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F A de Wolff

Publications and source records attributed to F A de Wolff.

At least 91 records · Page 5Linked to original sources
PubMed1986

Assessment of the therapeutic range of tiapride in patients with tardive dyskinesia.

Ten patients with tardive dyskinesia were treated with tiapride at an increasing dosage to establish the dose-concentration relationship and the dose-effect relationship. The effect was scored with the Abnormal Involuntary Movement Scale (AIMS) and the Doppler-radar method. The intra individual dosage-serum concentration correlation coefficients varied from 0.86 to 0.99 and the slopes of the individual regression lines varied from 0.16 to 0.58. All patients showed a diminution of their involuntary movements during the treatment period. A negative correlation coefficient was found between the dosage of tiapride and the AIMS; range -0.22 till -0.93, mean: -0.65 +/- 0.23 (SD). The Doppler-radar method results were inconclusive. No side-effects were observed.

Aged↗
PubMed1985

Intestinal absorption of aluminium in rats.

To study the mechanism of intestinal aluminium (Al) absorption, an experimental investigation into the uptake of Al from the rat gut was undertaken. The small intestine was perfused in situ for 60 min with isotonic media containing 4.63, 9.25, and 18.50 mmol/l Al chloride at pH 4.0 and 7.0. Portal and systemic blood were sampled and analysed for its Al content by flameless atomic absorption spectrophotometry. It was found that the intestinal absorption of Al in rats is concentration and pH dependent.

Aluminum↗
PubMed1985

Distribution of aluminium between plasma and erythrocytes.

It is common use to monitor body burdens of toxic trace metals by measuring concentrations in whole blood. To monitor aluminium (Al) body burden in renal patients on haemodialysis, which is a high-risk group for Al poisoning, the concentrations of Al in plasma (AlP) or serum (AlS) are determined rather than Al in whole blood (AlB). To evaluate this custom, which exists in clinical laboratories, an investigation was made into the distribution of Al between the plasma and the blood-cell compartment and on the extent of binding of Al to the blood cells both in rats and in dialysed patients. The results show that Al is distributed between plasma and blood cells with only very small quantitative differences, that binding of Al to blood cells is very weak and that AlP and AlB have similar prognostic value for toxicity.

Aluminum↗
PubMed1985

Toxicological aspects of aluminum poisoning in clinical nephrology.

Several dialysis-related diseases can be ascribed to an increased body burden of aluminum (Al). Determination of this metal in clinical samples is of great assistance in the diagnosis, treatment and prevention of Al intoxication. As there are many pitfalls in the estimation of Al in biological fluids, the performance of these assays should be restricted to laboratories specializing in the human toxicology of metals, which are experienced in flameless atomic absorption spectrophotometry and which participate in an external quality assessment scheme. One laboratory can serve ten dialysis centers. Serum, plasma or blood are equivalent samples for the biological monitoring of Al. The assay should be performed once in a three month period, but when oral Al-containing medication is changed, toxic symptoms are suspected, or levels exceeding 100 micrograms/l are observed, Al should be determined much more frequently, e.g., once weekly. A high incidence of symptoms associated with Al poisoning is seen in patients with serum concentrations (AlS) greater than 100 micrograms/l, and it is therefore recommended to keep AlS well below this level. Scalp hair appears to be of no use for the assessment of the body burden of Al in the individual patient. For "environmental monitoring", regular analysis of the dialysis fluid is necessary. The concentration of Al in this fluid should not exceed 5 micrograms/l; higher levels lead to a positive Al balance during dialysis and may eventually result in poisoning.

Aluminum↗
PubMed1985

Measurement of aluminum in serum, blood, urine, and tissues of chronic hemodialyzed patients by use of electrothermal atomic absorption spectrometry.

We describe different methods of electrothermal atomic absorption spectrometry with automatic sampling for determining aluminum in human serum, blood, urine, and tissues. Contamination with Al originating from receptacles and reagents was minimized. Whole-blood Al concentrations were measured after hemolysis of EDTA-anticoagulated blood samples with Triton X-100. A straightforward method for tissue destruction was developed. Instrument settings of the graphite furnace and of the atomic absorption spectrometer were adjusted so as to obtain close agreement between direct and standard-additions methodologies. The result is a reliable direct method appropriate for use with multiple samples. Tissue Al measurements showed low detection limits and approximately 100% analytical recoveries. Al concentration in serum of 10 healthy volunteers and of 100 chronic hemodialysis patients were 2.0 (SD 0.4) and 77 (SD 70) micrograms/L, respectively. Blood Al concentrations of 10 controls and of 100 dialysis patients were 12.1 (SD 1.5) and 79 (SD 70) micrograms/L, respectively. Al concentrations in serum and blood of 47 chronic hemodialysis patients were not significantly different. Bone Al concentrations were 8.2 (SD 5.8) micrograms/g of fresh tissue for 10 chronic hemodialysis patients without osteomalacia, as compared with 51 (SD 20) micrograms/g for 10 chronic-dialysis patients with Al-induced osteomalacia.

Aluminum↗
PubMed1984

A method of studying the intestinal absorption of aluminium in the rat.

