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Biomedical subjects

W Riesen

Publications and source records attributed to W Riesen.

At least 73 records · Page 4Linked to original sources
PubMed1983

Digitoxin intoxication with severe thrombocytopenia: reversal by digoxin-specific antibodies.

As a result of overdosage a 77-year-old patient with heart disease developed digitoxin intoxication, associated with arrhythmias, extracardiac symptoms of intoxication and severe thrombocytopenia. Treatment with digoxin-specific antibody fragments relieved the signs and symptoms of intoxication within a few hours. The rise in platelet count from the pretreatment value of 26 000/mm3 to 47 000 within 12 h and to over 60 000/mm3 within 16 h of starting the antibody infusion may also be attributed to the treatment with antibodies. Such a rapid recovery from digitoxin-induced thrombocytopenia has not hitherto been described. Digoxin-specific antibodies, obtained by immunization of sheep with a digoxin-albumin conjugate, were used to treat intoxication with digitoxin, since cross-reaction had been demonstrated in vitro and in animal experiments. The present paper briefly discusses the mode of action and the general problems relating to the antibody therapy of digitalis poisoning.

Aged↗
PubMed1983

Digoxin-specific antibody fragments and a calcium antagonist for reversal of digoxin-induced mesenteric vasoconstriction.

The effect of digoxin-specific antibody fragments on glycoside-induced mesenteric vasoconstriction were investigated. Digoxin caused a sustained contraction of strips of isolated feline mesenteric artery lasting for several hours, while in anaesthetized cats it produced a significant decrease in blood flow and increase in resistance in the mesenteric artery. In-vitro, digoxin's contractile effect was inhibited by 'prophylactic' addition of antibody to the organ bath, but the clinical use for prophylaxis is not a practical proposition. When the antibodies were added with the contraction of the arterial strip in response to digoxin already established, the tone of the preparation decreased significantly over 3 h, but the effect of the glycoside was not fully reversible. In-vivo, control animals not treated with antibodies developed arrhythmias, mesenteric blood flow fell by more than 50% and resistance increased by more than 80% relative to the initial values. These animals died of ventricular fibrillation before the end of the experiment. Animals treated with digoxin-specific antibody fragments after receiving digoxin injections showed no further decrease in mesenteric blood flow and 90 min after the last dose of digoxin, the flow was recovering and mesenteric resistance decreasing. Furthermore, all the animals that had received antibodies remained in sinus rhythm to the end of the experiment. In view of the latent period to onset of action of the antibodies, valuable time may be lost in impaired mesenteric blood flow. To bridge the gap or, indeed, as primary treatment, calcium antagonists merit consideration; in our experiments mesenteric vasoconstriction was abolished within a few minutes by application of the dihydropyridine calcium antagonist 4-(2,1,3-benzo-oxadiazol-4-yl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylic aid, diethyl ester (PY 108-068).

Anesthesia↗
PubMed1983

[Clinical and pathogenic aspects of secondary hyperlipoproteinemias].

The secondary hyperlipoproteinemias are frequent in "civilized" countries. Through new methods, the interest for secondary hyperlipoproteinemias is increasing, on theoretical and practical points of view. This paper reviews the hyperlipoproteinemias of alcoholism, renal and hepatic diseases, diabetes mellitus, abnormal thyroid function, and those secondary to various medications. For each of them, the clinical, pathophysiologic and therapeutic aspects are described.

Alcoholism↗
PubMed1983

[Apolipoproteins: valuable indicators of atherogenicity in patients with coronary disease and normal blood lipids].

The lipid, lipoprotein and apolipoprotein B, A-I and A-II fractions in 20 young patients, (mean age 34.4 years) with myocardial infarction were compared with the results of a control group of 20 healthy men (mean age 35.8 years). The apolipoproteins B and A-I distinguished the myocardial infarction from the control patients. The patient group (who had slightly lower total and HDL cholesterol levels) had significantly higher apo B and lower A-I fractions than the controls. There was no significant difference in apo A-II fractions between the two groups. The measurement of the apo B and A-I fractions would appear to improve the lipid diagnosis by distinguishing the patients predisposed to atherosclerosis due to disorders of fat metabolism who may not be detected by less detailed lipid studies.

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

Serum lipoproteins in patients with mild renal disease treated with the diuretic muzolimine.

