Monoclonal antibody studies in the skin lesions of patients with anetoderma

Venencie, P. Y.

doi:10.1001/archderm.121.6.747

Cited by 11 publications

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“…Also, the presenee or absence of clinical inflammatory lesions at onset is not related to prognosis or to the occurrence of other diseases [1,13]. The similar histological and ultrastructural findings of both the inflammatory and non-inflammatory lesions found in our patient indicate that these morphologically distinct lesions represent different stages of the same disease, as was previously observed [12], and not a simple association [10].…”

Section: Discussionsupporting

confidence: 85%

Idiopathic anetoderma with concomitant lesions of the Jadassohn‐Pellizzari and the Schweninger‐Buzzi types

Haligah

Zouboulis

Abdel-Naser

et al. 1994

Acad Dermatol Venereol

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Anctoderma is a rare disease of unknown etiology, today classified as a subtype of the eircumseribed elastotic disorders. The elinical picture shows atrophic patches loeated mainly on the upper trunk which characteristically give the palpating finger the sensation of a hernial orifiee. Our patient with primary idiopathic anctoderma presented a rarely reported concomitance of the inflammatory type of lesions described by Jadassohn and Peliizzari together with the non-inflammatory Schweninger-Buzzi type. Histologieally and ultrastrueturally, both kinds of lesions revealed similar pictures with a scanty perivascular lymphomononuclear cell infiltrate, with rarefied, partly fragmented elastic fibres and normal eollagen fibrils. These findings indicate that these two types of lesions represent different stages of the same disease and not a simple assoeiation. Furthermore, they support the opinion that the elassification of anetoderma into two separate Jadassohn-Pellizzari and Schweninger-Buzzi types may be unnecessary. After treatment with orai tetraeyciine 1 g/day for 3 weeks, no new lesions appeared; however, no improvement of the already present lesions occurred during a 6-month foilow-up period.

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Section: Discussionsupporting

confidence: 85%

Idiopathic anetoderma with concomitant lesions of the Jadassohn‐Pellizzari and the Schweninger‐Buzzi types

Haligah

Zouboulis

Abdel-Naser

et al. 1994

Acad Dermatol Venereol

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“…In all clinical and/or laboratory, immunologic abnormalities were found: one with Graves' disease, lupus anticoagulant and autoimmune hemolysis; one had systemic scleroderma; most had positive direct immunofluorescence findings; all had serologic immunologic abnormalities, of which the most common was ANA. On the basis of this series of patients and the previously reported cases, together with the finding that in all PA specimens there was a lymphocytic infiltrate with a predominance of helper T-cells [25], we suggested that PA is not primary or idiopathic at all, but rather, represents a rare elastolytic disorder in which immunologic mechanisms are involved [24].…”

Section: Introductionsupporting

confidence: 58%

Primary Anetoderma and Antiphospholipid Antibodies—Review of the Literature

Hodak

David

2007

Clinic Rev Allerg Immunol

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Primary anetoderma (PA) is a rare elastolytic disorder that develops in clinically normal skin or following a nonspecific inflammatory process. The old literature contains numerous reports of the association between PA and lupus eryhtematosus, although the relationship has not been clearly established. In recent years, there has been a growing body of literature linking PA with a wide range of immunologic abnormalities, the most common of which is the presence of antiphospholipid antibodies, with or without antiphospholipid syndrome. The present review summarizes the literature, from the early descriptions pointing toward an immunologic basis of PA and up to the present recognition that PA is a cutaneous sign for autoimmune disorders, in general, and the presence of antiphospholipid in particular.

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“…In the early stage of an erythematous lesion, the elastic tissue may still appear normal [1], but long-standing, non-inflammatory lesions generally show a more or less complete loss of elastic tissue [4,17]. As in previously reported cases, a perivascular and periadnexal round cell infiltrate of varying intensity was invariably present so that differentiation into an inflamma tory or non-inflammatory type does not seem justified [2], In previous studies, inflammatory cell infiltrates have been reported to be predominantly T helper cells [18]. Early lesions may show signs of vasculitis [1]; we found vascu litis in 3 of our patients.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, it has been suggested that the basic abnor mality is focal elastolysis which may be secondary to the release of elastase from the inflammatory cells [2,4,181. It has also been suggested that complement activation might be involved since C3 is deposited on the remaining elastic fibres [3,4], On the other hand, it has recently been sug gested that decay-accelerating factor and vitronectin (an inhibitor of the membrane attack complex) may protect elastic fibres against this type of damage [20], The oq-antitrypsin deficiency found in a few of our patients examined is interesting since oq-antitrypsin is known to inhibit trypsin activity, but it is also active against e.g.…”

Section: Discussionmentioning

confidence: 99%

“…It has also been suggested that complement activation might be involved since C3 is deposited on the remaining elastic fibres [3,4], On the other hand, it has recently been sug gested that decay-accelerating factor and vitronectin (an inhibitor of the membrane attack complex) may protect elastic fibres against this type of damage [20], The oq-antitrypsin deficiency found in a few of our patients examined is interesting since oq-antitrypsin is known to inhibit trypsin activity, but it is also active against e.g. neutrophil elastase, pancreatic elastase, serine proteases and collagenases [21 ].…”

Section: Discussionmentioning

confidence: 99%

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Antiphospholipid Antibodies and Anetoderma: Are They Associated?

Stephansson

Niemi

1995

Dermatology

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Background: Macular atrophy or anetoderma is a rare skin disease of unknown pathogenesis, characterised by wrinkled or flaccid skin. Objective: The finding of anetoderma in 5 patients followed up because of false-positive seroreactions of syphilis prompted us to study the occurrence of antiphospholipid (aPL) antibodies in anetoderma. Methods: 14 unselected patients with primary anetoderma (PA) were collected from hospital records and clinical, immunological and histological findings were compared in the two patient groups. Results: Of the 5 patients, 3 fulfilled the criteria for antiphospholipid syndrome. In two cases, it was secondary to systemic lupus erythematosus (SLE). Of the 14 PA patients 1 had aPL antibodies and 4 had borrelia antibodies. Two patients had thyroid antibodies; 1 of them developed SLE. In several biopsy specimens, microthromboses were seen in both patient groups. Conclusion: On the basis of this study and our previous findings, it seems that anetoderma is more often associated with aPL-positive SLE or lupus-like disease than with aPL-negative disease. Immunological mechanisms play an important role in both primary and secondary anetoderma. The meaning of false-positive serological tests for syphilis or borrelia and aPL antibodies is not clear, but they may be reacting to some still unidentified antigen. Probably, various systemic as well as local inflammatory and non-inflammatory processes, e.g. microthromboses, can trigger anetoderma via still unknown pathomechanisms.

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Monoclonal antibody studies in the skin lesions of patients with anetoderma

Cited by 11 publications

References 0 publications

Idiopathic anetoderma with concomitant lesions of the Jadassohn‐Pellizzari and the Schweninger‐Buzzi types

Idiopathic anetoderma with concomitant lesions of the Jadassohn‐Pellizzari and the Schweninger‐Buzzi types

Primary Anetoderma and Antiphospholipid Antibodies—Review of the Literature

Antiphospholipid Antibodies and Anetoderma: Are They Associated?

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