Violations of skin pigmentation (vitiligo, albinism, melasma): causes, symptoms, diagnosis, treatment

Distortions of pigmentation can be primary, as well as secondary, arising at the site of resolved primary vysypnyh elements (papules, pustules, vesicles, blisters).

Primary hyperpigmentation may be limited (melasma, freckles) or have a generalized character. Common hyperpigmentation is observed in Addison's disease (bronze skin tone), diseases of the hepatobiliary system (skin color from straw-yellow to dark-yellow and olive), chronic intoxications, chronic protein deficiency and vitamin B12 (hyperpigmented spots of dirty brown color on skin of the trunk, hypermelanosis around the small joints of the hands in combination with premature graying of the hair).

In general, pigment disorders are divided into epidermal depigmentation (leukoderma), epidermal hyperpigmentation (melanoderma) and color change to gray or blue (ceruloderma). Each of the listed violations are divided into primary and secondary.

The primary epidermal depigmentations include vitiligo, albinism, chronic idiopathic drop-shaped hypomelanosis (see photoaging ), and other diseases. Among secondary leukoderma, depigmentation is indicated after acute and chronic inflammatory dermatoses (allergic dermatitis, eczema, atopic dermatitis, psoriasis, etc.), after burns and injuries, post-parasitic and syphilitic leukoderma. Secondary depigmentation may occur after the use of hydroquinone (confetti-like leukoderma), against the background of long-term and uncontrolled therapy with topical glucocorticosteroids, in contact with the salts of mercury, rubber, sandalwood oil.

Primary melanoderma include melasma, freckles, lentigo, nevus Becker, some photodermatoses, and to secondary - hyperpigmentation after acute and chronic inflammatory dermatoses, cryodestruction, laser destruction, dermabrasion, sclerotherapy of veins, etc.

To primary ceruloderma include neva Ota and Ito, melasma, melilosis Ryla and other diseases. Secondary ceruloderma may occur after a number of chronic inflammatory dermatoses (eg, red flat-borne lichen), against the background of taking certain medications (eg, fixed sulfanilamide erythema).

Epidermal depigmentation can be associated with a decrease in the number or absence of melanocytes (melanocytopenic) or with a decrease or lack of melanin synthesis (melanopenic). The causes of melasma and ceruloderma are an increase in the production of melanin or the amount of melanocytes. With secondary cerulodermia, it is also possible to deposit hemosiderin in the dermis.

Vitiligo

Vitiligo is a chronic progressive disease of unclear etiology, manifested by the formation of depigmented spots in different parts of the skin and associated with the destruction of melanocytes. Etiology and pathogenesis are not known. They are referred to primary melanocytonic depigmentation. For the development of the disease, hereditary predisposition and the effect of provoking factors (stress, trauma, sunburn) are important. It is believed that the cause of the development of vitiligo is the destruction of melanocytes by toxic precursors of melanin or lymphocytes. It is known that antibodies to normal melanocytes are detected with vitiligo. The debut of vitiligo is observed at 10-30 years of age.

Symptoms of Vitiligo

Characterized by the appearance of rounded, oblong and irregularly shaped spots with clear boundaries, milky white, ranging in size from 5 millimeters to several centimeters. Due to peripheral growth, the spots can merge and reach large sizes, up to complete depigmentation of the skin. Most spots are localized around the mouth, eyes, extensor surfaces of limbs, around the elbows and knee joints, on the hands, underarms, lower back, genital area. Some depigmented spots may appear perifollicular. Perhaps a linear (zosteriform) location of the rash along the nerve. The disease can be accompanied by depigmentation of the hair (leukotrichia) in the affected area.

Diagnosis of vitiligo

Diagnosis of vitiligo is based on history, a typical clinical picture and a histological examination of the skin, in which the absence of melanocytes in lesions is detected, as well as in the examination in the rays of a lamp under a Wood filter.

Differential diagnosis of vitiligo is carried out with syphilitic leukoderma, post-parasitic leukoderma with pityriasis, sclerotrophic lichen, depigmented foci of cicatricial atrophy after discoid and disseminated lupus erythematosus, incomplete albinism, drug leukoderma and other dermatoses.