Patients with renal functional impairment are prone to develop hypertension and hyperlipidemia, and both abnormalities tend to occur already at an early stage of kidney disease. In 18 patients with mild renal disease (glomerular filtration rate 65 +/- 5 ml/min) and hypertension (mean blood pressure 126 +/- 4 mm Hg), the effect of six weeks of treatment with the loop-diuretic muzolimine on serum lipoproteins was assessed. Compared to placebo values, the diuretic significantly increased serum low-density lipoprotein cholesterol (LDL-C) and apoprotein B (+ 18 and 11%, respectively, P less than 0.005) in 13 men or postmenopausal women, but not in 5 premenopausal women. Serum high-density lipoprotein cholesterol (HDL-C), and total triglycerides or lipoprotein triglyceride fractions were not consistently changed in both subgroups. Thus, the ratio LDL-C/HDL-C was increased from 3.2 +/- 0.3 to 3.9 +/- 0.3 (P less than 0.05) in the men or postmenopausal women, while no such tendency occurred in the premenopausal women (4.1 +/- 0.6 to 3.7 +/- 0.6). Changes in serum LDL-C were not associated with hemoconcentration or alterations in carbohydrate metabolism and were not related to variations in serum potassium or blood pressure. Increased serum levels of the atherogenic LDL-C fraction during diuretic treatment in men or postmenopausal women with renal disease may represent a potentially undesirable effect, particularly since such patients may tend to have hyperlipidemia in the untreated state.

Female↗
PubMed1982

[Changes in serum lipoproteins in kidney diseases].

Secondary hyperlipoproteinemias frequently occur in patients with conservatively treated chronic uremia, under hemodialysis, after renal transplantation and notably in patients with the nephrotic syndrome. In chronic uremia patients conservatively treated or under hemodialysis, hypertriglyceridemia (type IV-pattern) is predominant whereas after renal transplantation and in the nephrotic syndrome hypercholesterolemia (type II-pattern) is more frequent. With the exception of hyperlipoproteinemia in the nephrotic syndrome, these hyperlipoproteinemias are associated with markedly reduced levels of the protective HDL. They therefore represent a relevant atherogenic risk. Lipoprotein disorders in chronic uremia are mainly due to disturbed catabolism of triglyceride-rich lipoproteins; treatment with corticosteroids may be the major underlying pathogenic mechanism of hyperlipoproteinemia after renal transplantation, whereas in the nephrotic syndrome increased hepatic lipoprotein production is observed.

Arteriosclerosis↗
PubMed1982

Suicidal digoxin poisoning: conventional treatment and antibody therapy.

A 66-year-old mand suffering from severe coronary heart disease took digoxin with suicidal intent an was treated for the ensuing complete atrioventricular block with digoxin-specific antibody fragments. Two and a half hours after intravenous infusion of the antibody fragments, the signs of intoxication passed off, and atrial fibrillation with a normal ventricular rate was reinstated. Antibody therapy is capable of permanently abolishing the signs of symptoms of digitalis poisoning after a matter of hours. Such a rapid or complete response cannot be achieved by any conventional form of treatment. This advantage must be weighed against the risks (immunologic reactions, loss of the therapeutic effect of the cardiac glycoside if an overdose of antibody is given). Moreover, antibody therapy does not take effect immediately, as is understandable in view of the mechanism of action. It should therefore be instituted in good time in potentially life-threatening cases of intoxication.

Aged↗
PubMed1982

[Behavior of high-density lipoproteins in drug lipid-lowering treatment].

Changes in serum lipids, the individual lipoprotein fractions after ultracentrifugation and the apoproteins B, A1 and A2 were studied in 66 patients with primary hypercholesterolemia under treatment with different lipid-lowering agents. After 3 months with dietary treatment alone and a 4-week placebo period the patients were given bezafibrate (3 X 200 mg daily), colestipol (2 X 10 g per day) or probucol (2 X 500 mg daily) for 12 months, followed by another 4-week placebo period at the end of the study. Colestipol showed the best lipid-lowering effect (total and LDL cholesterol were decreased by 20% and 23% respectively) but satisfactory total and LDL cholesterol lowering results were also obtained with the other substances. However, the changes in HDL differed widely among the three substances: bezafibrate increased HDL cholesterol and the HDL apoproteins A1 and A2 significantly, colestipol did not alter these parameters, while probucol treatment was followed by a significant decrease in both HDL-cholesterol and the apoproteins A1 and A2.

Adult↗
PubMed1982

"Low dose" colestipol in children, adolescents and young adults with familial hypercholesterolemia.

The effect of colestipol on plasma lipids and lipoproteins was studied in children, adolescents and young adults with familial hypercholesterolemia. O.125 g or 0.25 g/kg body weight were given in randomized sequence for period of 4 weeks. Total cholesterol was lowered by 13 and 18% with the smaller and larger dose , respectively, and LDL cholesterol lowered by 15% with the smaller and 12% with the larger dose. HDL cholesterol rose by 18 an 32%. LDL composition before and during the study was abnormal due to a markedly reduced triglyceride content. "Low-dose" colestipol is less effective lowering total plasma and LDL cholesterol than conventional doses but may, due to very few side effects, by advantageously used in cases of familial hypercholesterolemia when plasma cholesterol levels after dietary management are only 15-20% above normal.

Adolescent↗
PubMed1982

Reversal or prevention of diuretic-induced alterations in serum lipoproteins with betablockers.

