1977
DOI: 10.1001/archderm.113.10.1424
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Scleroderma-like changes in chronic graft vs host disease

Abstract: A case of chronic graft vs host disease had scleroderma-like skin changes. Clinical progression was from poikiloderma to scleroderma, and histopathological changes and results of direct immunofluorescence were noted. It is probable that both cell-mediated (T-cell) and humoral (B-cell) mechanisms contribute to the pathogenesis of the graft vs host reaction.

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Cited by 17 publications
(10 citation statements)
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“…Newly emerging techniques for determining when and where the synthesis of PDGF polypeptides and PDGF receptors occurs in situ should aid in a more systematic search for etiologic agents behind the development of diseases such as SSc. Particularly attractive in this context is the possibility that the increase in PDGF receptor expression demonstrated herein and the indirectly indicated increase in PDGF synthesis and release may represent a final common pathway which, in genetically susceptible individuals (27,28), can be reached both via pure immunologic stimulation (such as in the chronic graft-versus-host reaction [6]) and by the influence of environmental agents (such as silica [29] or polyvinyl chloride [30]).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Newly emerging techniques for determining when and where the synthesis of PDGF polypeptides and PDGF receptors occurs in situ should aid in a more systematic search for etiologic agents behind the development of diseases such as SSc. Particularly attractive in this context is the possibility that the increase in PDGF receptor expression demonstrated herein and the indirectly indicated increase in PDGF synthesis and release may represent a final common pathway which, in genetically susceptible individuals (27,28), can be reached both via pure immunologic stimulation (such as in the chronic graft-versus-host reaction [6]) and by the influence of environmental agents (such as silica [29] or polyvinyl chloride [30]).…”
Section: Discussionmentioning
confidence: 99%
“…Its pathogenic molecular mechanisms remain largely unknown (1). The demonstration of infiltrating T cells and macrophages in the skin of patients with recent-onset SSc has indicated that cell-mediated immune reactions may be involved in some stage of the pathogenesis of this disease (2-5), a notion that is supported by the appearance of scleroderma-like lesions in some patients with chronic graft-versus-host disease secondary to bone marrow transplantation (6). However, there are presently few suggestions on how immunologic events may, on a molecular level, be related to the changes in connective tissue cell behavior that constitute the main characteristics of SSc.…”
mentioning
confidence: 99%
“…GvHD is classically viewed as caused by histoincompatibility between donor lymphocytes and host tissues [16, 17]with a predominance of suppressor-type lymphocytes in peripheral blood and both epidermal and dermal skin compartments [4]. Epithelial damage is the most prominent feature in GvHD and is likely to be caused by alloreactive cytotoxic T cells.…”
Section: Discussionmentioning
confidence: 99%
“…Chronic skin lesions of homologous disease show extreme epidermal atrophy with markedly increased thickening and collagenization of the dermis• An inflammatory reaction, if present, is usually mild in such lesions. Similarly chronic graft-vs.-host disease (GVHD) after bone marrow transplantation has been found to have scleroderma-like features in humans (7,8,32). Spielvogel et al (7) have noted that patients with chronic GVHD have cutaneous abnormalities including degeneration and loss of cellularity of surface epithelium, hyperkerotosis, hyperpigmentation, and an infiltrate of the mid and deep dermis by monocytes, histiocytes, and fibroblasts (7).…”
Section: Discussionmentioning
confidence: 99%