Hepatitis C‐associated autoimmunity in patients coinfected with HIV

Woitas, Rainer P.; Stoschus, Bodo; Terjung, Birgit; Vogel, Martin; Kupfer, Bernd; Brackmann, H.‐H.; Rockstroh, Jürgen K.; Sauerbruch, Tilman; Spengler, Ulrich

doi:10.1111/j.1478-3231.2005.01159.x

Cited by 16 publications

(10 citation statements)

References 38 publications

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“…A recent retrospective analysis of the United Network for Organ Sharing (UNOS) database showed that although the 2 year survival of HIV patients (n = 138) was inferior to HIV -ve patients (70% vs 81%), the survival was similar in HIV -ve patients and HIV +ve patients without HCV or HBV co-infection [89] . Similar poor outcome in HIV patients with concomitant HCV infection has been observed in other studies [88,[90][91][92][93][94][95] . Survival of co-infected patients was inferior to HCV mono-infected patients at 1 year, 3 years, and 5 years (68%-80% vs 76%-87%, 56%-57% vs 72%-81%, and 33%-51% vs 72%-81%, respectively) [88,93,94] .…”

Section: Management Of Hiv-hcv Co-infected Patients With Endstage LIVsupporting

confidence: 68%

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Singal¹,

Anand²

2009

WJG

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N e a r l y o n e fo u r t h o f i n d i v i d u a l s w i t h h u m a n immunodeficiency virus (HIV) infection have hepatitis C virus (HCV) infection in the US and Western Europe. With the availability of highly active antiretroviral therapy and the consequent reduction in opportunistic infections, resulting in the prolongation of the life span of HIV-infected patients, HCV co-infection has emerged as a significant factor influencing the survival of HIV patients. Patients with HIV/HCV co-infection have a faster rate of fibrosis progression resulting in more frequent occurrences of cirrhosis, end-stage liver disease, and hepatocellular carcinoma. However, the mechanism of interaction between the two viruses is not completely understood. The treatment for HCV in co-infected patients is similar to that of HCV monoinfection; i.e., a combination of pegylated interferon and ribavirin. The presence of any barriers to anti-HCV therapy should be identified and eliminated in order to recruit all eligible patients. The response to treatment in co-infected patients is inferior compared to the response in patients with HCV mono-infection. The sustained virologic response rate is only 38% for genotype-1 and 75% for genotype-2 and -3 infections. Liver transplantation is no longer considered a contraindication for end-stage liver disease in coinfected patients. However, the 5 year survival rate is lower in co-infected patients compared to patients with HCV mono-infection (33% vs 72%, P = 0.07). A better understanding of liver disease in co-infected patients is needed to derive new strategies for improving outcome and survival.

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Section: Management Of Hiv-hcv Co-infected Patients With Endstage LIVsupporting

confidence: 68%

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Singal¹,

Anand²

2009

WJG

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“…Only one recent study has compared cryoglobulinaemic features in patients with HCV-HIV and those with HCV infection alone. Woitas et al [22] studied 98 coinfected patients and 78 patients with HCV infection alone and found that coinfected patients had a lower frequency of cryoglobulinaemia, higher levels of cryocrit and positive RF. This low cryoglobulinaemic expression in HCV-HIV coinfected patients with respect to those with HCV infection alone suggests that HIV may attenuate the symptomatic expression of cryoglobulinaemia in patients with chronic HCV infection.…”

Section: Discussionmentioning

confidence: 99%

Cryoglobulinaemia associated with hepatitis C virus: influence of HCV genotypes, HCV‐RNA viraemia and HIV coinfection

