Decalving folliculitis Kenko, as the cause of alopecia
Last reviewed: 19.10.2021
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Decalting folliculitis (synonym: sycosiform atrophic head folliculitis (folliculitis sycosiformis atrophicans capitis, Hoffmann E. 1931) was first described by Quinoquaud (ChE.E. 1889), a very rare dermatosis is a chronic bacterial folliculitis of the scalp that ends with an atrophic alopecia, decalvo, bald), other skin areas, especially those covered with bristly and long hair, may be affected.The same process described in the same years on the face, in the area of growth of the beard (sycosis lupoides, Brocq L., 1888), scarring sycosiform erythema (ulerythema sycosiforme, Unna P., 1889; ovkr (Greek) = ule (lat.) = scar), sycosiform atrophy folliculitis (folliculitis sycosiforme atrophicans barbae, Hoffmann E., 1931).
Thus, different scientists gave different names to the same dermatosis, in which the main, from their point of view, characteristic features were distinguished: chronic folliculitis, which has a similarity in the course and outcome with discoid lupus erythematosus (atrophy); erythema with sycosis-form manifestations and scarring; chronic folliculitis, similar to sycosis, but leading to atrophy. Already in the first descriptions of decalculating folliculitis and lupoid sycosis, common features for both dermatoses that determine their clinical manifestations were revealed: chronic folliculitis leading to high resistance to therapy without pustulization and ulceration to atrophy and persistent baldness. Differences are in the distribution of chronic folliculitis (folliculitis, grouped into small foci - in comparison with the large individual foci formed) and their preferential location (on the scalp or skin of the face). Later it turned out that in addition to facial skin, lupoid sycosis (LS) can affect both the scalp skin, as well as the skin of the pubic and axillary areas. Only many years later it became finally clear that the lupoid sycosis described by Brock is not an independent nosological form but duplicates the same disease - decalving folliculitis is a peculiar and rare clinical variant.
Causes of Decalvinating Folliculitis
The causative agent is Staphylococcus aureus, and colonization of hair follicles with gram-negative microflora is additionally possible. However, treatment with antibiotics with a wide spectrum of action gives only a temporary therapeutic effect, clearly limited by the duration of the course. This confirms the dominant role of the macroorganism, a change in its reactivity and a decrease in immune defense.
Pathogenesis
Predisposing to this dermatosis can be seborrheic condition, decreased resistance due to diabetes mellitus, chronic nephritis, dysproteinemia, other factors leading to suppression of the immune system. Cases of spontaneous cure of decalving folliculitis (DF) after removal of carious teeth complicated by periodontitis are described. Colonization of hair follicles by bacteria is in all probability only a pathogenetic link. Until now, the reason why chronic folliculitis ends with skin atrophy and persistent hair loss remains unclear. In patients with decalovirus folliculitis, or lupoid sycosis, modern research methods always manage to detect specific and significant disorders in the function of the immune system, internal organs and other body systems.
Symptoms of decalving folliculitis Kenko
Decalverting folliculitis usually occurs isolated on the scalp, mainly in the temporal and parietal regions, in the frontal region, lesions are located on the border of hair growth and resemble ophiasis. In some cases, axillary and pubic regions are also affected. Eruptions of inflammatory follicular nodules are less common - pustules usually do not cause subjective sensations and are therefore often seen. The magnitude of the elements rash ranges from pinhead to lentil. In the center, papular and pustular cells are permeated with unchanged or broken hair, and in their circumference a small corolla of hyperemia is seen. Characteristically extremely slow development of folliculitis; they last for a long time without noticeable dynamics and often do not end with the formation of pustules. Individual follicular pustules appear only after a long evolution of follicular papules ("secondary pustule" according to Mashkileyson LN, 1931). In the center of small grouped foci gradually forms a delicate cicatricial atrophy with persistent alopecia. When several nearby foci merge, larger foci of cicatricial alopecia form, within which individual hairs are sometimes retained. In the border zone, new follicular nodules and pustules, scales, crusts continue to appear, causing slow peripheral growth. Thus decalving folliculitis leads to the formation of different in size and shape foci of atrophic alopecia (pseudopelada state). The course of dermatosis is chronic, lasting for many years and even decades. At times, the number of new folliculitis appearing in the circumference of the foci of atrophic alopecia is reduced to a minimum. Dekulviruyuschy folliculitis of the scalp can be combined with foci of lupoid sycosis (LS) on the skin of the face or other localizations.
