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Biomedical subjects

H J Gilfrich

Publications and source records attributed to H J Gilfrich.

At least 37 records · Page 2Linked to original sources
PubMed1981

Magnesium concentration in saliva -- an indicator of digitalis toxicity. ?

In a prospective study salivary magnesium was measured by atomic absorption spectrophotometry in 168 patients on chronic digoxin therapy. Magnesium concentration in saliva was correlated with clinical data and plasma digoxin levels. A significant elevation in salivary magnesium concentration was caused by digoxin therapy (0.58 +/- 0.39 mmol/l, n = 93) in comparison to patients with no digitalis treatment (0.17 +/- 0.07 mmol/l, n = 35). Magnesium concentrations in saliva were significantly higher in toxic patients (1.1 +/- 0.68 mmol/l, n = 32) than in nontoxic patients. Possibly toxic patients showed a magnesium level of saliva of 0.63 +/- 0.39 mmol/l (n = 40). In 89% of the intoxicated patients salivary magnesium concentrations were higher than 1.0 mmol/l. The overlap of magnesium between toxic and nontoxic patients was less as compared to calcium and potassium concentrations in saliva. No changes were noted in serum magnesium levels. Magnesium concentration in saliva was influenced by chronic digoxin therapy only. No significant increase of magnesium in saliva was observed within 24 h after i.v. injection of 1.0 mg digoxin in four healthy volunteers. It is concluded that salivary magnesium concentration is a valid method for monitoring digoxin therapy in addition to plasma digoxin levels.

Digoxin↗
PubMed1981

Plasma protein binding of azapropazone in patients with kidney and liver disease.

1 The free fraction of azapropazone in the plasma of 37 healthy volunteers ranged from 0.0027 to 0.0070 (0.0044 +/- 0.0009, mean +/- s.d.). The principal binding protein was found to be albumin. 2 In 27 patients with various degrees of renal failure the free fraction values of azapropazone were markedly enhanced (0.0260 +/- 0.0239, mean +/- s.d.) and increased more than tenfold in some patients. There was a weak correlation (r = 0.46, P less than 0.05) between the free fraction and the clearance of endogenous creatinine. Such correlation was not found for serum creatinine, serum albumin, serum uric acid and serum urea nitrogen. 3 In 32 patients with chronic liver disease the free fraction values of azapropazone were also markedly higher (0.0210 +/- 0.0242, mean +/- s.d.) than in healthy subjects. There were statistical significant correlation between free fraction values and the prothrombin complex activity in the plasma (r = 0.40, P less than 0.05) and the total bilirubin concentration in the plasma (r = 0.90, P less than 0.001), respectively. Such correlation was not found for serum albumin, serum glutamic oxalacetic transaminase, serum gamma-glutamyl transpeptidase and serum alkaline phosphatase. 4 In patients with kidney and liver disease the free fraction values of azapropazone correlated well with those of the anticoagulant drug phenprocoumon (r = 0.93, P less than 0.001). However, the binding of the latter drug was less impaired. Bilirubin, when added in vitro, displaced both drugs from plasma proteins but this displacing effect was much smaller than the binding changes observed in patients with liver disease. 5 Kidney and liver disease caused a marked impairment of the plasma protein binding of azapropazone. In patients with kidney disease the degree of impairment of azapropazone binding cannot or only poorly (creatinine clearance) be predicted from the biochemical parameters of kidney function whereas in patients with chronic liver disease the total bilirubin concentration in the plasma may serve as an index of the binding defect.

Adolescent↗
PubMed1980

Transthoracic electrical impedance during extracorporeal hemodialysis in acute respiratory failure ("Shocked Lung syndrome").

The alteration (delta Z0) of transthoracic electrical impedance (TEI) during extracorporeal hemodialysis (EHD) was investigated in two Groups of patients with acute renal and acute respiratory failure, that differed with respect to the severity of respiratory insufficiency. Group I had moderate respiratory failure (FiO2 0.31 +/- 0.10, PaO2 84 +/- 14 mmHg), and Group II had severe respiratory failure (FiO2 0.75 +/- 0.17, PaO2 77 +/- 14 mmHg). There was a significant correlation between increase in TEI (delta Z0) and decrease in body weight (delta BW) in each individual patient, but the slope of regression lines was remarkably flattened in Group II. In Group I, delta TEI was 1.9 +/- 0.9 omega, the calculated TEI for 500 gr decrease in BW (delta Z0-500 gr) was 0.59 +/- 0.21 omega, and a significant correlation existed between pooled data of delta Z0 and delta BW. In Group II TEI increased less significantly, delta TEI was 0.6 +/- 0.3 omega (P less than 0.001), delta Z0-500 gr was 0.26 +/- 0.27 omega (P less than 0.01), and there was no correlation between pooled data of delta Z0 and delta BW. Increase of TEI in Group II could be completely attributed to increase in hematocrit. It is concluded that patients of Group I with acute renal failure and moderate respiratory failure lost intrathoracic fluid during EHD, whereas patients of Group II with severe respiratory failure did not. TEI during EHD may serve as a test for detection of fixed fluid within the pulmonary interstitium indicating a poor prognosis of the acute respiratory failure.

