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01 September 2005

Hepatitis C virus associated arthritis in absence of clinical, biochemical and histological evidence of liver disease - responding to interferon therapy. In reply Leter to the Editor

Shigemasa Sawada

Med Sci Monit 2005; 11(9): LE10-10 :: ID: 428460


Dear Editor, It is my great pleasure to read Newsletter of Medical ScienceMonitor Publication which is the July 2005 issue. Especially, I was most impressed an article subscribedby Akhtar AJ and Funnye AS entitled 'Hepatitis C virus associated arthritis in absence of clinical, biochemicaland histological evidence of liver disease-responding to interferon therapy' [1]. They reported thatseronegative and non erosive polyarthritis with hepatitis C type 1b, having very high viral load, wasimproved by the interferon therapy. This report strongly suggests that the cause of chronic arthritisis due to virus probable hepatitis C virus in some arthritis patient, and encourages us who investigateon the viral etiology for chronic arthritis. As author described, a comprehensive evaluation, includingMRI joint examination, synovial fluid PCR studies, the HCV-RNA in situ hybridization studies and HCVrelated protein studies of synovial cells will help to reveal the etiology for this arthritis. Nontherless,it is curious that a liver biopsy revealed normal liver histology, without evidence of inflammation.But this is suggesting that this virus may have a different RNA sequences, comparing with usual hepatitisC virus and may infect and proliferate in the synovial tissue which is very unusual but this might beas an alternative idea. Another event, this patient's immune system should be remained as investigation.The evidences for the relation with virus and arthritis are accumulating. Especially, Parvovirus B 19[2] and Epstein Barr virus are strong candidate for rheumatoid arthritis etiology. Epstein-Barr virus(EBV) has been a strong candidate about for over 25 years as environmental infectious agent(s). Thereare many circumstantial evidence for association between EBV and RA, but definite evidence is wanting.We reviewed an increase circumstantial proof which has been investigated so far and demonstrate directevidence for the presence of EBV in inflamed synovial cells in patients with RA and abnormal evidenceson the recent finding of signaling lymphocytic-activation molecule (SLAM)-associated protein (SAP), whichopened a new approach to understand on impaired function of cytotoxic T cell for EBV in patients withRA [3].We have several experience which arthritis activity was improved by the Aciclovir for Herpes Zosterin patients with rheumatoid arthritis. This means that some patients from rheumatoid arthritis are stronglyassociated with Herpes group virus as well as Akhtar AJ's arthritis patient is also strongly associatedwith hepatitis C virus because of an improvement by the interferon therapy. Eventhogh, Akhtar AJ's paientis seronegative, this may become seropositive in the future. Murai et al reported that Sixty seven casesshowing acute inflammatory polyarthritis from January 1990 to June 1990 were examined and followed upfor six years. Among them, 12 (9 female and 3 male) exhibited IgM anti-B19 antibodies. PCR, followedby a Southern blot analysis also showed the presence of B19 DNA in all 12 cases with IgM anti-B19 antibodies,but did not in the remainder. Initially, rheumatoid factor (RF) was negative in all B19 positive casesexcept one, but became positive in four, two to four months after the infection. We are learning nowthat Infliximab (Remicade) and etanercept (Enbrel): causes the serious infections and tuberculosis. Thereason why on the serious infection by anti cytokine therapy for arthritis is due to a very severe immunesuppression. The investigation on the etiology for chronic arthritis may establish an ideal therapy withoutside effect. References: 1.Abbasi J, Akhtar, Allen S, Funnyé AS: Hepatitis C virus associated arthritisin absence of clinical, biochemical and histological evidence of liver disease - responding to interferontherapy. Med Sci Monit, 2005; 11(7): CS37-CS39 2.Murai C et al: Rheumatoid arthritis after human parvovirusB19 infection. Ann Rheum Dis, 1999; 58(2): 130-32 3.Sawada S, Takei M: Epstein-Barr virus etiology inrheumatiod arthritis. Autoimmun Rev, 2005; 4(2): 106-10.

Keywords: Antiviral Agents - therapeutic use, Arthritis, Infectious - etiology, Hepatitis C - drug therapy, Interferon Type I - therapeutic use, RNA, Viral - isolation & purification, Recombinant Proteins



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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750