Lupoid sycosis affects mainly middle-aged and elderly people. The usual localization of one or two lesions of the medicine are the lateral surfaces of the hair-covered cheeks, whiskey, less often - the chin and upper lip (Milman IS, 1929). The lesion is more often one-sided and is located in the area of hair growth in the temporal region or on the cheek above the horizontal and ascending branches of the lower jaw. The focus of LS can appear isolated in the form of a large single lesion and on the scalp. Initially, on the background of hyperemia, grouping inflammatory follicular nodules and pustules appear on the same site, as well as small follicularly located light yellow crusts and grayish scales, which are easily removed when scraping. These elements merge and form a clearly limited round or oval inflammatory plaque 2-3 cm in diameter and larger, wine-red in color (as with erysipeloide) with a flat, painless infiltration in the base. Gradually, in its central part, the skin pales, thinens, becomes smooth, hairless and slightly sinks: a characteristic feature of the formed focus of lupoid sycosis - central atrophy develops. Within its limits, new rashes no longer arise and individual hair or tufts of hair growing from one or more follicles can be preserved. The peripheral zone of the focus, about 1 cm wide, is slightly elevated, more saturated with red, and moderately infiltrated. It contains numerous follicular papules with rare follicular pustules, some of which are perceived as vesicles. In the center of these elements are still preserved hair, some of which are broken off, as well as a significant number of easily removable follicular crusts and scales. The focus is slowly increasing in size due to the appearance in the peripheral zone of new folliculitis and individual follicular pustules. Sometimes the growth of the hearth prevails in one of its foci, which changes round outlines. With the diascopy of the edge of the focus, the symptom of "apple jelly" is not determined. The drug runs chronically for many months and years. Clinical manifestations of lupoid sycosis of the scalp are more smoothed. In the formed focus dominated by a smooth, hairless atrophic zone. In the peripheral hour, the raised cushion is absent, there are only individual, long-term folliculitis and pustules surrounded by a narrow corolla of hyperemia and also single small scales and crusts. Thus, on the scalp, the manifestations of lupoid sycosis and decalving folliculitis are virtually indistinguishable. The general condition of patients is not violated, subjective sensations are usually absent, complaints are limited only to a cosmetic defect.
Gistopathology
In the epidermis, a small focal hyperkeratosis, the unfurled horny masses, pronounced acanthosis. Cells of the thorny layer are dramatically changed, features in the lower rows, where there are signs of pronounced vacuolar dystrophy. The mouth of the hair follicles is considerably enlarged, made of horny masses. In the dermis, dense perivascular and perifollicular lymphohistiocytic infiltrate, less frequent are plasma mast cells and neutrophils. In some cases, the infiltrate is almost entirely composed of plasma cells. In the final atrophic stage, the pathomorphological picture differs little from the changes characteristic of the pseudo-pelagic state in the late stage.
Diagnosis of decalving folliculitis Kenko
On the scalp of the manifestation of the decalving folliculitis or lupoid sycosis, differentiate primarily with those diseases that manifest themselves with chronic folliculitis and follicular pustules and lead to a pseudo-peloid condition. Therefore, when the focus of atrophy is not formed in the central part of the atrophy, the AF (or LS) is differentiated from the mycosis of the scalp, including the scutulary of the favus form, vulgar sycosis, and later with necrotic acne, folliculitis and perifolliculitis abscessing and undermining Hoffmann's head, histiocytosis from Langerhans cells and erosive pustular dermatosis. Since follicular papules and tubercles on the scalp may resemble chronic folliculitis and pustules. Differentiate also with the follicular form of the red flat lichen, red lupus, lupus tuberculosis, lupoid form of leishmaniasis and tubercular syphilis. Essential aid in establishing the final diagnosis is the histological examination of typical elements of the rash (folliculitis, pustules, etc.) from the active peripheral zone of the focus.
