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

We investigated the incidence of chronic graft-versus-host disease (GVHD) and skin and oral lesions in chronic GVHD in 90 Japanese leukemia patients surviving over 100 days after bone marrow transplantation (BMT) from HLA-compatible siblings. The clinical characteristics of chronic cutaneous GVHD occurring in eight of these patients are summarized. There were some differences from previous reports in the USA and Europe. The incidence (8/29: 28%) of skin lesions in chronic GVHD was low in contrast to the previously reported high incidence (79-90%). Cutaneous manifestations in six out of eight patients with chronic GVHD tended to be mild, and lichen-planus-like eruptions in the skin and scleroderma-like lesions, which are well known as representative cutaneous manifestations of chronic GVHD, were rare. Furthermore, our statistical analysis indicated that there was no relationship between pretransplant total body irradiation and GVHD prophylaxis or acute GVHD and the onset of chronic cutaneous GVHD. The present study suggests that the differences from previous reports in the USA and Europe concerning chronic cutaneous GVHD may be attributable to differing genetic backgrounds in Japanese and western populations.
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PMID:Clinical characteristics of chronic cutaneous graft-versus-host disease in Japanese leukemia patients after bone marrow transplantation: low incidence and mild manifestations of skin lesions. 142 88

Lichenoid dermatosis is a pattern description of a variety of cutaneous lesions which primarily affect the dermoepidermal junction. Involvement of skin appendages has been restricted to hair follicles in lichen planopilaris and discoid lupus erythematosus. Sweat gland involvement has not been described in the four common members of this group, namely, lichen planus, discoid lupus erythematosus, fixed drug eruptions and erythema multiforme, although structural abnormalities have been reported in graft-versus-host disease. In a detailed morphological study of 59 cases, including lichen planus (12), discoid lupus erythematosus (18), fixed drug eruption (14) and erythema multiforme (15), 78% (47/59) showed sweat, gland abnormalities. The abnormalities included vacuolation of cell cytoplasm, with and without lymphocytic infiltration, apoptosis of basal cells and basal cell hyperplasia of the excretory ducts which predominantly affected the portion of the duct adjoining the acrosyringium. The portion of the duct close to the secretory gland was only involved in continuity and the secretory glands were unaffected. These abnormalities of the sweat gland mostly constitute primary involvement by the disease process in contrast to structural abnormalities secondary to fibrosis.
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PMID:Sweat gland abnormalities in lichenoid dermatosis. 183 38

Syngeneic rat radiation chimeras treated transiently with cyclosporine (CsA) often develop a GVHD-like syndrome after discontinuing the drug. CsA also causes medullary involution and loss of medullary epithelium in the thymus. Chronic graft-versus-host disease (GVHD), a late occurring syndrome following bone marrow transplantation with many features of autoimmune diseases, is thought by many to result from a thymic deficiency leading to a failure to develop specific tolerance for the host. A direct connection between a thymic deficiency and chronic GVHD was tested by transferring thymocytes from CsA-treated syngeneic Lewis chimeras into irradiated Lewis secondary recipients. Nine of 10 of these recipients had evidence of chronic GVHD in skin biopsies taken at 3 weeks posttransplant or in the autopsies at 5 weeks. Changes included characteristic lichen planuslike infiltrates and sclerodermalike changes in the skin, characteristic infiltrates and myositis of the tongue, often chronic hepatitis with bile duct injury, and interstitial and ductal infiltrates in the serous salivary glands. Immunoperoxidase stains of the skin and tongue infiltrates showed a marked predominance of W3/25+:OX8- lymphocytes. The hair follicles had increased expression of Ia antigen. The thymus in the secondary recipient had variable thymocyte reconstitution of the cortex and a mild to marked reduction in the relative size of the medulla. Stains for cytokeratin showed a moderate to marked reduction of cortical epithelium and marked to total loss of the medullary epithelium. These studies demonstrate that the features of post-CsA syngeneic GVHD resembling chronic GVHD result from an abnormal thymic microenvironment. They also provide additional evidence linking a thymus deficiency with chronic GVHD.
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PMID:Transfer of cyclosporine-associated syngeneic graft-versus-host disease by thymocytes. Resemblance to chronic graft-versus-host disease. 325 8

