Anetoderma Schweninger-Buzzi: Two Case Reports

Abstract

BACKGROUND: Anetodermas are rare disorders of connective tissue with a focal loss of elastic fibres in the upper and mid dermis. Two types are separated, inflammatory and non-inflammatory.
 CASE REPORTS: We report two cases of acquired anetoderma Schweniger-Buzzi type. This non-inflammatory subtype is characterised by skin-coloured or whitish atrophic sac-like protrusions of trunk skin in adult males. Chronic infections and autoimmune disorders have been excluded. The diagnosis had been confirmed by characteristic histopathology.
 CONCLUSIONS: Anetodermas are symptomless disorders. They can be easily overlooked. The knowledge of such conditions is of importance to identify patients with a risk of thromboembolic events and underlying infections or autoimmune connective tissue diseases.

The Risk of Thrombotic Events in Anetoderma Affecting Young Patients

“…[5][6][7] Another theory considers anetoderma as primary when it is associated with connective tissue diseases or APLS and anti-thrombin III deficiency, explaining the high risk of thromboembolic events. 8 In this view, secondary anetoderma has been diagnosed in patients suffering from variable other diseases, without knowing exactly if there is a coincidence or a causative relation.…”

“…Secondary anetoderma has been linked to infections: Lyme borreliosis, 9 syphilis, 10 HIV infection, leprosy 8 ; granuloma annulare, pilomatricoma, Sweet syndrome, Stevens-Johnson syndrome, drug intake (penicillamine or penicillin), Wilson's disease; or associated with neoplasia (Reed syndrome, cutaneous lymphomas, xanthogranuloma). 8 Thus, a long list of diseases diagnosed in patients with anetoderma has been updated.…”

“…Increased phagocytosis of elastic fibers by macrophages could be another explanation for the destruction of elastic fibers in anetoderma and could support another classification: inflammatory and non-inflammatory anetoderma. 8 If all patients diagnosed with anetoderma have prothrombotic anomalies, the deterioration of dermal elastic fibers could be explained by focal ischemia. 13 Other theories are based on the high level of gelatinases in the anetoderma-skin or a similar epitope in the elastic fibers and phospholipids (β2-glycoprotein 1), which can explain the occurrence of APLS in anetoderma cases.…”

A case of primary anetoderma of Schweninger–Buzzi type

“…1,2 Anetoderma is classically divided into two forms: primary anetoderma, in which the elastolysis develops in clinically normal skin, and secondary anetoderma that arises at the site of various well-defined skin diseases, such as acne and varicella. 3,4 Primary anetoderma has historically been subdivided into two subtypes: the Jadassohn-Pellizzari type, with preceding inflammation and the Schweninger-Buzzi type, which appears spontaneously without inflammation. 4,5 A 24-year-old woman presented with increasing numbers of multiple atrophic and sac-like whitish macules on her back for 1 year (Figure 1a,b).…”

“…The dominant histopathologic findings are loss of elastic tissue in the reticular dermis and occasionally in the papillary dermis, with some degree of lymphohistiocytic infiltrate. 3,6 There is no known effective treatment for established anetoderma lesions. Primary anetoderma lesions can evolve gradually and can remain unchanged thereafter for life.…”