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Biomedical subjects

H Kaffarnik

Publications and source records attributed to H Kaffarnik.

At least 55 records · Page 3Linked to original sources
PubMed1985

Lipoprotein fractions, lipoprotein lipase and hepatic triglyceride lipase during short-term and long-term uptake of ethanol in healthy subjects.

In short-term experiments, healthy fasting persons were given a basic dose of 0.5 g of ethanol/kg body weight, followed by hourly maintenance doses of 0.15 g of ethanol/kg body weight. After 10 h there was a significant increase of triglycerides in the VLDL, LDL, and HDL, the main rise (from 42 to 92 mg/dl) being found in the VLDL triglycerides. Other subjects, who received nourishment isocaloric with ethanol, likewise showed a significant rise of triglycerides in all lipoprotein fractions. Chylomicron triglycerides increased from 9.3 to 35.5 mg/dl. There was no significant change in postheparin HTGL, but postheparin LPL activity decreased after 10 h from 17.9 to 12.2 mmol FFA/ml/h in the fasting subjects, and from 28.5 to 10.2 mmol/FFA/ml/h in the persons receiving food. In long-term experiments after 4 weeks of 70 - 80 g of ethanol and isocaloric food daily, triglycerides increased, especially in the VLDL (from 50 to 82 mg/dl). The increase in the HDL, however, was also significant. After 4 weeks of ethanol, the chylomicron triglycerides in the plasma of the fasting subjects reached a value of 29.3 mg/100 ml, LDL cholesterol decreased, and HDL cholesterol increased. After 4 weeks of ethanol there was an increase in the lipoprotein lipase of the adipose tissue.

Adult↗
PubMed1984

Apolipoprotein E phenotypes and hyperlipidemia.

Apolipoprotein E phenotypes were determined in 361 patients with hyperlipidemia and in controls. The E2 isoform was significantly more frequent in the group of hyperlipidemics (P less than 0.0005). This was not due to a higher frequency of E-2/2 homozygotes with type III hyperlipoproteinemia, but rather to a significantly higher frequency of E2 heterozygotes (P less than 0.0005). Subgrouping of hyperlipidemics into patients with a) hypertriglyceridemia, b) hypercholesterolemia and c) mixed hyperlipidemia revealed i) that isoform E2 was significantly more frequent in patients with hypertriglyceridemia (0.001 greater than P greater than 0.005), ii) that isoform E4 was significantly more frequent in patients with hypercholesterolemia (0.01 greater than P greater than 0.005) and iii) that isoforms E2 (P less than 0.005) and E4 (0.05 greater than P greater than 0.025) were both more frequent in patients with mixed hyperlipidemia. Roughly 20% of patients with mixed hyperlipidemia had one of the rare phenotypes E-4/4, -4/2 or -2/2. We conclude that alleles epsilon 2 and epsilon 4 both contribute to the susceptibility for, and/or phenotypic expression of hyperlipidemia. Whereas the gene epsilon 2 seems to exert its influence on plasma lipoproteins by an abnormal gene product (E2) that has reduced binding activity to lipoprotein receptors, the mechanism underlying the association of the epsilon 4 gene with hyperlipidemia is presently unclear.

Apolipoproteins↗
PubMed1984

[Sex hormones and fertility following portacaval anastomosis in rats].

Portocaval anastomosis (PCA) in the normal male rat causes profound alterations in testicular morphology and function and in plasma levels of sex steroids as well as of gonadotropins. Testicular atrophy is accompanied by a significant decrease of plasma testosterone (0.03 ng/ml versus 0.99 ng/ml) and an increase of estradiol (76.2 pg/ml versus 39.7 pg/ml) and estrone (68. pg/ml versus 45.5 pg/ml). Plasma levels of gonadotropins (LH, FSH) and prolactin are lowered too (LH: 15 ng/ml versus 28.5 ng/ml, FSH:119 versus 182 ng/ml, prolactin:53 versus 109 ng/ml). The altered sex hormone metabolism is reflected in marked changes of the morphology and nucleic acid content of the metabolizing organs i.e. liver, gonades and kidney. The results of this study are consistent with the hypothesis that portosystemic shunt per se plays an important role in the pathogenesis of the disturbed metabolism of sex hormones observed in patients with liver cirrhosis and portal hypertension.

Adrenal Glands↗
PubMed1983

Ethanol-induced hyperlipoproteinemia. Crucial role of preceding ethanol intake in the removal of chylomicrons.

