Hyperpigmentation of the skin

Violation of melanogenesis leads either to excessive formation of melanin, or to a significant decrease in its content or its complete disappearance - depigmentation.

[1], [2], [3], [4], [5], [6], [7]

Pathogenesis

When histological examination of the skin, hyperkeratosis with horny plugs in the mouth of the hair follicles, sometimes atrophic changes in the epidermis and vacuolar degeneration of the basal layer cells are observed. In the dermis, as a rule, the degree of inflammatory reaction in the cells of the basal layer of the epidermis, as well as in melanocytes, the content of melanin is increased, especially its large number is found in the cytoplasm of macrophages of the upper third of the dermis, or melanophages. Surface capillaries are dilated, which is clinically manifested by telangiectasia. Around them are small infiltrates, consisting of the main lymphocytes with an admixture of tissue basophils.

[8], [9], [10], [11], [12], [13], [14], [15]

Symptoms of the hyperpigmentation of the skin

To limited hyperpigmentation include freckles, chloasma, "coffee with milk" pigment spots, simple and senile lentigo, Becker nevus, iatrogenous melanosis and post-inflammatory hyperpigmentation.

Freckles are small (2-4 mm), pigmented spots of tan color with fuzzy outlines. Appear at any age in the open areas of the skin, especially in fair-haired and white people, under the influence of sunlight darkens, in winter - disappear.

Pathomorphology. Hyperpigmentation of epidermal cells, especially of the basal layer, is determined. There is no proliferation of melanocytes.

Histogenesis. Under the influence of ultraviolet irradiation, there is an increase in the synthesis of melanin in the epidermis and its accumulation in melanocytes and in keratinocytes.

Chloasma is the larger pigmented spots that occur when the liver function, endocrine pathology, pregnancy and diseases of the appendages in women are disturbed.

Pathomorphology. An increased content of melanin in epidermal cells is noted.

Lentigo simple - patchy element with a diameter of 1 to 3 mm, with clear contours, dark brown or black. Appears in any age, including childhood, in open areas of the body.

Pathomorphology. In the basal layer of the epidermis, the amount of melanocytes is increased, but unlike the border nevus, they do not form nests. In this case, melanocytes usually increase in size. Simultaneously, there is an increase in the number and lengthening of epidermal outgrowths (lentiginous epidermal hyperplasia). The melanin content in the basal layer is increased. In the dermis - small lymphocytic infiltrates and single melanophages.

Histogenesis. The basis of hyperpigmentation of the skin is local proliferation of melanocytes.

A widespread lentiginous hyperpigmentation is observed with pigment xeroderma, peri-lateral lentiginosis.

Pigment xeroderma is a heterogeneous, mainly autosomal recessive disease characterized by increased photosensitivity, development of skin pigmentation and atrophy, photophobia, neurological symptoms, progressive course with a very high risk of developing skin tumors. The increased sensitivity of cells to ultraviolet rays is due to a violation of DNA repair, and the inadequacy of endonuclease excision of pyrimidine dimers is possible. Some patients experience neuropsychiatric symptoms and hypogonadism (de Sanctis-Kakkione syndrome).

Pathomorphology. The histological picture in the initial stage of the disease is nonspecific. Hyperkeratosis, thinning of the Malpighian epidermis layer with atrophy of some epithelial cells and an increase in the volume of others, accompanied by uneven melanin accumulation in the basal layer cells and an increase in the number of melanocytes are noted. In the dermis, a small lymphocytic infiltrate is seen. In the stage of hyperpigmentation and atrophic changes, hyperkeratosis and pigmentation are more pronounced. The epidermis is atrophic in some areas and thickened in others. There is a violation of the location of the nuclei of epithelial cells, an increase in their volume, there are atypical forms, as a result of which the picture resembles sunny keratosis. In the dermis - dystrophic changes, similar to those in solar dermatitis, characterized by basophilia of collagen fibers and elastosis. In the late stages of the disease, atypical growths of the epidermis join the changes described above, and in some foci, squamous cell carcinoma, and sometimes basal cell carcinoma, develops.

