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A combined use of hormones may reduce cholesterol levels in postmenopausal women. A two-year study of 113 women who had already experienced menopause revealed that a combination of 17-beta-estradiol and norethindrone acetate may reduce total blood cholesterol and low-density lipoprotein (LDL) cholesterol levels. The combined hormones may also reduce high-density lipoprotein (HDL) cholesterol concentrations when the hormones are administered continuously, cancelling out the beneficial increase in HDL concentrations usually obtained by estrogen replacement therapy. The reduced LDL cholesterol concentrations may reduce the incidence of coronary heart disease in postmenopausal women. When the hormones were administered one after the other rather than in combination, they did not effectively lower LDL levels, but increased triglyceride levels.

A method for determination of high-density lipoprotein cholesterol (HDL-C) is evaluated: after precipitation of low and very low lipoprotein cholesterol in serum by magnesium dextransulphate, HDL-C is determined by an enzymatic method. The precision of the method was good: coefficient of variation 4%. The accuracy was good, evaluated by correlating HDL-C results from the present assay to the results obtained from three other HDL-C assays (n=17): ultracentrifugation r=0.91, phosphotungstate/MgCl2 r=0.98, and α-lipoprotein determination by electrophoresis r=0.91 (p<0.01). Repeated analysis showed that serum may be kept at 4 °C for 1 month, at -20 °C for 2 months, and requires -80 °C for longer storage. Ten patients with acute myocardial infarction showed significantly lower HDL-C from day 4 in the acute phase and during the first 3 months follow up (p<0·05). Eighty patients with peripheral vascular disease, who were compared to a group of matched controls, also showed significantly decreased serum HDL-C (p<0·01). The present HDL-C assay is easy, fast and reliable and is considered a valuable clinical test.

Radiolabelled low-density lipoproteins (LDL), obtained from a patient with heterozygous, familial hypercholesterolaemia and from a normal subject, were injected into the patient and two normal subjects. Two approaches were made to evaluate the kinetics of metabolism of these LDL: (1) by serial measurements of radioactivity in serum, urine and the whole body; (2) by observing the density of the labelled LDL from serum using density-gradient ultracentrifugation. No significant change was seen in the modal density of the LDL in either the patient or the normal subjects, but there were changes in the skewness of the radioactivity peaks. This contrasts with previously published findings in the guinea pig, in which LDL radioactivity gradually accumulated in the densest particles. The guinea pig findings suggested that lipoproteins in the LDL region are structurally modified during their intravascular circulation. The present study indicates that modification leading to changes in density does not occur to any significant degree in the human, whose LDL represent the end product of intravascular metabolism of apolipoprotein B-containing lipoproteins.

Acute pancreatitis verified at laparotomy occurred in the 37th week in 1 of 4 women who developed excessive hypertriglyceridemia (type V hyperlipoproteinemia) during pregnancy. The hypertriglyceridemia was associated with and possibly caused by deficiency of lipoprotein lipase, measured as the NaCl sensitive component of post-heparin lipase activity. A severely fat-restricted diet controlled the hypertriglyceridemia in 1 of the patients, followed during a second pregnancy.