In the absence of changes in clinical chemical parameters, tumor necrosis factor-alpha, interleukin-6, and acute-phase reactant proteins, these results confirm in a clinical setting the upregulation of endothelial adhesiveness observed in experimental hypercholesterolemia and suggest a direct role for cholesterol in regulating this phenomenon, at least in familial hypercholesterolemia.

Hepatitis C viruses (HCV) present in 110 Italian patients were characterized by genotype-specific PCRs. Among the 65 cases of community-acquired hepatitis, HCV genotype IT was dominant (60%o), followed by genotypes IV (15%), m (11%), and I (3%). Among the 45 hemophilia-associated cases, the distribution of the

Background-HDL molecules have an established role in the regression processes of atherosclerosis as well as a putative role as antiinflammatory agents. Our study investigated whether familial hypoalphalipoproteinemia, a genetic form of dyslipidemia characterized by very low HDL levels, might be associated with increased inflammation markers such as C-reactive protein. Key Words: lipoproteins Ⅲ C-reactive protein Ⅲ hypolipoproteinemia Ⅲ inflammation Ⅲ atherosclerosis T he hypothesis that elevated levels of plasma high-density lipoprotein (HDL) protect against coronary atherosclerotic disease (CAD) was initially proposed by Barr et al 1 in the 1950s and is now firmly established. 2 Conversely, equally well-established evidence shows that low plasma HDL levels lead to atherosclerosis and are also recognized to be a major independent risk factor for CAD. 2 Thus, HDL molecules can be considered the 2-faced Janus of the atherosclerotic process, which, in turn, is increasingly believed to be an inflammatory phenomenon. Atherosclerotic lesions show activation and proliferation of macrophages and T-lymphocytes, cytokine production, and oxidized lowdensity lipoprotein (LDL) accumulation. 3,4 We hypothesized that the link between low HDL levels and atherosclerosis may depend on an upregulation of inflammation mechanisms putatively induced by low HDL, which has been shown to act as a proinflammatory agent. 5,6 Therefore, we measured C-reactive protein (CRP) in a group of patients affected by familial hypoalphalipoproteinemia (Hypoalpha), an autosomal-dominant genetic trait. Hypoalpha subjects are characterized by extremely low plasma levels of HDL (Ͻ10th percentile), 7-9 together with reduced or normal LDL levels and normal or high triglyceride (TG) levels. Hypoalpha patients have greater susceptibility to early, severe coronary atherosclerosis. 10 -12 In the general population this trait has a prevalence of Ϸ0.5%, and it is 10 to 20 times more frequent in subjects with CAD who are Ͻ60 years of age.CRP is a well-established, sensitive marker of systemic inflammation and represents an independent risk factor for cardiovascular events in population studies as well as in angina patients. 13,14 Also, CRP seems to add predictive value to total cholesterol (TC) and HDL levels with regard to the risk of future myocardial infarction in subjects with hyperlipemia and elevated concentrations of CRP. 15 The hepatic synthesis of CRP is induced by cytokines such as interleukin-6 16 ; it accumulates in the arterial wall during the atheroscle- rotic process, stimulates production of the tissue factor by monocytes, 17 and induces the synthesis of adhesion molecules in endothelial cells. Hypoalpha subjects were compared with a group of healthy controls and divided according to the presence or absence of CAD, as documented by coronary angiography, to provide a model in which to photograph the inflammatory state before and after the occurrence of clinical vascular damage. Methods PatientsThe patients recruited for the study consisted of 50 c...