Lentiginosis peri-official (syn: Peitsa-Egepca-Turena syndrome) is a neuromesisenchymal dysplasia caused by a gene mutation. Transmitted autosomal dominantly. The disease develops in the first years of life, but can exist from birth, rarely occurs in adults. Clinically, they detect multiple, small pigmented spots from light brown to black, oval or rounded outlines, densely located around the mouth, on the lips, especially the lower, perinasal, periorbital and mucosa of the oral cavity. Less often - on the limbs (palms, soles, back surface of the fingers). A.V. Braits and G.M. Bolshakova (1960) described the generalized lentiginous eruptions. The periodic lentigo is combined with polyposis of the intestine, predominantly of the small intestine, prone to transformation into adenocarcinoma.

Pathomorphology. There is an increase in the amount of pigment in the cells of the basal layer, accompanied by an increase in the number of melanocytes. In the upper parts of the dermis, a large number of melanophages are found, the pigment melanin is sometimes located extracellularly.

Lentigo senile (syn: solar lentigo) appears in people of middle age and elderly after repeated exposure to ultraviolet radiation, especially after sunburn. Preferred location - open areas of the body, the skin in the area of the shoulder girdle and upper back. The sizes of the lentiginous elements are from 4 to 10 mm, the color is from light brown to dark brown and even black, the outlines are blurred, uneven,

Pathomorphology. Lentiginous hyperplasia of the epidermis, hyperpigmentation of the keratinocytes of the basal layer, insignificant proliferation of melanocytes. In the dermis - dystrophic changes of collagen fibers, manifested by their basophilia (solar elastosis).

Spots "coffee with milk" - congenital or appearing soon after birth large pigment spots of a yellowish-brown color. Their surface is smooth, outlines are often oval. With age, the number and size of the spots increase. Multiple patches are pathognomonic for neurofibromatosis, observed in other geno- dermatoses, such as tuberous sclerosis, Albright's disease, but single cells can also occur in healthy individuals.

Pathomorphology. Hyperpigmentation of the basal layer of the epidermis, ADPA-positive melanocytes reveal giant granules (macromelanosomes).

Nevus Becker (syn: unformed Bekker melanosis) is a local lesion of the skin, usually in the region of the shoulder girdle, manifested by a portion of hyperpigmentation of a saturated brown color, usually in combination with pronounced hypertrichosis within the nevus. It is a developmental defect, observed predominantly in males, a complete clinical picture develops in adolescence, pigmentation is enhanced by exposure to ultraviolet rays.

Pathomorphology. Hyperpigmentation of the basal layer, acanthosis and hypertrichosis. Often there is a combination with the underlying smooth-muscle hamartoma, changes in collagen fibers in the area of the nevus are described, which gives reason to consider it an organoid nevus.

Hyperpigmentation secondary appears on the site of the primary morphological elements of the rash - papules, tubercles, vesicles, pustules, as well as secondary elements - erosions and ulcerative lesions, after an acute or chronic inflammatory process. This kind of pigmentation is based on an increase in the amount of pigment in the cells of the basal layer of the epidermis and melanocytes, which remains after the disappearance of the inflammation.

Pathomorphology. An increase in the pigment content in the basal layer is noted, the thickness of which depending on the nature of the former element may be different.

[16], [17], [18], [19]

Forms

Hyperpigmentation can be widespread and limited, congenital and acquired.

Acquired skin hyperpigmentation is observed with cachexia due to exhausting diseases (cancer, tuberculosis, etc.), with avitaminosis (pellagra, scurvy), adrenal pathology (Addison's disease).

Often occurring skin diseases that occur with increasing melanogenesis are melanodermia, developing on the basis of intoxication, mostly of a professional nature (contact with fuels and lubricants). These include Ryla melanosis, or Sivatt's reticulum poikiloderma, toxic Haberman-Hoffmann toxic melasma. This affects the skin of the face, neck, chest and rear of the hand, clinically characterized by a bluish-brown, generalized or limited, diffuse or net pigmentation.

[20], [21]