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Two families with anetoderma are described. Unlike previous reports of familial anetoderma, the disease process seemed to be limited to the skin, and there were no associated ocular, gastrointestinal, or orthopedic anomalies in the affected patients or in any other family members. Although infrequently reported, anetoderma may occur in families, and patients must be examined for associated systemic abnormalities for a thorough assessment of their skin disorder.
Anetoderma in premature infants is an uncommon lesion that may be associated with the use of various types of monitoring leads. In 2 infants multiple papules of anetoderma occurred on the forehead in association with the use of gel electrocardiographic electrodes. It is postulated that the cause of these papules was a local hypoxemia caused by pressure from the electrodes. Growth-restricted infants may be particularly predisposed to iatrogenic anetoderma.
Anetoderma is characterized by a loss of normal elastic tissue that presents clinically as localized areas of wrinkled or flaccid skin. We describe the case of a 30-year-old woman with systemic lupus erythematosus-associated anetoderma and positive anti-phospholipid antibodies. We discuss the possible role of these antibodies in the pathogenesis of anetoderma, and, when detected, the need to check for an associated anti-phospholipid syndrome in such patients.
Current views on etiopathogenesis of anetoderma have been presented on the grounds of literature data. Disorders of elastin metabolism are distinctive for the disease causing elastin fibres becoming disintegrated and atrophied. Apart from mechanism of anetoderma plaques evolution clinical observation and full diagnostication of systemic collagenosis seems to be important. Despite of numerous therapeutic trials it appears that medication of anetoderma lesions is inefficacious.
A middle-aged HIV infected man receiving treatment for pulmonary tuberculosis, presented with a febrile illness along with evanescent, erythematous nodular lesions all over the body. On examination, he had features suggestive of lepromatous leprosy with lesions of erythema nodosum leprosum. In addition, there were multiple small, circumscribed areas of slack skin, clinically and histopathologically suggestive of anetoderma. Both leprosy and HIV infection are known to give rise to lesions of anetoderma. Pathogenesis of anetoderma in these infectious conditions is discussed.
BACKGROUND AND DESIGN: Primary anetoderma is a rare cutaneous elastolytic disorder, the etiopathogenesis of which has not yet been established. Six patients with primary anetoderma were studied in an attempt to assess the role of the immunologic system in the elastolytic process. The investigation included the medical history, physical examination, routine blood tests, specific tests for collagen diseases, prothrombin time, activated partial thromboplastin time, thyroxine, indirect immunofluorescence test, and skin biopsies for histopathologic study and direct immunofluorescence. RESULTS: Two of the patients presented with autoimmune disorders: the first had Graves' disease, lupus anticoagulant, and autoimmune hemolysis, and the second had systemic scleroderma. There were positive direct immunofluorescence findings in most of the patients. Furthermore, all of them were found to have serologic immunologic abnormalities, of which the most common was a positive antinuclear factor. CONCLUSIONS: These findings indicate that there is an immunologic involvement in primary anetoderma.
Two cases of anetoderma and lupus erythematosus (LE) were studied. The first one showed secondary anetoderma and subacute LE. There was leucocytoplastic angitis in involved skin besides generalized lacking of elastic fibers (EF). The second one is a Schweninger Buzzi anetoderma with face and scalp lesions of LE tumidus. In new lesions angitis and immunoglobulin deposits of EF were seen. Another cases, pathogenic and characteristics of this unusual association were analyzed we pointed out: 1) leucocytoplastic angitis presence; 2) immunoglobulin deposits on EF finding; 3) angitis seems to play a principal rol in elastic fibers disappearance.
We reviewed the histopathologic findings in 34 biopsy specimens from 15 patients with anetoderma. Focal loss of normal elastic fibers, necessary for the diagnosis of anetoderma, was found in all 15 cases. The persistence of fine, irregular, or twisted elastic fibers is common. A perivascular infiltrate composed of lymphocytes was found in all specimens. Plasma cells were observed in specimens from six patients, and histiocytes with some granuloma formation were found in specimens from six patients. Variations in the intensity of inflammation or in the loss of elastic tissue were not related to the clinical findings, course, or associated diseases. All anetoderma lesions appeared to have an inflammatory pathogenesis.
Three patients with localized cutaneous lesions characteristic of anetoderma were studied. Clinically, the onset of the disease was between the ages of 17 and 25, and numerous flaccid, saclike skin lesions developed over several subsequent years. Histologically, the lesions were characterized by paucity and fragmentation of the elastic fibers. Electron microscopy demonstrated that the elastic fibers, both in papillary and deep reticular dermis in the lesional skin, were fragmented and irregular in appearance. The concentration of elastin, determined by a radioimmunoassay of desmosine, an elastin-specific cross-link compound, was markedly reduced in the lesions, as compared with unaffected skin from the same patients or with normal skin from unrelated control subjects. In contrast, the concentrations of hydroxyproline, an index of collagen, or deoxyribonucleic acid (DNA), a measure of cellularity, were not changed in the lesions. Thus, the results indicate that in the three patients studied, the elastic fibers are defective and reduced in quantity. These observations suggest that the deficiency of elastin in the dermis may lead to development of the cutaneous lesions of anetoderma.
