Actinic elastosis (elastoidosis): causes, symptoms, diagnosis, treatment

Actinic elastosis (elastoidosis) occurs with prolonged exposure to ultraviolet rays, usually observed in senile age (senile elastosis). It can also develop in children and young people with increased sensitivity to ultraviolet radiation. Clinically, on the face, neck, hands and forearms there are pale yellow patches with diamond-shaped slits and grooves, especially on the neck (cutis rhomboidale nuchae). Sometimes de- or hyperpigmentation, telangiectasia, poikilodermia, as well as precancerous changes, or squamous cell carcinoma, are observed. On the face, especially around the eyes, in the temporal regions and on the neck there may be pockets of skin tightening with the expansion of the pores, which gives the skin some resemblance to the lemon peel. Often, simultaneously there are milky-like and deep cystic formations, multiple comedones, hyperkeratosis (elastoidosis cutis nodularis cystica et comedoniea).

Pathomorphology of actinic elastosis (elastoidosis). There is atrophy of the epidermis, which is separated from a wide zone of elastosis, located in the upper parts of the dermis, a narrow strip of normal collagen. When stained with hematoxylin and eosin, the elastosis zone is sharply basophilic (basophilic dystrophy). Collagen fibers are located in it in the form of narrow eosinic, often fragmented fibers. In coloring according to the Weygert method, elastic fibers are found in this zone, mostly fragmented, thickened, sometimes densely adjacent to each other, forming an amorphous mass. Histochemically, a large amount of glycosaminoglycans is detected in these areas.

Histogenesis. It is shown that the elastosis is based on proliferation of elastic fibers with subsequent dystrophic changes in them. There are data on the increased transcriptional activity of the gene encoding elastin in the lesions. Previously it was believed that the main pathological process is the destruction of collagen and elastic fibers. It was also suggested that these actinic changes occur due to the increased proliferative activity of fibroblasts. Dystrophic changes are more pronounced than in ordinary senile atrophy, and are of a qualitatively different nature. They are preceded by a chronic inflammation, by which a slowly progressing thinning of the skin of the open areas of the body, dyschromia, and telangiectasia develop. The prolonged impact of unfavorable meteorological factors contributes to the earlier development of atrophic processes. Electron microscopic examination of elastic fibers showed that the thick fibers of the elastomeric material consist of two structural components, a fine-grained matrix of average electron density and the homogeneous, electronically dense, irregular forms of inclusions formed during the condensation of the granular matrix. Around this type of elastomeric material, amorphous masses and a large number of collagen fibrils can be seen. The number of fibers is reduced, at the edges they have a seemingly oblate appearance. Fibroblasts with signs of increased synthetic activity are often surrounded by granular material and elastotic fibers. The latter have histochemical properties, resembling those of normal collagen fibers, contain a large number of glycosaminoglycans such as hyaluronic acid.

[1], [2], [3]