Prevalence of Active Hepatitis C Virus Infection in Patients with Systemic Lupus Erythematosus

Ahmed, M. M.; Berney, S.M.; Wolf, Robert; Hearth-Holmes, Michelene; Hayat, Samina; Mubashir, E.; Vanderheyde, Henri; Chang, W. L. William; King, John W.

doi:10.1097/00000441-200605000-00003

Cited by 38 publications

(8 citation statements)

References 24 publications

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“…SVR patients achieved a sustained virological response (SVR) to pegylated interferon plus ribavirin (PR) therapy; non-SVR patients did not achieve SVR to PR therapy. compared to the control group (1.0-1.3%) 11,12 , which suggests a potential interaction between HCV infection and SLE. Patients with SLE and CHC share many common immunological features, such as hypocomplementemia and the presence of antinuclear and anticardiolipin antibodies 13 .…”

Section: Discussionmentioning

confidence: 81%

Sustained virological response to hepatitis C therapy does not decrease the incidence of systemic lupus erythematosus or rheumatoid arthritis

Hsu

Chen

Tseng³

et al. 2020

Sci Rep

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Section: Discussionmentioning

confidence: 81%

Sustained virological response to hepatitis C therapy does not decrease the incidence of systemic lupus erythematosus or rheumatoid arthritis

Hsu

Chen

Tseng³

et al. 2020

Sci Rep

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“…Ahmed et al substantiated this hypothesis by demonstrating an increased prevalence of Hepatitis C Virus in SLE patients [38]. …”

Section: Hepatobiliary Malignanciesmentioning

confidence: 99%

Malignancies in systemic lupus erythematosus

Goobie

Bernatsky

Ramsey‐Goldman

et al. 2015

Current Opinion in Rheumatology

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Purpose of Review Patients with systemic lupus erythematosus (SLE) have altered incidences of certain malignancies as compared to the general population. This review summarizes the recent literature on risk of malignancy in SLE and proposed mechanisms for these altered susceptibilities. Recent Findings Recent studies have confirmed previous data showing an increased risk of non-Hodgkin’s lymphoma, lung, liver, vulvar/vaginal, and thyroid malignancies, while demonstrating a decreased risk of breast and prostate cancer. Lymphomagenesis in SLE has been linked to increased activity of multiple inflammatory cytokines as well as possible viral etiologies. The decreased rates of hormone-sensitive cancers such as breast and prostate is speculated to be related to the presence of lupus autoantibodies and down-regulation of certain proteins in SLE. This knowledge has been utilized to investigate new therapeutic modalities for these malignancies. Summary Recent data confirm previously reported altered malignancy rates in SLE. Most striking in recent years are publications further elucidating mechanisms underlying cancer development in SLE, and subsequent investigations of potential therapeutics modulating these pathways.

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“…The occurrence of SLE in the setting of HCV and INF administration is now well established [1]-[3] and represents an accentuation of the underlying cytokine changes described in SLE pathogenesis [4,5]. Development of SLE is favoured by both reduced tumour necrosis factor (TNF) α following anti-TNF therapy or by increased IFNα.…”

Section: Discussionmentioning

confidence: 99%

“…PEG-IFN is commonly associated with development of autoantibodies and with autoimmune disorders in 4% to 19% of patients, and SLE-like syndromes have been reported in 0.15% to 0.7% of patients on INF therapy [1], with the onset ranging from one month to seven years after INF administration. Most present with arthralgia and a highly elevated ANA.…”

Section: Discussionmentioning

confidence: 99%

Development and management of systemic lupus erythematosus in an HIV-infected man with hepatitis C and B co-infection following interferon therapy: a case report

et al. 2009

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IntroductionThe association of human immunodeficiency virus and immune dysfunction leading to development of autoimmune markers is well described, but human immunodeficiency virus infection is relatively protective for the development of systemic lupus erythematosus. In contrast, development of systemic lupus erythematosus with hepatitis C and with interferon therapy is well described in a number of case reports. We here describe the first case of systemic lupus erythematosus developing in a man infected with human immunodeficiency virus, hepatitis C and hepatitis B co-infection where the onset seems to have been temporally related to interferon therapy.Case presentationWe report the occurrence of systemic lupus erythematosus complicating interferon-α therapy for hepatitis C in a 47-year-old asplenic male with haemophilia co-infected with human immunodeficiency virus and hepatitis B. He presented with a truncal rash, abdominal pains and headache and later developed grade IV lupus nephritis requiring haemodialysis, mycophenolate mofetil and steroid therapy. We were able to successfully withdraw dialysis and mycophenolate while maintaining stable renal function.ConclusionInterferon-α is critical in antiviral immunity against hepatitis C but also acts as a pathogenic mediator for systemic lupus erythematosus, a condition associated with activation of plasmacytoid dendritic cells that are depleted in human immunodeficiency virus infection. The occurrence of auto-antibodies and lupus-like features in the coinfections with hepatitis C require careful assessment. Immunosuppressant therapy for lupus risks exacerbating underlying infections in patients with concurrent human immunodeficiency virus, hepatitis B and C.

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Prevalence of Active Hepatitis C Virus Infection in Patients with Systemic Lupus Erythematosus

Cited by 38 publications

References 24 publications

Sustained virological response to hepatitis C therapy does not decrease the incidence of systemic lupus erythematosus or rheumatoid arthritis

Sustained virological response to hepatitis C therapy does not decrease the incidence of systemic lupus erythematosus or rheumatoid arthritis

Malignancies in systemic lupus erythematosus

Development and management of systemic lupus erythematosus in an HIV-infected man with hepatitis C and B co-infection following interferon therapy: a case report

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