Hypopigmentation and skin depigmentation: causes, symptoms, diagnosis, treatment
Last reviewed: 23.04.2024
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Hypopigmentation and depigmentation of the skin are accompanied by a significant decrease or complete disappearance of melanin. They can be congenital and acquired, limited and diffuse. An example of depigmentation of a congenital nature is albinism.
Albinism of the dermal-ocular is a heterogeneous disease characterized by the absence or sharp decrease in pigment in the skin, hair and iris of the eyes. Two forms of skin-eye albinism - tyrosinase-negative and tyrosinase-positive - are associated with the lack or inadequacy of tyrosinase activity. The mechanism of development of other forms (syndromes Chediak-Higashi, Germanic-Pudlak, etc.) has not yet been clarified.
Pathomorphology. Pigment melanin is not found. Melanocytes have normal morphology, are evenly distributed (except for the syndrome "black curl - albinism - deafness"), but their pigment-synthesizing function is reduced. In the tyrosinase-negative variant, melanosomes are found on I, less frequently in stage II of ripening, with tyrosinase-positive at stage III. With the syndromes of the German-Pudlak and Chediak-Higashi, giant melanosomes are described. In addition, in the Chediak-Higashi syndrome, large cytoplasmic inclusions (color toluidine blue) are found in the mast cells of the skin.
To limited depigmentation include vitiligo, which is characterized by skin hypomelanosis, caused by the absence of melanocytes.
Vitiligo. The nature of dermatosis is unknown, but there are data on the role of immune and metabolic disorders, neuroendocrine disorders, exposure to ultraviolet rays (sunburn). The presence of family cases indicates a possible role of the genetic factor. It can also manifest as paraneoplasia, be the result of exogenous, including professional, diseases. Clinically characterized by the presence of spots of various sizes and shapes, milky white, surrounded by normal skin or a strip of hyperpigmentation. The disappearance of the pigment can be complete or partial, in the form of reticulation or small spot spots. Depigmentation may be preceded by the stage of erythema. Very often at first the brushes are affected, which is not observed in autosomal dominant congenital vitiligo (piebaldism). Lesions of lesions can be localized on the entire skin. Depending on the prevalence of the process, focal, segmental and generalized forms are isolated.
Pathomorphology. In the lesions, large changes are usually not observed. Epidermis of usual thickness or slightly thinned, outgrowths smoothed. The horny layer is mostly thickened, the granular layer consists of a single row of cells with scant granularity. Chypovaty layer without any changes, the cells of the basal layer almost do not contain pigment. However, with hypopigmentation, it is found in some cases, although in small amounts. Melanocytes in depigmented skin are almost not found, in hypopigmented areas there are fewer than in normal. In the dermis, swelling and homogenization of individual collagen fibers is observed, the elastic network without any changes. Vessels, as a rule, are dilated, their walls are thickened, cluster clusters of fibroblasts, histiocytes and tissue basophils are located around them. Epithelial hair follicles in the depigmentation sites are somewhat atrophic, their mouths are widened, filled with horny masses, sebaceous glands are also atrophic. Electron microscopic examination of the skin at the border of the vitiligo focus shows an increase in the number of epidermal macrophages and destructive changes in melanocytes relating to all structures of these cells. Melanocytes and melanin-containing structures in epithelial cells are absent in the foci of long-term vitiligo. The number of epidermal macrophages, according to some authors, in the foci of vitiligo is increased, their activity significantly increased. In areas of externally healthy skin, melanocytes contain melanosomes and premelosinosomes, but not a complex of melanosomes, which are the highest degree of organization of melanin granules. This indicates a lack of function of melanocytes.
The histogenesis of vitiligo remains unclear. Some authors associate vitiligo with a violation of the function of the autonomic nervous system, others - with a decrease in the production of melanocyte-stimulating hormone. R.S. Babayants and Yu.I. Lonshakov (1978) considered melanocytes in this disease to be inferior and incapable of responding to the action of melanocyte-stimulating hormone, Yu.N. Koshevenko (1986) obtained data indicating the presence of cellular immune responses in the depigmented skin with the participation of the complement C3-component, capable of causing melanocyte damage.
Acquired depigmentation can be observed with occupational hazards (professional leukoderma), the use of medicinal products (medicinal leucoderma), on the site of inflammatory elements (psoriasis, sarcoidosis, leprosy) with syphilis, multi-colored lichen (secondary leukoderma).
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