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)

The serum level of total interferon (IFN) was measured in 15 male patients with systemic lupus erythematosus (SLE) in the active phase and in remission, before and during corticotherapy. The values found were correlated with the clinical and humoral signs of disease. The IFN titer was high in the active phase of disease and was correlated with fever, extension of skin rash, polyarthritis, myositis, autoimmune hemolysis, cardiac and cerebral involvement as well as with ESR, reacting protein C, CIC, ANF and the percentage of LE cells. Isolated LE nephropathy without rapidly progressive or advanced renal failure was not associated with high IFN titer.
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PMID:Correlation of serum interferon with some clinical and humoral signs of systemic lupus erythematosus. 171 46

Cytokines have been shown to be potent inducers of major histocompatibility complexes (MHC) class I and II as well as of cell adhesion molecules in muscle tissue cultures, indicating that cytokines may play a role in mediating muscle fiber damage in inflammatory myopathies. We found in 21 cases of autoimmune myositis various amounts of inflammatory cells expressing interleukin (IL)-1 alpha and -beta, IL-2, IL-4, tumor necrosis factor (TNF) -alpha and -beta, and interferon (IFN)-gamma and its receptor. Muscle fibers displayed enhanced expression of IL-1 alpha and -beta, IL-2, and TNF-alpha. Upregulation of cytokines was strongest at sites of cellular infiltration typical for the respective myositis subtype. There was no correlation between the cytokine expression and the grade of inflammation. To a lesser extent, cytokines were also present in Duchenne muscular dystrophy expressed by muscle fibers positive for TNF-alpha and by phagocytic mononuclear cells. Expression of cytokines by the muscle fiber may enable the muscle fiber to induce and mediate the process of autoimmunization and antigen-expression by itself without primary presence of inflammatory cells. Cytokine-expressing muscle fibers may enhance the cytolytic potential of cytotoxic cells and the muscle fiber may serve as source and target.
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PMID:Cytokine expression profile in idiopathic inflammatory myopathies. 878 92

Polymyositis is a systemic autoimmune disorder characterised by proximal muscle weakness which most frequently involves the limbs, neck and trunk. Alpha interferon is an antiviral molecule with well-known immunomodulatory and antiproliferative effects, but its use is often associated with a variety of side effects, in particular autoimmune phenomena. We report the occurrence of polymyositis during treatment with alpha-interferon in a patient affected by malignant melanoma. Indirect evidence suggests that in this case the patient's myositis was not linked to her neoplasia, since the melanoma was confirmed to be in remission both at the time of the diagnosis of the muscle disease and again after more than one year of follow-up.
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PMID:Polymyositis occurring during alpha-interferon treatment for malignant melanoma: a case report and review of the literature. 1065 Oct 86

Inclusion-body myositis (IBM) is an inflammatory muscle disease that has proven resistant to treatment. Tumor necrosis factor molecules have been detected in muscle biopsies from patients with IBM. Etanercept is a TNFalpha receptor fusion protein that binds and inactivates tumor necrosis factor. Nine patients were treated with etanercept at a dose of 25 mg, two times a week for an average of 17 +/- 6.1 months. Each patient was evaluated using quantitative strength testing. Their data were compared to two different control groups. The first control group consisted of patients who participated in trials of beta-interferon-1A and had received placebo. There was no significant difference. The second control group was a natural history cohort of IBM patients. There was no statistically significant difference between the treated group and the natural history group at 6 and 12 months when looking at elbow flexors, or 6 months when looking at hand grip. In the treated patients there was a small but significant improvement (p = 0.002) in handgrip at 12 months.
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PMID:Pilot trial of etanercept in the treatment of inclusion-body myositis. 1643 40

Juvenile dermatomyositis (JDM) is a rare, presumably autoimmune illness that causes proximal muscle weakness and a variety of typical cutaneous features. The study of this illness has been hampered by its rarity but, in recent years, important developments have increased our understanding of JDM. Genetic factors are likely important in the pathogenesis of JDM. These include several Human Leukocyte Antigen alleles, in particular those associated with the 8.1 ancestral haplotype and the tumor necrosis factor-alpha gene 308 polymorphism. Microchimerism, activation of plasmacytoid dendritic cells, and upregulation of type-1 interferon inducible genes also appear to play an important role in the pathogenesis of JDM. The study of JDM has also been limited by a lack of validated assessment tools. Recent work has validated the Childhood Myositis Assessment Scale and the Childhood Health Assessment Questionnaire as measures of muscle strength and function, and the Cutaneous Assessment Tool as a measure of skin disease activity and damage. Development of core sets of tools that should be used in all JDM studies has also been an important step. The use of magnetic resonance imaging and novel laboratory assessments (such as type-1 interferon inducible gene products, peripheral blood B cell and natural killer cell numbers, and myositis-associated and myositis-specific autoantibodies) are also playing an increasing role in the diagnosis and assessment of JDM. Current treatment is with corticosteroids, frequently in combination with other medications such as methotrexate or intravenous gammaglobulin. Newer therapies, such as anti-tumor necrosis factor agents and rituximab are currently being evaluated; it is not clear what role these medications will have in the future.
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PMID:Juvenile dermatomyositis: advances in pathogenesis, evaluation, and treatment. 1987 22