Ramos-Casals¹,

Forns²,

Brito-Zerón³

et al. 2007

Journal of Viral Hepatitis

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To determine whether the clinical and immunological expression of patients with cryoglobulinaemia associated with chronic hepatitis C virus (HCV) infection varied according to HCV-RNA load, HCV genotype or human immunodeficiency virus (HIV) coinfection. We studied 340 HCV patients (188 women and 152 men, with a mean age of 49 years) consecutively diagnosed with cryoglobulinaemia between 1993 and 2003 in our hospital. HCV infection was confirmed by serum HCV-RNA determination in all patients. Two hundred and forty-eight (73%) patients had asymptomatic cryoglobulinaemia and 92 (27%) presented cryoglobulinaemic symptoms. Patients with genotype 1 had a higher mean age at diagnosis of cryoglobulinaemia (48.2 vs 40.2 yrs, P < 0.001) and a higher prevalence of cryoglobulinaemic symptoms (25%vs 10%, P = 0.02), especially of vasculitic features (19%vs 5%, P = 0.014). In comparison with monoinfected HCV patients, those with HIV coinfection had a lower mean age at diagnosis of cryoglobulinaemia (40.4 vs 52.8 years, P < 0.001), a lower prevalence of cryoglobulinaemic symptoms (15%vs 34%, P < 0.001), vasculitis (10%vs 28%, P < 0.001), associated systemic autoimmune disease (3%vs 14%, P = 0.001), rheumatoid factor (30%vs 70%, P = 0.001) and hypocomplementaemia (50%vs 78%, P = 0.01). In HCV-HIV patients, a high viral load was associated with a high frequency of symptomatic cryoglobulinaemia, especially in patients with a high viral load of the two viruses (50%vs 7%, P = 0.001) A higher frequency of cryoglobulinaemic symptoms (especially vasculitis) was found in patients with HCV monoinfection and in those carrying HCV genotype 1. In contrast, patients with HIV coinfection presented a threefold lower prevalence of vasculitis. Associated HIV infection significantly attenuated the clinical and immunological expression of cryoglobulinaemia, except in coinfected patients with high viral loads for the two viruses.

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“…It is not entirely clear whether HIV infection itself can trigger an autoimmune phenomenon and associated autoimmune hepatitis, but in some HIV/HCV co‐infected patients, the features of an autoimmune‐like hepatitis can be seen. It has been shown recently that HIV may differentially modulate HCV‐associated autoimmunity, as manifested by the presence and frequency of various auto‐antibodies (thyroglobulin, cardiolipin, for example), but it appears that, even in the presence of auto‐antibodies, the manifestations of autoimmunity are not clinically significant (44).…”

Section: Histopathologic Findings In Hiv/hcv Co‐infectionmentioning

confidence: 99%

HIV/HCV co‐infection: histopathologic findings, natural history, fibrosis, and impact of antiretroviral treatment: a review article

Petrovic

2007

Liver International

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Human immunodeficiency virus/hepatitis C virus (HIV/HCV) co-infection has emerged as a leading cause of liver morbidity in the last two decades. Liver failure is also frequently a cause of death in HIV/HCV co-infected patients. Highly active antiretroviral treatment (HAART) has revolutionized the HIV treatment, leading to a significantly decreased morbidity, prolonged survival, and an overall better outcome of HIV infection. Hepatotoxicity associated with antiretroviral treatment, however, has been recognized as one of the serious complications of the treatment. The effects of HIV infection on the natural history and progression of HCV-associated chronic liver disease that had been well documented in the pre-HAART treatment era have been changing, and there are now many indications that HIV/HCV co-infection should be recognized as an evolving and a challenging disease entity.

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Hepatitis C‐associated autoimmunity in patients coinfected with HIV

Abstract: HIV coinfection appears to differentially modulate the frequency of HCV-related autoimmunity. However, autoimmunity is rarely accompanied by clinical manifestations.

Cited by 16 publications

References 38 publications

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Cryoglobulinaemia associated with hepatitis C virus: influence of HCV genotypes, HCV‐RNA viraemia and HIV coinfection

HIV/HCV co‐infection: histopathologic findings, natural history, fibrosis, and impact of antiretroviral treatment: a review article

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