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Biomedical subjects

E Farish

Publications and source records attributed to E Farish.

At least 19 recordsLinked to original sources
PubMed1999

Effects of tibolone on serum lipoprotein and apolipoprotein levels compared with a cyclical estrogen/progestogen regimen.

OBJECTIVE: The purpose of the study was to examine the effects of tibolone, a synthetic steroid that alleviates climacteric symptoms and prevents bone loss without inducing monthly bleeds, on lipoprotein cardiovascular risk markers and to compare the effects with those of a standard combined estrogen/progestogen preparation. DESIGN: Ninety-seven postmenopausal women were randomly allocated to receive either tibolone 2.5 mg/day or conjugated equine estrogens 0.625 mg/day with norgestrel 0.15 mg/day for 12 of each 28 days. Fasting serum levels of lipids, lipoproteins, and apolipoproteins (Apo) were monitored during 18 months of treatment. Women on the cyclical preparation had levels determined during both estrogen-only and combined phases. RESULTS: Tibolone caused reductions in triglycerides (33%, p < 0.001), very low density lipoprotein (VLDL) cholesterol (43%, p < 0.001), and high density lipoprotein (HDL) cholesterol (18%, p < 0.001). The HDL2/HDL3 ratio fell by 22% (p < 0.001). Levels of Apo AI and AII were reduced by 18 and 8%, respectively (p < 0.001). The combined preparation caused reductions in VLDL cholesterol (23%, p < 0.001) and low density lipoprotein cholesterol (15%, p < 0.001). There were small reductions in HDL3 cholesterol and in Apo AII and Apo B. All parameters, except for Apo AII and Apo B and lipoprotein (a) [Lp (a)], showed cyclical changes. Lp (a) levels were reduced significantly by both treatments. CONCLUSIONS: The cyclical preparation had potentially beneficial effects on LP risk markers. The reduction in HDL induced by tibolone constitutes a potentially adverse change, which may be offset by the substantial falls in triglycerides, VLDL cholesterol, and Lp (a).

Anabolic Agents↗
PubMed1998

Long-term effects of continuous combined HRT on bone turnover and lipid metabolism in postmenopausal women.

This study was undertaken to investigate the effect of 10 years of hormone replacement therapy (HRT) on bone turnover and lipid metabolism in postmenopausal women. The single-centre trial was initiated as a 1-year, double-masked, randomized, parallel-group study of continuous combined HRT with 2 mg 17 beta-estradiol and 1 mg norethisterone acetate administered once daily with or without 1 mg estriol. Following preliminary results which showed no difference between the addition and omission of estriol, patients continued on an open-label extension phase of continuous combined HRT without estriol for a further 9 years. Of the 52 women who entered the original double-masked study, 32 entered the open-label extension phase. The 10-year analysis was based on 27 patients. Major increases in bone mineral density (BMD) of the lumbar spine were seen during the first 3 years of treatment, remaining statistically significant compared with baseline at all visits throughout the 10-year follow-up (p < or = 0.025). Statistical modelling confirmed that there were no decreases in BMD after these initial increases. BMD remained 5.5% higher than baseline values after 10 years of continuous combined HRT. Mean total cholesterol levels were significantly reduced after 10 years of therapy (p = 0.012), with no significant changes in serum triglyceride and low-density lipoprotein (LDL)-cholesterol levels from baseline values at this time. High-density lipoprotein (HDL)-cholesterol levels, however, were reduced by 15.4% (p < 0.001). In conclusion, 10 years of continuous combined HRT resulted in a significant and sustained increase in BMD. This treatment regimen therefore appears to be well suited for the long-term prevention of osteoporosis in postmenopausal women.

Adult↗
PubMed1996

Effects of postmenopausal hormone replacement therapy on lipoproteins including lipoprotein(a) and LDL subfractions.

