Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Patients with systemic lupus erythematosus (SLE) have a 25-50% chance of developing abnormal liver tests in their lifetime. This percentage does not include unconjugated hyperbilirubinaemia due to haemolysis associated with SLE, or elevated aspartate-aminotransferase caused by SLE-associated myositis. The most common cause is drug-induced hepatitis, while mild, predominantly lobular-but sometimes also portal and periportal-hepatitis reflecting SLE activity is another possibility. Other liver disease in SLE can be related to thrombotic events, whether or not associated with the lupus anticoagulant, including Budd-Chiari syndrome and veno-occlusive disease. Other liver abnormalities have been more or less frequently associated with SLE, such as nodular regenerative hyperplasia, perihepatitis, and hepatic or splenic rupture. Also viral hepatitis, obstructive jaundice, autoimmune hepatitis, primary biliary cirrhosis, granulomatous hepatitis, cryptococcus infection of the liver, chronic hepatitis with IgA or IgD deficiency, porphyria or idiopathic portal hypertension co-existing with SLE have been described.
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PMID:The spectrum of liver disease in systemic lupus erythematosus. 871 47

We report a case of myositis associated with chronic hepatitis C virus infection. Muscle biopsy and immunohistochemistry showed perifascicular atrophy, few necrotic and regenerating fibres, scarce perivascular infiltrates, deposits of immunoglobulin G, C3, fibrinogen and MAC in muscle vessel walls, and non-uniform expression of major histocompatibility complex-I antigens among muscle fibres. Hepatitis C virus NS3 antigen and hepatitis C virus RNA were detected in infiltrating cells but not within muscle fibres or endothelial cells. Our findings suggest that humoral-mediated immune mechanisms, not directly related to hepatitis C virus infection of muscle structures, may sustain the local inflammatory reaction in this patient.
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PMID:Hepatitis C virus infection and myositis: a virus localization study. 1246 35

We report the case of an ABO-incompatible kidney transplant recipient who died suddenly following a good transplant course of 12 years. For 10 years after transplantation, the graft function had been stable (s-Cr: 1.0-1.5 mg/dL), although chronic hepatitis C had developed, with elevation of transaminase. In the 11th year, he was admitted into the hospital with low-grade fever and general fatigue. Jaundice and anaemia progressed, and he died 2 months after admission. The autopsy diagnosis was: (1) post-renal transplantation state, (2) phlegmonous enterocolitis with septic infarction, (3) cellulitis and necrotic myositis, and (4) sepsis. The transplanted kidney graft showed well-preserved glomeruli and tubules, corresponding to chronic allograft nephropathy (CAN) grade Iota (ci1, ct1, cv1), according to the Banff classification. The pathological changes observed in this long-surviving ABO-incompatible kidney graft were similar to those of an ABO-compatible graft, although its degree was milder.
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PMID:An autopsy case of bacterial septic shock 12 years following ABO-incompatible renal transplantation. 1519 73

We report the first case of inclusion body myositis (IBM) which occurred after interferon-alpha treatment for chronic hepatitis C. A 63-year-old man contracted hepatitis C virus (HCV) and human T cell leukemia virus type 1 (HTLV-1) from a blood transfusion at age of 18. At age 57, he was treated with interferon-alpha (IFN alpha) for chronic hepatitis C. A month later, he developed muscle weakness in the proximal part of his lower extremities. IBM was diagnosed after a muscle biopsy at age 62. Steroid therapy improved his muscle power. One year later, worsening of his hepatic condition required re-administration of IFN alpha after gradual decrease and discontinuation of prednisolone. However, several days later, he rapidly became weaker and required a cane to walk. Elevated serum creatine kinase (2,199IU/L) and abnormal intensity in his MRI of thigh were demonstrated. The second muscle biopsy, performed after obtaining the informed consent from our patient, confirmed relapse of IBM. His symptoms improved again after discontinuation of IFN alpha and re-induction of prednisolone. Although a few cases each of IBM associated with HCV or HTLV-1 have been reported, the pathogenesis of virus-associated inflammatory myositis has not been clearly understood. Moreover, there has been no description on IBM associated with IFN alpha treatment, though several cases of polymyositis have been reported. Our case suggests that infection of HCV and HTLV-1 may be immunologically involved in the development of IBM and that IFN alpha can be directly related to onset and relapse of IBM.
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PMID:[Inclusion body myositis after interferon-alpha treatment in a patient with HCV and HTLV-1 infection]. 1551 4

Dermatomyositis is a rare and idiopathic inflammatory myopathy with characteristic cutaneous manifestations. In recent years, some researchers have showed the cause of dermatomyositis might be due to an autoimmune response induced by viral infections. However, chronic hepatitis C virus (HCV) infection associated with dermatomyositis is very rare. In this report, we present a patient with dematomyositis with abnormal liver function test results and elevated alfa-fetoprotein level. After excluding multiple viral infections known to cause myositis, the case was proven to be chronic hepatitis C by positive HCV-RNA in the serum. Abdominal computed tomography showed a liver tumor on the right lobe and needle biopsy proved it to be hepatocellular carcinoma. Chronic hepatitis C or hepatocellular carcinoma might cause dermatomyositis by inducing the formation of autoantibodies. Chronic hepatitis C or hepatocellular carcinoma should be considered in patients of dermatomyositis if no other cause is found.
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PMID:Chronic hepatitis C virus infection associated with dermatomyositis and hepatocellular carcinoma. 1579 60

