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Biomedical subjects

J Prandota

Publications and source records attributed to J Prandota.

At least 19 recordsLinked to original sources
PubMed1992

[A case of histiocytosis of Langerhans cells].

A lethal case is presented of disseminated for of histiocytosis of Langerhans cells in 16-month-old girl. In the clinical course predominated high fever, opportunistic infections, cell-mediated and humoral immunity disturbances, and gross hepatocellular damage which made impossible carrying out of the treatment with cytostatics. The advances in immunological investigations in these patients are more widely discussed as well as the use of thymus hormones.

Female↗
PubMed1991

Diuretic effect and disposition of furosemide in cystic fibrosis.

The pharmacodynamics and kinetics of single oral and intravenous doses of furosemide were studied in 9 patients (mean age 18.5 y) with cystic fibrosis. The diuretic effect of furosemide lasted for 6 h after oral administration and 2 h following intravenous injection of the drug. The patients with cystic fibrosis had a more pronounced diuretic response both to the oral and intravenous treatments than that reported in normals. Furosemide caused a marked decrease in urine pH for 5 h following the oral dose and between the 2nd and 3rd h after i.v. injection. The baseline nocturnal urine flow rate in 7 of the 9 patients given furosemide orally was increased by 30.6% compared to that reported in healthy subjects. The bioavailability of furosemide, its mean absorption rate and the mean plasma and urinary elimination half-lives both of the oral and the intravenous drug were similar to those reported in normal subjects. The patients with cystic fibrosis showed, however, about double normal mean total clearance after both the oral and i.v. treatments, and its renal clearance was almost half the plasma clearance. Nonrenal clearance was markedly increased in the patients, which agreed with a considerable decrease in the renal excretion of the drug. The mean apparent volume of distribution was also markedly increased compared to data in the literature. Oral furosemide resulted in a moderate increase in haematocrit and haemoglobin levels in 7 of 9 patients with cystic fibrosis and marked hypokalemia developed in 6 of the 9 patients 6 h after dosing. Pulmonary function tests performed at that time were changed in an inconsistent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

High doses of furosemide in children with acute renal failure. A preliminary retrospective study.

The diuretic effect of high doses of furosemide alone and furosemide plus mannitol was analysed retrospectively in 30 children with acute renal failure. In 10 children (Group 1) renal failure developed mainly during glomerulonephritis, and in 20 children (Group 2) the cause was gastroenteritis. The diuretic effects of furosemide and furosemide plus mannitol were evaluated measuring the 24-hour urine volume at the time of anuria, oliguria or normal diuresis. The highest mean single intravenous doses of furosemide were 6.5 and 14 mg/kg in Groups 1 and 2, respectively; the highest average daily doses were 10.1 and 25.5 mg/kg, respectively. A broad relationship was observed between single i.v. dose and diuretic response following administration of furosemide (1.2 to 30.8 mg/kg). In both groups of patients a statistically significant negative linear correlation was found between the daily intravenous dose of furosemide and the 24-hour urine volume. Calculations based on the obtained regression equations showed that the expected 24-hour urine volumes corresponding to daily diuresis normal for age could be obtained after administration of daily 2.8 to 1.4 mg/kg furosemide in Group 1 and 9.3 to 2.3 in Group 2. It is therefore suggested that the total daily dose of furosemide should not exceed 100 mg in children with acute renal failure. Administration of furosemide plus mannitol did not result in higher daily diuresis as compared to 24-hour urine volume obtained when furosemide was given alone. Furosemide was well tolerated. Electrolyte disturbances, especially in Group 2, were the most frequent side effects due to high doses of furosemide.

Acute Kidney Injury↗
PubMed1991

Pharmacokinetic, biliary excretion, and metabolic studies of 14C-furosemide in the rat.

