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)

(1) We evaluated efficacy of several treatments for HTLV-I-associated myelopathy (HAM) on the basis of our study on 254 HAM patients and of literature review. Improvement of motor disability more than fair response was obtained as follows: 82% in prednisolone, 69% in interferon-alpha, 92% in fosfomycin, 82% in high-dose vitamin C, 72% in blood purification therapy, 70% in heparin, 59% in salazosulfapyridine, 56% in thyrotropin-releasing hormone, 55% in erythromycin, 50% in mizoribine. (2) In the absence of clear guideline, the efficacy of zidovudine in the AIDS dementia complex has been demonstrated. There are also efficacy of amytriptylinein controlling HIV headache, corticosteroid in mononeuritis multiple and inflammatory myositis, hydrocortisone in autonomic neuropathy and plasmapheresis in distal sensory neuropathy respectively. Otherwise, it is emphasized that ddI, ddC and d4T have peripheral neuropathy as major, dose related side effect.
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PMID:[Therapy for HAM/TSP and AIDS]. 799 4

A 57-year-old woman was admitted with symmetrical proximal muscle weakness, liver dysfunction, abnormal muscle enzymes, and she was an antibody to hepatitis B e (anti-HBe) positive hepatitis B virus (HBV) carrier. Biopsy of her left quadriceps femoris showed myositis, so prednisolone was started at 40 mg/day. However, her hepatic function deteriorated and liver biopsy after 4 months showed acute hepatitis with partial submassive necrosis. Treatment with interferon-alpha and cyclosporin A progressively reduced the transaminase and HBV-DNA levels. Early treatment with interferon-alpha plus cyclosporin A can control exacerbation of hepatitis B.
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PMID:Antibody to hepatitis B e positive hepatitis induced by withdrawal of steroid therapy for polymyositis: response to interferon-alpha and cyclosporin A. 967 85

The age-related acquisition of resistance to fatal Sindbis virus infection was examined using a molecularly cloned laboratory strain of the AR339 isolate designated TRSB. TRSB caused 100% mortality in mice up to 5 days of age. Resistance to fatal infection developed abruptly between 5 and 9 days of age. Lethal Sindbis virus infection of mice inoculated at 4 days of age was characterized by high levels of virus replication, induction of high levels of interferon-alpha/beta and TNF-alpha and severe thymic involution indicative of a systemic stress response. These changes correlated with predominantly noninflammatory lesions. In contrast, TRSB infection of older mice was characterized by survival, more limited virus replication, reduced cytokine induction, and the development of inflammatory responses leading to encephalitis, myositis, and myocarditis. Previous studies utilized infections of neonatal mice with TRSB and an attenuated mutant of TRSB to compare fatal and nonfatal Sindbis infection (Trgovcich et al., 1996. Virology 224, 73-83). The experiments reported here utilize mouse age at the time of infection to create conditions for examination of fatal and nonfatal TRSB infections. Both experiments suggest that fatal infection is associated with a shock-like syndrome and little or no inflammatory pathology, while survival is correlated with greatly reduced cytokine levels and inflammatory lesions.
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PMID:TNFalpha, interferon, and stress response induction as a function of age-related susceptibility to fatal Sindbis virus infection of mice. 1054 7

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

Polymyositis (PM) and dermatomyositis (DM) are rare idiopathic inflammatory myopathies (IIM) with a presumed autoimmune pathogenesis. Typical features are subacute onset, proximal, symmetric muscle weakness, elevated serum creatine kinase, and mononuclear cell infiltrates in the muscle biopsy. Strong support for an autoimmune pathogenesis comes from histopathological findings in biopsies of affected muscles. Furthermore, the association with autoantibodies supports the notion that immune-mediated inflammation is involved. PM and DM may occur in isolation or in connection with a connective tissue disease or cancer. The current treatment for IIM consists of first-line high-dose steroids and various conventional second-line treatments. Improvements in treatment for IIM are hampered by difficulties in the design of trials and the low incidence and prevalence of the disease. Cytokines and chemokines are factors involved in the inflammatory process in IIM, and are candidates for future therapeutic targets. Preliminary data with anti-tumour necrosis factor therapy are not very promising, but results of blockers of the lymphotoxin signalling pathway are to be awaited. Anti-B cell therapy may be a valuable therapeutic option for treatment of refractory IIM. The effects of anti-interferon-alpha in IIM are to be awaited, as are results of other anti-cytokine therapies and anti-chemokine therapy. Outcome measures to be used in clinical trials in II M include at present the core sets of outcome proposed by the International Myositis Assessment Clinical Study Group (IMACS).
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PMID:Dermatomyositis and polymyositis: new treatment targets on the horizon. 2205 60