Differential diagnosis with mycosis of the scalp. The reason for carrying out mycological examinations is the presence on the skin of the scalp of the scalp, altered hair, yellow scales-crusts, follicular pustules, inflammatory follicular nodules and nodes, purulent-bloody crusts with fragments of hair and foci of cicatrical alopecia of different sizes. In the presence of these manifestations, especially in children and elderly patients, it is advisable to exclude mycosis of the scalp. When examining other areas of the skin, attention is drawn to the condition of the nail plates of the hands and feet. It is necessary to carry out luminescent research of hair, microscopic and cultural research of the changed hair, skin and nail flakes, crusts, purulent discharge. The fastest and most informative is microscopic examination of altered hair (broken at the skin level, having the appearance of "black dots", and at a height of 3-5 mm, with a case at the bases, gray, dim, deformed in the form of "stained", "exclamation mark" ). Detection of fungal elements, elucidation of the characteristics of the damage to the hair allow the doctor to diagnose mycosis of the scalp and get an idea of the genus of the pathogen and the probable epidemiology of the disease.
From vulgar sycosis, lupoid sycosis (LS, or - DF) is distinguished by the dominance of long-term folliculitis, only a small part of which is completed by the formation of follicular pustules, the presence of 1 or 2 (with DF-more) clearly restricted foci with slow peripheral growth and the existence in them 2 zones (except foci on the scalp): a central, wide zone of cicatricial atrophy, and peripheral - narrow, serpiginiruyuschey in the form of a red cushion, where new folliculitis is formed. The characteristic localization of the drug is also another-the temporal region and the side surface of the cheek, the scalp and, much less often, the region of the chin and upper lip, which are favored for vulgar sycosis. It should also take into account the greater resistance of drugs (or DF) to treatment, compared with vulgar sycosis, as well as differences in the pathomorphological pattern. Important for clinical and histological diagnostics, the active peripheral zone with DF (or LS) of the scalp is poorly expressed and is represented only by individual folliculitis and follicular pustules. This decalting folliculitis, or lupoid sycosis, differs from many other dermatoses of the scalp, leading to a pseudo-peloid condition.
Decalverting folliculitis (or lupoid sycosis) of the scalp needs to be differentiated with necrotic acne (NU), or necrotic folliculitis of this localization. With a common primary voiding element (folliculitis) and a chronic course of these rare dermatoses, they differ in the localization and distribution of folliculitis, as well as in the tempo and peculiarities of their evolution. For DF, or LS, unlike necrotic acne, long-existing follicular papules 2-5 mm in diameter are characterized, which slowly transform into single pustules without central necrosis and dirty-brown necrotic caps. With DF, or LS, chronic folliculitis group, peripherally grow and merge without pustulization, central necrosis and itching, leading to the formation of smooth foci of atrophic alopecia (pseudo-pelpal state). With NU, for example, the favorite location is the forehead skin along the border of hair growth (a zone several centimeters wide and inside from the hair growth line), temporal areas, the back surface of the neck, rarely rashes can spread to the ears, nose, central areas of the chest and back. With necrotic acne folliculitis occurs in elderly people usually against the background of seborrheic status, accompanied by itching and quickly transformed into papulo-pustular, then into papulo-necrotic elements. They are always located in isolation, are delimited from each other, do not grow peripherally and therefore do not merge into larger foci. With NU, crimson-red follicular papules and papules-pustules 2-4 mm in diameter are rapidly necrotic in the center and covered with dirty brown necrotic crusts. They are tightly attached, long-lasting, so they dominate in clinical manifestations and are most characteristic of necrotic acne, or necrotic folliculitis. After leaving the crusts on the skin, there are isolated stamped, ossicular-like scars that resemble the scars after papulonecrotic tuberculosis or grouped tubercular syphilis. On the scalp, the scars after NU are subtle and do not lead to the formation of rapidly detectable foci of cicatricial atrophy. There are also histological changes in these dermatoses. A feature of the histological picture with necrotic acne is the location of the granulocyte abscess inside the follicle with necrosis of the epithelium of the funnel of the hair follicle. Perifollicular infiltrate consists of neutrophils, lymphocytes and mast cells, in the peripheral inflammatory zone there are thromboses of the vessels.
