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Biomedical subjects

H Kaffarnik

Publications and source records attributed to H Kaffarnik.

At least 91 records · Page 5Linked to original sources
PubMed1976

[Human ethanol-induced hyperlipoproteinemia (author's transl)].

Reversible hyperlipoproteinemia may be observed after ethanol loads in healthy man before any ethanol-induced disease is being established. Different pathogenetic ways to this acute ethanol-induced hyperlipoproteinemia have been investigated or postulated in recent years. Two main sites have appeared: changes in the metabolism of lipids and their precursors which depend from acutal oxidation of ethanol in the liver, and ethanol-induced activation of lipolysis in adipose tissue, transmitted by the sympathico-adrenal system. The changes in liver metabolism during ethanol oxidation have been well confirmed in many experiments, they nevertheless do not seem to lead to hyperlipoproteinemia in many experimental designs in animals and after drinkable amounts of ethanol in healthy man when lipolysis of adipose tissue is blocked and no food is ingested. After the intake of a fatty meal these triglycerides are becoming importance as a source of fatty acids. A possible increased de novo synthesis of palmitic acid may to a minor degree contribute to hypertriglyceridemia.

Adipose Tissue↗
PubMed1976

[Fatty acid patterns and glucose tolerance in Huntington's chorea (author's transl)].

Fatty acid patterns of plasma lipids and glucose-tolerance in Huntington's chorea. 25 patients with Huntington's chorea of various manifestation (9 predisposed symptomefree, 5 with light and 11 with severe manifestation) had studies of carbohydrate and lipid metabolism. These studies measured glucose-tolerance tests, insulin-, HGH-secretion, serum lipids and plasma fatty acid conposition of the cholesterylesters, triglycerides and phospholipids. The reactive insulin- but not HGH-levels were significantly raised, 32 % of the patients with Huntington's chorea had abnormal glucose-tolerance tests, compared with 3.2 % in a control group. Duration of symptoms correlated with higher cholesterol levels. Minor deviations were found in the fatty acid patterns in various lipid clases.

Cholesterol↗
PubMed1976

[Changes of triglycerid-fatty acids in healthy volunteers during acute ethanol ingestion with and without blocking peripheral lipolysis (author's transl)].

This investigation decided to answer the question of the origin of fatty acids for the increased synthesis of triglycerides in acute ethanol-induced hyperlipoproteinemia. Healthy persons ingested 0.5 g of ethanol/kg body weight initially and 0,15 g of ethanol/kg and hour for 12 hours. The fatty acids of plasma triglycerides were determined before and after ingestion of ethanol in persons fasting and nourished isocaloricaly, with and without blocking peripheral lipolysis by nicotinic acid and with addition of glucose. The fasting persons triglycerides fatty acids increased to 165.7 % of the initial value after 12 hours of ethanol ingestion, with a preferential increase in palmitic-, oleic- and stearic acid. When lipolysis in adipose tissue was blocked by 0.5 g of nicotinic adic/hour the triglyceride-fatty acids reached only 116.2% after 12 hours, with a decrease in oleic acid, which is present in adipose tissue to a higher degree than in plasma triglycerides. When nourished isocaloricaly, the enhancement of plasma triglyceride-fatty acids could not be suppressed by nicotinic acid. The changes in concentration and pattern of triglyceride-fatty acids announce that the fatty acids used for increased synthesis of triglycerides in fasting persons come from adipose tissue preferentially. In contrast ethanol-ingested hyperlipoproteinemia during ingestion of a food which cannot be suppressed by nicotinic acid, seems to orginate from fatty acids of the food and for de novo synthesis of fatty acids in the liver.

Adipose Tissue↗
PubMed1976

Alteration of plasma lipids and intermediates of lipid metabolism in healthy fasting volunteers by ethanol and fructose.

