Evaluation of nitric oxide (NO) levels in hepatitis C virus (HCV)
infection: Relationship to schistosomiasis and liver cirrhosis among Egyptian
patients
Affiliations: Oncology Diagnostic Unit, Biochemistry Department,
and | Department of General Medicine, Faculty of Medicine,
Ain Shams University, Cairo, Egypt
Note: [] Address for correspondence: Mahmoud I. Hassan, M.D., Ph.D.,
Oncology Diagnostic Unit, Biochemistry Department, Ain Shams Faculty of
Medicine, Abbassia, Cairo 11566, Egypt. Tel.: 202 685 8940; Fax: 202 685 9928
Abstract: Nitric oxide (NO), a recently discovered free radical, is
overproduced in liver cirrhosis. Hepatitis C virus (HCV) might increase NO
levels via increased inducible NO synthase (iNOS). This work was carried out to
study the effect of HCV-induced liver cirrhosis on NO levels among Egyptian
patients. The study included 46 patients with liver cirrhosis, and 30 healthy
individuals of matched age and sex. NO levels determined as the stable
endproduct nitrate, showed a statistically significant increase among patients
compared to the control group (P<0.001). Furthermore, NO levels increased
proportionally with the severity of liver cirrhosis as assessed by Child's
classification (P<0.05). Moreover, schistosomial infection enhanced NO
levels in cirrhotic patients with HCV infection compared to non-bilharzial
patients (P<0.001). Polymerase chain reaction (PCR) and branched DNA assays
were used for detection of HCV RNA positivity, and measurement of the virus
load, respectively. Both showed a positive correlation with the NO levels
(P<0.001). At a nitrate cutoff value of 70 μmol/L, the sensitivity and
specificity were 83.0% analysis showed a significant correlation between ALT
levels and both HCV RNA positivity by polymerase chain reaction (PCR)
(P<0.02), and virus load (P<0.05). Interestingly enough, there was a
significant positive correlation between HCV RNA and schistosomal antibody
titer as measured by hemaglutination inhibition assay (HAI) (P<0.05). The
data presented in this report indicated an association between NO levels and
the development and progression of liver cirrhosis. Furthermore, the findings
obtained from this study demonstrated that schistomiasis is an important risk
factor involved in enhancement of NO levels and virus replication. The latter
may aggravate liver cell injury and hence the development of cirrhosis.