[1]

Treatment of vitiligo

Treatment and prevention of vitiligo - adequate photoprotection, the use of special masking cosmetics. Use local photochemotherapy, electrophoresis with a solution of copper sulphate on the lesions, preparations that stimulate melanogenesis. Scientific developments of recent years have shown the effectiveness of transplantation into the affected area of its own melanocytes. Systemically prescribed vitamins of group B, preparations of zinc, iron.

Albinism

Albinism is a hereditary dermatosis associated with a disruption of tyrosinase synthesis and is manifested by depigmentation of the skin, eyes and hair.

They are referred to primary melanopenic depigmentation.

[2]

The causes and pathogenesis of albinism

It was found that albinism is caused by a disruption in tyrosinase synthesis, which is necessary for normal melanogenesis. There are total and incomplete albinism. Total albinism is inherited autosomally-recessively, manifests itself immediately after birth and is characterized by depigmentation of the entire skin, hair and eye membranes. Incomplete albinism is congenital, inherited by an autosomal dominant type.

Symptoms of albinism

Depigmented spots are localized in limited areas of hands and feet, as well as on the skin of the trunk. Typically, the appearance of white strands of hair on the head in front. Eye color may not vary.

Differential diagnosis is carried out with vitiligo, depigmentation after chronic inflammatory dermatoses.

Treatment and prevention of albinism

Using sunscreen products with maximum protection against ultraviolet rays A and B, beta-carotene inside at a dose of 30-60 mg three times a day.

Melasma

Melasma (from the Greek, melas - black), or chloasma, - acquired uneven pigmentation in the face and, rarely, the neck.

Causes and pathogenesis of melasma

The main factors contributing to the development of melasma are ultraviolet irradiation and genetic predisposition. Essential role is played by the hormonal background. So, natural and synthetic estrogens and progesterone are involved in the pathogenesis of melasma when it appears during pregnancy, when taking oral contraceptives, in the perimenopause and in ovarian tumors. Melanocyte-stimulating hormone does not matter in the development of this disease. Important in the emergence of dermatosis is also considered the use of photosensitizing agents that make up the composition of external cosmetic preparations and the ingestion of certain photosensitizers.

[3], [4], [5], [6]

Symptoms of Melasma

When melasma affects mainly the skin of the face and neck, the mucous membranes are not involved in the process. Women are more often ill. The rashes are characterized by uneven pigmentation of brownish-yellow color in the central part of the forehead, above the upper lip, chin, cheeks and cheekbones, in the angle of the lower jaw.

Depending on the location of the rash, three clinical forms of melasma are distinguished:

1. centrofacial - pigmentation is localized in the region of the central part of the forehead, on the cheeks, upper lip, dorsum of the nose and chin.
2. molar - the pigmentation is localized in the region of the cheeks (in the projection of molars) and the nose;
3. Mandibular - the pigmentation is localized in the angular region of the lower jaw.

Diagnosis of melasma

When diagnosing melasma, it is extremely important to examine the skin with a Wood filter. This technique allows the doctor to determine the depth of the process, develop tactics and predict the results of further treatment, as the external changes on the skin detected by examination under the Wood luminescent lamp correlate with the histological data. Based on the examination, one of the three histological types of melasma can be diagnosed.

[7], [8]

Epidermal type of melasma

With this type of lesions become more vivid and contrast when viewed under a fluorescent lamp Wood. It is this phenomenon that is associated with the predominant localization of melanin in the epidermis. This type is prognostically most favorable.

[9], [10], [11], [12]

Dermal type of melasma

When viewed in the rays of a fluorescent lamp under a Wood filter, the pigmentation does not increase, its contrast with the surrounding unaffected skin does not become more pronounced. This type corresponds to the predominant localization of melanophages within the dermis, which indicates an unfavorable prognosis in treatment.

[13], [14]

Mixed type of melasma

With this type, some areas become brighter and more contrasting, and some - vice versa. Accordingly, the localization of the pigment both in the epidermis and in the dermis. Adequate therapeutic tactics can only lead to partial regression.

