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...

Objective: To test the working hypothesis that inflammation underlying precocious and severe coronary atherosclerotic disease in familial hypoalphalipoproteinaemia (FH) can be mediated by up regulation of the innate immune response. Conclusions: Increased concentrations of sICAM-1, C3c, and C4 co-express with high concentrations of CRP in FH. The lack of signs and symptoms of inflammation in these patients may suggest that the immune response is up regulated as part of the pro-inflammatory mechanisms that are activated in this atherogenic condition.

The clinical and pathological data of a case of cavernous haemangioma of the spleen are reported. The diagnostic value of scanning in the present case is discussed.

The rubidium and lithium ions are known to have opposite effects on a wide range of biochemical and behavioral parameters in experimental animals. Based on the proven effectiveness of lithium as an antimanic agent, several trials have been conducted with rubidium in the acute treatment of the depressive phase of bipolar illness. The results to date are promising. However, the 30- to 60-day biologic half-life of rubidium has mandated careful studies of potential toxicity before engaging in long-term administration of this ion to depressive subjects. One area of potential concern is the possibility of renal toxicity, which could be expressed as unexpectedly increased retention of rubidium. The data in this paper show that after 15 days of rubidium administration, there are no changes beyond the normal range in a variety of kidney function tests, including in four enzymes which are specific markers of tubule cell function.

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