Anetoderma after disseminated Mpox.

Anetoderma or macular atrophy is a rare skin condition of unclear pathogenesis, often associated with autoimmune diseases and skin damage from various infections. Human immunodeficiency virus (HIV), syphilis, and poxviruses have been implicated in the development of anetoderma. A 37-year-old male patient with HIV and recent unprotected sexual encounters presented with more than 400 skin lesions, consistent with Mpox. Symptomatic treatment for Mpox resulted in acute symptom resolution. However, 8 months later he developed papular anetoderma lesions in areas previously affected by Mpox. Biopsy confirmed the loss of elastic fibers in the affected skin areas, leading to the diagnosis of Mpox-induced anetoderma. This report presents a unique case of anetoderma following Mpox in an HIV-positive patient.

Cutaneous manifestations of antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is an acquired thrombophilic disorder in which autoantibodies are produced against a variety of phospholipids and phospholipid-binding proteins. The purpose of this article is to review cutaneous findings in patients with APS diagnosis. An overview regarding prevalence, description, pathogenesis and histopathology, are described for cutaneous manifestations of APS.

Anetodermia asociada a síndrome antifosfolipídico / Anetoderma associated with antiphospholipid syndrome

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Japanese familial anetoderma: A report of two cases and review of the published work.

Anetoderma is a rare cutaneous disorder characterized by focal loss of dermal elastic tissue, resulting in macular atrophy or herniated saclike skin. Some families with hereditary anetoderma have been described, but there have been no reports on Japanese familial anetoderma so far. We herein report two Japanese sibling cases of primary anetoderma. A healthy 13-year-old Japanese girl and a healthy 15-year-old Japanese girl presented to our hospital with a 6-month history of small atrophic pittings on their arms and trunks. All lesions were less than 0.5 cm in diameter, which are relatively small for non-familial anetoderma. Preceding infections or skin lesions were not observed. A skin biopsy revealed a focal, complete loss of elastic tissue in the superficial to mid-dermis which was surrounded by fine, irregular or twisted elastic fibers. Based on these findings, the diagnosis of anetoderma was made. Review of published works demonstrated that the mode of inheritance of familial anetoderma is not simple, suggesting that it is important to survey any family member of the patients with anetoderma.

Bullous sweet syndrome healing with prominent secondary anetoderma.

A 15-month-old boy presented with 1-4 cm, pink edematous plaques with overlying round erosions and hemorrhagic bullae in the setting of a gastrointestinal illness and was ultimately diagnosed with bullous-type Sweet syndrome. Despite appropriate treatment with oral steroids, the patient's cutaneous lesions healed with secondary anetoderma. This case should prompt practitioners to be aware of bullous-type Sweet syndrome and the possibility of lesions healing with postinflammatory scarring.

Cutaneous disorders characterized by elastolysis or loss of elastic tissue.

Along with collagen, elastic fibers are integral components of cutaneous connective tissue. A decrease in elastic fibers or loss thereof has been described in a number of clinically distinct skin diseases, both hereditary and acquired. In disorders associated with inflammation, elastophagocytosis is an important histological hallmark. Treatment is generally difficult.

Ultrastructural aspects of primary anetoderma.

Anetoderma is a rare cutaneous disorder characterized by focal loss of dermal elastic tissue due to unknown mechanisms. Primary anetoderma develops on clinical normal skin, without any preceding dermatosis and it can be associated with autoimmune conditions. Secondary anetoderma develops on the same area of a previous disorder, such as infectious, neoplastic or inflammatory diseases. A 37-year-old female patient noticed for 4 years circumscribed, normochromic, asymptomatic herniated plaques on the trunk and upper limbs. Family history was negative. Only a positive antinuclear factor (ANF) test, with titer of 1:160 and nuclear homogeneous pattern was found. Light microscopy with Weigert staining showed a lessening of elastic fibers with fragmentation; the oxytalanic fibers were also affected or absent. Transmission electron microscopy showed fragmentation and granular degeneration of elastic fibers. With greater magnification, fragments similar to those seen with optical microscopy were identified. The collagen fibers did not present any alteration. The examination of the dermis with scanning electron microscopy also identified fragmentation and significant fissures of the elastic tissue, granular degeneration was also observed. With greater magnification fragmented elastic fibers were seen.