The initial manifestations of folliculitis and perifolliculitis abscessed and undermining Goffmann (FPAP) of the scalp may resemble decalvulatory folliculitis (DF, or lupoid sycosis). However, with established clinical manifestations, these dermatoses have little similarity, which is limited only by chronic inflammation of the hair follicle and a prolonged persistent course leading to cicatrical alopecia. The depth of the lesion, inflammatory changes in the area of the hair follicle, the main vyplypnoy element and its evolution are different. With DF (or LS), superficial chronic folliculitis of the scalp is grouped and merged into foci without pustulization, without the formation of subcutaneous abscessing nodes and without the formation of fistulous holes with purulent-bloody discharge and crusts. In the central, largest in the area, the focus zone forms a smooth, shiny, thin atrophic scar (the state of the pseudo-pancake). Follicular papules with individual pustules and corolla of hyperemia in their circumference predominate in the focal zone of the focus, as well as easily separating scales and crusts. In FPAP, in contrast to DF (or LS), the deepening nodes are from 0.5 to 1.5 cm in diameter, which merge, abscess and perforate tissues. They arise as a result of the evolution of deep abscessing and undermining folliculitis and perifolliculitis. With abscessing of nodes, numerous subcutaneous fistulas are formed, which, as it were, undermine the skin and open on the surface with numerous apertures. At pressure on the infiltrated site with a bumpy surface of several fistulous holes separated from each other, a purulent and bloody discharge is identified that is considered characteristic of this rare dermatosis. It is noteworthy that the penetrating lesion (deep to the tendon helmet) is not accompanied by pronounced hyperemia of the skin of the scalp and remains slightly painful. FPAP occurs only in men aged 20-30 years with marked seborrheic status. In a number of cases, this dermatosis is combined with globose and inverse acne. After scarring of individual foci of FPAP, not only atrophic alopecia remains, but also hypertrophic, uneven scars, especially in the occipital region.
In some cases, histiocytosis from Langerhans cells of the scalp is clinically very similar to the manifestation of devalued folliculitis, or lupoid sycosis, of this localization. These diseases proceed chronically, steadily progressing and lead to the state of the pseudo-peloid, within which the characteristic manifestations of the preceding dermatosis do not persist. In some patients, the lesions of the scalp with histiocytosis are isolated, but more often it is a fragment of systemic changes caused by the proliferation of Langerhans cells in the skin and visible mucous membranes or proliferation of macrophages in other tissues (in the bones, central nervous system, liver, intraorbital, ). In these cases, in addition to the common manifestations of histiocytosis on the skin (they may also recall the manifestations of other dermatoses: Darya's disease, decalving folliculitis, necrotic acne, etc.), there are other characteristic manifestations of this very rare disease. Thus, the most common lesions are lung lesions, foci of destruction in the bones (especially the skull), damage to the posterior lobe of the pituitary gland (which is manifested by symptoms of diabetes insipidus), exophthalmus caused by retrobulbar infiltration of fatty tissue, infiltration and gingival edema, ulceration, loosening and loss of teeth). In some cases, clinical manifestations of DF and histiocytosis of the scalp are very similar.
With a great similarity of the clinical manifestations of these dermatoses on the scalp, it is possible to identify individual symptoms that are not characteristic of DF. The most significant difference is the presence in the histiocytosis of the skin of the scalp in the active zone of papulo-pustular and pustular elements that are not associated with the hair follicles, as well as individual surface erosions and ulcers of the elongated form that are revealed after the removal of the crusts. These painless surface defects have an elongated shape (up to 0.5 cm in width and up to 1 cm in length), an uneven surface and several protruding above the skin level. The evolution of these elements leads to the development of areas of skin atrophy of varying size and shape, located in the circumference of a continuous atrophic foci of alopecia, sometimes in the form of laces, which causes: significant rarefaction of hair in this zone. Perhaps, in some patients DF. Which was diagnosed without histological confirmation.