Immunohistochemical analysis of oral lichen-planus-like eruption (LPLE) in graft-versus-host disease (GVHD) using monoclonal antibodies (MoAbs) was performed on five patients after allogeneic bone marrow transplantation (BMT) for leukemia. In the mucosal lesions of LPLE in GVHD, the major population of infiltrated lymphocytes in the areas of upper lamina propria (Lp), basal cell layer (Bc), and epithelium above the basal cell layer (Ep) were T-cells (Leu-1+, Leu-4+) and expressed the phenotype associated with suppressor/cytotoxic T-cells (Leu-2a+) rather than helper/inducer T-cells (Leu-3a+). Some of the infiltrated lymphocytes in the areas of Lp, Bc, and satellite cell necrosis (SCN) bore interleukin-2 (IL-2) receptor. HLA-DR antigen was expressed on keratinocytes in the LPLE lesions. Immunoelectron micrographs showed various degrees of degeneration of keratinocytes to which Leu-2a+ cells attached, whereas those with accidentally attached Leu-3a+ cells preserved normal structures. These findings suggest that cellular immunity mediated by cytotoxic T-cells may play a major role in the pathogenesis of oral LPLE in GVHD.
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PMID:Immunohistochemical analysis of oral lichen-planus-like eruption in graft-versus-host disease after allogeneic bone marrow transplantation. 327 80

Ia antigen (HLA-DR in man) has been demonstrated in keratinocytes in graft versus host disease. This study investigates the occurrence of HLA-DR in keratinocytes in the following dermatoses: eczematous dermatitis, discoid lupus erythematosus, with immunoglobulin and non-exposed skin from cases of systemic lupus erythematosus with immunoglobulin deposits, lichen planus, lichen simplex, bullous pemphigoid, pemphigus vulgaris, 'toxic erthema', tuberculid and chillblain. Keratinocyte staining was found in a variety of conditions. The unifying features of the instances of its occurrence was lymphoid infiltration and usually some focal evidence of keratinocyte damage. Thus in eczema the staining was mid-epidermal, while in discoid lupus erythematosus and lichen planus it was basal. HLA-DR staining was absent in bullous pemphigoid and pemphigus vulgaris, which is consistent with the hypothesis that in these conditions the damage is mediated by autoantibodies and complement in the absence of cellular immune attack.
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PMID:Expression of HLA-DR (Ia like) antigen on epidermal keratinocytes in human dermatoses. 620 2

A 45-year-old female patient with CML underwent allogeneic BMT and developed two episodes of acute GVHD. The first episode of acute cutaneous GVHD grade II (day +17) responded well to systemic CsA and steroids. During the second episode (around day +60) the patient developed erythroderma (grade III), and subsequently signs of lichen-planus-like GVHD. The patient did not respond to increased dosages of prednisolone and CsA. On day +89 extracorporeal photochemotherapy (ECP) was initiated. After four cycles, a significant improvement of erythroderma and lichen-planus-like lesions was documented, and after 12 cycles, a lasting complete remission was achieved. To our knowledge this is the first report of successful treatment of early-onset, lichen-planus-like GVHD after allogeneic BMT with ECP.
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PMID:Complete remission of lichen-planus-like graft-versus-host disease (GVHD) with extracorporeal photochemotherapy (ECP). 905 23

