The authors report a study of 28 cases of hyperlipemia due to alcohol. Clinically, they emphasize the predominance of the male sex, the high incidence of digestive disturbances, weight loss and hepatomegaly and the rarity of cardiovascular involvement. From the biochemical point of view, the majority of cases present an endogenous hyperlipemia of the same type as that induced by carbohydrates. Attention is also drawn to the disturbed glucose balance and the frequent hyperuricemia. Moreover, demonstration of lipid anomalies in the relatives of 11 cases out of 15 suggests a genetic predisposition rather analogous to that in carbohydrate hyperlipemia. Treatment by simple withdrawal of alcohol is always effective, but very unreliably adhered to by these patients.
The aim of our study was to estimate the potential relationship between smoking behavior and other coronary heart disease risk factors in 250 hyperlipidemic patients. We present data obtained through self-reporting of the number of cigarettes smoked per day, measurements of three tobacco markers, and data on dietary habits and lipid variables. We measured cotinine (by HPLC) and thiocyanate and used a recent colorimetric assay for the indirect evaluation of the nicotine metabolites in a single urine specimen. Mean values of nicotine metabolites, expressed as cotinine equivalents, were 6.7, 39.9, and 79.4 mumol/L, respectively, for nonsmokers, light smokers (7.7 cigarettes per day), and heavy smokers (25.8 cigarettes per day). We found that light smokers have higher concentrations of cotinine and nicotine metabolites in proportion to the number of cigarettes smoked per day than do heavy smokers. Thus, the simple colorimetric assay can accurately evaluate smoking status. Hyperlipidemia and smoking are linked by an intricate network of multiple relations. The concentration of high-density lipoprotein (HDL) cholesterol is lower in heavy smokers, and the concentrations of triglycerides and cholesterol are higher. The 0.11 mmol/L difference in HDL cholesterol between light and heavy smokers is close to the results of previous papers; however, when gender, dietary habits (including alcohol intake), and data on body mass index are included in a multiple regression analysis, there is no longer an association between HDL cholesterol concentrations and smoking status. Therefore, these different dietary habits may be confounding factors that partly explain the pattern of lipid variables.
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