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D J Gawkrodger – One of the best experts on this subject based on the ideXlab platform.

  • Hamartomatous congenital melanocytic nevi showing secondary Anetoderma-like changes.
    Journal of the American Academy of Dermatology, 1998
    Co-Authors: S E Cockayne, D J Gawkrodger

    Abstract:

    A 47-year-old man had multiple large congenital melanocytic nevi associated with striking atrophic changes. Biopsy specimens showed a prominent reduction and fragmentation of elastic fibers in the papillary dermis. The Anetoderma-like changes may have been secondary to a past inflammatory process but more likely represent a hamartoma.

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  • Hamartomatous congenital melanocytic nevi showing secondary Anetoderma-like changes
    Journal of the American Academy of Dermatology, 1998
    Co-Authors: S E Cockayne, D J Gawkrodger

    Abstract:

    Abstract A 47-year-old man had multiple large congenital melanocytic nevi associated with striking atrophic changes. Biopsy specimens showed a prominent reduction and fragmentation of elastic fibers in the papillary dermis. The Anetoderma-like changes may have been secondary to a past inflammatory process but more likely represent a hamartoma. (J Am Acad Dermatol 1998;39:843-5.)

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Harald Gollnick – One of the best experts on this subject based on the ideXlab platform.

  • idiopathic Anetoderma with concomitant lesions of the jadassohn pellizzari and the schweninger buzzi types
    Journal of The European Academy of Dermatology and Venereology, 1994
    Co-Authors: Charles E.k. Haligah, Christos C. Zouboulis, Michael Detmar, Günther Ehlers, Mohamed Badawy Abdelnaser, Harald Gollnick

    Abstract:

    Anetoderma is a rare disease of unknown etiology, today classified as a subtype of the circumscribed elastotic disorders. The clinical picture shows atrophic patches located mainly on the upper trunk which characteristically give the palpating finger the sensation of a hernial orifice. Our patient with primary idiopathic Anetoderma presented a rarely reported concomitance of the inflammatory type of lesions described by Jadassohn and Pellizzari together with the non-inflammatory Schweninger-Buxzi type. Historically and ultrastructurally, both kinds of lesions revealed similar pictures with a scanty perivascular lymphomononuclear cell infiltrate, with rarefied, partly fragmented elastic fibres and normal collagen fibrils. These findings indicate that these two types of lesions represent different stages of the same disease and not a simple association. Furthermore, they support the opinion that the classification of Anetoderma into two separate Jadassohn-Pellixzari and Schweninger-Buzzi types may he unnecessary. After treatment with oral tetracycline 1 g/day for 3 weeks, no new lesions appeared; however, no improvement of the already present lesions occurred during a 6-month follow-up period.

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  • Idiopathic Anetoderma with concomitant lesions of the Jadassohn‐Pellizzari and the Schweninger‐Buzzi types
    Journal of the European Academy of Dermatology and Venereology, 1994
    Co-Authors: Charles E.k. Haligah, Christos C. Zouboulis, Mohamed Badawy Abdel-naser, Michael Detmar, Günther Ehlers, Harald Gollnick

    Abstract:

    Anetoderma is a rare disease of unknown etiology, today classified as a subtype of the circumscribed elastotic disorders. The clinical picture shows atrophic patches located mainly on the upper trunk which characteristically give the palpating finger the sensation of a hernial orifice. Our patient with primary idiopathic Anetoderma presented a rarely reported concomitance of the inflammatory type of lesions described by Jadassohn and Pellizzari together with the non-inflammatory Schweninger-Buxzi type. Historically and ultrastructurally, both kinds of lesions revealed similar pictures with a scanty perivascular lymphomononuclear cell infiltrate, with rarefied, partly fragmented elastic fibres and normal collagen fibrils. These findings indicate that these two types of lesions represent different stages of the same disease and not a simple association. Furthermore, they support the opinion that the classification of Anetoderma into two separate Jadassohn-Pellixzari and Schweninger-Buzzi types may he unnecessary. After treatment with oral tetracycline 1 g/day for 3 weeks, no new lesions appeared; however, no improvement of the already present lesions occurred during a 6-month follow-up period.

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Emmilia Hodak – One of the best experts on this subject based on the ideXlab platform.

  • Anetodermic Primary Cutaneous B-Cell Lymphoma: A Unique Clinicopathological Presentation of Lymphoma Possibly Associated With Antiphospholipid Antibodies
    Archives of dermatology, 2010
    Co-Authors: Emmilia Hodak, Hana Feuerman, Aviv Barzilai, Michael David, Lorenzo Cerroni, Meora Feinmesser

    Abstract:

    Background Primary cutaneous B-cell lymphoma manifested by Anetoderma has been reported in 7 cases. In all, the secondary Anetoderma developed in lesions of marginal-zone lymphoma or posttransplant lymphoproliferative disorder resembling marginal-zone lymphoma. The mechanisms underlying the destruction of elastic tissue in Anetoderma are unclear. However, there is growing evidence linking primary Anetoderma with a wide range of immunologic abnormalities, the most common being the presence of antiphospholipid antibodies. Observations We analyzed data from 5 patients (3 male, 2 female) with clinical and histopathological features of anetodermic primary cutaneous B-cell lymphoma. Three had marginal-zone lymphoma and 2 had follicle-center cell lymphoma. In all, secondary Anetoderma developed in self-regressing nodules/plaques of the lymphoma. Two patients also had lesions clinically and histopathologically compatible with primary Anetoderma. Associated immunologic diseases were systemic lupus erythematosus–like disease and rheumatoid arthritis (1 patient each; not in patients with primary Anetoderma). Antiphospholipid antibodies were found in 4 patients. Conclusions Anetodermic primary cutaneous B-cell lymphoma is a rare and unique clinicopathological manifestation not only of marginal-zone lymphoma, as previously described, but also of follicle-center cell lymphoma. This type of secondary Anetoderma, like primary Anetoderma, might be associated with immunologic disorders, particularly antiphospholipid antibodies.

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  • Immunologic Abnormalities Associated With Primary Anetoderma
    Archives of dermatology, 1992
    Co-Authors: Emmilia Hodak, Michael David, Orna Shamai-lubovitz, Bilha Hazaz, Meir Lahav, Varda Katzenelson-weissman, Miriam Sandbank

    Abstract:

    • 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. ( Arch Dermatol. 1992;128:799-803)

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  • Primary Anetoderma associated with a wide spectrum of autoimmune abnormalities.
    Journal of the American Academy of Dermatology, 1991
    Co-Authors: Emmilia Hodak, Michael David, Orna Shamai-lubovitz, Bilha Hazaz, Meir Lahav, Miriam Sandbank

    Abstract:

    Although the underlying pathologic mechanisms of primary Anetoderma have not yet been identified, data suggest the participation of an immunologic mechanism in some cases. In a woman with clinical and histopathologic features of primary Anetoderma (Jadassohn-Pellizzari type) of 30 years’ duration, laboratory investigation disclosed positive antinuclear factor, hypocomplementemia, hypergammaglobulinemia, granular deposits of immunoreactants along the dermoepidermal junction, and fibrillar deposits in the papillary dermis. In addition, she was found to have autoimmune hemolysis and circulating lupus anticoagulant associated with recurrent deep-vein thrombosis and a history of Graves’ disease (starting 5 years after onset of primary Anetoderma). To our knowledge, none of the latter three autoimmune conditions has been previously associated with primary Anetoderma.

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