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Biomedical subjects

K Rasmussen

Publications and source records attributed to K Rasmussen.

At least 397 records · Page 22Linked to original sources
PubMed1980

[Propionacidemia].

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Acetyl-CoA Carboxylase↗
PubMed1980

Excretion pattern of branched-chain amino acid metabolites during the course of acute infections in a patient with methylmalonic acidaemia.

A 1-year-old boy with a typical B12-responsive form of methylmalonic acidaemia was hospitalized twice due to acute bacterial infections. On both occasions, the child was lethargic with a severe ketoacidosis on admission. Intensive therapy with protein restriction, intravenous administration of electrolytes and antibiotics was effective within 4 days on both occasions. The urinary excretion of organic acids showed the same pattern on both occasions. There were rising excretion concentrations, reaching a peak value within the first 24-hour period, for the following compounds: 3-hydroxybutyric acid, 3-hydroxypropionic acid, 3-hydroxyisobutyric acid and 3-hydroxyisovaleric acid. Excretion concentrations of the following rose for 48 h: isobutyric acid, 2-methylbutyric acid, isovaleric acid, lactic acid and the 2-oxo-acids. There was no increase until 12-24 h after the onset of severe illness in the excretion of propionic acid and methylmalonic acid. Propionic acid excretion was maximal at about 48 h, while peak excretion of methylmalonic acid was delayed until about 72 h after the onset of severe illness; at this time there was clinical improvement. The biochemical implications of this excretion pattern are discussed.

Acute Disease↗
PubMed1980

Biochemical studies in a patient with defects in the metabolism of acyl-CoA and sarcosine: another possible case of glutaric aciduria type II.

The clinical and biochemical abnormalities in a neonate, who died in coma accompanied by severe hypoglycaemia at the age of 3 days, are described. The study of the urinary metabolic profiles of organic acids and amino acids revealed that the excretion rates of glutaric acid, isovaleric acid, isovalerylglycine, 3-hydroxyisovaleric acid and isobutyric acid were very high. Increased excretion rates were also found for 2-methylbutyric acid, adipic acid, caproylglycine, 5-hydroxycaproic acid, caproic acid and butyric acid. The amino acid, sarcosine, was excreted in enhanced amounts and the patient had lactic aciduria, whereas the excretion of 3-hydroxybutyric acid was only moderately increased. This abnormal excretion pattern is consistent with a defect in the metabolism of acyl-CoAs and sarcosine. Normal activity of glutaryl-CoA dehydrogenase was found, excluding glutaryl-CoA dehydrogenase deficiency (glutaric aciduria type I).

Acyl Coenzyme A↗
PubMed1980

The antihypertensive effect of prazosin on mild to moderate hypertension, changes in plasma volume, extracellular volume and glomerular filtration rate.

Changes in blood pressure, plasma volume (PV) (125I-albumin space), extracellular volume (ECV) (82Br-space) and glomerular filtration rate (GFR) (51Cr-EDTA clearance) were measured in 12 patients with mild to moderate essential hypertension on placebo and during long-term treatment with prazosin. During the study, BP decreased from an average of 172/107 to 166/102 mmHg (n.s.). PV increased from 3278 to 3324 ml (n.s.) and ECV from 18360 to 18639 ml (n.s.). GFR was almost unchanged, 95 and 93 ml/min, prespectively. An inverse significant correlation was found between the changes in mean BP and changes in ECV, i.e. fluid retention was demonstrated in patients with the smallest BP reduction. It is concluded that inadequate BP response during treatment with prazosin may in part be due to fluid retention. It is therefor suggested that prazosin should in principle be used together with a diuretic in order to prevent fluid retention.

Adult↗
PubMed1979

Treatment of glutaryl-CoA dehydrogenase deficiency (glutaric aciduria). Experience with diet, riboflavin, and GABA analogue.

The autosomal recessive inherited disorder glutaryl-CoA dehydrogenase deficiency (glutaric aciduria) runs a progressive course with severe choreoathetosis and dystonia, eventually leading to total helplessness and early death. Theree patients were observed during therapeutic trials with a protein-low diet, riboflavin and GABA analogue. Diet and riboflavin had a slight-to-moderate effect on the clinical symptoms; the excretion of glutaric acid and 2-amino-adipic acid decreased considerably during treatment. Regression of neurologic symptoms was observed during treatment with GABA analogue. It is concluded that the patients should be treated as early as possible with protein-low diet, riboflavin, and GABA analogue.

2-Aminoadipic Acid↗
PubMed1979

Influence of high plasma concentrations of free-fatty acids on heart rhythm in healthy fasting men.

Ten healthy male student in regular sinus rhythm fasted for 66 hours. Their overnight fasting plasma concentration of free fatty acids (FFA) was 455 +/- 104 micro mol/1 (mean +/- S.E.M., n=7), the reference value of our laboratory, measured in another normal population of young men, being 344 +/- 28 micro mol/1 (n=10). After 42 and 66 hours of fasting, the plasma concentration of FFA rose to 1198 +/- 181 (p less than 0.01, n=10) and 1471 +/- 89 micro mol/1 (p less than 0.001, n=10), respectively. During the last 24 hours of fasting, the heart rate rhythm was monitored continuously by means of a Holter recorder and computer. No arrhythmias were observed, indicating that elevated plasma concentrations of FFA, exceeding those reported in patients with acute myocardial infarction, are well tolerated by the healthy human myocardium.

Adult↗