Apart from decalting folliculitis (DF), discoid lupus erythematosus also leads to the pseudopelada state . In the active stage, dermatoses differ in different types of primary vysypnogo element. In DF, the primary voiding element is a small follicular inflammatory papula (2-5 mm in diameter), the evolution of which does not always result in the formation of a follicular pustule. In the center, these elements permeate the hair (sometimes broken), and in the circumference there is a narrow corolla of hyperemia. Scraping of rashes does not cause severe soreness, and grayish scales and light yellow follicles are easily separated from the affected surface. In the central part of the focus there is a superficial atrophy of the skin with hair loss without the formation of new rashes within it. DF is characterized by a long, chronic course outside the connection with the season and the absence of exacerbations after insolation. The lesion is more often isolated, without foci in other localizations. In typical cases of discoid lupus erythematosus, the primary efflorescence is an inflammatory spot that transforms into a plaque with hyperkeratosis, leading to atrophy. On its surface there are firmly attached hyperkeratotic scales with unevenly located horn corks. Scraping foci is painful, scales are separated from the surface with difficulty. On the periphery of the growing foci there is a hyperemic corolla, and in the center comparatively fast develops skin atrophy with telangiectasias and hair loss. Relapses of dermatosis often occur on old atrophied areas of the skin. In addition to scalp, the centers of lupus erythematosus usually appear on the auricles, the back of the nose, the cheekbone part of the cheeks, etc. With these dermatoses, the histological changes in the lesions are also significantly different.
Dekulviruyuschy folliculitis (or lupoid sycosis) differs from follicular decalcifying red depriving the appearance of the primary vysypny element, which can be seen only in the active stage of the disease. At the edges of the focus of atrophic alopecia in AF there are small follicular inflammatory papules with a long evolution leading to single follicular pustules. The defeat of the scalp with these dermatoses is usually isolated, occasionally lupoid sycosis (or DF) can also affect the temporal region and the lateral surface of the cheeks. In follicular decalcifying red lichen, the primary voiding element is a small, follicular, conical papule with a horn spinule in the center, leading to atrophic alopecia. Detection in other areas of the skin (including axillary and pubic regions), on the mucous membrane of the mouth and nails characteristic for red flattened lesions facilitates a preliminary diagnosis. It is important to confirm it with the help of a histological examination of the affected skin; Pathomorphological changes in these dermatoses have been previously reported.
From the lupous tuberculosis of the skin (serpiginating form), the focus of the decalting folliculitis (DF, or lupose sycosis-LS) is distinguished by the primary element of the rash. Lupose tuberculosis (LT), which rarely affects the scalp, is characterized by flat merging tubercles, yellowish-red, soft consistency with a positive symptom of "apple jelly" with diascopy. Bumps are not associated with hair follicles, there are also no pustules. With DF (or LS) in the nocturnal area of the focus around follicular papules and single pustules, hyperemia is more pronounced in the form of a narrow border, and in the central zone there is a smooth, superficial atrophy of the skin with alopecia without new active rashes. When LT, which is often localized on the face, against the background of skin atrophy, there are fresh tubercles (relapses on the rumen), it is also possible their ulceration, which does not happen with DF (or LS). Dermatoses have a different histological pattern. Intrafollicular microabscesses and perifollicular, predominantly lymphohistiocytic infiltrates in the dermis are characteristic of DF. With LT, the tubercle granuloma lies in the dermis and consists of clusters of epithelioid cells with foci of necrobiosis, several giant cells located among the epithelioid, and the shaft of lymphoid cells in the circumference.