The purpose of this study was to examine the effects on lipoprotein risk markers for CHD of oestradiol given alone and in combination with the androgenic progestogen, norethisterone. Eighty postmenopausal women were randomly allocated to receive oestradiol (2 mg/day) alone or with continuous norethisterone (1 mg/day). Serum lipoprotein levels, including lipoprotein(a), were monitored during 12 months on treatment in all the women, and in a sub-set of 32 patients cholesterol was measured in the two major density subfractions of LDL. Oestradiol caused a transient rise in triglycerides, a small decrease in LDL cholesterol (significant only at 3 and 6 months, P < 0.05) and a consistent significant increase in HDL cholesterol (16%, P < 0.01). There was a downward trend in lipoprotein(a) levels which did not achieve statistical significance. The combined preparation caused significant, sustained decreases in triglycerides (31%, P < 0.01), total cholesterol (15%, P < 0.001), VLDL (42%, P < 0.01), LDL (9%, P < 0.05) and HDL (11%, P < 0.001). Lipoprotein(a) was also reduced (39%, P < 0.05). In the sub-set of patients in which LDL subfractions were measured, the reduction in LDL induced by oestradiol monotherapy was significant only at the 3-month visit (6%, P < 0.05). This was due to a decrease in the 'light' (1.025 < d < 1.044 g/ml) subfraction (10%, P < 0.05) and resulted in an apparent shift in subfraction distribution towards the 'heavy' (1.044 < d < 1.060 g/ml) subfraction, although there was no absolute increase in the latter. None of these changes was statistically significant at 12 months. Oestradiol/norethisterone caused sustained decreases in both 'light' (15%, P < 0.05) and 'heavy' (29%, P < 0.05) subfractions, with no significant change in the relative amounts. The changes in 'light' and 'heavy' LDL in this group were highly correlated with changes in triglyceride levels (r = -0.57, P < 0.05 and r = 0.82, P < 0.01 respectively). Therefore, at the end of 1 year's treatment with unopposed oestradiol the only statistically significant change was an increase in HDL cholesterol. Addition of norethisterone to the preparation reversed this potentially beneficial change, but favourably influenced triglycerides, VLDL, LDL subfraction profile and lipoprotein(a), which may counteract the adverse effect on HDL.

Adult↗
PubMed1996

Thyroid function in idiopathic oedema.

BACKGROUND: The role of abnormal thyroid function in the aetiology of idiopathic oedema is unclear. Previous studies of small samples of patients have suggested a high prevalence of latent hypothyroidism and a possible deiodination defect in the conversion of T4 to T3 in this condition. There is a need to clarify the possible significance of abnormal thyroid function in a larger sample of idiopathic oedema patients. OBJECTIVE: The study was undertaken to compare basal thyroid function in idiopathic oedema patients and in an age and sex-matched control group. PATIENTS AND DESIGN: After excluding one idiopathic oedema patient and three control subjects with abnormal thyroid function, basal thyroid function was compared in 44 idiopathic oedema patients and in 44 age and sex-matched controls. MEASUREMENTS: Basal thyroid function was assessed in patient and control groups by measuring serum T4, fT4, T3, fT3 and TSH by standard methods. RESULTS: There were no significant differences in basal thyroid function between patient and control groups except for an elevated mean fT4 concentration in the idiopathic oedema group (P = 0.03). Exclusion of patients and controls taking oestrogen abolished this difference. T4:T3 ratios were similar in patient and control groups. CONCLUSION: Abnormalities of basal thyroid function are uncommon in patients with idiopathic oedema and appear unrelated to the pathogenesis of this disorder. Similar T4:T3 ratios between patient and control groups exclude a deiodination defect in idiopathic oedema.

Adult↗
PubMed1994

Artificial ultraviolet whole-body radiation does not modify serum lipoprotein, plasma fibrinogen, plasminogen or antithrombin III concentrations in post-myocardial infarction patients.

The relationship of ischaemic heart disease (IHD) to seasonal and latitude variation has prompted speculation that exposure to the ultraviolet component of solar radiation may reduce IHD risk. This hypothesis was partially tested by exposing 14 post-myocardial infarction patients to a 6 week course of artificial whole-body ultraviolet radiation (UVR). Serum lipoprotein and plasma coagulation factor concentrations were measured before and after the course of UVR. Results were compared with similar measurements from a placebo-controlled group of 13 post-myocardial patients. Despite a more than two-fold rise in mean serum 25-OHD, serum lipoprotein and plasma fibrinogen, antithrombin III and plasminogen concentrations did not change significantly in the UVR group. Significant but minor change in prothrombin time and thrombin time in the placebo group appear unlikely to be of biological significance. Seasonal and latitude variation in these IHD risk factors appear unrelated to corresponding variation in solar UVR exposure.

