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Biomedical subjects

P Cremer

Publications and source records attributed to P Cremer.

At least 55 records · Page 3Linked to original sources
PubMed1988

[Serum lipid and lipoprotein concentrations in pregnancy and at onset of labor in normal and complicated pregnancies caused by hypertensive gestosis and fetal growth retardation].

Cholesterol triglyceride and lipoprotein concentrations were determined in the sera of 220 pregnant women at different periods of their pregnancy. In 197 healthy pregnant women we found besides an increase in cholesterol level and in particular an increase in the beta-lipoprotein fractions, a marked increase in pre-beta-lipoprotein levels and more than twice as high triglyceride concentration in the course of the first to the third trimenon. Nothing abnormal was found on comparing the lipid and lipoprotein parameters of 13 pregnant women having hypertensive toxaemia, with those of healthy gravidae, with the exception of a marked increase in the pre-beta-lipoprotein levels in those patients who suffered from toxaemia. No connection was seen between infantile deficient development below the tenth percentile and the serum lipid and lipoprotein concentrations (n = 10) in the mother. Examinations carried out in 233 pregnant women and their children at the time of birth did not yield any connections between maternal and infantile protein patterns. All infants had definitely lower parameter concentrations than their mothers.

Adolescent↗
PubMed1988

Incidence rates of fatal and nonfatal myocardial infarction in relation to the lipoprotein profile: first prospective results from the Göttingen Risk, Incidence, and Prevalence Study (GRIPS).

In a screening investigation in 1982, which included medical history, clinical examination, general laboratory investigation, and quantification of lipids, lipoproteins, and apoproteins A1 and B, 5020 male subjects aged 40 to 59 years took part. All subjects were free of any heart or vascular disease at the basic examination. Of them 40 suffered fatal or nonfatal myocardial infarction (MI) during the first 3-year observation period between January 1982 and December 1984 (incidence cases), the others remained free of heart or vascular diseases (reference group). Comparison with the reference group revealed a strong relationship between MI-incidence rate and LDL cholesterol (correlation coefficient according to univariate regression analysis r = +0.248; P value according to Chi-square test P less than 0.001). The relationship was less strong but significant for age (r = +0.189; P less than 0.001), total serum cholesterol (r = +0.197; P less than 0.001), and apoprotein B (r = +0.195; P less than 0.001). Although statistically significant, the relationships to the MI-incidence rate were comparatively weak for HDL cholesterol (r = -0.09; P less than 0.01), apo-A1 (r = -0.09; P less than 0.01), systolic blood pressure (r = +0.067; P less than 0.05), and blood glucose level (r = +0.066; P less than 0.05). Body mass index, diastolic blood pressure, and plasma levels of uric acid, triglycerides, and VLDL did not exert relevant influences on the MI-incidence rate in our study population.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Medroxyprogesterone acetate and lipid metabolic changes.

Lipid metabolic changes under oral treatment with medroxyprogesterone acetate (MPA) were investigated in four groups of patients: group I; 10 patients aged 25-45 (mean 38) years received 50 mg MPA daily for pelvic endometriosis. Group II; 21 patients aged 55-77 (mean 62) years received 200 mg MPA daily for surgically treated endometrial carcinoma stage I. Group III; 14 praemenopausal patients aged 37-52 (mean 47) years received 1000 mg MPA daily for metastasized breast cancer. Group IV; 27 post-menopausal patients aged 53-78 (mean 68) years were treated with 1000 mg MPA daily for metastatic breast cancer as well. A fifth group of initially 86 patients aged 40-86 (mean 63) years after surgery for endometrial carcinoma stage I served as untreated control for groups II and IV. Cholesterol and triglyceride concentrations were measured enzymatically lipoproteins were determined by quantitative electrophoresis and precipitation and apolipoproteins A1 and B were quantified by kinetic rate nephelometry. Whereas in patients of group I no changes of lipid and lipoprotein parameters were observed, daily oral doses of 200 mg MPA and more led to a marked fall in alpha-lipoprotein-, HDL-cholesterol and apolipoprotein A1 levels. beta-Lipoprotein-, LDL-cholesterol and apolipoprotein B concentrations rose significantly in Groups III and IV. The relevance of these findings in terms of athero-genicity is discussed.

Adult↗
PubMed1986

The association between serum Lp(a) concentrations and angiographically assessed coronary atherosclerosis. Dependence on serum LDL levels.

Lipoprotein(a) concentrations were measured by radial immunodiffusion in a cohort of 40-60 year males who had been classified by coronary angiography as CAD+ with 50% stenosis of one or more of the major coronary arteries or CAD- with no signs of coronary lesions. Sample odds ratios were calculated as a measure of association between serum Lp(a) values and the presence of coronary artery disease. An odds ratio of 2.706 (P less than 0.001) was derived for elevated (greater than or equal to 30 mg/dl) Lp(a) levels vs low (less than 5 mg/dl) Lp(a) levels indicating a strong association between the presence of coronary artery disease and elevated Lp(a) concentrations. This association was independent of the known risk factors smoking, hypertension and diabetes as well as the serum concentrations of total triglycerides, HDL-cholesterol, alpha-Lp-cholesterol and pre-beta-Lp-cholesterol. In contrast to these variables the association between Lp(a) and coronary artery disease was dependent upon the serum concentrations of LDL-cholesterol, beta-Lp-cholesterol and total cholesterol. At concentrations below the respective median for each variable, odds ratios of between 1.42 and 1.67 were calculated whereas at concentrations above the respective medians the odds ratios ranged from 4.50 to 6.33 (P less than 0.001). Our data, therefore, suggest that increasing LDL concentrations markedly increase the risk of coronary artery disease due to elevated Lp(a) levels.