Yellow fever (YF) vaccines (17D-204 and 17DD) are well tolerated and cause very low rates of severe adverse events (YEL-SAE), such as serious allergic reactions, neurotropic adverse diseases (YEL-AND), and viscerotropic diseases (YEL-AVD). Viral and host factors have been postulated to explain the basis of YEL-SAE. However, the mechanisms underlying the occurrence of YEL-SAE remain unknown. The present report provides a detailed immunological analysis of a 23-year-old female patient. The patient developed a suspected case of severe YEL-AVD with encephalitis, as well as with pancreatitis and myositis, following receipt of a 17D-204 YF vaccination. The patient exhibited a decreased level of expression of Fc-gammaR in monocytes (CD16, CD32, and CD64), along with increased levels of NK T cells (an increased CD3(+) CD16(+/-) CD56(+/-)/CD3(+) ratio), activated T cells (CD4(+) and CD8(+) cells), and B lymphocytes. Enhanced levels of plasmatic cytokines (interleukin-6 [IL-6], IL-17, IL-4, IL-5, and IL-10) as well as an exacerbated ex vivo intracytoplasmic cytokine pattern, mainly observed within NK cells (gamma interferon positive [IFN-gamma(+)], tumor necrosis factor alpha positive [TNF-alpha(+)], and IL-4 positive [IL-4(+)]), CD8(+) T cells (IL-4(+) and IL-5(+)), and B lymphocytes (TNF-alpha(+), IL-4(+), and IL-10(+)). The analysis of CD4(+) T cells revealed a complex profile that consisted of an increased frequency of IL-12(+) and IFN-gamma(+) cells and a decreased percentage of TNF-alpha(+), IL-4(+), and IL-5(+) cells. Depressed cytokine synthesis was observed in monocytes (TNF-alpha(+)) following the provision of antigenic stimuli in vitro. These results support the hypothesis that a strong adaptive response and abnormalities in the innate immune system may be involved in the establishment of YEL-AND and YEL-AVD.
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PMID:Clinical and immunological insights on severe, adverse neurotropic and viscerotropic disease following 17D yellow fever vaccination. 1990 94

Polymyositis (PM), dermatomyositis (DM) and inclusion body myositis (IBM) are chronic inflammatory diseases that are characterized by muscle weakness and inflammatory cells in muscle tissue. Autoantibodies are common, some of them are specific for myositis, the most frequent being the anti-Jo-1 antibody which is associated not only with myositis but also with interstitial lung disease and arthritis. A role of type I interferons in disease mechanisms of myositis was first supported by the reported onset of PM and DM during treatment with type I interferon. More recently an interferon signature has been reported in muscle tissue of DM and PM patients both as gene and protein expression, and type I IFN expression in peripheral blood cells seems to correlate with disease activity. Different mechanisms could induce type I interferon in PM and DM like viral infections or endogenous factors as suggested by the observation that sera from myositis patients with anti-Jo-1 antibodies as well as anti-SSA and anti-SSB antibodies have an interferon inducible capacity. Accumulating data indicate a role of the type I interferon in myositis, particularly in juvenile and adult DM and in anti-Jo-1 or anti-SSA positive PM.
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PMID:The type I interferon system in idiopathic inflammatory myopathies. 2018 2

Myositis during interferon therapy is a known but rare adverse event. However the clinician may overlook the symptom-complex of proximal muscle weakness and myalgia, seen in myositis, since myalgia is a commonly reported side effect of therapy. In this context then, is there a role for monitoring muscle enzymes to detect subclinical myositis in patients on interferon therapy? We prospectively monitored the creatine kinase (CK) and lactate dehydrogenase (LD) levels in all our patients who reported myalgia during treatment and noted that muscle enzymes remained within normal range throughout the duration of treatment. This excluded the possibility of subclinical myositis in myalgic patients and thus led us to conclude that routine monitoring of muscles enzymes is neither necessary nor beneficial.
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PMID:Myalgia during interferon therapy--does it warrant monitoring muscle enzymes? 2030 56

Chikungunya virus is a mosquito-borne arthrogenic alphavirus that has recently reemerged to produce the largest epidemic ever documented for this virus. Here we describe a new adult wild-type mouse model of chikungunya virus arthritis, which recapitulates the self-limiting arthritis, tenosynovitis, and myositis seen in humans. Rheumatic disease was associated with a prolific infiltrate of monocytes, macrophages, and NK cells and the production of monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor alpha (TNF-alpha), and gamma interferon (IFN-gamma). Infection with a virus isolate from the recent Reunion Island epidemic induced significantly more mononuclear infiltrates, proinflammatory mediators, and foot swelling than did an Asian isolate from the 1960s. Primary mouse macrophages were shown to be productively infected with chikungunya virus; however, the depletion of macrophages ameliorated rheumatic disease and prolonged the viremia. Only 1 microg of an unadjuvanted, inactivated, whole-virus vaccine derived from the Asian isolate completely protected against viremia and arthritis induced by the Reunion Island isolate, illustrating that protection is not strain specific and that low levels of immunity are sufficient to mediate protection. IFN-alpha treatment was able to prevent arthritis only if given before infection, suggesting that IFN-alpha is not a viable therapy. Prior infection with Ross River virus, a related arthrogenic alphavirus, and anti-Ross River virus antibodies protected mice against chikungunya virus disease, suggesting that individuals previously exposed to Ross River virus should be protected from chikungunya virus disease. This new mouse model of chikungunya virus disease thus provides insights into pathogenesis and a simple and convenient system to test potential new interventions.
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PMID:Chikungunya virus arthritis in adult wild-type mice. 2051 86

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


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