Alterazioni neurovascolari nell'epatite cronica C: uno studio caso-controllo

Summary Introduction Hepatitis C is a major health problem: approximately 170 million people are infected with the hepatitis C virus worldwide. It is unclear whether chronic hepatitis C affects atherosclerosis and whether it can cause endothelial and/or autonomic nervous system (ANS) dysfunction. Materials and methods From April 2008 through April 2009, we studied 76 patients with biopsy-confirmed chronic hepatitis C and no evidence of cirrhosis, ascites, portal hypertension, encephalopathy, or hepatocellular carcinoma. The age-, sex-, BMI- and cardiovascular risk factor-matched control group comprised 76 healthy, HCV-negative individuals with no evidence of liver, autoimmune, or immunoproliferative diseases and no history of cardiovascular events. Twenty five of the hepatitis C patients were treatment-naive; the other 51 had been treated with interferon (but only 25 had persistent virological responses). Color Doppler sonography was used to measure the intima-media-thickness (IMT) of the common and internal carotid arteries. Endothelial function was assessed in the brachial artery with the flow-mediated-dilatation (FMD) test. The ANS was assessed with the tilt, laying to standing, Valsalva, hand grip, deep breath, and stroop tests. Results The case group (mean age 52 ± 13 years) had a significantly higher internal carotid IMT (0.86 ± 0.3 vs 0.67 ± 0.1 mm for controls; p = 0.002). Chronic hepatitis C was also associated with an odds ratio for carotid plaque formation (reflected by an IMT ≥ 1.3 mm) of 2.15. Cases also had significantly reduced FMD in the brachial artery (0.46 ± 0.9 vs 0.76 ± 0.7 for controls; p = 0.005) and significantly altered sympathetic and parasympathetic function (p = 0.001 vs controls in the Valsalva, hand grip, deep breath, and stroop tests). Within the case group, all alterations were more severe in patients with significant viremia. Discussion Our findings suggest that chronic hepatitis C may be a nonclassic cardiovascular risk factor since it seems to influence the onset of pre-atherosclerotic lesions and to promote atherosclerotic plaque formation in patients with pre-existing increases in carotid IMT. It also seems to cause dysfunctions of the vascular endothelium and ANS. Conclusions Chronic hepatitis C may increase cardiovascular risk and promote ANS dysfunctions, particularly when patients have experienced treatment failure and have persistent viremia. These patients may require cardiovascular and neurologic follow-up

Recurrent thromboembolism in cancer patients: incidence and risk factors.

I.F.2,49

An antifibrinolytic effect associated with an anti-factor V antibody in a patient with severe thrombophilia

I.F. = 5.03

Postthrombotic syndrome

Revie

Diagnosis and follow-up of thrombotic thrombocytopenic purpura by means of von Willebrand factor collagen binding assay.

Thrombotic thrombocytopenic purpura (TTP) is characterized by intravascular thrombosis leading to consumption of large or unusually large von Willebrand factor (VWF) multimers. The usefulness of VWF collagen binding (VWF:CB) assay was assessed in detecting the decrease/absence of large VWF multimers or the presence of abnormally large forms in patients with TTP. Nine patients with TTP were studied during the acute phase of the disorder and the absence of large VWF multimers was demonstrated by means of the VWF:CB assay. These findings were confirmed by VWF multimer pattern analysis; VWF:CB deficiency appeared to correlate with abnormalities in large VWF multimers. The diagnostic potency of VWF:CB was especially evident when the values were expressed as VWF:CB/VWF:Ag ratio. VWF:CB was also used during the follow-up of the disorder to document improvement or restoration of large VWF multimers. VWF:CB was able to detect the absence or decrease of large VWF multimers better than VWF ristocetin cofactor (VWF:RCo); in fact, VWF:CB was defective when large VWF multimers persisted to be decreased, in contrast with what observed with VWF:RCo. In conclusion, VWF:CB is a simple test that appears to be useful, together with clinical symptoms and reduced platelet count, for the diagnosis and follow-up of TTP