Acute polymyositis during treatment of acute hepatitis C with pegylated interferon alpha-2b

Venezia, G.; Licata, Anna; Marco, Vito Di; Craxı̀, Antonio; Almasio, Piero Luigi

doi:10.1016/j.dld.2005.06.010

Cited by 20 publications

(8 citation statements)

References 37 publications

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“…In fact, type I IFN appears to be involved in both adult and juvenile DM, because muscle biopsy specimens display up-regulation of type I IFN-induced genes, induction of IFN␣/␤-inducible human myxovirus resistance 1 (MX-1) protein, and the presence of plasmacytoid dendritic cells (PDCs), the major type I IFN producers (9,10). An additional role for IFN␣ in PM is suggested by the induction of this disease in patients treated with IFN␣ (11)(12)(13).…”

mentioning

confidence: 99%

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

Eloranta

Helmers

Ulfgren

et al. 2007

Arthritis & Rheumatism

164

128

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Objective. To investigate type I interferon (IFN) system activation and its correlation with autoantibodies and organ manifestations in polymyositis (PM), dermatomyositis (DM), and inclusion body myositis.Methods. Sera from 30 patients and 16 healthy controls, or purified IgG, were combined with material released from necrotized cells to stimulate Conclusion. Immune complexes containing antiJo-1 or anti-Ro 52/anti-Ro 60 autoantibodies and RNA may act as endogenous IFN␣ inducers that activate IFN␣ production in PDCs. These PDCs could be of importance for inducing myositis, whereas in DM patients without autoantibodies the presence of MX-1 protein in capillaries suggests another cellular IFN␣ source and induction mechanism. Consequently, the type I IFN system may be of importance in both PM and DM, but via different pathways.The idiopathic inflammatory myopathies polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM) are characterized by symmetric, proximal muscle weakness and decreased muscle endurance. Other organs are frequently involved, such as skin in DM and lungs in PM and DM. Shared classic histopathologic features are the presence of inflammatory cell infiltrates in skeletal muscle tissue, dominated by T cells and macrophages, and regenerating and degenerating muscle fibers (1). Another characteristic feature is the presence of autoantibodies, of which anti-histidyltransfer RNA synthetase (anti-HisRS or anti-Jo-1) is one of the most frequent (2). This autoantibody is considered myositis specific and is associated with a distinctive clinical phenotype, the so-called antisynthetase syndrome, which is characterized by myositis, Raynaud's phenomenon, interstitial lung disease (ILD),

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mentioning

confidence: 99%

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

Eloranta

Helmers

Ulfgren

et al. 2007

Arthritis & Rheumatism

164

128

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“…However, polymyositis associated with IFN therapy is still relatively rare. To the best of our knowledge, only four cases treated with conventional IFN [6][7][8][9] and only one case with PEG-IFN and ribavirin combination therapy have been reported to date [1].…”

Section: Discussionmentioning

confidence: 99%

A case of polymyositis in a chronic hepatitis C patient treated with peg-interferon-alpha 2b and ribavirin therapy

Okuma

Kimura

Saeki

et al. 2009

Clin J Gastroenterol

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Hepatitis C virus (HCV) infection may result in progression to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Interferon-based treatment in patients with chronic hepatitis C may achieve viral clearance, and as a consequence improve liver histology and prevent progression to hepatocellular carcinoma. At present, the recommended therapy for chronic hepatitis C is peg-interferon-alpha (PEG-IFN-α) in conjunction with the oral nucleoside analog ribavirin. In the current study, we report a case of polymyositis associated with chronic hepatitis C following PEG-IFN-α and ribavirin therapy. The patient, a 64-year-old female who was treated with combination therapy, demonstrated elevated serum CPK, AST, ALT and LDH levels at 28 weeks after treatment onset. As there was an elevation of the serum HCV-RNA levels, combination treatment was ceased at 24 weeks. The patient had received IFN therapy twice previously (IFN-α 2a and IFN-α 2b with ribavirin therapy); however, no adverse side effects were observed. Further laboratory examination, muscle biopsy and imaging data suggested polymyositis, possibly triggered by the PEG-IFN-α treatment. The patient was subsequently administered prednisolone and the dose tapered over 7 months. As a result the polymyositis has remained in remission. Although many autoimmune diseases have been associated with IFN therapy, the development of polymyositis is extremely rare.

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“…Mutations in the gene of the slow myosin heavy chain protein MYH7 on chromosome 14 have been found in several families with this disease and thus the name “myosin storage myopathy” was proposed 4, 14, 16, 21, 26. Linkage to chromosome 3p22 was found in another family with autosomal recessive inheritance, demonstrating that hyaline body myopathy is a genetically heterogeneous disorder 16.…”

Section: Discussionmentioning

confidence: 99%

Hyaline inclusion myopathy: Unmasked by statin therapy

Supala-Berger¹,

Fine²,

Heffner³

et al. 2009

Muscle and Nerve

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We report a case of a patient with history of alcohol abuse, treatment for hepatitis C and repeated strenuous physical activity who developed severe muscle pain and weakness during statin therapy. The symptoms persisted after discontinuation of the drug. The diagnosis of myopathy was made clinically and by electromyography. As his symptoms persisted a muscle biopsy was performed which showed inclusions consistent with hyaline inclusions. Hyaline inclusion myopathy is discussed in the context of this case with review of the literature.

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Acute polymyositis during treatment of acute hepatitis C with pegylated interferon alpha-2b

Cited by 20 publications

References 37 publications

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti–Jo‐1 or anti–Ro 52/anti–Ro 60 autoantibodies

A case of polymyositis in a chronic hepatitis C patient treated with peg-interferon-alpha 2b and ribavirin therapy

Hyaline inclusion myopathy: Unmasked by statin therapy

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