Skin of the scalp is almost not affected by leishmaniasis, since the hair covering protects against mosquito bites. However, at the borderline of hair growth, infection and the development of late ulcerative (anthroponous) leishmaniasis, cutting - severely necrosisable (zoonotic) type, and even less frequent - chronically leupoid (tuberculous) leishmaniasis of the skin (LLK) can occur. All forms of the disease lead to scar formation and persistent baldness within it. The manifestations of the lupoid form of skin leishmaniasis may resemble the focus of decalving folliculitis (or lupoid sycosis). When differentiating, it is necessary to determine the type of primary vysypny element, find out from the anamnesis of residence earlier in endemic for leishmaniasis places and transferred in the past leishmaniasis of the skin. In contrast to DF (LS), for LLK characterized by small yellowish-brown tubercles, not associated with hair follicles and arising around the scarring or healed leishmanioma. The bumps are usually located on the face and the size, color, consistency and positive symptom of the "apple jelly" are completely identical to the clinical manifestations of the flat shape of the lupoid skin tuberculosis. Therefore, DF (LS) otherwise differentiate with lupoid leishmaniasis of the skin in the same way as with lupous tuberculosis. With the help of histological examination, LLK is detected with granuloma, but a small number of pathogens with this rare form of the disease makes diagnosis difficult. It is possible to detect leishmania in the LLK lesion with repeated bacterioscopic studies of thin smears prepared from scrapes of tubercle tissue and stained using the Gimza-Romanovsky method.
From the serigyning tubercular syphilis of the scalp (BS), the decalving folliculitis (or LS) is distinguished by a primary voiding element and its different evolution. At DF in the peripheral zone of the focus there are small (2-5 mm) inflammatory follicular papules and individual follicular pustules, scales, crusts. In the tubercular serigiviruyuschem syphilide in the peripheral part of the focus are visible tubercles the size of lentils, dark red, smooth, hemispherical, dense, not associated with hair follicles. At the edges of the hearth, they are closely grouped and merge, some of them ulcerate, forming round And oval ulcers with cylindrical. Steeply breaking edges, greasy bottom or bloody crusts on the surface. Such manifestations do not occur with DF (or LS), as well as the continuous, uneven, cellular atrophic cicatrix with scalloped outlines and pigmentation along the periphery remaining after suture scarring. There are also pathomorphological changes in the lesions. With tubercular syphilidae, in contrast to DF, a granulomatous infiltrate is found in the dermis.
Erosive pustular dermatosis head knives is a very rare disease of unexplained etiology, described recently in old women. Dermatosis has a prolonged chronic recurrent course and also leads to a pseudo-peloid condition. However, the clinical manifestations of EPD and DF differ. Thus, with EPD, flat pustules appear on the scalp that are not associated with hair follicles, erosive and ulcerative skin defects and purulent-bloody crusts. It should also be taken into account that DF, or drugs, are ill after puberty both women and men. The pathomorphological picture of these dermatoses is also different. Unlike intra-follicular microabscesses with perifollicular and perivascular lymphobstiocytic infiltrates in the dermis, characteristic for DF, with EG, nonspecific inflammation in the dermis is accompanied by necrosis of the epidermis and its appendages, acanthosis and subcorneal pustules. The dermal infiltrate is dominated by plasma cells; In the initial phase there are signs of leukocytoclastic vasculitis. However, direct immunofluorescence is usually negative.
Treatment of patients with decalovirus folliculitis
Patients with suspected decalculating folliculitis (or lupoid sycosis) should be examined in detail to verify the diagnosis (including biopsy of the affected skin) and to elucidate the specific pathogenesis of reduced resistance (chronic foci of infection, decompensated diabetes mellitus, chronic nephritis, dysproteinemia, etc.). General and external treatment of patients with this dermatosis is fundamentally little different from the treatment of vulgar (staphylococcal) sycosis. Prescribe systemic antibiotics, taking into account the tolerability of patients and the sensitivity of the bacterial flora. Antiseptic, disinfectant antimicrobial agents are applied topically: 0.1% chlorhexidine bigluconate solution, dioxidine solution, 0.01% myramistin solution, Fukortzin solution, as well as 2% mpyrozin or 10% mafenide in the form of ointment, etc. In the active peripheral zone focuses hair removal from the affected hair follicles. If the effectiveness of these drugs is insufficient, the use of combined antibiotics with glucocorticosteroid in the form of a spray, lotion, and cream is indicated. Treatment is prescribed to patients with exacerbations, spend it for a long time, with courses, with a change of drugs. Now almost do not appoint X-ray therapy, which was used before with a good, though not always long, therapeutic effect on the lesions. Comparison of the pictures-copies of the foci in the dynamics makes it possible to determine the progression of the disease in a timely manner and to prescribe rational therapy.
