Skin pigmentation disorders (vitiligo, albinism, melasma): causes, symptoms, diagnosis, treatment

Pigmentation disorders can be primary or secondary, occurring at the site of resolved primary rash elements (papules, pustules, vesicles, blisters).

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

In general, pigment disorders are divided into epidermal depigmentation (leukoderma), epidermal hyperpigmentation (melasma), and discoloration to gray or blue (ceruloderma). Each of these disorders is divided into primary and secondary.

Primary epidermal depigmentations include vitiligo, albinism, chronic idiopathic guttate hypomelanosis (see photoaging ) and other diseases. Secondary leukodermas include depigmentation after acute and chronic inflammatory dermatoses (allergic dermatitis, eczema, atopic dermatitis, psoriasis, etc.), after burns and injuries, postparasitic and syphilitic leukoderma. Secondary depigmentation can occur after the use of hydroquinone (confetti-like leukoderma), against the background of long-term and uncontrolled therapy with topical glucocorticosteroids, upon skin contact with mercury salts, rubber, sandalwood oil.

Primary melasma includes melasma, freckles, lentigo, Becker's nevus, some photodermatoses, and secondary melasma includes hyperpigmentation after acute and chronic inflammatory dermatoses, cryodestruction, laser destruction, dermabrasion, vein sclerotherapy, etc.

Primary ceruloderma includes nevi of Ota and Ito, melasma, melanosis of Riehl and other diseases. Secondary ceruloderma can occur after a number of chronic inflammatory dermatoses (for example, lichen planus), against the background of taking certain medications (for example, fixed sulfanilamide erythema).

Epidermal depigmentation may be due to a decrease in the number or absence of melanocytes (melanocytopenic) or to a decrease or absence of melanin synthesis (melanopenic). The causes of melasma and ceruloderma are an increase in melanin production or the number of melanocytes. In secondary ceruloderma, hemosiderin deposition in the dermis is also possible.

Vitiligo

Vitiligo is a chronic progressive disease of unclear etiology, manifested by the formation of depigmented spots on different areas of the skin and associated with the destruction of melanocytes. The etiology and pathogenesis are unknown. It is classified as a primary melanocytonic depigmentation. Hereditary predisposition and the action of provoking factors (stress, trauma, sunburn) are important for the development of the disease. It is believed that the cause of vitiligo is the destruction of melanocytes by toxic melanin precursors or lymphocytes. It is known that antibodies to normal melanocytes are found in vitiligo. The onset of vitiligo is observed at the age of 10-30 years.

Symptoms of Vitiligo

The appearance of round, oblong and irregularly shaped spots with clear boundaries, milky white in color, ranging in size from 5 millimeters to several centimeters is characteristic. Due to peripheral growth, the spots can merge and reach large sizes, up to complete depigmentation of the skin. Most often, spots are localized around the mouth, eyes, on the extensor surfaces of the limbs, around the elbow and knee joints, on the hands, in the armpits, lower back, and genital area. Some depigmented spots can occur perifollicularly. Linear (zosteriform) arrangement of rashes along the nerve is possible. The disease can be accompanied by depigmentation of hair (leukotrichia) in the affected area.

Diagnosis of vitiligo

Diagnosis of vitiligo is based on anamnesis data, typical clinical picture and histological examination of the skin, which reveals the absence of melanocytes in the lesions, as well as examination under a lamp with a Wood's filter.

Differential diagnostics of vitiligo is carried out with syphilitic leukoderma, postparasitic leukoderma in pityriasis versicolor, scleroatrophic lichen, depigmented foci of cicatricial atrophy after discoid and disseminated lupus erythematosus, incomplete albinism, drug-induced leukoderma and other dermatoses.

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Treatment of vitiligo

Treatment and prevention of vitiligo - adequate photoprotection, use of special masking cosmetics. Local photochemotherapy, electrophoresis with copper sulfate solution on the lesions, drugs that stimulate melanogenesis are used. Scientific developments in recent years have shown the effectiveness of transplanting one's own melanocytes into the affected area. Vitamins of group B, zinc and iron preparations are prescribed systemically.

Albinism

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

It is classified as a primary melanopenic depigmentation.

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Causes and pathogenesis of albinism

It has been established that albinism is caused by a disruption in the synthesis of tyrosinase, which is necessary for normal melanogenesis. A distinction is made between total and incomplete albinism. Total albinism is inherited in an autosomal recessive manner, manifests itself immediately after birth and is characterized by depigmentation of the entire skin, hair and eye membranes. Incomplete albinism is congenital, inherited in an autosomal dominant manner.

Symptoms of Albinism

Depigmented spots are localized on limited areas of the arms and legs, as well as on the skin of the trunk. The appearance of white strands of hair on the head in front is typical. Eye color may not change.

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

Treatment and prevention of albinism

Use of sunscreens with maximum protection from ultraviolet rays A and B, beta-carotene orally in a dose of 30-60 mg three times a day.