Antithrombin III↗
PubMed1994

Effects of tibolone on lipoprotein(a) and HDL subfractions.

OBJECTIVE: To determine the effects of tibolone, a synthetic steroid used to alleviate climacteric symptoms and prevent osteoporosis, on lipoprotein metabolism, with particular reference to lipoprotein(a) levels and HDL subfraction profiles. DESIGN: Thirty nine postmenopausal women were treated with tibolone (Livial) 2.5 mg/day for 6 months and fasting serum lipoprotein levels were estimated at 0, 2, 4 and 6 months. RESULTS: Lipoprotein(a) levels were reduced significantly over the 6 months from a median level of 245 (range < 60-780) mg/l to 152 (range < 60-530) mg/l, a reduction of 39% in the median level. A decrease was observed in approximately two thirds of the women. Reductions were noted in all 6 subjects whose pretreatment levels were high, although concentrations remained at a level associated with increased risk in all but one. There were significant decreases in triglycerides and VLDL cholesterol and no significant change in LDL cholesterol. There was a significant reduction of 18% in HDL cholesterol and a 26% reduction in the HDL2-HDL3 ratio. CONCLUSION: The reduction in lipoprotein(a) levels may have a beneficial effect on cardiovascular risk, which could go some way towards balancing the potentially adverse effect on the cardiovascular system caused by the reduction in HDL cholesterol.

Adult↗
PubMed1993

Response of plasma low density lipoprotein subfractions to oestrogen replacement therapy following surgical menopause.

OBJECTIVE: Epidemiological studies suggest that postmenopausal oestrogen replacement reduces the incidence of cardiovascular disease. The purpose of this study was to establish the effects of oestrogen replacement therapy on subfractions of plasma low density lipoprotein in bilaterally oophorectomized women. DESIGN: In a placebo controlled, double-blind study, patients were randomized on a two to one basis to receive either oestradiol valerate (2 mg/day) or placebo respectively for a period of 16 weeks. PATIENTS: Seventeen women aged 28-51 years who had all had hysterectomy and bilateral oophorectomy at least 2 months before recruitment were assigned to either the active (n = 12) or placebo (n = 5) group. MEASUREMENTS: Plasma lipids, lipoproteins, apolipoproteins and LDL subfractions were determined immediately before and after the treatment period. LDL subfractions were isolated directly from plasma by density gradient ultracentrifugation within 24 hours. Non-parametric statistical analysis was carried out within each group using Wilcoxon's signed rank test for matched pairs. RESULTS: After 16 weeks of treatment, HDL cholesterol, apo A-I and HDL-2 were increased in the group receiving oestrogen (HDL cholesterol +12%, P < 0.01; apo A-I +14%, P < 0.01; HDL-2 +24% P < 0.01). While there were no significant changes in serum cholesterol, LDL cholesterol or triglycerides, the proportion and concentration of the least dense LDL-I subfraction was decreased significantly (-27%, P < 0.05). The LDL subfraction of intermediate density (LDL-II) was decreased in eight subjects, while small, dense LDL-III was unaffected. Overall, these changes resulted in an apparent shift in the distribution of LDL subfractions towards small, dense LDL-III, although there was no net increase in the latter. CONCLUSION: In view of a similar and characteristic response of LDL subfractions to hypolipidaemic drugs that enhance the clearance of LDL via the LDL receptor, the present findings suggest that oestrogen promotes the preferential removal of LDL-I and II by activating LDL receptors. As this effect is normally associated with a reduction in the circulating level of LDL, it should not be regarded as an unfavourable response to oestrogen replacement therapy.

Adult↗
PubMed1993

Lipoprotein(a) and postmenopausal oestrogen.