Ethanol produces a number of effects in different steps of lipid metabolism which have been suggested to be responsible for the common phenomenon of ethanol-induced hyperlipoproteinemia in man. The occurrence of hyperchylomicronemia has been attributed to an ethanol-specific disturbance of the clearing mechanism of triglyceride-rich lipoproteins. However, the reports on lipolytic activities and the clearance of chylomicrons after ethanol ingestion are contradictory. In this investigation the short-term excess of serum lipoproteins and the lipolytic activities in healthy volunteers were studied after single and prolonged ethanol ingestion followed by an intravenous lipid load. One hour after a single oral dose of ethanol, the intravenous fat tolerance test was unchanged. After an ethanol load over a 5 hr period, the fat tolerance was reduced, although the same ethanol levels at the time of infusion were maintained. In addition, the lipolytic activities of the serum were significantly reduced after 5 hr of ethanol ingestion followed by intravenous fat load. Hence the time relations between ethanol and fat loads determine whether a defect in chylomicron catabolism can be observed or not. A striking difference in the situations when the fat infusions were performed was the development of endogenous hypertriglyceridemia after 5 hr of ethanol ingestion. Since ethanol-dependent differences in the absorption of fat are ruled out by our experimental design, we attribute our findings to a competitive inhibition of chylomicron degradation by VLDL and partial depletion of the lipolytic system by combined endogenous and exogenous hypertriglyceridemia.

Adult↗
PubMed1982

[Alcohol and plasma lipoproteins in acute and long-term studies].

The influence of ethanol on plasma lipids, lipoproteins and on the activity of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL), the major enzymes in the catabolism of triglyceride rich lipoproteins, was studied in 14 healthy young volunteers who were given 50 g ethanol daily for 4 weeks together with a standardized isocaloric diet. Marked hypertriglyceridemia occurred initially, mainly due to increased VLDL, but chylomicronaemia was also present in all probands. While HTGL activity remained unaltered there was a marked decrease in LPL activity. At the end of the study serum triglycerides and VLDL almost returned to initial levels, while Chylomicronaemia had totally disappeared. Furthermore, there was no atherogenic plasma lipoprotein alteration: LDL were not increased and the possibly antiatherogenic HDL were even significantly increased after the four weeks' study period. Again, HTGL activity remained unchanged but that of LPL reached its maximum after 4 weeks. It is therefore suggested that regular alcohol intake may increase LPL activity and hence may lead to a more rapid catabolism of triglyceride-rich lipoproteins in plasma.

Adult↗
PubMed1982

Apolipoprotein AIMarburg: studies on two kindreds with a mutant of human apolipoprotein AI.

Three probands heterozygous for a mutant of apolipoprotein AI (apo AIMarburg, Utermann et al. 1982a) were detected by screening of 2282 unrelated individuals resulting an a frequency estimate of about 1/750 in the German population. All three probands with apo AIMarburg had hypertriglyceridemia (triglyceride above 250 mg/dl) and subnormal HDL-cholesterol (below 30 mg/dl), but no other lipoprotein abnormalities. The kindreds of two probands with AIMarburg were studied. The family data are consistent with an autosomal codominant inheritance of the trait. A total of 16 heterozygous blood relatives with the mutant AIMarburg were detected in these kindreds. Analysis of the plasma lipid and lipoprotein levels in relation to the apo AI phenotype was complicated by the high prevalence of diabetes mellitus and thyroid disease in one kindred and of hyperlipidemia in both kindreds. No consistent relationship between plasma lipid and lipoprotein levels, and the mutant apo AI could be demonstrated. Instead the mutant apo AI and the dyslipoproteinemia seem to co-exist independently in these kindreds. Three sibs with the homozygous apo E-2/2 phenotype were detected in one kindred, and all three sibs had subnormal LDL-cholesterol and beta-VLDL, e.g., the lipoprotein abnormality characterizing primary dysbetalipoproteinemia. Genetic apo E phenotypes and the apo AI mutant segregated independently, indicating that the structural gene loci for apo E and apo AI are not closely linked.

Adult↗
PubMed1980

[Blood coagulation disorders in liver cirrhosis in relation to the degree of portal hypertension].

