The Effect of Viral Hepatitis ON APTT, PT, TT, Fibrinogen and Platelet among Blood Donors at FMC, Umuahia

Abstract

The effect of viral hepatitis on some coagulation parameters APTT, PT,TT,Fibrinogen and platelets were determined among blood donors at FMC Umuahia. One hundred and sixty three blood donors were sampled comprising One hundred and thirteen as follows; (HAV 16, HBV 65 and HCV 32) and fifty non hepatitis subjects who served as control. The parameters were analysed using standard haematology technique. Results obtained showed no statistical significant changes in the coagulation parameters in HAV subjects (32.8±2.6) secs, 12.4±1.5 (secs), 16.7±1.3 secs, 2.9±0.2g/L and 249±73 10 9 /L when compared with control group 34.1±3.1 secs 13.4±1.7 secs 16.7±1.5 secs 2.5±0.6g/L and (263±74) 10 9 /L respectively for the parameters as stated above (P > 0.05), significant change in HBV infection 42.4±5.8 (secs); 22.3±10.7 (secs); 23.9±4.7 (secs); 1.8±1.1(g/L); and 162±144(10 9 /L) when compared with the control 34.1±3.1 (secs); 13.4±171 (secs); 16.7±1.5 (secs); 2.5±0.6 g/L); 26. ±74 (10 9 /L) respectively at P<0.05. The HCV infection showed the same significant changes in all the coagulation factors estimated; 45.0±6.3 (secs); 20.9±4.9 (secs); 24.6±5.6 (secs); 1.6±0.6 (g/L) and 170±61 (10 9 g/L) when compared with the same control group. The APTT showed a positive relationship with PT and TT and a negative relationship with fibrinogen and platelets. PT had a strong positive correlation with TT and a negative relationship with fibrinogen and platelet. TT showed a strong negative relationship with fibrinogen and platelet. The result showed an alteration in the levels of coagulation factors following viral infection of the liver.

Assessment of Factor V Gene G1691A Mutation (Factor V Leiden) among Chronic Hepatitis C Patients with Thrombocytopenia

“…Moreover, the present study showed a biological increase in aPPT in HCV chronically infected patients when compared to controls, but this change did not reach a signifi cant value (p = 0.214). By contrast, this result disagrees with the former study conducted by Leticia OI, et al [4], who referred to a signifi cant increase in aPPT in chronic hepatitis C patients when compared to controls. Generally, the prolongation of PT and aPTT as a consequence of viral hepatitis with thrombocytopenia was explained due to the loss of integrity of both the extrinsic and common pathways concerned with the coagulation process [4,37].…”

“…In the current study, HCV chronically infected patients showed a signifi cant increase in Prothrombin Time (PT) as a coagulation marker. This result is in agreement with Leticia OI, et al [4], who studied the eff ect of HCV infection on PT and Activated Partial Where: N = Number. The chi-Square test was applied to analyze the data.…”

“…Thrombocytopenia is more noticeable in chronic hepatitis C patients than in patients with other types of Chronic Liver Disease (CLD) at a comparable stage of severity [10,38]. In the present study, the marked thrombocytopenia in HCV chronically infected patients may be explained by the impairment in hepatic synthesis of thrombopoietin, which is the major physiological regulator of platelet production in the liver [4,39]. Some reports highlighted the decrease in thrombopoietin levels concerning the progression of liver disease, but others referred to its normal level in chronic hepatitis C patients compared with controls [10,40,41].…”

“…Chronic humoral immunity activation against HCV and the inability to clear this viral infection can result in recurrent exposure to a self-reactive antibody and, as a result, organ damage [3,4]. Also, a strong T-cell reaction is induced by HCV, generating diff erent cytokines including interleukin 2 (IL-2), Tumor Necrosis Factor-Alpha (TNF alpha), and interferongamma (IFN-gamma), which in particular correlate with liver infl ammation and fi brosis [3,4] and cause hepatic dysfunction [4]. Thrombocytopenia results from a decreased level of platelets and is a fundamental health problem in chronic HCV infection.…”

“…Generally, chronic viral hepatitis may lead to thromboembolism, especially Portal Vein Thrombosis (PVT) [4], which refers to portal vein obstruction by a blood clot [8,9]. Therefore, special attention has been given to the Hepatitis C Virus (HCV) infection due to its ability to activate hemostais in several ways during its course of pathogenicity [10], which involves a serious liver injury that leads to Chronic Liver Disease (CLD).…”