After healthy persons, aged between 20 and 35 years, had consumed either ethanol or ethanol and fructose, triglycerides, free glycerol, FFA, phospholipids and total cholesterol were determined. After a basic dosage of 0.5 g ethanol/kg body weight, each person received a maeintenance dosage of 0.1 g ethanol/kg body weight and hour. Control experiments were carried out on persons receiving only fructose and on fasting persons who consumed no ethanol. After 8 hrs, triglycerides rose in the ethanol group by 107 %, in the ethanol-fructose group by 63 %. FFA exhibited in both ethanol and ethanol-fructose groups an initial decrease, with a secondary increase in the ethanol group. The initial decrease was greater in the ethanol-fructose group. A significant rise in free glycerol by 419 % was observed 30 min after the intake of combined ethanol/fructose. Free glycerol rose under ethanol alone by 144%. The ohospholipids exhibited a slight rise in the ethanol group; no significant changes occured in the cholesterol. The blood ethanol level was lower under ethanol-fructose than under ethanol alone. The addition of fructose diminishes the ethanol-induced hypertriglyceridemia. Our investigations give further proof that, under short-term ethanol load, the fatty acids necessary for the increased triglyceride synthesis in the liver, originate predominantly from a peripheral lipolysis, and that changes in liver metabolism depending on the oxidation of ethanol are not of less importance for the development of the acute ethanol-induced hyperlipidemia.

Adult↗
PubMed1976

[Field study on the decrease of lipids using etofibrate].

A field-trial on Etofibrat was performed on 4405 patients suffering from primary and secondary hyperlipoproteinemia. The results were proved statistically. After a 3 to 4 weeks treatment the concentration of cholesterol as well as tryglicerides in the serum decreased significantly. After 6 to 8 weeks treatment the lipid-lowering effect was even stronger. Nearly 90% of the patients investigated gave a positive response to the treatment. Part of the population had undergone a treatment with other lipid-lowering agents before-most likely without sufficient success-in these cases a further lipid-lowering effect due to Etofibrat could be shown. Under-dosage in premedication cannot be excluded. The stratification of the patients in different groups of diagnosis showed a nearly similarity of both blood lipids independent of the diagnosis. This could also be confirmed for the group of patients suffering from diabetes. To prove the lipid-lowering efficacy of Etofibrat a population was withdrawn from treatment. Cholesterol as well as tryglicerides increased significantly during the interval without treatment. During a long-term study both lipid fractions could be kept down without increasing of the daily Etofibrat dose. The tolerance of Etofibrat was stated to be good up to very good. Objectively the measured enzymes SGOT, SGPT and gamma-GT showed a decrease of the means. Subjectively the occurrence of an often intermediate heat sensation and/or rubedo was of relevance. The low daily dose compared with other lipid-lowering agents gives indication for a better pharmacocinetic behaviour of the drug;

Alanine Transaminase↗
PubMed1976

[Beta-sitosterin in unsuccessfully pretreated patients with hypercholesteremia. Simultaneously, a contribution to dose dependence].

To 9 patients with hyperlipoproteinemia type II and treated with different hypolipidemic drugs without success, sitosterol was given for a period of 4 to 16 months. The effective dose was 10.56 to 21.12g beta-sitosterol corresponding to 12 to 24g granulate. One patient developed a serious diarrhoe and dropped out. 4 patients showed an impressive decrease of serum cholesterol levels.

Adult↗
PubMed1976

[Post-heparin-lipolytic activity in acute ethanol-induced hyperlipoproteinemia (author's transl)].

Post-heparin lipolytic-activity (PHLA) was studied in 10 healthy volunteers ingesting 0.5 g of ethanol/kg body weight initially and 0.1 g/kg body weight and hour over 5 hours. This dose led to enhancement in plasma triglycerides to about 170% of the pre-ethanol values. PHLA was determined before, 15 min, 1 and 5 hours after intake of the initial dose and showed no significant changes. These findings are compared with the results of earlier investigations. It is concluded that acute ethanol induced hyperlipoproteinemia in healthy man seems to be due mainly to enhanced hepatic synthesis of triglycerides and release of very low density lipoproteins and not to decrease catabolism of triglyceride rich lipoproteins.