Melasma

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

Causes and pathogenesis of melasma

The main factors contributing to the development of melasma are ultraviolet radiation and genetic predisposition. Hormonal levels play a significant role. Thus, natural and synthetic estrogens and progesterone are involved in the pathogenesis of melasma when it appears during pregnancy, when taking oral contraceptives, during perimenopause, and with ovarian tumors. Melanocyte-stimulating hormone is not important in the development of this disease. The use of photosensitizing agents included in external cosmetics and the ingestion of certain photosensitizers are also considered important in the development of dermatosis.

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Symptoms of Melasma

Melasma mainly affects the skin of the face and neck, the mucous membranes are not involved in the process. Women are more often affected. The rash is characterized by uneven pigmentation of a brownish-yellow color in the central part of the forehead, above the upper lip, chin, on the cheeks and cheekbones, in the area of the corners 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 area of the central part of the forehead, on the cheeks, upper lip, bridge of the nose and chin.
2. molar - pigmentation is localized in the area of the cheeks (in the projection of the molars) and nose;
3. mandibular - pigmentation is localized in the area of the angles of the lower jaw.

Diagnosis of melasma

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

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Epidermal type of melasma

With this type, the lesions become brighter and more contrasting when examined under a Wood's fluorescent lamp. This phenomenon is associated with the predominant localization of melanin in the epidermis. This type is prognostically the most favorable.

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Dermal type of melasma

When examined under fluorescent lamps under a Wood filter, pigmentation does not increase, and its contrast with the surrounding unaffected skin does not become more obvious. This type corresponds to the predominant localization of melanophages inside the dermis, which indicates an unfavorable prognosis for treatment.

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Mixed type melasma

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

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

Treatment of melasma

It is necessary to find out individually what factor was predisposing to the development of the disease. It is recommended to stop taking oral contraceptives, a detailed examination by a gynecologist-endocrinologist. It is also recommended to study liver function, prescribe hepatic protectors (vitamin E, Essentiale). Effective photoprotection using sunscreens with maximum protection from ultraviolet rays A and B is mandatory. Patients are advised to wear hats, avoid sun exposure, especially from 10 am to 4 pm (even with adequate photoprotection), and refuse to visit a solarium. The above measures aimed at reducing exposure to UV radiation should be especially observed during pregnancy and the first months after childbirth. For external therapy, long courses of azelaic acid, topical retinoids, benzoyl peroxide, ascorbic acid, resorcinol (gamma Iklen, Merck Medication Familial), chemical peels with hydroxy acids (alpha-, beta- and polyhydroxy acids) or trichloroacetic acid, hydroquinone and other drugs are used. Laser skin "polishing", photorejuvenation and dermabrasion can give a good cosmetic result. Ascorbic acid (vitamin C) and tocopherol (vitamin E) are prescribed internally to inhibit the formation of melanin.

Prevention of melasma

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

Becker's nevus

Becker's nevus is a non-melanoma-prone pigmented lesion.

Causes of Becker's Nevus

Causes and pathogenesis are unknown. It occurs in 0.5% of men in the population. In women it is rare and can be combined with various stigmas of dysembryogenesis (breast hypoplasia, spina bifida, etc.).

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Symptoms of Becker's nevus

The disease begins in adolescence. A light-brown lesion is characteristic on the skin of the shoulder, anterior chest, and back. The skin of the face and neck is rarely affected. The lesion is usually linear or segmental. Dark hair subsequently appears against the background of the spot. Histologically, an increase in the amount of melanin in melanocytes is detected, they contain giant melanosomes, and 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 hamartoma).

Diagnosis of Becker's nevus

The diagnosis is established based on the characteristic clinical picture. Differential diagnostics are performed with a giant pigmented nevus, a dispersed nevus, and café au lait spots in Recklinghausen's disease.

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Treatment of Becker's nevus

Traditional whitening methods, peelings, laser destruction, dermabrasion usually give a negative aesthetic result. Camouflage is recommended.

Nevi of Ota and Ito

Nevi of Ota and Ito are primary ceruloderma. Nevi of Ota (dark blue orbitomaxillary nevus) and Ito were described in the middle of the last century in the Japanese. However, they can also be found in people of other nationalities.

Causes of nevi of Ota and Ito

The causes and pathogenesis are unknown.

Symptoms of nevi of Ota and Ito

The disease begins in childhood or adolescence. Characteristic is a grayish-blue pigmentation with unclear boundaries on the temporal region and eyelids (nevus of Oga) or in the brachiocephalic region - along the neck and shoulder (nevus of Ito), asymmetrical. With nevus of Ota, skin lesions are combined with ocular hypermelanosis - grayish coloration of the sclera of the eye. Histologically, melanocytes rich in melanin with processes are detected in the dermis.

Diagnosis of nevi of Ota and Ito

Clinical diagnostics is not difficult. It is differentiated from post-traumatic hematoma, melasma, fixed erythema.

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Treatment of nevi of Ota and Ito

Cryodestruction, laser destruction, microdermabrasion are recommended. Due to the incomplete effectiveness of these methods, dermatological camouflage is indicated.