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Increased systemic sST2 in patients with end stage renal disease contributes to milder liver damage during HCV
Ruzica Lukic1, Maja Cupic2, Nevena Gajovic3
1Department of Microbiology, Faculty of Medicine Foča, University of East Sarajevo, Foča, Bosnia and Herzegovina. l.ruzica@yahoo.com.
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Elevated soluble ST2 (sST2) levels in patients with end-stage renal disease (ESRD) and Hepatitis C Virus (HCV) infection may indicate reduced liver damage. This suggests the IL-33/ST2 pathway influences liver disease severity in these patients.
Area of Science:
- Immunology
- Hepatology
- Nephrology
Background:
- Hepatitis C Virus (HCV) is a major cause of chronic liver disease globally.
- HCV infection is common in end-stage renal disease (ESRD) patients due to factors like blood exposure and hemodialysis.
- The IL-33/ST2 signaling pathway's role in HCV and ESRD co-infection is not well understood.
Purpose of the Study:
- To investigate the impact of the IL-33/ST2 signaling pathway on liver disease severity in ESRD patients with HCV infection.
- To compare sST2 levels and ratios with inflammatory cytokines in different patient groups.
Main Methods:
- Blood samples were collected from 20 ESRD HCV+ patients, 20 HCV+ patients, and 20 healthy controls.
- Biochemical parameters, serum cytokine concentrations (including sST2), and HCV molecular diagnostics were analyzed.
Main Results:
- Serum sST2 levels positively correlated with urea and creatinine.
- sST2 levels were significantly higher in ESRD HCV+ patients compared to HCV+ patients.
- Ratios of sST2 to IL-1, IL-4, and IL-23 were elevated in ESRD HCV+ patients, indicating altered pathway activity.
Conclusions:
- Elevated sST2, potentially due to renal failure, may be associated with less liver destruction in HCV infection.
- The IL-33/ST2 pathway plays a role in modulating liver disease severity in co-infected ESRD patients.
Introduction:
Hepatitis C Virus (HCV) is the leading cause of chronic liver disease and is a serious global health problem. Hepatitis C infection is highly prevalent in patients with end stage renal disease (ESRD), due to frequent exposure to blood and blood products, nosocomial transmission of HCV, and prolong hemodialysis duration. The aim of the study was to evaluate the influence of IL-33/ST2 signaling pathway on severity of the liver disease in ESRD HCV+ patients.
Methodology:
Blood samples from patients with end stage renal disease (ESRD) and hepatitis C infection (HCV), 20 patients with HCV infection, 20 patients with ESRD and 20 healthy control donor patients were taken for the examination of biochemical parameters, for the determination of the serum cytokine concentration, and for the molecular diagnostics of HCV.
Results:
Systemic sST2 positively correlated with serum level of urea and creatinine, respectively. Serum sST2 was significantly increased in ESRD HCV+ patients in comparison to HCV+ group. sST2/IL-1, sST2/IL-4 and sST2/IL-23 ratios were significantly increased in serum of ESRD HCV+ patients in comparison to HCV+ patients. Significantly higher systemic level of sST2 and sST2/IL-1 and sST2/IL-4 ratios were measured in ESRD patients compared to non-ESRD patients.
Conclusion:
These results suggested that elevated level sST2, as the consequence of renal failure, causes less destruction of liver in HCV infection.
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