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Anetoderma: causes, symptoms, diagnosis, treatment
Last reviewed: 07.07.2025

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Anetoderma (synonym: macular cutaneous atrophy) is a type of skin atrophy characterized by the absence of elastic tissue.
The causes and pathogenesis of the disease have not been fully established. There is evidence of the causal role of endocrine and nervous disorders. The influence of neuroendocrine effects is indicated. The role of infection (spirochetes) is not excluded, as evidenced by cases of the disease developing after tick bites. The good therapeutic effect of penicillin therapy allowed some authors to put forward an infectious theory of the disease. Histochemical studies have established that the occurrence of anetoderma may be explained by the release of elastase from the cells of the inflammation focus, which causes elastolysis.
Symptoms of spotted skin atrophy (anetoderma). Clinically, several variants are distinguished: foci of atrophy that arose during the preceding erythematous stage (Jadassohn-Thiberge type), at the site of urticarioedematous elements (Pellizari type) and on clinically unchanged skin (Schwenninger-Buzzi type). Different variants can be present in the same patient. Foci of atrophy can be located on any part of the skin, most often on the upper half of the body, on the arms and face, they are small, on average 1-2 cm in diameter, have round or oval outlines, a whitish-bluish color, a shiny wrinkled surface. Some elements bulge like a hernia, when pressing on them with a finger there is a feeling of falling into emptiness, other elements, on the contrary, sink. Anetoderma is a component of Blegvad-Haxthausen syndrome (atrophic spots, blue sclera, brittle bones, cataracts).
The disease most often occurs in women aged 20-40 years, more often in central Europe. This is probably due in some cases to the association of anetoderma with chronic atrophic acrodermatitis caused by Br. burdorferi.
Clinically, several variants of anetoderma are distinguished: foci of atrophy that arise after the preceding erythematous stage (classical Yatzasson type); on outwardly unchanged skin (Schwenninger-Buzzi type) and at the site of urticarial-edematous elements (Pellisari type).
In the classic type of Jadassohn's anetoderma, single or multiple spots of irregular oval or round shape, up to 0.5-1 cm in diameter, pink or yellowish-pink in color appear. The lesions are most often localized on the trunk, upper and lower extremities, neck and face, but skin lesions in other areas are possible. The palms and soles are usually free of rashes. The spot increases in size and within 1-2 weeks its size reaches 2-3 cm. Erythematous plaques and even large nodes have been described. Gradually, without any subjective sensations, atrophy develops at the site of the erythematous spot, which begins in the center of the spot. The skin in these areas becomes pale, wrinkled, resembling crumpled tissue paper; the lesion slightly protrudes above the level of the surrounding skin in the form of a soft hernia-like protrusion of the skin. When pressing a finger on this area of skin, it creates the impression of emptiness (the finger falls "deep"). Hence the name of the disease: anetos - emptiness.
In anetoderma of the Schwenninger-Buzzi type, hernia-like protruding atrophic spots also appear on the back and upper limbs. However, unlike the classical type of anetoderma of Jadassohn, the foci of atrophy protrude significantly more above the surrounding skin, there may be telangiectasias on their surface and the first inflammatory stage is always absent.
In the urticarial type, anetoderma develops at the site of blisters, there are no subjective sensations. When pressing on the element, the finger seems to fall into the void.
In all types of anetoderma, a sharp thinning of the epidermis, complete disappearance of elastic fibers and dystrophic changes in collagen fibers are observed in the area of atrophy.
A distinction is made between primary and secondary anetoderma. The cause of primary anetoderma is unknown. However, it is often combined with diseases such as scleroderma, hypocomplementemia, HIV infection, etc. Secondary anetoderma occurs after the resolution of spotted and papular elements in secondary syphilis, lupus erythematosus, leprosy, sarcoidosis, acne vulgaris, etc.
Premature anetoderma (anetoderma prematura) is described, developing in infants born prematurely. The development of this type is explained by chemical, metabolic changes in the skin of the fetus. A case of fetal anetoderma development in intrauterine life is described, when the mother suffered from intrauterine borreliosis. Such a case indicates the existence of congenital anetoderma.
Pathomorphology. In the initial (inflammatory) stage, histological changes are nonspecific and are characterized by the presence of perivascular infiltrates in the dermis, consisting of lymphocytes and neutrophilic granulocytes. In older elements, epidermal atrophy, a decrease in the infiltrate in the dermis and dystrophic changes in collagen fibers (atrophy stage) can be seen. This disease is characterized by focal or complete absence of elastic fibers. The epidermis is usually thinned. Electron microscopic examination of skin lesions revealed changes in the elastic fibers in the form of a sharp thinning and decrease in their number. According to these authors, the remaining thin elastic fibers consist of a centrally located amorphous substance of low electron density without fibrils, but with their presence along the periphery of the fiber. Large-fibrillar masses are found in which microfibrils are detected in places, sometimes in the form of tubules. Vacuolar dystrophy is observed inside some fibers. Collagen fibers are unchanged. Most fibroblasts show signs of activation of the synthetic function. Macrophages alternate with lymphocytes, among which are the remains of dead macrophages, sometimes plasma cells and individual tissue basophils are found here. J. Pierre et al. (1984) believe that the presence of thin fibers indicates new synthesis of elastic fibers after elastolysis, which occurs in this disease.
Histogenesis. The sharp decrease in elastic fibers in the lesions is explained, on the one hand, by the possibility of a primary molecular defect consisting of a decrease in the synthesis of elastin or the microfibrillar component of elastic fibers or a disturbance in the formation of desmosine; on the other hand, it is possible that the destruction of elastic fibers is caused by elastase released from the cells of the inflammatory infiltrate, primarily such as neutrophilic granulocytes and macrophages. The possibility of increased elastolysis is indicated, in particular due to an increase in the elastase/antielastase ratio, as is noted in other diseases based on damage to elastic fibers. There is evidence in favor of immune mechanisms in the pathogenesis of anetoderma, as indicated by the frequent detection of plasma cells in infiltrates and a large number of T-lymphocytes with a predominance of T-helpers among them, as well as signs of leukocytic vasculitis with perivascular deposits of IgG, IgM and the C3 component of complement. Taking into account the development of spotted atrophy of the skin in such various conditions as urticaria pigmentosa, xanthomatosis, long-term use of corticosteroids, penicillin, regression of many dermatoses (tertiary syphilis, tuberculosis, leprosy), it can be assumed that anetoderma is a heterogeneous condition, the basis of which is the death of elastic fibers under the influence of a variety of causes. In addition, there is evidence indicating the existence of not only cutaneous forms of anetoderma, but also lesions of other organs, which is confirmed by the combination of anetoderma with cutis laxa.
Treatment of spotted skin atrophy (anetoderma). Penicillin and antifibrinolytic (aminocaproic acid) agents and general tonic (vitamins, biostimulants) preparations are recommended.
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