Apoprotein D in a healthy, male population and in male myocardial infarction patients and their male, first-degree relatives.

This report examines the correlation of serum apoprotein D with other lipoprotein lipids and apoproteins in a healthy, male population and compares the levels of high density lipoprotein apoprotein D of this control population with 2 samples composed of male, acute myocardial infarction patients and their healthy, male, first-degree relatives. Highly significant correlations were observed with very low density lipoprotein lipids (negative), high density lipoprotein lipids (positive) and serum triglycerides (negative). Serum and low density lipoprotein apoprotein B was not correlated with serum apoprotein D, whereas apoprotein A-I from serum and high density lipoproteins was strongly correlated with apoprotein D. A significant reduction in high density lipoprotein apoprotein D was observed in male, myocardial infarction patients. Their male, first-degree relatives also had lower apoprotein D levels, but the difference was not significant.

HDL cholesterol levels in patients with myocardial infarction and their families.

The present study using a quartile distribution of myocardial infarction patients demonstrated that the first-degree relatives of the myocardial infarction patients with the lowest HDL cholesterol have similarly the lowest HDL cholesterol. Low HDL cholesterol among these relatives was not secondary to increased VLDL triglycerides, as it persisted when subjects with hyper VLDL triglycerides were excluded. Familial low HDL cholesterol could not be attributed to known environmental factors as their levels did not differ significantly between the groups compaired. There was a significant correlation between HDL cholesterol levels of the parents and that of their younger offspring. The correlation was not significant with the offspring aged 20 and over. It appeared that there was a familial trend in low HDL cholesterol levels, more apparent among the young offspring than among the adult offspring, who may possibly not share any more the parental environment for factors liable to influence HDL cholesterol. This finding is compatible with a hereditary trait.

Liver glycerokinase deficiency in man with hyperglycerolaemia and hypertriglyceridaemia.

Hyperglycerolaemia and glyceroluria is described in a patient who presented transient dietary-induced hypertriglyceridaemia. The increased glycerol in blood and urine was related to glycerokinase deficiency as evidenced by a hepatic tissue glycerokinase activity of one tenth (4.8 X 10(-5) mmol g-1 min-1) of that of normoglycerolaemic subjects (5.9 X 10(-4) ). As triglycerides are routinely determined by an enzymatic method after hydrolysis to glycerol, the differential diagnosis between true hypertriglyceridaemia and hyperglycerolaemia may prove difficult. Persisting "hypertriglyceridaemia' despite adequate dietary and drug treatment should suggest the existence of undiagnosed hyperglycerolaemia .

[HDL-cholesterol and family incidence of coronary disease in the Genevan population]. / Cholestérol HDL et anamnèse familiale de maladie coronarienne dans la population genevoise.

In a healthy population, comparison of the lipoprotein lipid profile between subjects who were aware of the existence of cardiovascular disease among their relatives with the subjects who were not showed that the men in the former group had lower HDL cholesterol (1.3 mmol/l p less than 0.05) than men without a familial history of CHD (1.41 mmol/l). The difference was not significant in women. The values were within the normal range and there was an overlap of individual HDL cholesterol levels between the groups. This observation did however demonstrate that familial history of CHD was associated with lower HDL cholesterol and that low HDL cholesterol could play a significant role in certain families at risk.

[Reversible acquired acanthocytosis and hemolytic anemia associated with hypobetalipoproteinemia in a chronic alcoholic]. / Acanthocytose acquise et anémie hémolytique réversibles associées à une hypobétalipoprotéinémie chez un alcoolique chronique.

A 38-year-old male chronic alcoholic developed spur-cell anemia during an episode of non-A, non-B hepatitis. Lipid evaluation showed a marked decrease in cholesterol (1.98 mmol/l), in triglycerides (0.41 mmol/l) and in phospholipids (1.38 mmol/l) in total serum as well as in VLDL and LDL. Serum apolipoprotein B was also low. Cholesterol (C) and phospholipid (PH) content of the erythrocytic membrane was increased, as was the intraerythrocytic C/PH ratio. Hemolysis ceased with correction of the hypobetalipoproteinemia. The relationship between acquired acanthocytosis and lipid disorders is discussed.

Lipid, lipoprotein and APO-A and APO-B lipoprotein distribution in Italian and Swiss schoolchildren. The Geneva survey.