We describe two men with multiple erythematous dermal nodules which were clinically and histologically consistent with a diagnosis of primary cutaneous immunocytoma. Both patients exhibited the very unusual feature of secondary anetoderma occurring in spontaneously resolving lesions. There is one previous report of anetoderma in association with a plasmacytoma. The pathogenesis remains unknown but release of cytokines such as interleukin-6 may be implicated.
We describe an 11-year-old girl with secondary anetoderma involving a pilomatricoma. She presented with a soft, wrinkled pedunculated lesion overlying a firm subcutaneous mass on her right anterior shoulder. Pathologic examination revealed a pilomatricoma in the subcutaneous tissue, with focal loss of elastic fibers in the overlying dermis. Secondary anetoderma has been reported to involve various infections, inflammatory disorders, and tumors, but the association with pilomatricoma is very rare.
A fifty-nine-year-old healthy male presented with fifteen round pouches around his bilateral shoulders and proximal thighs, at which elasticity was lost on palpation. Histopathological examinations demonstrated that the lesional dermis was thinner than normal skin and there was loss of elastic fibers and mild inflammatory cell infiltration. Because there was no preceding inflammatory skin lesion or associated diseases, the patient was diagnosed with primary anetoderma. This is a rare case of primary anetoderma that showed loss of elastic fibers and the thinner dermis. In addition, a modified classification is proposed considering associated diseases with a review of literature.
Primary anetoderma (PA) has occasionally been described in association with lupus erythematosus (LE). The present study was performed to elucidate a possible causal link between PA and LE by the use of direct and indirect immunofluorescence (IF) methods. Two patients with PA were studied. Biopsy specimens were obtained from early inflammatory and atrophic anetoderma lesions and from the exposed and unexposed uninvolved skin of each patient. The pattern of immune deposits observed in one patient was indistinguishable from that which is often seen in systemic LE, and in the other patient from that which may be observed in chronic cutaneous LE. The direct IF study also showed fibrillar immune deposits in the dermis that resembled elastic fibres morphologically. The indirect IF study, however, failed to demonstrate anti-elastic fibre antibodies in the patients' sera. The results of this study and a review of the literature suggest that some cases of PA have direct IF findings similar to those of either chronic cutaneous or systemic LE. However, these findings, along with the serological findings, are insufficient to establish a diagnosis of LE in most of these PA cases.
We report a 22-year-old female with a 2-year history of increasingly numerous well-circumscribed, asymptomatic skin lesions. The clinical and histological features were consistent with anetoderma and investigations failed to reveal any associated underlying disorders. Electron microscopy of abnormal skin showed phagocytosis of elastic fibres by macrophages. Although the aetiology of primary anetoderma remains unknown, this finding suggests that phagocytic destruction of elastic fibres plays a major role in its pathogenesis.
Two boys, age 7 and 9 years, with the diagnosis of primary anetoderma are presented. In one patient a growing number of indolent lesions developed for one year on the neck. The other boy complained of single lesions appearing over four months on the arms, feet, and chest wall. Individual lesions measured up to 1 cm in diameter and showed a palpable herniation phenomenon and wrinkled surface. The lesions did not have an inflammatory onset. Histologically, in both patients the diagnosis of anetoderma was verified by loss of elastic fibers and a lympho-histiocytic infiltration in the middermis. Administration of oral penicillin for three weeks did not result in marked improvement, and atrophic macules continued to appear in the younger boy. Although no autoimmunologic abnormalities or other associated diseases have arisen in our patients, long-term follow-up is mandatory to detect autoimmune disorders that are reported to occur in the course of the disease.
Anetoderma is a rare elastolytic disorder included within the group of cutaneous atrophies. Its pathogenesis is not yet clearly established, but immunological mechanisms could play an important role in dermal elastolysis. It has been associated with different autoantibodies and autoimmune disorders. We present a case of anetoderma in a systemic lupus erythematosus patient with anti-proliferating-cell-nuclear-antigen and antiphospholipid antibodies, highlighting the peculiarities of such an association.
We report the case of a woman with a primary Sjögren's syndrome who developed asymptomatic anetoderma lesions with no other pathology responsible. This dermatosis has been associated with many autoimmune disorders, in particular lupus erythematosus and lupus-like syndromes. Our literature review found only one previous description of primary anetoderma associated with primary Sjögren's syndrome.
Anetoderma is an uncommon disorder characterized by the loss of elastic fibres in the dermis histologically and herniation of subcutaneous tissue clinically. Recent studies indicate that immunologic mechanisms may play a role in this process. Here we report a 33-year-old woman with numerous well-circumscribed, asymptomatic skin lesions in whom clinical and histopathologic features were consistent with anetoderma. Additionally, history and investigations revealed antiphospholipid syndrome and systemic lupus erythematosus. It has been speculated that immune deposits in the dermis or within the capillary walls may lead to ischaemia and subsequent degeneration of the elastic fibres.