Differential diagnosis of melasma should be carried out with secondary hyperpigmentation (for example, after simple dermatitis from sunburn, peeling, etc.), Sivatta poikiloderma, dermatitis, Ryll melanosis, poikiloderma skin lymphoma, Ota nevus, pigment xeroderma and a number of other dermatoses.

Treatment of melasma

It is necessary to find out individually what factor was not available in the development of the disease. It is recommended to stop taking oral contraceptives, a detailed examination of a gynecologist-endocrinologist. There is also a study of liver function, the appointment of hepatorotectors (vitamin E, essential). Obligatory effective photoprotection using sunscreens with maximum protection against ultraviolet rays A and B. Patients are advised to wear hats, avoid sun exposure, especially from 10 am to 16 pm (even with adequate photoprotection), to refuse visits to the solarium. These measures aimed at reducing the exposure of UFOs, especially should be observed during pregnancy and during the first months after childbirth. For external therapy, use long courses of azelaic acid, topical retinoids, benzoyl peroxide, ascorbic acid, resorcinol (gamma Iklen, Merk Medikasion Familihal), chemical peelings with hydroxy acids (alpha, beta and polyhydroxy acids) or trichloroacetic acid, hydroquinone and other drugs . A good cosmetic result can be given by laser skin resurfacing, photorejuvenation and dermabrasion. Inside with the goal of inhibiting the formation of melanin is prescribed ascorbic acid (vitamin C) and tocopherol (vitamin E).

Prevention of melasma

Prevention of the disease includes effective photoprotection In pregnant women, women taking oral contraceptives, and the perimenopause period, as well as in individuals with hereditary predisposition to melasma.

Nevus Becker

Nevus Becker is a non-melanoma pigmented formation.

Causes of Becker nevus

Causes and pathogenesis are not known. It occurs in 0.5% of men in the population. In women, it is rare and can be combined with various stigmata of disembriogenesis (hypoplasia of the breast, spina bifida, etc.).

[15]

Symptoms of nevus Becker

The onset of the disease in adolescence. A focus of light brown color on the skin of the shoulder, front surface of the thorax, back is characteristic. Rarely affects the skin of the face and neck. The hearth has, as a rule, a linear or segmental arrangement. In the future, dark hair appears on the background of the spot. Histologically, an increase in the amount of melanin in melanocytes is revealed, there are giant melanosomes, there may be an increase in the number of melanocytes. Sometimes a large number of smooth muscle cells are detected (in this case, the formation is diagnosed as a smooth muscle gammarth).

Diagnosis of nevus Becker

The diagnosis is made on the basis of a characteristic clinical picture. Differential diagnosis is carried out with a giant pigmented nevus, nebulized nebulis, "coffee and milk" spots in Recklinghausen's disease.

[16], [17], [18]

Treatment of nevus Becker

Traditional methods of bleaching, peeling, laser-construction, dermabrasion give, as a rule, a negative aesthetic result. Recommend camouflage.

Nevus Ota and Ito

Nevus Ota and Ito belong to the primary ceruloderma. Nevus Ota (dark blue ophthalmic-maxillary nevus) and Ito are described in the middle of the last century by the Japanese. However, they can also occur in people of other nationalities.

The causes of nevuses Ota and Ito

Causes and pathogenesis are not known.

Symptoms of nevuses Ota and Ito

The disease begins in childhood or adolescence. Characteristic grayish-blue pigmentation with fuzzy boundaries on the coca of the temporal region and eyelids (nevus Oga) or in the brachiocephalic region - along the neck and shoulder (nevi Ito), asymmetric. With nevus Ota lesions on the skin are combined with ocular hypermelanosis - grayish staining of the sclera of the eye. Histologically, melanocyte-rich melanocytes, which have processes, are revealed in the dermis.

Diagnosis of nevuses Ota and Ito

Clinical diagnosis is not difficult. Differentiate from post-traumatic hematoma, melasma, fixed erythema.

[19], [20], [21], [22]

Treatment of nevuses Ota and Ito

Recommend cryodestruction, laser destruction, microdermabrasion. Due to the incomplete effectiveness of these methods, dermatological camouflage is shown.