Tactics of a doctor with a pseudo-pellet
When examining a patient with a pseudo-peloid, the first task is to establish a nosological form of dermatosis, which led to focal atrophic alopecia. It is rational at first to exclude those diseases that most often lead to the condition of the psedopelada: atrophic forms of red flat lichen, discoid or disseminated lupus erythematosus, scleroderma, decalving folliculitis, atrophic forms of mycosis of the skin, etc. On the way to the diagnosis of a doctor, difficulties due to a number of objective factors . So, in a number of cases, active manifestations of dermatosis on the skin of the scalp are missing or little informative. This may be due to the onset of remission of the disease or hidden ("smoldering") of its course. With the primary damage to the deep layers of the dermis of the scalp, inflammatory changes on the surface of the skin are not noticeable. Therefore, the characteristic manifestations of different atrophying dermatoses in this localization are smoothed, which causes a decrease in their clinical differences. A common and dominant eruption is focal atrophy of the skin with baldness. This objectively makes it difficult to diagnose dermatosis, which led to the development of pseudo-pancreas, especially in cases where it is limited to the scalp.
To establish the diagnosis, you need anamnesis data, an objective examination not only of the scalp, but also of the rest of the skin surface, as well as hair, nails, visible mucous membranes and laboratory examination (primarily mycological and histological). Based on the history of the patient's age, in which focal atrophic alopecia was observed. So. The existence of a skin defect on the scalp from birth and the absence of progression in the future, allow one to suspect a developmental flaw - congenital aplasia of the skin. Some genodermatosis often occurs in children and can lead to a pseudo-peloid condition (for example, congenital and vulgar ichthyosis, congenital bullous dystrophic epidermolysis, pigment retention (in girls), or Simens' follicular keratosis (in boys), etc.
When examining the affected skin of the scalp, special attention is paid to the zone bordering with the atrophic focus of alopecia, as well as to the remaining bundles of hair in the region of the pseudo-peloid. In the active stage of the disease in these areas, you can find a typical primary element of the rash and secondary rashes. The doctor must consistently establish the morphology of the primary and secondary elements of the rash and their characteristics (color, size, shape, connection with the hair follicle, the presence of a horn spine in the center, possible hair changes, etc.). In cases where the primary voiding element can not be detected, it is important to investigate secondary eruptions (erosions or ulcers, crusts - purulent, bloody, serous or necrotic, etc.), which are the consequence of the evolution of the primary element and therefore indirectly help in its determination. Taking into account the type of the primary element of the rash, differential diagnosis is performed among dermatoses, which are manifested by the same or similar rashes (see the algorithms for diagnosing dermatoses that lead to the pseudo-peloid state).
After the objective study of the pseudo-peloid area and the formation of a preliminary opinion on the genesis of the initial dermatosis, the doctor proceeds to a thorough examination of the patient. Examine the entire surface of the skin, the condition of its appendages and visible mucous membranes. If there are rashes in other locations (except the scalp), their morphology and nosology are consistently established. Atrophic dermatoses retain their characteristic clinical features outside the scalp. This applies equally to pathological changes in the skin. Depending on the clinical manifestations, the necessary laboratory tests (mycological, bacteriological, histological, immunological, etc.) are carried out.
In most cases, the condition of the pseudo-pellet and skin lesions in other locations are caused by the same dermatosis. Therefore, clarifying the morphology and nosology of the rashes on smooth skin (or mucous membrane) practically predetermines the diagnosis of the underlying disease that led to the pseudo-peloid. In each case of the progressive pseudo-pellet, a histological examination of the affected skin is necessary, since only on the basis of the clinical picture is it possible to establish a reliable diagnosis unrealistically. A skin biopsy is advisable to do in a zone where there are characteristic primary elements of the rash. The conclusion about the pathomorphological structure of the primary vysypny element is an important and decisive link in the verification of diagnosis.