In 18 patients with essential hypertension serum low density lipoprotein cholesterol (LDL-C) was significantly (P less than 0.001) increased following short-term chlorthalidone therapy, but not during combination therapy with chlorthalidone and a betablocker. This tendency was similar in two subgroups which were studied with an inverse sequence of drug administration. In Group I (11 men), a 22% increase (P less than 0.01) in LDL-C during chlorthalidone monotherapy was restored to normal 6 weeks after addition to a betablocker to the diuretic; in Group II (5 men, 2 postmenopausal women) LDL-C levels were increased by 41% (P less than 0.05) 6 weeks after withdrawal of the betablocker from the combination therapy. No significant changes occurred during either the treatment phase in high density lipoprotein cholesterol or apoprotein B levels. It is concluded that combination therapy with a betablocker may prevent or reverse an increase in serum LDL-C associated with short-term chlorthalidone monotherapy.

Adolescent↗
PubMed1982

Reversal of diuretic-induced increases in serum low-density-lipoprotein cholesterol by the betablocker pindolol.

Seventeen patients with mild to moderate essential hypertension received during three consecutive 4 wk periods a matched placebo, the thiazide-like diuretic, clopamide in a low dosage of 5 mg/day, or this diuretic combined with the betablocker, pindolol in a low dosage of 10 mg/day. Compared to placebo conditions, clopamide monotherapy significantly increased serum low-density lipoprotein cholesterol (LDL-C) by 13% (p less than 0.025). Following addition of pindolol, serum LDL-C was restored to control values. These variations in serum LDL-C were unrelated to concomitant changes in blood pressure, plasma potassium, renin activity or aldosterone levels. Blood pressure in the supine position was reduced from 152/99 +/- 13/9 mm Hg (+ SD) to 141/93 +/- 15/7 mm Hg following diuretic-monotherapy and to 139/90 +/- 12/9 mm Hg following diuretic-betablocker combination treatment. These findings suggest that antihypertensive combination treatment with low doses of clopamide and pindolol is not only effective and well tolerated, but may also avoid the increase in serum LDL-C levels occurring when the thiazide-like diuretic is given alone.

Adult↗
PubMed1982

Menopause-dependent plasma lipoprotein alterations in diuretic-treated women.

The effects of chlorthalidone, 100 mg/d given for 6 weeks, on serum lipids and lipoproteins were assessed in 22 premenopausal and 18 postmenopausal women. In the latter, chlorthalidone significantly increased total serum cholesterol (13%, p less than 0.001), low-density-lipoprotein (LDL) cholesterol (21%, p less than 0.001) and apoprotein B (16%, p less than 0.05). In contrast, these values were not altered in the premenopausal group. Levels of LDL cholesterol, high-density-lipoprotein cholesterol, total and very-low-density triglycerides, apoproteins A1 and A2, and plasma volume, plasma glucose, insulin, epinephrine, estradiol, and free fatty acids were unchanged in both groups. Chlorthalidone-induced changes in levels of LDL cholesterol did not correlate significantly with variations in blood pressure, plasma potassium, uric acid, renin, aldosterone, or norepinephrine levels. These findings indicate that the thiazide-like diuretic chlorthalidone increases serum LDL cholesterol in postmenopausal but not in premenopausal women.

Adult↗
PubMed1981

Diuretic treatment and serum lipoproteins: effects of tienilic acid and indapamide.

Treatment with the commonly used diuretic, chlorthalidone, has previously been found to increase the serum low-density-lipoprotein cholesterol (LDL-C) fraction. Therefore, the effects of two new agents, tienilic acid (a combined diuretic-uricosuric) and indapamide on serum lipid and lipoprotein levels were assessed. Six weeks of treatment with tienilic acid, 250 mg/day, markedly decreased serum uric acid and significantly increased LDL-C and triglycerides in 16 men. In contrast, indapamide 2.5 mg/day, had no apparent influence on serum lipids or lipoproteins in 18 men.

Diuretics↗
PubMed1981

[HDL--the unknown with great significance].

The high density lipoproteins (HDL) play an important role in lipoprotein metabolism. In view of the results of various epidemiologic and experimental studies, their antiatherogenic potency appears to be confirmed. The antiatherogenic effect of the HDL can be chiefly explained by the following mechanisms: 1. inhibition of uptake of cholesterol-rich low density lipoproteins (LDL) by the smooth muscle cells in the arterial wall, 2. mobilization of cholesterol deposits from the cells of the arterial wall, and 3. an important role in the catabolism of triglyceride-rich lipoproteins. There are many unanswered questions concerning the role of HDL in lipoprotein metabolism. Furthermore, methodological problems with HDL determination at present reduce their clinical relevance. Determination of HDL-cholesterol should therefore be confined to borderline cases of hypercholesteremia (cholesterol 240-300 mg/100 ml) to provide a further argument for or against lipid-lowering treatment.

Alcohol Drinking↗