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Biomedical subjects

M Worthington

Publications and source records attributed to M Worthington.

At least 19 recordsLinked to original sources
PubMed1995

Body fat distribution, rather than overall adiposity, influences serum lipids and lipoproteins in healthy men independently of age.

PURPOSE: We investigated the relationships between the amount and distribution of body fat and fasting serum lipids and lipoproteins to explore whether coronary artery disease (CAD) risk may be mediated through effects on the serum lipid profile. PATIENTS AND METHODS: We determined serum total cholesterol and triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein (HDL) cholesterol, and HDL subfractions 2 and 3 in 103 healthy men, aged 21 to 77 years (mean 48.7). The amount and distribution of fat were determined directly by dual energy X-ray absorptiometry. Adiposity was determined as the ratio between total body fat tissue and total body lean tissue, while fat distribution was taken as the ratio between the mass of fat tissue in the android (central) and gynoid (hip and thigh) regions. RESULTS: Univariate analysis showed both adiposity and fat distribution to be correlated with total serum cholesterol and triglyceride concentrations (adiposity r = .20, .21; both P < 0.05: fat distribution r = .25, .38; P < 0.05, P < 0.001, respectively). Fat distribution was also negatively correlated with HDL2 cholesterol (r = -.20, P < 0.05). In multiple linear regression analysis, neither age nor adiposity was significantly correlated with any serum lipid or lipoprotein concentration, while increasing android-to-gynoid ratio was independently associated with elevated total serum triglyceride (r = .40, P < 0.01) and decreased HDL2 (r = -.25, P < 0.05) concentrations. CONCLUSIONS: The association of both age and overall adiposity with the fasting serum lipid profile are mediated via their correlations with body fat distribution. In men, the distribution, rather than the amount, of body fat is related to adverse changes in serum lipids and lipoproteins, and hence potentially to increased CAD risk.

Absorptiometry, Photon↗
PubMed1994

Effect of continuous combined estrogen and desogestrel hormone replacement therapy on serum lipids and lipoproteins.

OBJECTIVE: To determine the effects of continuous combined hormone replacement therapy with desogestrel and 17 beta-estradiol (E2) on serum lipids and lipoproteins. METHODS: Fifty-seven healthy postmenopausal women of less than 60 years of age were studied prospectively and treated with oral desogestrel 0.15 mg/day and micronized 17 beta-E2 1 mg/day, both taken continuously. Fasting venous blood samples for serum lipids and lipoproteins were taken before and after 6 and 12 months of treatment. RESULTS: Thirty-two women completed the study. Levels of all serum lipids and lipoproteins fell significantly by 6 months and remained low at 12 months. The mean percentage reduction after 12 months of treatment was 12.8% for high-density lipoprotein (HDL) cholesterol, which largely resulted from a reduction in the HDL2 subfraction, which fell by 25.7%. The mean percentage reduction for both low-density lipoprotein (LDL) cholesterol and triglycerides was 7.7%. The median percentage reduction for lipoprotein (a) was 17.6%. CONCLUSIONS: This combination of hormone replacement therapy had profound effects on serum lipids and lipoproteins. According to current concepts, reductions in total and LDL cholesterol, triglycerides, and lipoprotein (a) may reduce cardiovascular disease risk. The reduction in HDL was unexpected, given the rise in HDL that has been demonstrated when desogestrel is combined with ethinyl estradiol in the contraceptive pill. The lowering of HDL observed in this study is undesirable and may be potentially harmful. Our results indicate that when desogestrel 0.15 mg/day is combined with micronized 17 beta-E2 1 mg/day in a continuous manner, the effects of the progestogen on HDL predominate and cause a reduction in HDL and the HDL2 subfraction.

Cholesterol, HDL↗
PubMed1993

A comparative metabolic study of two low-estrogen-dose oral contraceptives containing desogestrel or gestodene progestins.

OBJECTIVES: Our objective was to compare the effects of low-estrogen-dose oral contraceptives containing desogestrel or gestodene progestins on metabolic risk markers for coronary heart disease. STUDY DESIGN: A cross-sectional comparison of 70 women who used a formulation that contained 30 micrograms ethinyl estradiol and 150 micrograms desogestrel, 43 women who used a formulation that contained 30 micrograms ethinyl estradiol and 75 micrograms gestodene, and 54 women who did not use steroidal contraceptives was performed. RESULTS: Oral contraceptive users had higher concentrations of high-density lipoproteins than did women in the control group (+10% to +20%, p < 0.001) primarily because of increases in high-density lipoprotein subfraction 3. High-density lipoprotein subfraction 2 concentrations were higher in users of the desogestrel formulation. Low-density lipoprotein cholesterol concentrations were normal in oral contraceptive users, but triglyceride concentrations were high (+80% to +100%, p < 0.001). Fasting glucose, insulin, and C-peptide concentrations were similar in the three groups, but their responses to a glucose load were higher in oral contraceptive users than in controls (p < 0.01 to p < 0.001). The late plasma insulin response to glucose was higher in the women who used the gestodene formulation than in those who used the desogestrel formulation. CONCLUSIONS: The metabolic profiles induced by these oral contraceptives were remarkably similar and may reflect the activity of the estrogen component.

