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Biomedical subjects

H Greten

Publications and source records attributed to H Greten.

At least 217 records · Page 12Linked to original sources
PubMed1978

[Coronary heart disease in patients with primary type V hyperlipoproteinemia (author's transl)].

In two patients with primary Type V hyperlipoproteinemia with typical clinical features including recurrent bouts of abdominal pain a myocardial infarction was diagnosed. In both cases coronary angiography revealed a severe three vessel disease. The case reports demonstrate that the incidence of ischemic heart disease in patients with Type V hyperlipoproteinemia is higher than reported in the literature. In each case of severe abdominal pain, even in younger Type V patients, a myocardial infarction has to be excluded, In both patients a selective depression in the activity of lipoprotein lipase was found. The possible pathogenetic implication of this finding will be discussed.

Aged↗
PubMed1978

[Comparison between combination therapy with clofibrate and beta-pyridylcarbinol and clofibrate monotherapy (author's transl].

In order to determine whether the lipid-lowering effect of combined treatment with clofibrate and beta-Pyridylcarbinol exceeds that of clofibrate monotherapy, a double-blind crossover study was performed. 17 patients with primary hyperlipoproteinemia of Type IIa and 10 patients with primary hyperlipoproteinemia of Type IIb received either Lipofacton (1.000 mg clofibrate and 50 mg beta-pyridylcarbinol per day) or clofibrate (1.500 mg per day) for a period of 6 weeks each. Before beginning therapy and between both periods of medication, placebo was administered for 14 days. In both total plasma and in the LDL fraction the cholesterol level was lowered by less than 10% for both substances. In patients with hyperlipoproteinemia of Type IIb, the triglyceride levels were lowered by about 40%.

Adolescent↗
PubMed1978

[Mechanism of action of synthetic heparinoids: results in patients with hypertriglyceridaemia (author's transl)].

The effect of two synthetic heparinoids, SP-54 and Depot-Thrombocid, on serum lipids was studied in 17 patients with primary hyperlipidaemia (types IIb, IV and V of Fredrickson) and 15 healthy persons. SP-54 had no lipid-lowering effect, neither on oral nor rectal suppository application. Intramuscular injection of Depot-Thrombocid, however, resulted in a decrease of serum triglyceride concentrations of maximally 50% after six hours. There was a marked increase in the activity of the two lipolytic enzymes, lipoprotein lipase and hepatic triglyceride lipase in plasma, as well as an increase in free fatty acids and an extension of thrombin time and PTT. Twenty-four hours after injection all values returned to pretreatment levels. Intramuscular administration of Depot-Thrombocid two or three times a week for seven weeks had no lasting effect on serum lipids. However, there were considerable side effects such as haemorrhagic diatheses, hair loss and thrombocytopenia.

Administration, Oral↗
PubMed1978

[Drug treatment of primary hyperlipoproteinemia (author's transl)].

Cardiovascular disease has become the major cause of death in the Western countries. There is strong evidence that elevations of serum lipids contribute to the pathogenesis of premature atherosclerosis. The classification of the hyperlipoproteinemias has been most beneficial as a guide to development of dietary and pharmacological regimens for lowering serum lipid concentrations. The results of dietary and drug prevention trials are discussed. Insight into the mechanisms involved in lipoprotein metabolism as well as the mode of action and of side-effects of hypolipidemic drugs is reviewed. Using present knowledge of heart disease research, it is reasonable to suggest dietary and drug treatments for the high risk patient.

Anion Exchange Resins↗
PubMed1978

Secondary type II hyperlipoproteinemia in patients with anorexia nervosa.

In 18 patients with anorexia nervosa, plasma cholesterol and triglyceride concentral concentrations were repeatedly determined over a period of 14 mo. In 11 patients elevated cholesterol concentrations were found which were due to an increase of low-density lipoprotein cholesterol, whereas high-density lipoprotein and very low density lipoprotein cholesterol levels were in the normal range. The elevated cholesterol values did not correlate with clinical and laboratory parameters such as the degree of weight loss and thyroid function tests. In follow-up studies it could be shown that in patients who regained their original weight, elevated plasma cholesterol concentrations fell to normal levels parallel to weight increase. In patients who showed no change in weight, however, cholesterol levels remained high. The cause for this secondary type II hyperlipoproteinemia in anorexia nervosa is not known. Hepatic triglyceride lipase and lipoprotein lipase activities in post-heparin plasma were found to be low despite normal triglyceride concentrations.

Adolescent↗
PubMed1978

[Metabolic diseases and idiopathic ischemic necrosis of the femoral head in adults (author's transl)].

100 patients suffering from osteonecroses (including 95 with necroses of the head of the femur) were subjected to comprehensive clinical, roentgenologic and chemical laboratory examination. A triangle was established from the range of factors considered as pathogenetically important by various authors. These three outstanding factors were: disturbance of lipid metabolism, found in 41% of the patients, deviation of the liver function data, and, finally, abuse of alcohol as discovered on the basis of the case history. The statistically significant correlation of these factors makes it probable that there is actually a pathogenetic chain abuse of alcohol--hyperlipoproteinemia--arteriosclerosis--osteonecrosis. No specific importance of the uric acid and glucose metabolism could be established, since the metabolic disturbances associated with these processes are mostly linked with the observed hyperlipoproteinemia. Deliberations regarding the genesis of necrosis of the head of the femur must also take into account, over and above the relation between metabolic disturbances and stenosing vascular processes, the presence of a locally predisposing factor, such as mechanical strain or the state of enzymatic supply of the osseous tissue.

