Association of HIV Infection and HIV/HCV Coinfection With C-Reactive Protein Levels

Reingold, Jason; Wanke, Christine; Kotler, Donald P.; Lewis, Cora E.; Tracy, Russell P.; Heymsfield, Steven B.; Tien, Phyllis C.; Bacchetti, Peter; Scherzer, Rebecca; Grünfeld, Carl; Shlipak, Michael G.

doi:10.1097/qai.0b013e3181685727

Cited by 98 publications

(49 citation statements)

References 41 publications

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“…In our cohort of women, median CRP levels were 46–74% and 24% lower than those reported in other cohort studies of HIV-infected women [10], [31] and HIV/HCV-infected women [10], respectively. Our study was conducted in the era of potent antiretroviral therapy, which is reflected in high median CD4 counts (>500 cells/ml) and could explain the lower IL-6 and CRP levels than reported in other studies.…”

Section: Discussioncontrasting

confidence: 77%

“…Among the HIV-monoinfected women, current smoking and marijuana use were associated with higher CRP levels, as was a higher CD4 count. Smoking has been associated with higher CRP levels [10]; whether or not there is a direct association of marijuana with higher CRP levels is unclear. Although unexpected, the association of higher CD4 could represent a restoration to health, and thus restoration of fat stores and higher CRP levels.…”

Section: Discussionmentioning

confidence: 99%

“…[9, 10] Liver fibrosis severity and HCV replication are postulated mechanisms for the attenuated CRP level. The paucity of data describing the effect of liver fibrosis severity on IL-6 and CRP levels likely reflects the difficulties of pursuing liver biopsy in large numbers of patients.…”

Section: Introductionmentioning

confidence: 99%

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Association of HIV, hepatitis C virus and liver fibrosis severity with interleukin-6 and C-reactive protein levels

Shah¹,

Ma²,

Scherzer

et al. 2015

Aids

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Background Hepatitis C infection (HCV) is associated with chronic inflammation; yet studies show greater IL-6 but lower CRP levels. We determined whether liver fibrosis severity and HCV replication affect the ability of IL-6 to stimulate production of CRP from the liver. Methods We used multivariable generalized linear regression to examine the association of HIV, HCV and transient elastography-measured liver stiffness (LS) with IL-6 and CRP in participants (164 HIV-monoinfected; 10 HCV-monoinfected; 73 HIV/HCV-coinfected; 59 neither infection) of the Women's Interagency HIV Study. Significant fibrosis was defined as LS>7.1 kiloPascals. Results IL-6 was positively correlated with CRP levels in all women, but CRP levels were lower in HCV-infected women (with and without HIV infection) at all levels of IL-6. HCV-infected women with fibrosis had nearly 2.7-fold higher IL-6 levels compared to controls (95% Confidence Interval [CI]:146%, 447%); HCV-infected women without fibrosis had IL-6 levels that were similar to controls. By contrast, CRP was 28% lower in HCV-infected women with fibrosis (95% CI:-55%, 15%) and 47% lower in HCV-infected women without fibrosis (95% CI:-68%,-12%). Among the HCV-infected women, higher HCV RNA levels were associated with 9% lower CRP levels per doubling (95% CI: -18%, 0%). Conclusion Liver fibrosis severity is associated with greater IL-6 levels, but the stimulatory effect of IL-6 on CRP appears to be blunted by HCV replication rather than by liver fibrosis severity. Investigation of the potential CRP rebound after HCV RNA eradication and persistent liver fibrosis on organ injury is needed.

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Section: Discussioncontrasting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

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Association of HIV, hepatitis C virus and liver fibrosis severity with interleukin-6 and C-reactive protein levels

Shah¹,

Ma²,

Scherzer

et al. 2015

Aids

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“…Data from HIV studies also support a hypothesized HIV-mediated reduction in hepatocyte synthetic function. Levels of C-reactive protein (CRP), an acute phase reactant released by hepatocytes, were modestly higher among HIV mono-infected individuals and actually lower among those with HIV/HCV co-infection, when compared to uninfected controls [66]. In addition, while IL-6 and D-dimer levels decline with initiation of ART, CRP levels fail to improve or actually increase in some studies [67, 68].…”

Section: Altered Composition Of Coagulation Factorsmentioning

confidence: 99%

Chronic HIV disease and activation of the coagulation system

Baker

2013

Thrombosis Research

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With current effective antiretroviral treatment, the spectrum of morbidity and mortality during chronic HIV disease has shifted away from AIDS defining clinical events. Persistent abnormalities in coagulation appear to contribute to excess risk for a broad spectrum of non-AIDS defining complications, including, but not limited to, venous and arterial thrombotic disease. Mechanisms specific to HIV disease, antiretroviral therapy, and lifestyle or behavioral factors contribute to a pro-coagulant state, in part, through increased tissue factor activity coupled with a paradoxical decline in the anti-coagulant response. Alterations in coagulation biology in the context of HIV disease appear to be largely a consequence of persistent systemic immune activation, micro- and macro-vascular disease, and, potentially, impaired hepatic synthesis of coagulation factors. The clinical consequences of HIV-related changes in coagulation biology, the degree to which they are unique to HIV disease, and whether they can be mitigated through adjunct treatments, remains a focus of current research.

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“…112140–45 In the Strategic Management of Anti-Retroviral Therapy Study (SMART), it has been shown that hsCRP and IL-6 levels are associated with HIV viral replication and CVD and all-cause mortality risk. 81446 In SMART, higher levels of hsCRP and IL-6 at baseline were strongly associated with increased risk for mortality both over the short- and long-term (CVD and non-CVD related).…”

Section: Markers Of Inflammationmentioning

confidence: 99%

Biomarkers and HIV-associated cardiovascular disease

Baker

Duprez

2010

Current Opinion in HIV and AIDS

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Purpose of Review Our goal is to summarize recent literature on biomarkers of cardiovascular disease (CVD) in the setting of HIV infection with an emphasis on those associated with clinical events. Recent Findings Epidemiological data have demonstrated that HIV-infection is associated with increases in well-established markers of inflammation and thrombosis, and levels of hsCRP, IL-6, D-dimer and fibrinogen predict CVD and mortality risk in HIV cohorts. Levels of IL-6, D-dimer and endothelial adhesion molecules increase when antiretroviral therapy is interrupted, suggesting HIV replication may be driving CVD risk in this context. However, data on changes in many CVD biomarkers after starting ART are inconsistent or lacking. Finally, assessment of high-density lipoprotein particle concentration may provide important information specific to HIV-related CVD risk beyond that apparent from traditional measures of serum cholesterol. Summary Biomarkers of inflammation and thrombosis have the potential to improve CVD risk stratification beyond traditional and HIV-specific factors, and may prove useful for evaluating CVD prevention strategies for individuals with HIV infection.

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Association of HIV Infection and HIV/HCV Coinfection With C-Reactive Protein Levels

Abstract: In the absence of HCV coinfection, HIV infection is associated with higher CRP levels in men. HCV coinfection is associated with lower CRP levels in men and women.

Cited by 98 publications

References 41 publications

Association of HIV, hepatitis C virus and liver fibrosis severity with interleukin-6 and C-reactive protein levels

Association of HIV, hepatitis C virus and liver fibrosis severity with interleukin-6 and C-reactive protein levels

Chronic HIV disease and activation of the coagulation system

Biomarkers and HIV-associated cardiovascular disease

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