Adult↗
PubMed1975

[Swollen lymph nodes of the neck as a cardinal symptom of lymphoepithelioma (Schmincke-Regaud) (author's transl)].

Of two cases of lymphoepithelioma (Schmincke-Regaud) is given report. Swollen lymph nodes of the neck, which in the beginning have been thought to be inflammatory, persisted in the first case five years, at the second patient one year before diagnosis. In both cases the tumor originated from the epipharynx. After X-raying both patients since 2 1/2 years are free of recidivation.

Adult↗
PubMed1975

[Insulin and proinsulin secretion under contraceptive steroid administration (author's transl)].

An ivestigation has been performed in 49 women about the influence exerted on the glucose-tolerance, insulin and proinsulin secretion by hormonal contraceptives of different types and compositions. A disturbed dynamics of the insulin secretion with elevated values in the OGTT at two and three hours has been proven at a nearly equal degree using combined preparations (Anacyclin, Eugynon, Neogynon, Mikrogynon) or sequential preparations (Kombiquens, Ovanon). Though there has been interference with the glucose tolerance, the serum proinsulin in the OGTT showed increased levels too. When a combined preparation was applied, the proinsulin values were significantyl higher compared to a sequential type contraceptive. The observed disturbance of the insulin and proinsulin secretion is explained by a decreased sensitivity to insulin in the peripheral fat tissue. The actual dose of the estrogen-gestagen components has no influence on the described changes. Elevated insulin levels are demonstrable already during the first treatment cycle. The degree of the disturbance is independent of the duration of the medicamentous application during the first 6 contraceptive months. After withdrawal of the respective contraceptive steroid the insulin secretion showed nearly normal dynamics during the subseqeunt menstrual cycle.

Blood Glucose↗
PubMed1975

[Basal and reactive proinsulin and insulin secretion in overweight women (author's transl)].

Serum proinsulin and insulin levels were measured on 55 normal or overweight women before and after oral glucose administration. The proinsulin proportion of basal total insulin was 70% in women of normal weight. With increasing overweight the relation shifted in favour of insulin. After stimulation with glucose, proinsulin levels were significantly raised, analogous to total insulin, but les marked than the latter. The increased total insulin excretion in obesity was, therefore, largely due to insulin and less to proinsulin. The greater the overweight the later maximal insulin levels were reached after oral glucose administration: proinsulin peaks occurred later than insulin peaks. Measurement of areas from single values and corresponding times for proinsulin and insulin, after stimulation, indicated their significant correlation with the degree of overweight. In women of more than 70% overweight (Broca index), reactive proinsulin and insulin excretion decreased again despite an increase in body weight. They had a definitely reduced carbohydrate tolerance. After reduction in body weight previously increased proinsulin levels fell again. The significance of higher proinsulin levels in fasting subjects, which increased after stimulation and with overweight but were in percentage terms less than those of reactive insulin, remains unexplained.

Adult↗
PubMed1975

Haemolytic anaemia with hereditary pyruvate kinase instability developing acute leukaemia.

The case of a 27-year-old woman with pancytopenia, revealing acute monocytic leukaemia and haemolytic anaemia, is described in detail. The underlying cause for the red cell destruction was found to be a pyruvate kinase (PK) instability. Further investigation into three generations of her family (n = 12) disclosed a hereditary PK instability. This was proven by performing biochemical studies to elucidate mutants representing a structurally defective enzyme. Since conversions of pancytopenia with acquired red cell enzyme deficiency into leukaemia have been described, our observation emphasizes that hereditary red cell enzymopathy might also be associated with adult acute leukaemia.

Adenosine Triphosphate↗