Dermatomyositis (DM) is an idiopathic inflammatory myopathy (IIM) with typical cutaneous manifestations. It has been proposed that DM may be caused by autoimmune responses to viral infections, and previous studies have also shown that an association between DM and malignancy. However, chronic hepatitis B virus (HBV) infection associated with DM and hepatocellular carcinoma (HCC) is rarely encountered. The authors report a case of DM and HCC in a patient with a HBV infection. A 58-year-old man presented erythematous skin rashes on a sun-exposed area of 2 year's duration, and recent proximal muscle weakness. His medical history revealed that he had a chronic HBV infection. A diagnosis of DM relies on proximal muscle weakness, elevated muscle enzymes, myopathic changes (demonstrated by electromyography), muscle biopsy evidence of myositis, and its characteristic cutaneous findings. A Liver mass in the left lobe visualized by abdominal computed tomography was confirmed histologically as HCC. This case suggests that DM associated with HCC might be caused by a HBV infection.
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PMID:Dermatomyositis associated with hepatitis B virus-related hepatocellular carcinoma. 1880 99

A 62-year-old woman with a past history of chronic hepatitis C virus infection presented an atypical predominantly painful polymyositis following a flu-like syndrome, persisting despite the withdrawal of PEG-interferon alpha-2b therapy. Clinical assessment, then immunological, electrophysiological and iconographic investigations including myositis antibodies, electromyography, pulmonary functions assessment and thoracic CT-scan found respectively "mechanic hands", arthralgia, presence of antisynthetase anti-PL7 antibody, typical myographic features of hip and shoulder girdles involvement, pulmonary fibrosis and restrictive syndrome features. A deltoid muscle biopsy revealed an unclassified myositis getting closer to anti-J0-1 and connective tissue disease associated myositis featuring: some components of polymyositis, dermatomyositis, and the following peculiar pathological aspects: noncaseous granulomatous infiltrate, endomysial microangiopathy and vascular and sarcolemic deposition of complement membrane attack complex. The diagnosis of interferon induced anti-PL7 antisynthetase syndrome with microangiopathic and granulomatous overlap myositis was retained. A treatment associating intravenous immunoglobulin and moderate tapered oral corticosteroids allowed a complete long-term resolution of myositis and a clear improvement of pulmonary involvement. This case points out the wide range of interferon alpha-associated disorders and call for a precise and detailed immunopathological analysis of myositis, instead of the usual vague classification as idiopathic polymyositis or dermatomyositis about antisynthetase syndrome.
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PMID:Anti-PL7 antisynthetase syndrome under interferon therapy. 2085 61

In dogs with symptomatic or asymptomatic leishmaniasis, Leishmania infantum appears to induce a mixed Th1/Th2 immune response that in the sick dog may eventually result in tissue damage via different pathomechanisms, notably granulomatous inflammation (eg, nodular dermatitis, osteomyelitis), immune complex deposition (eg, glomerulonephritis), and/or autoantibody production (eg, polymyositis). This is a compensatory but detrimental mechanism generated mainly because of the insufficient killing capacity of macrophages against the parasite in the susceptible dog. Clinical disease is typically exemplified as exfoliative and/or ulcerative dermatitis, with or without nasodigital hyperkeratosis and onychogryphosis, glomerulonephritis, atrophic myositis of masticatory muscles, anterior uveitis, keratoconjunctivitis sicca, epistaxis, and/or polyarthritis, appearing alone or in various combinations. The pathogenesis of these clinical conditions has recently been highlighted, to a greater or lesser extent. The usually subclinical conditions expressed as chronic colitis, chronic hepatitis, vasculitis, myocarditis, osteomyelitis, orchiepididymitis, and meningoencephalomyelitis, though uncommon, are of pathologic importance from a differential point of view. The leading cause of death among canine leishmaniasis patients is chronic proteinuric nephritis that may progress to end-stage kidney disease, nephrotic syndrome, and/or systemic hypertension. However, even the asymptomatic proteinuria, when profuse, may be a serious problem because it predisposes to arterial thromboembolism and eventually contributes to the deterioration of the body condition.
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PMID:Pathologic mechanisms underlying the clinical findings in canine leishmaniasis due to Leishmania infantum/chagasi. 2451 Sep 47

Polymyositis (PM) is an inflammatory condition of skeletal muscle and is believed to be a paraneoplastic syndrome associated with various types of cancer. PM associated with chronic hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) is very rare. We report a case of advanced HCC with chronic HBV cirrhosis that presented with proximal muscle weakness. Further investigation showed elevation of muscle enzymes, myopathic pattern of electromyography (EMG), and evidence of myositis compatible with PM. Lamivudine and 1 mg/kg of oral prednisolone were given. Two sessions of transcatheter arterial chemoembolization (TACE) were performed and sorafenib was started. Muscle enzymes normalized after 6 weeks of treatment. Unfortunately, 5 months after treatment, patient was readmitted and died of severe bacterial pneumonia.
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PMID:Polymyositis Associated with Hepatitis B Virus Cirrhosis and Advanced Hepatocellular Carcinoma. 2615 63


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