Several antibodies, including anticardiolipin antibodies (ACA), have been detected among chronically infected hepatitis C virus (HCV) patients. The present work aimed at ascertaining the clinical significance of ACA levels among HCV infection associated with two commonly encountered diseases, thrombocytopenia and arteriovenous-shunt malfunction. Six groups were studied, 11 HCV-positive thrombocytopenic patients (group I), 14 HCV-positive non-thrombocytopenic patients (group II) and 15 healthy controls (group III), 11 anti-HCV-positive hemodialysis patients with non-functioning shunt (group IV), 14 anti-HCV-positive hemodialysis patients with patent shunt (group V) (Bain Medical Equipment Co., China) and 15 healthy controls (group VI). Anticardiolipin antibody (ACA) assay was performed on all patients and controls whereas tumor necrosis factor α (TNF-α) assay was carried out on thrombocytopenic patients and controls. Thrombocytopenic groups presented an inverse correlation between IgG ACA levels and both thrombocytopenia and TNF-α levels. During the follow-up period, no other clinical manifestations related to ACA were developed. Hemodialysis groups showed a significant elevation in IgG ACA levels in groups IV and V compared to the controls, with statistically higher levels in group IV than group V. Three group IV patients were hypercholesterolemic. We can conclude that induction of proinflammatory cytokines such as TNF-α by persistent HCV infection may promote the generation of ACA. Complications of HCV, including thrombocytopenia and thrombosis in arteriovenous shunt, are more strongly correlated with IgG ACA than with IgM ACA.

Hepatitis C virus (HCV) patients commonly have low platelet counts; however, the exact role of HCV infection in thrombocytopenia is unknown. This work aimed to study the serum levels of interleukins (IL) 10 and 12 in patients with mild and moderate thrombocytopenia associated with chronic hepatitis C infection. Our study included 15 patients with chronic HCV infection and newly diagnosed isolated autoimmune thrombocytopenia (Group I) and 15 patients with chronic HCV infection and normal platelet count as controls (Group II). All patients were examined for personal history and clinical aspects, complete blood count, bone marrow aspiration, liver function tests, HCV antibody assay by ELISA and polymerase chain reaction (PCR), abdominal ultrasound, Helicobacter pylori stool antigen test, evaluation of serum levels of IL-10, IL-12 and platelet specific antibodies. Our results revealed that eight patients from Group l had mild thrombocytopenia and seven patients had moderate thrombocytopenia. Serum IL-10 level was significantly elevated (t = 9.301, p < 0.001) while serum IL-12 showed a significant decrease (t = 6.502, p < 0.001) in Group I compared to the control group. No correlation was detected between platelet counts and the serum levels of either IL-10 [r = 0.454, p = 0.089 (Group I), r = 0.038, p = 0.89 (Group II)] or IL-12 [r = 0.497, p = 0.06 (Group I), r = 0.499, p = 0.058 (Group II)]. However, in Group I, a significant correlation was present only between moderate thrombocytopenia and serum levels of either IL-10 (r = 0.794, p = 0.033) or IL-12 (r = 0.967, p = 0.001), while no correlation was detected between these interleukin parameters and mild thrombocytopenia (r = 0.311 and p = 0.453 for IL-10 and r = -0.08 and p = 0.851 for IL-12). Based on our data, we may conclude that interleukins 10 and 12 are involved in low platelet levels.