Aluminium (Al) intoxication in dialysis patients is held to be caused not only by Al in the dialysis fluid but also by Al from orally administered phosphate binders. Studies on Al absorption in patients and healthy individuals as well as in animals are still scarce, and do not provide sufficient data to characterize the absorption process. This paper presents a method of studying the process of Al absorption in a perfusion system of rat small intestine in vivo, in combination with a cannulation system of the portal vein for serial blood sampling. Determination of concentrations of an absorbed substance in samples of both the perfusion medium and the portal blood, collected during the perfusion medium and the portal blood, collected during the perfusion period, may clarify the nature of the absorption process. Although this method appears to be useful for the study of the intestinal absorption of any substance, it was adapted for the study of the intestinal absorption of Al compounds. The usefulness of this method for studying Al absorption was demonstrated in an experiment in which Al chloride (0.5 g/l) in buffered media of pH 7.0, 7.5, and 8.0 was perfused through the rat small intestine over a period of at least 30 min. The results of this experiment indicate that a decrease in pH of the perfusion medium leads to an increase in absorption of Al in the portal blood.

Aluminum↗
PubMed1984

Food does not effect in bioavailability of theophylline from Theolin Retard.

The absorption of theophylline from a sustained release tablet preparation ( Theolin Retard 300 mg) was studied in 10 subjects both when fasting and immediately after a standardized breakfast. Intravenous aminophylline was used as the reference material. Food did not influence the absorption from Theolin Retard. The bioavailability was complete (93% after 30 h) both with and without food, and no difference was found in the time to peak of the plasma concentration curve (7 h), or the mean residence time (14 h). The absorption characteristics, with predominantly zero order kinetics, did not change with concomitant intake of breakfast.

Adult↗
PubMed1984

Amitriptyline metabolism in relation to antidepressive effect.

The relationship between amitriptyline (AT) metabolism and clinical response was studied in 14 outpatients treated with a daily dose of 150 mg AT. Riboflavin was added to the medication to check compliance. On days 0, 2, and 7 and at 3, 6, 9, and 13 wk after onset of therapy, blood samples were drawn from the patients 3 (+/- 0.5) hr after the first morning dose and a sample of the first morning urine was taken to check riboflavin. Serum levels of AT and its metabolites, nortriptyline (NT), E- and Z-10-hydroxynortriptyline (E- and Z-10-OH-NT), total (E + Z) 10-hydroxyamitriptyline (tot-10-OH-AT), and desmethylnortriptyline (DNT), were measured by means of HPLC while minimizing adsorption onto glass. On day 0 and after 6 and 13 wk the severity of the depressive disorder was scored by means of the self-rating depression scale of Zung.28 Mean steady-state concentrations of AT, NT, and E-10-OH-NT were in the order of 100 micrograms/l and tot-10-OH-AT and Z-10-OH-NT approximated 20 micrograms/l. DNT concentrations were under 15 micrograms/l. There was great variation in metabolic pattern between patients. After 6 wk concentrations of all compounds were approximately 15% lower than at 3 wk, indicating a weak autoinducible effect of AT or its metabolites. Steady-state concentrations of AT correlated well with that of NT (r = 0.64; P less than 0.05) but not with that of E-10-OH-NT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

[Cave fungos!].

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Adult↗
PubMed1983

The effects of valproic acid on liver function.

To study a possible enzyme-inducing potency of valproic acid (VPA) in children, serum gamma-glutamyltranspeptidase (GGT) activity in serum and D-glucaric acid (GLA) excretion in urine were measured in 32 epileptic children who were on sodium valproate monotherapy (29.6 +/- 10.3 mg/kg/day). VPA did not affect GGT activity, but it selectively enhanced GLA excretion. To approach this phenomenon experimentally an attempt was made to induce a similar effect in animals. In guinea pigs it was possible to provoke a VPA induced rise in GLA excretion. In addition, vacuolisation of the cytoplasm of the hepatic parenchymal cells was observed. The question of the possible relationship between VPA hepatotoxicity and stimulation of GLA excretion remains to be answered.

Animals↗
PubMed1983

Impairment of phenytoin parahydroxylation as a cause of severe intoxication.

A case history is presented of a patient who developed a severe phenytoin intoxication on a "therapeutic" dose of 300 mg/day. This phenomenon could be ascribed to a poor oxidative metabolizing capacity of this patient for phenytoin, as demonstrated by a low para-hydroxyphenyl-phenylhydantoin to phenytoin ratio in the urine. To characterize the specificity of this metabolic defect, debrisoquine and antipyrine oxidation were also studied. Contrary to expectations, this patient was shown to be an extensive debrisoquine metabolizer; the antipyrine clearance was even higher than normal. These findings suggest that phenytoin para-hydroxylation is regulated by an oxidative enzyme complex different from those which oxidize debrisoquine and antipyrine.

Aged↗
PubMed1983

Experience with a screening method for laxative abuse.

1 Abuse of laxatives may lead to a variety of serious disorders which are usually difficult to recognize because of the heterogenicity of the toxic effects. 2 In order to facilitate the diagnosis of chronic laxative poisoning, a laboratory screening method for the detection of colonic stimulants in urine has been designed and has been applied in practice over a three-year-period. 3 During this period, 157 samples from 81 patients were sent to the laboratory. Fifteen patients (18.5%) were definitely shown to use self-prescribed laxatives. 4 Next to the diphenolic compounds: bisacodyl, phenolphthalein and bisoxatin, the anthraquinone derivative rhein, a metabolite of vegetable laxatives, was found in several cases. In the urine of three patients a substance resembling rhein was found, which was shown to be aloe-emodin. 5 It is concluded that chronic self-poisoning with laxatives is a fairly common disorder than can easily be overlooked. Laboratory screening of the urine of suspected patients is an economic and reliable method for its diagnosis.

Cathartics↗