Study of the effect of antiviral therapy on homocysteinemia in hepatitis C virus- infected patients

Abstract

BackgroundHepatitis C virus (HCV) infection is one of the leading causes of chronic liver disease (CLD). About 80% of those exposed to the virus develop a chronic infection. Hyperhomocysteinemia, which is an independent risk factor for atherosclerotic vascular disease and thromboembolism, may develop in HCV-infected patients although altered alanine amino transferase (ALT) enzyme levels are generally associated with damage to liver cells. The gold standard therapy for chronic hepatitis C patients is pegylated interferon combined with an anti-viral drug (ribavirin). The current study aimed to investigate the effect of antiviral therapy on plasma homocysteine (Hcy) levels in HCV patients in addition to other parameters.Methods532 HCV-infected patients and 70 healthy controls were recruited for the study. All patients were subjected to laboratory investigations including HCV-RNA levels, complete blood cell counts, serum levels of homocysteine, ALT, alkaline phosphatase (ALP), lipid profile and liver ultrasonographic examination. The outcome of treatment with pegylated interferon α plus ribavirin treatment and sustained virologic response (SVR) was determined 6–9 months post-therapy.ResultsHyperhomocysteinemia was found in 91.35% of HCV-infected patients. The difference in plasma Hcy concentrations reached statistical significance between the patient and control groups. ALT, cholesterol and triglycerides (TGs) levels were found higher than normal in the patients group. After receiving a combined therapy for 24 weeks, 43.66% patients showed an SVR (responders); 30.98% patients were non-responders while 25.35% patients initially responded to therapy but again retrieved positive status of HCV infection six months post-therapy (relapse-cirrhotic patients). The mean levels of plasma Hcy, ALT and ALP were significantly reduced in responders within 10 weeks of therapy when compared with non-responders and relapse-cirrhotic patients.ConclusionElevated homocysteine levels in serum due to HCV infection can be reduced to normal range with the standard interferon α plus ribavirin treatment. This study highlights the significance of the measurement of serum homocysteine levels in the diagnosis and monitoring of HCV infection treatment in addition to other laboratory parameters.

Assessment of serum Homocysteine levels in congenital heart disease and with rubella infection: A hospital- based case-control study in North Indian population

“…pneumonia and cytomegalovirus showed signi cant association with increased serum Hcy levels (hyperhomocysteinemia) and several other studies also investigated the association of serum homocysteine levels and viral infections. [20][21][22][23][24][25] In the current study, we found signi cant higher levels of serum homocysteine in rubella seropositive cases as compared to rubella seronegative cases among CHD cases.…”

Lean Body Mass Harbors Sensing Mechanisms that Allow Safeguarding of Methionine Homeostasis

“…That working hypothesis should be confirmed by the demonstration of a negative correlation between rising Hcy values and declining TTR plasma levels [ 25 , 26 ] in aged subjects. The liver may similarly endure toxic exposure and varying inflammatory, autoimmune, and degenerative processes associated with HHcy states, as described in viral hepatitis [ 62 ], cirrhosis [ 63 ], and nonalcoholic steatosis [ 64 ]. The replacement of normal parenchymal cells by fatty, fibrotic, or inflammatory material would lead to marked intrahepatic dysregulation of Met metabolism, as recently documented in mouse experiments showing that diet-induced steatofibrosis is associated with HHcy status and a 30% depletion of the intrahepatic Met pool size [ 65 ].…”

Viral infections in cardiometabolic risk and disease between old acquaintances and new enemies

“…In particular, this lipids disarrangement [e.g., increase in lipid biosynthesis, hepatic levels of triglycerides, cholesterol esters, and sphingolipids, but also reduction of mitochondrial oxidation, lipid degradation, and apolipoproteins export, in particular very-low-density lipoproteins (VLDL)] lead to circulatory hypocholesterolemia and hypo-lipoproteinemia, steatosis and lipotoxicity [121,122]. Steatosis is in turns a well recognized CV risk factor, as it promotes IR, adiponectin elevation, metabolic syndrome, oxidative stress, hyperhomocysteinemia, and TNF-α [122][123][124][125]. Clearly, alteration in the lipid asset may also be secondary to worsened liver function induced by HCV, in addition to direct HCV effects.…”