Search PubMed⌕ Search

Biomedical subjects

E Farish

Publications and source records attributed to E Farish.

51 records · Page 3Linked to original sources

Ten years post-menopausal hormone replacement therapy--effect on lipoproteins.

Serum lipoproteins were measured in 72 post-menopausal women, 40 of whom had been taking the synthetic oestrogen, mestranol, for a period of 10 yr and 32 of whom had been taking identical placebo tablets. Mestranol therapy was found to increase serum triglycerides, decrease low density lipoprotein (LDL) cholesterol and increase high density lipoprotein (HDL) cholesterol. The increase in HDL cholesterol was due principally to a marked increase in the cardioprotective HDL2 fraction. It is concluded that long-term mestranol therapy has a beneficial effect on serum lipoproteins which may help to protect post-menopausal women against fatal ischaemic heart disease.

Cholesterol↗

Effect on lipoproteins of Trisequens, a combined hormone preparation.

Lipoprotein concentrations were measured in 31 post-menopausal women during 1 yr of treatment with Trisequens, a natural oestrogen-progestogen preparation. Serum triglyceride, high density lipoprotein and very low density lipoprotein cholesterol concentrations did not change significantly, but low density lipoprotein cholesterol concentrations fell over the first 6 mth. After 1 yr none of the lipoprotein fractions differed significantly in concentration from pre-treatment levels.

Adult↗

Calcitonin and postmenopausal osteoporosis.

Fasting serum calcitonin levels were measured in 54 postmenopausal women who had for 10 years been taking part in a double blind trial to assess the effect of the synthetic oestrogen, mestranol, on postmenopausal bone loss. There were no differences in calcitonin levels between mestranol treated and placebo groups. Fifteen of the women were challenged with a calcium infusion to measure the secretory reserve of calcitonin. Oestrogen treatment did not increase the calcitonin response to calcium infusion. The three patients who exhibited the greatest responses were placebo treated. Bone density was measured by gamma-ray absorptiometry over the ten year period and the annual rate of change of bone density calculated. No correlation could be found between basal calcitonin level or calcitonin reserve and change in bone density. Our results indicate that postmenopausal osteoporosis is not caused by a deficiency of calcitonin and that the action of oestrogen therapy to prevent bone loss does not involve calcitonin.

Calcitonin↗

Lipoprotein levels during hormone replacement therapy by vaginal ring pessaries.

Nineteen women who had had a surgical menopause had a vaginal ring pessary containing levonorgestrel and oestradiol in situ for a period of 3 months. Fasting lipoprotein levels were measured before, and after 1 and 3 months on therapy. After 3 months total triglyceride levels were significantly lower than baseline values (P less than 0.01) as were very-low-density-lipoprotein cholesterol (P less than 0.01), low-density-lipoprotein cholesterol (P less than 0.05) and high-density-lipoprotein cholesterol (P less than 0.001) levels. These changes suggest that in this preparation the effects of the progestogen component are dominant.

Adult↗

The effects of hormone implants on serum lipoproteins and steroid hormones in bilaterally oophorectomised women.

Serum lipoproteins were measured over a period of 6 months in 14 oophorectomised women treated with oestrogen implants (50 mg oestradiol-17 beta) and 17 oophorectomised women treated with oestrogen/testosterone implants (50 mg oestradiol-17 beta, 100 mg testosterone). Both types of implant caused only minimal changes in lipoprotein metabolism. Low density lipoprotein (LDL) cholesterol decreased with both types of implant and high density lipoprotein (HDL) cholesterol rose with the oestrogen implants. HDL subfractions were also measured. The oestrogen implants caused a transient rise in HDL2 cholesterol levels at 2 months and a slower rise in HDL3 cholesterol. The oestrogen/testosterone implants had no effect on HDL fractions. The results indicate that hormone implants do not cause the profound changes in lipoproteins associated with oral hormone therapy.

Adult↗

A long-term study of the effects of norethisterone on lipoprotein metabolism in menopausal women.

Long-term effects of the androgenic progestogen norethisterone on lipoprotein metabolism were studied by measuring lipoprotein concentrations in 21 women during one year on treatment for the relief of climacteric symptoms. There were significant reductions in total serum triglyceride (p less than 0.01), very low density lipoprotein (VLDL) cholesterol (p less than 0.01) and high density lipoprotein (HDL) cholesterol (p less than 0.001) after two months on treatment, all of which were still in evidence after one year. Low density lipoprotein (LDL) cholesterol levels climbed gradually becoming significantly higher than baseline after one year on treatment (p less than 0.01). Comparison of cholesterol concentrations in HDL subfractions in the one year treated subjects with those in a control group of untreated subjects suggests that the fall in HDL cholesterol is due to reductions in both the HDL2 and HDL3 fractions. We conclude that norethisterone adversely affects the important lipoprotein risk factors for coronary heart disease.

Adult↗

Metabolism of apolipoprotein A-I in healthy young adults.

The metabolism of 125I-labeled apolipoprotein A-I bound to high-density lipoproteins by an in vitro transfer procedure was studied in 10 healthy young adults (5 males and 5 females). Both sexes handled the labeled apolipoprotein similarly, and no statistically significant differences were found in the derived kinetic data. The mean (+/- 1 SD) plasma apolipoprotein A-I concentrations (males, 105 +/- 19 mg/dl; females, 111 +/- 13.8 mg/dl) and half-lives (males, 4.46 +/- 0.45 days; females, 4.64 +/- 0.70 days) were similar, as were the fractional rates of catabolism (FCR) of the apoprotein derived from the above data (FCR in males, 27% of intravascular pool/day; FCR in females, 25% of intravascular pool/day). The absolute catabolic rate of the apoprotein, equivalent under steady-state conditions to the synthetic rate, was 12.1 +/- 1.6 mg/kg/day in males and 11.9 +/- 2.4 mg/kg/day in females.

Adolescent↗

Chemical and kinetic study of the lipoproteins in abetalipoproteinaemic plasma.

Abetalipoproteinaemic plasma lipoproteins were fractionated by molecular sieve chromatography into two classes on the basis of size. Each class had the same chemical and immunochemical composition and seemed to be interconvertible in vitro, presumably as a result of aggregation/disaggregation. The low levels of circulating apolipoprotein A-I found in abetalipoproteinaemic subjects have been shown by kinetic analysis to result from reduced synthesis of the apoprotein and not from increased catabolism or redistribution between vascular and extravascular compartments.

Abetalipoproteinemia↗

Plasma apolipoprotein A levels in healthy human adults.

The apolipoprotein A concentration in the plasma of ten healthy human subjects was measured immunologically on three occasions at monthly intervals and the following results recorded. 1. There was no difference between fasting and non-fasting apoprotein A concentrations. 2. Apoliportein A levels were higher in females than in males (p less than 0.001). 3. The correlation coefficient calculated for high density lipoprotein cholesterol and apolipoprotein A was 0.62. 4. The apoprotein values varied widely between subjects and ther were considerable concentration differences from month to month in the plasma of each individual.

Adult↗