Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association of lichen planus and primary biliary cirrhosis in five patients is reported. The coexistence of the two diseases is probably more than coincidental and may be due to the fact that both conditions are based on an alteration of mechanisms. There is great similarity between primary biliary cirrhosis and chronic graft-versus-host disease and a common pathogenesis for the two entities has been postulated. Since lichen planus is one of the most common manifestations of graft-versus-host disease, its association with primary biliary cirrhosis is of significance, although not unexpected.
Br J Dermatol 1982 Jun
PMID:Lichen planus and primary biliary cirrhosis. 708 75

An ultrastructural study was performed on skin biopsies of eight patients with lichenoid eruption of chronic graft-versus-host disease (GVHD). The lichenoid eruption is similar to idiopathic lichen planus with the injury of the basal cells, the distribution of the numerous colloid bodies, and the presence of regenerative cells. Lymphocytes satellites of injured keratinocytes were observed in those lichenoid eruptions, as well as in the acute phase of GVHD. The numerous mast cells in the lichenoid eruption of GVHD may be related to the connective tissue changes of the patients progressing to a late sclerotic phase of chronic GVHD.
Ann Dermatol Venereol 1981
PMID:[Ultrastructural similarities between the planus-like reaction of the graft versus host disease and the idiopathic lichen planus (author's transl)]. 723 4

The pathogenetic mechanisms underlying common, and less common but severe, adverse cutaneous drug reactions are reviewed. Pharmacogenetic variability may account for a susceptibility to serious drug reactions to sulphonamides and anticonvulsants, as well as to lupus erythematosus (LE)-like syndrome. Exanthematous drug reactions may have an immunological basis. Cell mediated cutaneous drug reactions, including lichenoid reactions, LE-like syndrome, fixed drug eruption, erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis, will inevitably involve elements of the skin immune system. Graft-versus-host disease provides a useful model for aspects of these drug-induced disorders. Urticaria, angioedema, anaphylaxis and anaphylactoid reactions may involve Type I immunoglobulin (Ig)-mediated or Type III hypersensitivity, or may be caused by pharmacological, non-allergic means. Drug-induced vasculitis, serum sickness and the Arthus phenomenon are manifestations of the immune complex disease. Drug-induced pemphigus may involve immune dysregulation, but several thiol-containing drugs are able to cause antibody-independent acantholysis directly.
Australas J Dermatol 1995 Aug
PMID:Mechanisms of drug eruptions: Part I. 748 37

It has been suggested that the bulge of the hair follicle contains a pool of follicular stem cells that may serve as a target site of graft-versus-host disease and as a source of cells with carcinogenic potential. The bulge is prominent in the developing follicle although it is a subtle swelling in the adult follicle. In this paper, we studied the bulge in human fetal skin specimens. Ultrastructurally, the bulge cells, especially the interior cells, have abundant free ribosomes and glycogen particles, but almost no cytoplasmic organelles indicative of differentiation. Immunostaining with several specific anti-keratin antibodies demonstrated that the bulge cells express keratins of both stratified and simple epithelia. Melanocytes and Merkel cells, defined by immunohistochemical and ultrastructural criteria, are seen among bulge cells. Laser confocal microscopy revealed that primitive smooth muscle cells attached directly to the bulge initially at the mid-bulbous hair peg, the stage when the bulge is most prominent. K-laminin and type VII collagen are strongly expressed in the dermoepidermal junction of the bulge and between the matrix area of the bulb and the dermal papilla. Thus, the bulge of human hair follicle is not only an attachment site for arrector pili muscle, but also a pool of keratinocytes that are relatively undifferentiated.
J Invest Dermatol 1995 Dec
PMID:Characterization of hair follicle bulge in human fetal skin: the human fetal bulge is a pool of undifferentiated keratinocytes. 749 Apr 81

We report a patient with graft versus host disease (GVHD) with mixed chimerism (MC). The patient had chronic myelogenous leukemia and received bone marrow transplantation (BMT) from his elder sister. Eighty days after BMT, erythematous lesions appeared on his chest. Histological examination from the skin lesion revealed lymphocytic infiltration into the upper dermis. Eosinophilic necrotic keratinocytes were scattered through the epidermis. Liquefaction degeneration was also recognized. Sicca syndrome appeared from 110 days after BMT. Detection of host origin Y-chromosome-specific DNA by polymerase chain reaction (PCR) method in bone marrow and peripheral blood showed that all bone marrow samples obtained 6 months from BMT were positive for Y-specific DNA, while peripheral blood became positive in the 60th month after BMT. The host origin normal karyotype (46,XY) in the bone marrow samples was identified for the first time in the 60th month after BMT. These results indicate that host-origin hematopoietic cells survived after BMT.
J Dermatol 1995 Jul
PMID:Graft versus host disease with mixed chimerism. 756 Apr 40

Transfusion-associated graft-versus-host disease (TAGVHD) occurs in immunocompromised persons who receive nonirradiated blood products containing immunologically competent donor lymphocytes. TAGVHD occurs almost exclusively as an acute illness and has a very high mortality rate. We describe a patient with a long history of non-Hodgkin's lymphoma in whom acute TAGVHD developed after transfusion of packed red blood cells from two unrelated donors. TAGVHD developed despite pretreatment of the transfused units with white blood cell filters. The patient survived and subsequently had clinical manifestations typical of chronic cutaneous graft-versus-host disease. HLA phenotyping studies suggested that elements from both transfusion donors engrafted. TAGVHD is a rare but probably underdiagnosed disorder that, although usually fatal, may evolve into chronic graft-versus-host disease. Treatment of blood products with white blood cell filters does not appear adequate to prevent TAGVHD.
J Am Acad Dermatol 1995 Aug
PMID:Transfusion-associated chronic cutaneous graft-versus-host disease. 761 79