Investigated were the haemostasis of 45 patients with histologically confirmed liver cirrhosis. The patients were subdivided into three groups according to the extent of their porto caval collateral circulation as proved by laparoscopy, gastroscopy and radiology: I = no porto caval shunts (n = 10); II = moderate porto caval shunts (n = 13); III = distinct porto caval shunts (n = 14). A 4th group consisted of 8 patients with bleeding from oesophageal varices. The results indicated a significant decrease in the stages I-III of the coagulation factors produced in the liver (incl. factor XIII and AT III) and the thrombocytes. Unchanged remained the concentration of factor VIII, whereas the factor VIII associated antigen showed an increased activity depending on the severity of the disease (stages I-III). In patients with bleeding from oesophageal varices, values of about 300% of normal could be demonstrated. Depending on the stage of the porto caval collateral circulation, the concentration of fibrin(ogen) split products were also increased. For comparison, patients with pre- and posthepatic blockage were investigated, whose portal hypertension was not caused by liver cirrhosis. Besides a mild thrombopenia they only showed a secondary hyperfibrinolysis. The results, above all in the cases of liver cirrhosis, can be explained by pathophysiological mechanism: a decreased synthesis of clotting factors-a disturbed portal microcirculation with fibrin deposition-an impaired function of the liver RES.

Blood Coagulation Disorders↗
PubMed1980

[Longterm therapy and etofibrate (author's transl)].

The stabilization parameters of patients under routine care are differentiated. 20 hyperlipoproteinemic patients (types IIa, IIb and IV) who were difficult to stabilize were treated with 0.9 g etofibrate daily. In addition to the cholesterold and triglyceride levels, we followed up the laboratory control parameters in the serum, fasting blood sugar and differential blood count. During the treatment period the cholesterol levels fell to 18%, triglycerides to 50%. Tachyphylaxis was never seen. The good tolerance of etofibrate shows that the substance is suitable as a potent hypolipidemic agent for longterm treatment of hyperlipoproteinemia.

Anticholesteremic Agents↗
PubMed1980

Long-term treatment of hyperlipoproteinemia with etofibrate: clinical observations.

We investigated the changes in serum lipid concentrations of patients treated with Etofibrate as part of their routine management in the metabolic ambulatory care unit of the Medical Policlinic at the University of Marburg. In our study, 26 patients who had not responded well to prior treatment for Types IIa, IIb, III and IV hyperlipoproteinemia were given a daily dose of 900 mg Etofibrate for up to 48 months. As a result to this treatment, serum total cholesterol levels fell by up to 17,6% and triglyceride levels by up to 47,8%. We observed no tachyphylaxis toward Etofibrate. The results of standard laboratory parameters measured in parallel with drug treatment reflect a good tolerance for Etofibrate. This substance is highly suited as a potent lipid-lowering agent.

Adult↗
PubMed1980

[Effects of polymyxin B and E (colistin) on blood coagulation, thrombocyte function, and fibrin structure (author's transl)].

Polymyxins are known to form complexes with endotoxins and phospholipids. Therefore patients with septicaemia were treated in some studies with polymyxin. We investigated the effect of polymyxin B and E (colistin) on some blood coagulation parameters, spreading of platelets and fibrin polymerisation. With increased concentrations of polymyxin (1, 5, 10, 20, 100 mg%) we found a significant prolongation of prothrombin, partial thromboplastin and TEG reaction times. Spreading of platelets was also reduced. There was, however, no effect on fibrin polymerisation. The coagulation inhibitory effects of polymyxins could be reduced by adding phospholipids as procoagulant. These results indicate: 1. There are anticoagulant effects of polymyxins even in therapeutic doses and therefore it should not be applied in cases of haemorrhagic diathesis or renal insufficiency. 2. In septicaemia the disseminated intravascular coagulation can be prevented because due to consumption of polymyxin, endotoxinaemia persists.

Anticoagulants↗
PubMed1980

Clinical experience with bezafibrate.

We report on 41 patients with primary hyperlipoproteinemia (type IIa, IIb and IV) treated with 450 to 600 mg of bezafibrate for 12 months. Placebo periods of 8 weeks surrounded the treatment period. In types IIa and IIb total cholesterol decreased by up to 18,7%, triglycerides to 34,6%. In type IV serum triglycerides decreased up to 48,2 and cholesterol by 12,2%. In a second investigation we differentiated the cholesterol- and triglyceride-values of 16 patients regularly controlled. We found a significant decrease during the treatment period. Bezafibrate is a potent lipid-lowering agent of the new generation.

Bezafibrate↗