A 63-year-old male patient spontaneously developed severe erosive orogenital mucositis, palmoplantar and gluteal inflammatory lesions resistant to therapy. The skin lesions clinically and histologically resembled lichen-planus-like graft-versus-host disease. Investigation for an underlying autoimmune or malignant disorder revealed a centrocytic-centroblastic low-grade non-Hodgkin's lymphoma (according to the Kiel classification) in the bone marrow, mesenterial and iliacal lymphoma. Serological titers were intermittently positive for ANA, anti-Sm/U1RNP, anti-Ro and anti-dsDNA. Immunoprecipitation of lysates from radiolabeled human keratinocytes with the patient's serum revealed circulating antibodies against 210-kD (desmoplakin II), 190- and 170-kD antigens but none against the 230-kD antigen or 250-kD desmoplakin I. Under cytostatic chemotherapy the lymphomas showed complete and long-lasting remission, whereas the mucocutaneous lesions persisted. Six years after diagnosis, the mucocutaneous lesions are sufficiently controlled by immunosuppressive therapy. In the presented case, several features of lymphoma-associated dysimmunoreactivity are assumed that bring about the intrinsic production of various autoantibodies typical of paraneoplastic pemphigus and systemic lupus erythematosus.
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PMID:Graft-versus-host-like mucocutaneous eruptions with serological features of paraneoplastic pemphigus and systemic lupus erythematosus in a patient with non-Hodgkin's lymphoma. 969 95

Lichenoid dermatoses comprise a significant proportion of dermatologic conditions. The pathophysiologic mechanisms are unclear for many such dermatoses making treatment difficult. Ongoing research into these mechanisms is allowing more directed intervention possible. This article describes some of the recent experiences in the therapy of lichen planus, lichen nitidus, toxic epidermal necrolysis, and graft versus host disease.
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PMID:New and emerging therapies for lichenoid dermatoses. 1062 8

There are numerous dermatoses which may cause cicatricial alopecia when localized on the scalp, such as chronic discoid lupus erythematosus (DLE), lichen planus, graft-versus-host disease, dermatomyositis, scleroderma, cicatricial pemphigoid, porphyria cutanea tarda, follicular mucinosis, perifolliculitis capitis abscedens, lichen sclerosus et atrophicus, necrobiosis lipoidica, sarcoidosis, etc. Histologically, cicatricial alopecia is characterized by dermal scarring, along with absent or reduced hair follicles and reduced number of erector pili muscles. According to working classification of cicatricial alopecia by the North American Hair Society, primary cicatricial alopecia may be divided into the following categories: lymphocytic group (e.g., DLE, lichen planopilaris, classic pseudopelade (Brocq), central centrifugal cicatricial alopecia); neutrophilic group (e.g., folliculitis decalvans, dissecting cellulitis); and mixed group (e.g., folliculitis keloidalis). Over a 5-year period, 36 patients with cicatricial alopecia were hospitalized at our Department: DLE (n = 27), pseudopelade Brocq (n = 3), mucinosis follicularis (n = 2), and lichen planopilaris, folliculitis decalvans, folliculitis abscedens and folliculitis keloidalis (one patient each). Clinical evaluation was compared with histopathologic analysis of follicular architecture, as well as with the type, localization and extent of inflammatory infiltrate. Scalp biopsy was considered mandatory in all cases. Our experience indicates the need of more complex research to extend the knowledge about the etiopathogenesis and treatment options for cicatricial alopecia. We hope that this type of alopecia may attract more attention and research in the future.
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PMID:Cicatricial alopecia as a manifestation of different dermatoses. 1731 39

Interface dermatitis includes diseases in which the primary pathology involves the dermo-epidermal junction. The salient histological findings include basal cell vacuolization, apoptotic keratinocytes (colloid or Civatte bodies), and obscuring of the dermo-epidermal junction by inflammatory cells. Secondary changes of the epidermis and papillary dermis along with type, distribution and density of inflammatory cells are used for the differential diagnoses of the various diseases that exhibit interface changes. Lupus erythematosus, dermatomyositis, lichen planus, graft versus host disease, erythema multiforme, fixed drug eruptions, lichen striatus, and pityriasis lichenoides are considered major interface diseases. Several other diseases (inflammatory, infective, and neoplastic) may show interface changes.
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PMID:Interface dermatitis. 2361 39


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