We report a heart transplant recipient who developed graft-versus-host disease (GVHD) following blood transfusion. We consider that heart transplant recipients should be included in the category of immunosuppressed patients who may develop this disease after being treated with blood products. We also consider that, at the present time, irradiation of blood products is the only useful method of avoiding development of GVHD in these patients.
Br J Dermatol 1995 Apr
PMID:Transfusion-associated acute graft-versus-host disease in a heart transplant recipient. 774 58

An infant suffered from psoriasiform dermatitis complicated by severe constitutional symptoms. During his 12 months of hospitalization, the symptoms exacerbated periodically despite numerous therapeutic trials. Histologic findings revealed lichenoid psoriasiform dermatitis with striking eosinophilic necrosis of epidermal cells and satellite cell necrosis. Immunohistochemically, CD1+ Langerhans cells had almost disappeared, and CD8+ cytotoxic-suppressor T cells were predominant over CD4+ helper-inducer T cells in the epidermis. These findings in the skin biopsy specimens suggested some similarity to graft-versus-host disease but no known cause of that disorder was proved. Finally, methotrexate was effective. The patient became afebrile, and his skin lesions improved, leaving almost no scarring. This patient seems to have had specific clinical features that do not correspond with any of the known dermatitis. Clinical, histologic, and laboratory findings did not uncover any etiologic factors.
Pediatr Dermatol 1995 Mar
PMID:A case of infantile febrile psoriasiform dermatitis. 779 16

(C57BL/6 x DBA/2)F1 (B6D2F1) mice inoculated with parental DBA/2 (D2) splenocytes develop chronic stimulatory graft-versus-host reaction with many of the clinical manifestations of systemic lupus erythematosus. This investigation tested the ability of 8-methoxypsoralen (8-MOP) and ultraviolet A (UVA) light-treated D2 cells, primed to contain an expanded population of T cells specific for B6D2F1 major histocompatability complex antigens, to treat and/or prevent such systemic lupus erythematosus-like disease. 8-MOP/UVA-treated cells from B6D2F1-primed D2 donors were inoculated into B6D2F1 recipients weekly six to ten times, either before or after initiating graft-versus-host disease with normal D2 cells. A third group of B6D2F1 recipients were vaccinated weekly six times before disease initiation using 8-MOP/UVA-attenuated, B6D2F1-primed D2 cells that had been secondarily stimulated and expanded in vitro in the presence of irradiated B6D2F1 targets and interleukin-2. Control B6D2F1 mice were vaccinated with 8-MOP/UVA-treated D2 cells stimulated in vitro and/or in vivo with (C3H/HeJ x DBA/2)F1 cells. Only mice vaccinated with 8-MOP/UVA-attenuated D2-anti-B6D2F1 cells that were secondarily stimulated and expanded in vitro exhibited differences from controls when measured by the clinical parameters of ascites formation, and mean survival (p < 0.025). These groups also differed significantly in mean antinuclear antibody titer measured 14 weeks after disease initiation (p < 0.05). At 28 weeks, histologic evidence of systemic lupus erythematosus-like kidney disease was found only in the control group. These results indicate that photochemically attenuated D2-anti-B6D2F1 cells primed in vivo and secondarily stimulated and expanded in vitro are capable of vaccinating recipients against progression of graft-versus-host reaction-initiated systemic lupus erythematosus-like disease.
J Invest Dermatol 1995 Feb
PMID:Specific suppression of lupus-like graft-versus-host disease using extracorporeal photochemical attenuation of effector lymphocytes. 782 72

The skin is a major target organ for graft-versus-host disease (GVHD), the principal complication of allogeneic bone marrow transplantation. The purpose of the present study was to test whether mast cell degranulation might be related to early target cell injury in the development of acute GVHD. We employed two irradiated murine strain combinations, one in which disease was mediated by CD4+ effector T cells (B10.D2-->DBA/2), and the other by CD8+ effector T cells (B10.BR-->CBA). As compared to controls, both models exhibited mast cell degranulation of differing extents and patterns, as well as dyskeratosis in the epidermis before the influx of effector lymphocytes. These results suggested that factors produced and released by degranulated dermal mast cells might contribute to early target cell injury. Accordingly, the possible role of tumor necrosis factor (TNF)-alpha, a cytokine recently discovered in mast cell granules, was investigated by the injection of anti-TNF-alpha antibody during the course of disease mediated by either CD4+ or CD8+ T cells. Although overall survival of recipients undergoing CD4+ T-cell-mediated GVHD was only slightly improved and the extent of mast cell degranulation was not affected by anti-TNF-alpha antibody treatment, the skin exhibited a significant diminution in the number of dyskeratotic cells/linear mm at 3-4 weeks post-transplantation. In contrast, anti-TNF-alpha antibody failed to enhance survival or reduce the number of dyskeratotic cells in the skin during CD8+ T-cell-mediated disease. Finally, to determine whether CD8+ T-cell-mediated GVHD was at all dependent upon mast cell involvement, the C3H.SW-->B6WWv strain combination was utilized, in which recipients were genetically deficient in mast cells. Onset of GVHD was significantly delayed in B6WWv mice and was clearly correlated to the appearance and increase of de novo mast cells at later time points.
J Invest Dermatol 1994 Apr
PMID:Role of mast cells in early epithelial target cell injury in experimental acute graft-versus-host disease. 790 82


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>