Adult↗
PubMed1985

Effects of medrogestone and conjugated oestrogens on serum lipid and lipoprotein concentrations.

Twenty patients, aged 30-60 yr, who had undergone bilateral ovariectomy, were treated orally with 5 mg medrogestone (6,17-dimethylpregna-4,6-diene-3,20-dione) and 1.25 mg conjugated oestrogens per day, according to a constant dosage pattern during the cycle (22 + 6 days). The lipids and lipoproteins were determined twice before the start of therapy and 3, 6 and 12 mth thereafter. The lipids were quantified enzymatically and the lipoproteins by quantitative lipoprotein electrophoresis. Whilst cholesterol and triglyceride concentrations showed no detectable change, a slight but significant increase was seen in the high-density alphalipoprotein (HDL) cholesterol concentrations. The low-density beta-lipoprotein (LDL) cholesterol level showed a moderate fall. There was a resultant reduction in the beta/alpha-lipoprotein ratio. Accordingly, the apoprotein A1 concentrations were found to be elevated, while apoprotein B tended to fall to lower levels during therapy. When these changes are measured by the lipid metabolism risk criterion for the occurrence of coronary heart disease applicable to post-menopausal patients, the effects of the above-mentioned combination may be regarded as entirely favourable.

Adult↗
PubMed1985

[Changes in serum lipoproteins under hormonal therapy of breast carcinoma and other endocrine-dependent tumors].

The higher the low-density-lipoprotein cholesterol (beta lipoprotein) level, the greater the risk that coronary heart disease will develop, alpha-lipoprotein fractions (high-density-lipoproteins) are considered to be protective factors. Medroxyprogesterone acetate is responsible for characteristic changes of the lipoprotein patterns indicating enhanced coronary risks. Medroxyprogesterone acetate is applied in the therapy of breast, uterus and ovarian cancer. A statistically significant decrease was observed in alpha-lipoproteins whereas beta-lipoproteins increased without statistical significance. A similar reaction can be observed under the combination therapy of aminoglutethimide and medroxyprogesterone acetate, whereas the combination of cortisone and aminoglutethimide has a distinct influence on beta-lipoproteins but the alpha-lipoprotein level remains uninfluenced. According to these data the effect of an adjuvant application of these drugs must be carefully evaluated due to an increase of coronary risks.

Aminoglutethimide↗
PubMed1984

[Lipoprotein changes during hormonal treatment of endometriosis with lynestrenol and danazol].

The Lipoprotein profile of 24 patients with endometriosis was determined before, during and after the treatment with the two steroid hormones Lynestrenol (10 mg/day) and Danazol (600-800 mg/day). The total cholesterol triglycerides, beta-, prebeta-, and Alphalipo -protein bound to cholesterol were determined. Both hormones cause a marked lowering of the Alpha-Lp-cholesterin. In addition, the beta-LP-cholesterin was elevated and the beta-alpha-LP-ratio was elevated. In the dosage used by us, Lynestrenol showed less effect on the Lipoprotein profile. Danazol caused changed in the beta- and alpha-lipoprotein pattern of highly pathological atherogenic types. The total cholesterol was not influenced. Since women in the fertile age group will suffer a higher risk of arteriosclerosis from an elevation of the beta-LP-cholesterin, the treatment with Danazol calls for a sophisticated monitoring of the lipid metabolism and care in the indication for long term treatment with Danazol or with Lynestrenol.

Adult↗
PubMed1984

Influence of smoking on the plasma lipoprotein profile.

Smoking and hypercholesterolemia, or more specifically hyper-beta-lipoproteinemia, are well established risk factors for the early development of atherosclerotic disease. The presence of both factors augments the potential risk. The question arises, therefore, as to whether cigarette smoking has a direct effect on the plasma lipoproteins and, in particular, on the atherogenetic low density lipoproteins. In this study, the influence of cigarette smoking on the lipoprotein profile was investigated in a defined cohort of 6,543 male industrial workers aged 40-59 years, consisting of 2,434 smokers and 3,975 non-smokers. The effect of smoking on the lipoprotein profile showed no significant changes in LDL and only slight changes in the other lipoprotein fractions. Other factors, such as alcohol intake, body weight, and general life style seem to have a greater influence on HDL-cholesterol than smoking. It is concluded that smoking does not significantly alter lipid metabolism and that minor differences observed between smokers and non-smokers are due to a variety of factors, rather than a reflection of a direct metabolic relationship.

Adult↗
PubMed1982

Determination of apolipoprotein B by kinetic (rate) nephelometry.

Determination of apoB by rate nephelometry is a simple, rapid and precise method, which is also suitable for a routine laboratory. It can be standardized with lipoprotein-B or LDL fractions, but only if these fractions are diluted with fresh whole serum. The standardization is also valid for VLDL if the samples are diluted with hydroxypolyethoxydodecane (trade name: Thesit) in a concentration of 0.33 g/liter. Using rate nephelometry, a strong correlation between the contents of cholesterol and apoB of VLDL as well as of LDL can be demonstrated. Similar high correlations are achieved if apoB is determined chemically in isolated lipoprotein fractions. The ratio of apoB to cholesterol is constant but not the same in both VLDL and LDL. There is also a strong correlation between the concentration of apoB in whole serum with the LDL cholesterol values in a normotriglyceridemic population. Therefore, the assay of apoB in whole serum by rate nephelometry is proposed as a screening method for dyslipoproteinemia (increased concentrations of atherogenic lipoproteins at normal or elevated levels of cholesterol in plasma).

Cholesterol↗