Adolescent↗
PubMed1993

Effects of a low-estrogen, desogestrel-containing oral contraceptive on lipid and carbohydrate metabolism.

Fasting serum lipids, lipoproteins and apolipoproteins, and fasting plasma glucose, insulin and C-peptide were measured in 107 non-users and 83 users of an oral contraceptive containing the progestin desogestrel, combined with 20 micrograms ethinyl estradiol. Plasma glucose, insulin and C-peptide concentrations during an oral glucose tolerance test (OGTT) were measured in a subgroup of 69 non-users and 39 users. Compared with non-users, users had higher concentrations of total, high density lipoprotein (HDL), HDL subfraction 3 and very low density lipoprotein (VLDL) cholesterol, total triglycerides, VLDL triglycerides, apolipoproteins AI and AII and fasting plasma insulin. There were no differences in HDL subfraction 2, low density lipoprotein cholesterol and apolipoprotein B. OGTT glucose was 60% higher in the users and OGTT insulin response 19% higher. The OGTT C-peptide response did not differ. The effects of 20 micrograms ethinyl estradiol combined with 150 micrograms desogestrel on lipid, lipoprotein, glucose and insulin metabolism are similar to those described previously with a 30 micrograms ethinyl estradiol combination containing the same dose of desogestrel. The relatively favourable metabolic profile associated with the higher estrogen dose desogestrel combination is maintained at the lower dose.

Apolipoprotein A-I↗
PubMed1993

A randomized comparative study of the metabolic effects of two regimens of gestrinone in the treatment of endometriosis.

OBJECTIVE: To study some of the metabolic effects of oral gestrinone on plasma lipoprotein risk markers for cardiovascular disease and on bone density, a risk marker for osteoporosis. DESIGN: Randomized double-blind study. SETTING: All patients were referred to Gynaecology Clinic of Royal Free Hospital Medical School. PATIENTS: Twenty premenopausal women with laparoscopically confirmed endometriosis. INTERVENTIONS: Subjects were randomized in a double-blind fashion to receive either 1.25 mg or 2.5 mg gestrinone two times per week for 6 months. MAIN OUTCOME MEASURE: Laparoscopy was performed before treatment, and clinical responses were determined by second laparoscopy after 6 months. Plasma lipid and bone density measurements during and after therapy were compared with baseline. RESULT: Median total endometriosis scores decreased from 7.5 to 1.0 in the 1.25-mg group and from 7.0 to 0 in the 2.5-mg group. There were no significant between-group differences in endometriosis scores. At both doses, bone density in the spine and the proximal femur was conserved, but plasma concentrations of low-density lipoproteins rose by 13% and those of high-density lipoproteins fell by 40%. CONCLUSIONS: Reducing the dose of gestrinone to 1.25 mg appeared to maintain the therapeutic effectiveness of this treatment but was still associated with potentially unfavorable effects on lipids and lipoproteins.

Adult↗
PubMed1992

Effect of simvastatin on high density lipoprotein subfractions and apolipoproteins in type IIa hypercholesterolemia.

Changes in plasma concentrations of high density lipoproteins (HDL) and triglycerides may partly explain the ability of cholesterol-lowering drugs to decrease the incidence of coronary heart disease. We measured the response of fasting plasma lipids, lipoproteins, and apolipoproteins in 46 subjects with Type IIa hypercholesterolemia treated with simvastatin for 3 months. The initial dose of simvastatin (10 mg/day) was subsequently increased up to 40 mg/day if the plasma cholesterol concentration had not fallen below 5.2 mmol/l. Plasma concentrations of HDL cholesterol and of the apolipoproteins AI and AII were increased by simvastatin. The increase in HDL cholesterol (9%) was due to increases in both subfractions (HDL2 17%; HDL3 7%), changes that would be consistent with a beneficial effect on cardiovascular risk. Simvastatin decreased plasma triglyceride concentrations by 25%. Plasma total cholesterol concentrations fell by 35% after 3 months of treatment; this fall was proportional to the initial concentration and was due almost entirely to a 45% fall in low density lipoprotein cholesterol. In contrast, plasma concentrations of lipoprotein Lp(a) were not affected by simvastatin.

Anticholesteremic Agents↗
PubMed1992

Comparison of transdermal and oral estrogen-progestin replacement therapy: effects on serum lipids and lipoproteins.