Adolescent↗
PubMed1977

Selective deficiency of hepatic triglyceride lipase in uremic patients.

To investigate the pathogenesis of hypertriglyceridemia in patients with renal disease we measured plasma lipoprotein composition as well as hepatic triglyceride lipase and lipoprotein lipase in post-heparin plasma. Three groups with renal disease were studied: conservatively treated chronic uremia; patients undergoing maintenance hemodialysis; and renal-allograft recipients. A selective decrease of hepatic triglyceride lipase with normal lipoprotein lipase was found in conservatively treated uremia and in patients undergoing hemodialysis. Elevated levels of very-low-density lipoproteins and increased triglycerides in low-density lipoproteins occurred in these patients. In contrast, hepatic triglyceride lipase and lipoprotein lipase were both normal in patients after renal transplantation who had Type II hyperlipoproteinemia as a common lipoprotein pattern with increased low-density-lipoprotein cholesterol and decreased high-density-lipoprotein cholesterol concentrations. The accumulation of a triglyceride-rich low-density lipoprotein in the majority of patients with renal disease may be the consequence of low hepatic triglyceride lipase.

Adult↗
PubMed1977

[Lipid-protein-interactions of human apolipoproteins-structural aspects and models of lipoproteins (author's transl)].

The plasma lipoproteins are complex macromolecular structures which play an essential role in fat transport and in energy and membrane metabolism of higher organized organisms. Much has been learned in the last decade about the structural and functional interrelationships of the different lipoprotein classes. Their protein moieties, the so-called apolipoproteins, have been purified and characterized, the primary structure of four of them is known. Initial recombination experiments showed a considerable potential of the (unfractionated) lipoprotein protein to bind to lipids and to form particles similar to native lipoproteins. Further binding experiments performed in several laboratories with the purified A- and C-apolipoproteins and different physico-chemically well defined lipids have lead to the identification of lipid binding sites within the protein molecules and the formation of amphipathic helices upon and during lipid binding. This possible common mechanism of lipid-protein fractions forms the basis of a recently proposed model of one lipoprotein class, namely the high density lipoproteins (HDL). The significance of protein-protein-interactions in the formation and maintenance of these lipoprotein particles is still unknown. Whether disturbed lipid protein interactions lead to structural and/or functional alterations of the corresponding lipoproteins is a topic of discussion. The pertinent literature is listed in this paper and the physiological relevance of these studies and their clinical aspects will be presented.

Apolipoproteins↗
PubMed1977

Comparison of assay methods for selective measurement of plasma lipase. The effect of clofibrate on hepatic and lipoprotein lipase in normals and patients with hypertriglyceridemia.

Three different assays for selective measurement of plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) were compared. These were: an immunochemical method based on enzyme antibody precipitation (IM), a procedure in which both enzymes were separated by affinity chromatography on small heparin--Sepharose columns (HS), and an assay in which one enzyme was inhibited by protamine sulfate (PS). Good correlations were found between the immunochemical and the heparin--Sepharose method, but not between these and the protamine sulfate assay procedure. The IM was then used to evaluate the effect of clofibrate on the two lipolytic enzymes. It was found that both in normals and in patients with Type IV hyperlipoproteinemia, clofibrate treatment leads to a specific increase of plasma LPL while H-TGL activity remains almost unaffected. The magnitude of the LPL response was different in normals and in patients with endogenous hyperlipoproteinemia. Furthermore, in normals the maximal increase of LPL activity was already reached one week after drug treatment was begun, while in hypertriglyceridemic patients, this effect was not evident prior to four weeks of clofibrate treatment. The marked enzyme increase following clofibrate administration indicates that an increased peripheral removal rate for triglycerides is one major mechanism responsible for the lipid-lowering effect of this drug.

Adolescent↗
PubMed1977

Secondary hypertriglyceridaemia in patients with parenchymal liver disease.

Hypertriglyceridaemia occurring in patients with liver disease has been studied by measuring hepatic triglyceride lipase (H-TGL) and plasma lipoprotein lipase (LPL) by selective precipitation of H-TGL with specific antibodies. Lipid analysis, determination of lecithin-cholesterol-acyltransferase (LCAT) activity, and liver function tests were performed in parallel in fifty patients with acute hepatitis, twenty patients with chronic active or persistent hepatitis and fifty with cirrhosis of the liver. Total post-heparin lipolytic activity (PHLA) decreased with the severity of liver dysfunction. This decrease was due to low H-TGL and only to some degree to low LPL activity. With improvement over several weeks of hospitalization, hypertriglyceridaemia disappeared with a concomitant increase of H-TGL and LPL. It is concluded that impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.

Adolescent↗
PubMed1976

[Sitosterol in familial hyperlipoproteinemia type II. A randomized double-blind cross-over study].

The effect of beta-sitosterol on the lipid and lipoprotein level was evaluated in a randomised double-blind cross-over trial in 24 patients with primary familial type II hyperlipoproteinaemia over a period of 16 weeks. All patients completed the trial, however 10 of them had to be excluded from the evaluation due to fluctuations of their body weight or unreliable drug intake. Sitosterol lowered the total cholesterol level by 12.5% (P less than 0.01) from 9.96 mmol/l (3.69 g/l) to 8.37 mmol/l (3.23 g/l). The LDL-cholesterol level was lowered by 19.5% (P less than 0.05). The sitosterol concentration in plasma was consistently lower than 0.3% of total cholesterol. No side effects or tachyphylaxis was observed in the course of the trial. A return to normal of an increased serum cholesterol level by a combination of a lipid lowering diet and sitosterol monotherapy was only achieved in one patient.

Adolescent↗