Epidemiological studies have shown that postmenopausal oestrogen therapy substantially reduces the risk of cardiovascular and cerebrovascular disease and this is partly mediated by oestrogen-associated changes in lipoproteins, particularly high-density lipoprotein. In this study, we investigated whether changes in lipoprotein(a) might help to account for the reduction in coronary heart disease and stroke associated with postmenopausal oestrogen therapy. The study group consisted of 18 women who had hysterectomy and bilateral oophorectomy at least 2 months prior to recruitment and had received no previous hormonal therapy. Serum samples were collected for measurement of lipoprotein(a) before and after 4 months of treatment with oestradiol valerate (2 mg/day). Lipoprotein(a) levels ranged from 35 to 720 mg/l (median 180 mg/l) before treatment and from 55 to 780 mg/l (median 130 mg/l) after oestradiol treatment and showed no consistent pattern of change. It would appear, therefore, that treatment with unopposed oestrogen in relatively low doses not have a marked effect on lipoprotein(a), at least in the short term.

Adult↗
PubMed1992

Placebo-controlled trial of doxazosin in management of patients with hypertension and hypercholesterolaemia.

The blood pressure (BP)- and lipid-lowering activities of the alpha 1-antagonist, doxazosin, were investigated in hypertensive, hypercholesterolaemic patients. Thirty-one patients satisfactorily completed the study, and there was no significant difference between doxazosin and placebo in terms of reported adverse events. After 3-month treatment, BP was significantly reduced by doxazosin by 24/14 mm Hg supine and by 33/22 mm Hg erect as compared with corresponding reductions of 2/9 and 2/2 mm Hg with placebo. There were concomitant improvements in the plasma lipid profile with, in particular, significant net reductions of 30% for triglycerides and 20% for apoprotein B. There was no adverse effect on glucose metabolism. The principal aim of this study was assessment of the clinical utility and acceptability of doxazosin in a heterogeneous population of patients with several cardiovascular risk factors. The results confirm that doxazosin is an effective antihypertensive agent that has modest additional beneficial effects on the plasma lipid profile.

Aged↗
PubMed1992

Reversible menopause induced by the GnRH analogue buserelin: effects on lipoprotein metabolism.

GnRH agonists can induce a reversible pharmacological menopause and can be used to treat endometriosis, a fairly common gynaecological problem which responds well to oestrogen deprivation. Premature menopause is associated with adverse lipid changes and an increased risk of coronary heart disease. Therefore we set out to investigate changes in lipoprotein metabolism in a group of premenopausal women being treated with the GnRH analogue buserelin for active endometriosis. We monitored lipoprotein levels, high density lipoprotein subfractions and apolipoproteins AI, AII and B during a 12-month course of treatment and for 6 months afterwards. Treatment caused a sustained increase in HDL3 cholesterol levels and a small increase in low density lipoprotein cholesterol, which was significant at the six-month visit only. Apolipoprotein B levels rose significantly and there were marginal increases in apolipoproteins AI and AII. All changes and trends were reversed after cessation of treatment. We conclude that the treatment did not profoundly affect lipoprotein metabolism, neither LDL nor HDL cholesterol, the established important risk markers for coronary heart disease appreciably altered.

Adult↗
PubMed1992

Effects of nicardipine on the metabolic responses to food and exercise.

In a placebo-controlled, double-blind, randomised, cross-over study the metabolic and hormonal responses to standard food and exercise challenge have been evaluated in seven patients with mild to moderate essential hypertension after treatment with nicardipine 30 mg three times daily for four weeks. There were no significant differences between nicardipine and placebo for any of the measured hormonal and metabolic indices following food or exercise. These results indicate that nicardipine has no clinically important effects on serum lipids or hormonal or metabolic responses to food and exercise.

Adult↗
PubMed1992

Measurement of capillary cholesterol as an aid to the management of hypertensive patients with hyperlipidaemia--an assessment of the Reflotron.

The Reflotron dry chemistry method of capillary cholesterol measurement has been widely adopted as a rapid means of population screening. We attempted to use it to monitor changes in cholesterol in a trial of intensive dietary intervention in hyperlipidaemic hypertensives. Four hundred and eighty-nine capillary cholesterol levels measured by the Reflotron were compared with levels for venous samples obtained simultaneously and assayed by the Biochemistry Department using conventional laboratory methods. The mean difference between them was 0.3 mmol/l +/- 0.8 (SD). Approximately one-third of the variability in the difference between the two methods was explained by the variables, Reflotron machine used and time (R2 = 54%, adjusted R2 = 34%). We conclude that the Reflotron is not suitable for accurate assessment of the modest changes in cholesterol which occur in individual patients during dietary intervention.