1. Partition of furosemide into organic solvents at pH 3.8 was greatest for ethyl acetate (33:1) greater than 2-ethyl-1-hexanol (10:1) greater than ethyl ether (6:1). 2. Furosemide was highly bound to human, bovine, rabbit, and rat plasma or albumin (97.4-98.4%). 3. Furosemide was highly bound to rat tissues. One hour after i.p. injection of the drug, tissue to plasma concentration ratios were: adrenals (10:1), lung (4:1), kidney (4:1), spleen (3:1). 4. In rats with ligated renal pedicles, furosemide was excreted in bile, at least in part, by active transport. Hepatic clearance of a 1 mg/kg i.v. dose contributed 20% to total body clearance. Large doses (50 mg/kg and more) of furosemide exerted a choleretic effect. 5. Chromatography of bile showed that i.v. administration of 50 mg/kg and higher doses of furosemide to rats resulted in saturation of hepatic drug metabolism. 6. The bile of rats contained the parent drug, 4-chloro-5-sulphamoyl-anthranilic acid, and at least two unknown metabolites with the furan ring intact.

Adrenal Glands↗
PubMed1988

Dosage regimen of cimetidine reviewed. Possible drug accumulation after multiple oral doses.

The doses of cimetidine recommended differ in children, especially those with cystic fibrosis. These dosage regimens were derived from single-dose pharmacokinetic studies of the drug. Some authors showed, however, that after administration of repeated oral doses of cimetidine in healthy adults and children with cystic fibrosis, the elimination half-life of the drug was markedly prolonged. In view of the ability of cimetidine to inhibit metabolism of other drugs, it is suggested that the parent compound and/or it is metabolite(s) may inhibit its own metabolism during a prolonged course of treatment. Enterohepatic recirculation of the drug and/or its metabolite(s) may also contribute to prolongation of its elimination. One should therefore be cautious in using single-dose pharmacokinetic parameters to calculate repeated dose regimens and expected plasma steady-state concentrations.

Administration, Oral↗
PubMed1988

Clinical pharmacology of antibiotics and other drugs in cystic fibrosis.

The disposition of many drugs in cystic fibrosis is abnormal. In general, changes in pharmacokinetics include: increased volume of distribution, decreased plasma concentration, and enhanced renal and sometimes non-renal elimination of drugs. Pathophysiology of the disease important for drug disposition includes: (a) hypersecretion of gastric acid and duodenal secretions which are of small volume, viscous and low in bicarbonate; (b) increased intestinal permeability to some sugars and probe substances; (c) hypergammaglobulinaemia and sometimes hypoalbuminaemia; (d) significant elevation of free fatty palmitoleic acid level and decreased low-density and high-density serum lipoproteins; (e) an average increase by 30 to 45% in plasma volume in patients with cystic fibrosis who have moderately severe pulmonary disease, right ventricle hypertrophy and dilatation, which occurs in 15 to 35% of patients with a Shwachman score of 81 to 100; (f) abnormal bile acid metabolism and enterohepatic recirculation; and (g) enlarged kidneys and glomerulomegaly with increased glomerular filtration rate, tubular clearance and urine flow rate in some patients with cystic fibrosis. Delayed absorption from the gastrointestinal tract has been reported in patients with cystic fibrosis for cloxacillin, epicillin, clindamycin, ciprofloxacin and probably for cephalexin, para-aminobenzoic acid and chloramphenicol. A possible increased absorption was reported for cimetidine. Of 7 drugs studied only theophylline had significantly decreased plasma protein binding. An increased volume of distribution and increased renal clearance reported for several drugs is caused mainly by increases in plasma volume and urine flow rate in many of these patients. Possible increased elimination of some drugs in bile (which probably results from bile acid malabsorption) and in bronchial secretions (which are abundant in some cystic fibrosis patients with acute pulmonary infection) may explain enhanced non-renal elimination of these drugs. The metabolism of cimetidine in cystic fibrosis was reported not to be changed significantly compared to control subjects.

Anti-Bacterial Agents↗