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

Actinic elastosis (elastoidosis) occurs with prolonged exposure to ultraviolet rays, usually observed in old age (senile elastosis). It can also develop in children and young people with increased sensitivity to ultraviolet radiation. Clinically, pale yellow areas with diamond-shaped slits and grooves appear on the face, neck, hands and forearms, especially on the neck (cutis rhomboidale nuchae). Sometimes de- or hyperpigmentation, telangiectasias, poikiloderma, and precancerous changes, or squamous cell carcinoma, are observed. On the face, especially around the eyes, in the temporal areas and on the neck, foci of skin compaction with enlarged pores may appear, which gives the skin a certain resemblance to lemon peel. Often, milia-like and deep cystic formations, multiple comedones, and hyperkeratosis (elastoidosis cutis nodularis cystica et comedoniea) are present at the same time.

Pathomorphology of actinic elastosis (elastoidosis). Atrophy of the epidermis is observed, which is separated from the wide zone of elastosis, located in the upper parts of the dermis, by 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 eosin, often fragmented fibers. When stained using the Weigert method, elastic fibers are found in this zone, mostly fragmented, thickened, in places tightly adjacent to each other, forming an amorphous mass. Histochemically, a large content of glycosaminoglycans is found in these places.

Histogenesis. It has been shown that elastosis is based on the proliferation of elastic fibers with subsequent dystrophic changes in them. There is evidence of increased transcriptional activity of the gene encoding elastin in the lesions. Previously, it was believed that the main thing in the pathological process is the destruction of collagen and elastic fibers. It was also suggested that the above-mentioned actinic changes occur due to increased proliferative activity of fibroblasts. Dystrophic changes are more pronounced than in normal senile atrophy and are of a qualitatively different nature. They are preceded by chronic inflammation, after which slowly progressive thinning of the skin of exposed areas of the body, dyschromia, and telangiectasia develop. Long-term exposure to unfavorable meteorological factors contributes to the earlier development of atrophic processes. Electron microscopic examination of elastic fibers showed that thick fibers of the elastic material consist of two structural components, a fine-grained matrix of medium electron density and homogeneous, electron-dense, irregularly shaped inclusions formed during the condensation of the granular matrix. Amorphous masses and a large number of collagen fibrils can be seen around this type of elastic material. The number of fibers is reduced, and they have a flattened appearance at the edges. Fibroblasts with signs of increased synthetic activity are often surrounded by granular material and elastotic fibers. The latter have histochemical properties reminiscent of those of normal collagen fibers and contain a large number of glycosaminoglycans such as hyaluronic acid.

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