Immunohistochemical characterization of the 'intimal proliferation' phenomenon in Sneddon's syndrome and essential thrombocythaemia

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urn:nbn:de:bvb:355-epub-268878 Copy

Tamm, Ernst R. ; Jungkunz, W. ; Wolter, M. ; Marsch, W. C.

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Date of publication of this fulltext: 04 Dec 2012 07:14

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Item type:	Article
Journal or Publication Title:	The British journal of dermatology
Publisher:	Wiley-Blackwell
Volume:	131
Number of Issue or Book Chapter:	6
Page Range:	pp. 814-821
Date:	1994
Institutions:	Biology, Preclinical Medicine > Institut für Anatomie > Lehrstuhl für Humananatomie und Embryologie > Prof. Dr. Ernst Tamm
Identification Number:	Value Type 7857833 PubMed ID
Classification:	Notation Type Actins/analysis MESH Adult MESH Brain Ischemia/pathology MESH Desmin/analysis MESH Female MESH Humans MESH Immunohistochemistry MESH Middle Aged MESH Muscle, Smooth/pathology MESH Skin Diseases, Vascular/pathology MESH Syndrome MESH Thrombocytopenia/pathology MESH Tropomyosin/analysis MESH Vimentin/analysis MESH
Dewey Decimal Classification:	600 Technology > 610 Medical sciences Medicine
Status:	Published
Refereed:	Yes, this version has been refereed
Created at the University of Regensburg:	Unknown
Item ID:	26887

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Abstract

Cellular changes were immunocytochemically characterized in skin vessels of five patients with idiopathic generalized racemose livedo (Sneddon's syndrome), and one patient with localized racemose livedo associated with essential thrombocythaemia. Antibodies against alpha-smooth muscle-actin, tropomyosin, desmin, vimentin, factor VIII-related antigen, human endothelial cells (CD31), human ...

Abstract

Cellular changes were immunocytochemically characterized in skin vessels of five patients with idiopathic generalized racemose livedo (Sneddon's syndrome), and one patient with localized racemose livedo associated with essential thrombocythaemia. Antibodies against alpha-smooth muscle-actin, tropomyosin, desmin, vimentin, factor VIII-related antigen, human endothelial cells (CD31), human macrophages (CD68), and HLA-DR positive cells (CR3/43) were used. Conventional light microscopy showed, in all cases, intimal thickening of ascending arteries and arterioles as a result of an accumulation of cells and extracellular hyalinized material. None of the specimens showed infiltration with polymorphonuclear leucocytes or macrophages. The cells in the region of the intimal hyperplasia showed intense positive immunostaining for alpha-smooth muscle actin and tropomyosin. Staining for the intermediate filament desmin was localized to the resident smooth muscle cells of the media, whereas staining for vimentin was found in all types of cells in both the intima and media. Positive immunostaining for factor VIII-related antigen and CD31 was strictly confined to the endothelial cells lining the narrowed lumina of the vessels. No positive staining with either antibody was observed in totally occluded vessels. Cells in the subintimal space did not show reactivity for CD68 in any of the specimens, but two cases showed solitary cells with positive staining for HLA-DR in this region. There were no differences in staining pattern between Sneddon's syndrome and essential thrombocythaemia with any of the antibodies. Our results support the assumption that the 'intimal proliferation' in both diseases is caused by colonization of the subendothelial space with contractile cells of possible smooth muscle origin.(ABSTRACT TRUNCATED AT 250 WORDS)

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