Cholesterol and triglyceride lipid, lipoprotein as well as apolipoprotein A and B levels, are presented for Italian and Swiss schoolchildren of similar socio-economic origin, living in Geneva, and ranging in age from 8-9 and 14-15 years. This cross-sectional study revealed some differences associated with the ethnic origin of the participants. Furthermore subtle changes were related to age, associated with puberty and were sex-specific. Apolipoprotein A and B levels were found to be significantly related to age and less significantly to sex, whereas apolipoprotein A levels decrease with puberty, apolipoprotein B levels increase slightly. Of the 387 Italian and the 416 Swiss participants, 173 Italian and 193 Swiss children had a complete lipoprotein examination including apolipoprotein determination, whereas serum cholesterol and serum triglycerides were studied in the total group.

Relationship between plasma insulin levels and high density lipoprotein cholesterol levels in healthy men.

Insulin and high density lipoproteins are considered to play a role in the development of atherosclerosis. In order to study whether there was a relationship between endogenous plasma insulin response and high density lipoproteins, an acute intravenous glucose tolerance test (0.5 g glucose/kg body weight) was performed in 94 healthy men, aged 20-49 years. Cholesterol and triglyceride levels were measured in very low density lipoproteins, low density lipoproteins and high density lipoproteins isolated from fasting serum by preparative ultracentrifugation. The subjects were divided into quartiles according to their fasting and post-glucose load plasma insulin and high density lipoprotein cholesterol levels. The results obtained in the subjects of the upper quartiles were compared with the results obtained in the subjects of the lower quartiles. The mean glucose disappearance rates were within the normal range and did not differ between the upper and lower quartiles. Subjects with high fasting plasma insulin had lower high density lipoprotein cholesterol levels (1.11 +/- 0.34 mmol/l, p = 0.01) than men with low fasting plasma insulin (1.40 +/- 0.37 mmol/l). Higher mean post-glucose plasma insulin was associated with lower high density lipoprotein cholesterol levels (1.18 +/- 0.32 mmol/l, p less than 0.05) and increased high density lipoprotein triglyceride levels (0.14 +/- 0.07) mmol/l, p less than 0.01) when compared with the men with low post-glucose plasma insulin (1.40 +/- 0.36 mmol/l and 0.09 +/- 0.03 mmol/l respectively). These observations reflect the close relationship between endogenous insulin and lipoprotein metabolism.

[HDL and lipoproteins in the families of coronary patients]. / HDL et lipoprotéines dans les familles de malades coronariens.

Male first degree relatives of acute myocardial infarction patients differ from a control population by virtue of their low HDL cholesterol. The results are compared with those obtained previously in women and children who are first degree relatives of coronary patients. Low HDL cholesterol (Fig. 5) is a familial feature of first degree relatives of acute myocardial infarction patients. This observation is of considerable interest in view of the role of HDL cholesterol in the development of atherosclerosis.

Decreased HDL cholesterol in prepubertal and pubertal children of CHD patients.

Prepubertal boys and pubertal girls and boys selected because of the occurrence of acute myocardial infarction in their father or mother were characterized by a low HDL cholesterol when compared to healthy controls. This observation extends our previous observations of low HDL cholesterol in adult relatives of CHD patients to the children of the same patients. The occurrence of an HDL abnormality in young children demonstrates that the low HDL cholesterol precedes the occurrence of cardiovascular disease. Low HDL cholesterol was associated with increased VLDL cholesterol in prepubertal children and pubertal boys without significant increase in VLDL triglycerides. Smoking and drinking habits, and physical activity which are environmental factors known to affect HDL did not differ between these children and the controls and cannot account for the observed differences. The results show that the low HDL cholesterol is detectable early in life in close relatives of CHD patients, persists throughout the lifespan and is possibly genetically determined.

HDL lipids in close relatives of coronary heart disease patients. Environmental and genetic influences.

Female first-degree relatives of CHD patients differed, after the age of forty, from the normal control population by their low HDL cholesterol. Between the ages of 20 and 40 years a slight but significant increase in HDL triglycerides was observed. Except for hormonal contraception which induces significant lowering of HDL cholesterol in the first degree relatives, the observed differences in HDL lipids did not seem related to environmental factors but rather to be genetically determined. In contrast, the low HDL cholesterol observed in the wives of the CHD patients appeared to be related to differences in alcohol intake.