OBJECTIVE: We attempted to ascertain whether transdermal postmenopausal estrogen-progestin therapy has the typical effects of oral therapy on serum lipoprotein risk markers for cardiovascular disease. STUDY DESIGN: Sixty-one postmenopausal women were randomized to receive either transdermal continuous 17 beta-estradiol, 0.05 mg/day, with transdermal cyclic norethindrone acetate, 0.25 mg/day, or oral continuous conjugated equine estrogens, 0.625 mg/day, with oral cyclic dl-norgestrel, 0.15 mg/day. Twenty-nine untreated subjects served as controls. Lipoprotein profiles at 3 and 6 months were compared with baseline values by means of analysis of variance. RESULTS: In the estrogen-alone phase both therapies reduced serum levels of total and low-density lipoprotein cholesterol; high-density lipoproteins were largely unchanged. Oral therapy increased triglycerides whereas this lipid fell with transdermal therapy. In the combined phase of the cycle both therapies reduced triglycerides, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. CONCLUSION: Transdermal and oral therapies had similar effects on lipoprotein cholesterol but different effects on triglycerides.

Administration, Cutaneous↗
PubMed1989

Zoladex versus danazol in the treatment of pelvic endometriosis: effects on plasma lipid risk factors.

Plasma lipid risk markers for coronary heart disease (CHD) are influenced by sex steroid concentrations. Therapies that alter sex hormone levels have the potential to affect CHD risk. Zoladex had no effect on plasma lipids, but increased high density lipoprotein (HDL) subfraction 3, a lipoprotein of uncertain clinical significance. Danazol increased low density lipoprotein and decreased HDL concentrations to give a lipid profile associated with increased risk of CHD.

Buserelin↗
PubMed1988

3'-Azido-3'-deoxythymidine (AZT) inhibits proliferation in vitro of human haematopoietic progenitor cells.

Peripheral blood cytopenias are a serious, dose-limiting toxicity of AZT therapy in patients infected by HIV. To evaluate the mechanism by which cytopenias develop, AZT effects of haematopoietic differentiation and growth were measured in serum-free, nucleoside-depleted cultures of normal human bone marrow. In contrast to native thymidine, AZT suppressed the proliferation of erythroid, granulocyte/macrophage and primitive haematopoietic stem cells in a dose-related and time-dependent fashion. Relative progenitor sensitivity varied, with half-maximal concentrations of 1-5 microM and 20-40 microM AZT for inhibition of erythroid and nonerythroid progenitor cell growth, respectively. Inhibition was observed over full ranges of concentrations of haematopoietic tissue-specific regulators (human erythropoietin, colony-stimulating activity, interleukin-3 and lymphocyte conditioned medium) and of platelet-derived growth factor (PDGF), an agent that enhances erythropoiesis in vitro via accessory marrow stromal elements. Furthermore, suppression was similar in cultures of marrow cells that were depleted of accessory populations, suggesting that its action is directed at progenitors. Finally, when deoxythymidine was added in increasing amounts to cultures with a half-maximal concentration of AZT, inhibition was abrogated. We conclude that AZT is a potent inhibitor of haematopoiesis in vitro, and that erythroid progenitors are particularly sensitive to its action. These results may explain the marrow hypoplasia that occurs during AZT administration in vivo.

Antiviral Agents↗
PubMed1984

Tricuspid valve myxoma infected with dysgonic fermenter-2.

We have described a patient with an infected myxoma attached to the tricuspid valve. Unlike those previously reported, our patient had a significant underlying disease, chronic lymphocytic leukemia, and presented the problem of multiple pulmonary infiltrates in an immunosuppressed host, with persistently negative blood cultures. The infecting bacterium, isolated only at operation, was a recently described fastidious gram-negative rod belonging to the CDC group dysgonic fermenter-2.

Bacterial Infections↗
PubMed1984

Acquired immunodeficiency syndrome with progressive multifocal leukoencephalopathy and monoclonal B-cell proliferation.

A 34-year-old man who used intravenous drugs developed the acquired immunodeficiency syndrome with lymphadenopathy, Mycobacterium tuberculosis pneumonia, and progressive multifocal leukoencephalopathy. Early biopsy specimens of the lymph node showed hyperplasia without evidence of lymphoma. Later, immunologic analysis of peripheral blood lymphocytes showed inversion of the helper/suppressor T-lymphocyte ratio and persistent monoclonal B-cell proliferation without clinically overt lymphoma. The clinical course of this patient suggests that abnormal immune responses seen in the setting of the acquired immunodeficiency syndrome may evolve into lymphoproliferative disorders detectable by peripheral blood lymphocyte analysis.

Acquired Immunodeficiency Syndrome↗