Blood Chemical Analysis↗
PubMed1991

Long-term amiodarone therapy raises serum cholesterol.

Serum total cholesterol and triglyceride levels were measured in 12 patients before and 3.6 and 9 months after treatment with amiodarone. In addition, we monitored serum T4, T3, reverse T3 and TSH levels. Amiodarone and its desethyl metabolite levels were measured on each occasion. Serum total cholesterol and T4 levels rose from 5.95 mmol/l, and 102.7 mmol/l respectively at baseline to 6.95 and 115.8 at 6 months and reverse T3 increased at 3, 6 and 9 months from baseline. Serum triglycerides did not change. No relationship existed between cholesterol, T4 and T3 and amiodarone (or its metabolite) levels nor between cholesterol and thyroid hormone levels. These data demonstrate that amiodarone therapy is associated with an elevation in serum cholesterol. This may have clinical implications in view of the current widespread use of the drug.

Adult↗
PubMed1991

Short-term changes in lipoproteins and apoproteins during cyclical oestrogen-progestogen replacement therapy.

Lipoproteins and apoproteins were measured weekly in a group of 18 post-menopausal women treated with a cyclical hormone replacement regimen comprising 28 days on conjugated equine oestrogens (0.625 mg/day) with the addition of norgestrel (0.15 mg/day) for the last 12 days of the cycle. There were no significant changes in total triglyceride, very low-density-lipoprotein (VLDL) cholesterol or high-density-lipoprotein (HDL) cholesterol levels. Low-density lipoprotein (LDL) and total cholesterol levels fell, the differences being significant after two weeks. The LDL/HDL cholesterol ratio also fell significantly over 1 week of treatment. There were no significant changes in either HDL2 or HDL3 cholesterol. The HDL2/HDL3 cholesterol ratio did, however, alter significantly, increasing during the oestrogen-only phase. Apart from this ratio, none of the parameters measured showed any significant differences as between the oestrogen-only phases and the oestrogen/norgestrel phases. There were no significant changes from baseline values in the levels of apoproteins AI, AII or B. The apoprotein AI/AII ratio was significantly increased, the levels being higher during the oestrogen phase of the cycle. There was no significant change in the apoprotein B/AI ratio. The apoprotein B/LDL cholesterol ratio showed a statistically significant increase after 4 weeks. There was no evidence of any cyclical changes. We conclude that the results of this study are generally favourable with regard to coronary heart disease risk but that the change in the apoprotein B/LDL ratio merits further investigation.

Apoproteins↗
PubMed1991

Prevention of bone loss by hormone replacement therapy is probably not due to stimulation of calcitonin secretion.

Weekly fasting serum calcitonin levels and biochemical indices of bone metabolism were measured in 13 postmenopausal women being given hormone replacement therapy over a period of 8 weeks. All of the biochemical indices except urinary hydroxyproline creatinine ratios fell significantly, indicating that the treatments were effective in reducing bone turnover. Calcitonin levels fell significantly and, within the individual, levels were positively correlated with adjusted calcium levels. These findings do not support the theory that estrogen conserves bone by stimulating calcitonin secretion.

Alkaline Phosphatase↗
PubMed1991

Combined lipid-lowering and antihypertensive treatment as part of a strategy of multiple risk factor intervention.

Thirty-six patients with treated mild to moderate hypertension and hypercholesterolaemia (greater than 6.5 mmol/l) entered a 12 week study to evaluate the efficacy and patient tolerability of combined lipid-lowering and antihypertensive treatment as part of a strategy of multiple risk factor intervention. The principal effects on the plasma lipid profiles were significant reductions of 30-40% in total and LDL cholesterol. These reductions were achieved without loss of blood pressure control. There was no significant impact on HDL cholesterol or on lipoprotein Lp(a). These preliminary results suggest that substantial reductions in total and LDL cholesterol can be achieved without compromising blood pressure control which remained satisfactory at 144/82 supine and 143/80 mmHg standing. Furthermore, these changes were achieved without any problems of patient tolerability or interference with patient compliance with drug treatment. Overall, therefore, substantial reductions in CHD risk can be achieved with an acceptable combination of lipid lowering and antihypertensive treatments.

Aged↗