suppress the activity of the microsporia pathogen. Drugs in this group are not recommended for use by girls during pregnancy and lactation. Topical sprays are effective in treating large areas of ringworm. Modern formulations do not leave stains on the skin and are not absorbed into the fabric of clothing.

A severe inflammatory reaction is treated with a combination of antifungal and hormonal drugs. Patients will have to apply ointment applications to the affected areas. After this, the skin is treated with iodine solutions. The oral tablet intake schedule is formed by a dermatologist based on the clinical picture of the pathology.

The addition of a secondary infection to microsporia involves the use of drugs based on betamethasone, gentamicin or clotrimazole.

Symptoms

Ringworm on the face and body appears in the form of pink or red circles raised 1-3 mm above the surface of the skin. The lesions are characterized by clear boundaries, while pale areas of skin with red dots are visible inside. These spots quickly increase in size. Their number is growing over time.

The skin inside the lesions becomes covered with a white crust, which peels and itches. Ringworm on the scalp is characterized by split hair and hair loss. As the number of lesions increases, they begin to connect and overlap each other. Ringworm on the body occurs with increased symptoms when the pathogen gets inside existing lesions, and new fungal rings form in them.

Preventive measures

Prevention of ringworm is based on regular medical examinations of children attending preschool educational institutions. Parents should talk to their children about the inadmissibility of contact with stray animals. An important preventive measure is compliance with personal hygiene rules by patients of all age groups.

When purchasing pets, you must visit a veterinarian. The doctor will examine the cat or dog and give recommendations on how to eliminate any health problems with the pet. Following your veterinarian's advice will help prevent microscopic outbreaks within your family.

What is pityriasis rosea and why is it called pink dandruff?

The content of the article

Pink dandruff (Pityriasis rosea - PR) is an acute inflammatory disease of unknown etiology, characterized by the appearance of skin rashes mainly on the torso and limbs. It is an erythematous, scaly disease. The disease occurs seasonally. The etiology is most likely viral. The most likely factor is herpes virus type 7 (HHV7).

Most cases (75%) involve people aged 10 to 35 years, although there have been reports of cases diagnosed in a 3-month-old infant and in an 83-year-old man. The disease occurs throughout the world without any particular racial predilection.

Pityriasis rosea is a disease for which patients visit a dermatologist with a frequency of up to 2% of all visits per year. Occurs mainly in spring and autumn; in summer the level of symptoms decreases significantly.

The disease affects more women than men in a 2:1 ratio. The duration of the disease is 6 to 8 weeks, but is highly variable.

Many names - one face. Symptoms of pityriasis rosea

The first description of the disease as "ringed roseola" dates back to 1798. Uch. Robert William defined the disease as irregularly shaped spots consisting of small thin scales that never coalesce into scabs and are not accompanied by redness or signs of inflammation.

Other names for this disease: erythema annulatum, tonsurans maculosus, Herba, roseola squamosa (Nicolas, Chapard), pink lichen (Wilson), pityriasis versicolor (Horand), pseudoexanthemata nitoexanthemata, roseola furfuracea herpetiformis (Behrend) - mainly determined the morphological features and variability individual spots.

Pityriasis rosea

Only in 1860, the French physician Camille Melchior Gibert gave the name, which lasted almost 150 years. He wrote: “There is only one thing that can be described under the name of pityriasis rosea, and the characteristic features of this pathology are: small, branched spots, very faintly colored, no larger than a fingernail, numerous and tightly fitting ... the disease usually lasts up to 6 weeks or 2 months... in young people... ". Pityriasis means "bran" or "fine husk" and rosea translates to "pink".

The symptoms of pink dandruff are indeed quite characteristic. First, a heraldic lesion (the so-called mother plate) appears on the skin, most often on the torso. Usually it is several centimeters of red or dark pink erythema, covered with scales inside.

After a few days (and sometimes weeks), much smaller skin lesions of similar morphology are seeded. The rash occurs symmetrically, mainly on the torso and neck. There are no changes in the mucous membrane. Usually the skin lesions do not cause itching.

Possible variations of the rash:

• urticarial form of RL – blisters appear instead of plaques;
• vesicular form of RP - rashes in the form of small bubbles with clear or cloudy liquids;
• papular form of RL – protruding, cavity-free formations.

How do you know if pityriasis rosea is going away?

After a course of therapy, the spots disappear without scarring. In place of the plaques, clean skin remains, possibly lighter. Over time, the color evens out. In patients with atypical lichen, ulcers may form.

Complications during self-medication:

• infection of affected areas with bacteria;
• suppuration, ulcers;
• hyperpigmentation.

Hyperpigmentation
To prevent this development of the disease, at the first symptoms of pityriasis rosea, it is recommended to make an appointment with a dermatologist.