Acute Kidney Injury↗
PubMed1979

[Biological availability of digoxin and beta-acetyldigoxin after single-dose administration (author's transl)].

The biological availability of digoxin tablets (Lanicor) and beta-acetyldigoxin tablets (Novodigal) was tested after single-dose administration. Plasma levels over 48 hours, the area under the blood-level curves and the cumulative urinary excretion over seven days served as a measure of biological availability. The area under the blood-level curve after 1.0 mg digoxin by mouth was 40.7 +/- 1.7 ng . ml-1 . h and after 1.0 mg beta-acetyldigoxin by mouth 39.1 +/- 1.4 ng . ml-1 h, compared with 56.1 +/- 1.4 after 1.0 mg digoxin intravenously. Seven days later 0.67 +/- 0.12 mg digoxin of the orally administered digoxin, 0.68 +/- 0.12 mg digoxin of the orally administered beta-acetyldigoxin and 0.81 +/- 0.08 mg of the intravenously administered digoxin were excreted in the urine. There was no significant difference in the biological availability of the two drugs (P greater than 0.05).

Acetyldigoxins↗
PubMed1979

[Plasma levels, renal excretion and metabolism of orciprenaline after administration in sustained-release form (author's transl)].

A newly developed sustained-release form of orciprenaline-sulfate (Alupent) was tested in 13 patients. Determination of 3H-radioactivity in blood, urine and faeces was used to elucidate its pharmacokinetic properties. Maximum plasma levels of radioactivity were obtained between 8 and 12 h after administration. 10.7 +/- 2.5% of the administered radioactivity were excreted in urine over a period of 72 h. Orciprenaline was mainly excreted as the sulfate-conjugate. Approximately five percent of the radioactivity were excreted as 4,6,8-trihydroxy-N-isopropyl-tetrahydroisoquinoline--the condensation product of formaldehyde and orciprenaline.

Biotransformation↗
PubMed1979

Pharmacokinetics of azapropazone following single oral and intravenous doses.

The pharmacokinetics of azapropazone (Prolixan) was studied in 7 healthy volunters following single oral and i.v. doses of 600 mg. After i.v. injection plasma concentration declined biexponentially with time. The half-life of the beta-phase was 13.6 +/- 2.6 h (mean +/- SD), the apparent volume of distribution 11.9 +/- 3.5 l, and the total clearance 10.1 +/- 2.1 ml . min-1. Following oral administration peak plasma concentrations occurred between 3 and 6 h and declined with a beta-phase half-life of 14.3 +/- 2.8 h. The binding of azapropazone to plasma proteins was high (ranging from 99.52 to 99.67% at a total plasma concentration of 75 micrograms/ml). The bioavailability of azapropazone when administered as capsules was 83 +/- 19%.

Administration, Oral↗
PubMed1978

Digoxin and digitoxin elimination in man by charcoal hemoperfusion.

Since there is no widely used causal means of reducing the severity of massive digitalis intoxication the capability of hemoperfusion with coated activated charcoal to remove toxicologically relevant amounts of digoxin and digitoxin was evaluated in vitro and in man. At a blood flow rate of 100 ml/min the digoxin clearance by hemoperfusion in vitro was 51 +/- 8 ml/min in comparison to 24.3 +/- 11.3 ml/min by hemodialysis. The average hemoperfusion clearance of digitoxin was 31.7 +/- 13.4 ml/min, whereas almost no digitoxin was removed by hemodialysis. These clearance values point to the ability of hemoperfusion of eliminating digitalis glycosides from the blood. They do not clarify the essential question whether it is possible to lower the toxic concentrations in the tissues.

Charcoal↗
PubMed1978

Massive digoxin intoxication in childhood.

In a 10 year old boy 8 hours after taking about 16 mg beta-acetyl-digoxin a maximum serum digoxin level of 31.8 ng/ml was measured radioimmunologically. This is the highest digitalis level in childhood described to date. The serum potassium level rose to 7.4 mmol/l. Complete atrio-ventricular block, and salves of ventricular premature beats were the most serious rhythm disturbances. The absence of life threatening rhythm disturbances is attributed to the early use of diphenylhydantoin in small frequent doses.

Child↗
PubMed1978

Enhanced elimination of warfarin during treatment with cholestyramine.

1 The elimination and anticoagulant activity of a single intravenous dose of warfarin (1.0-1.2 mg/kg) without and with concomitant cholestyramine treatment (about 4 g three times daily) was studied in five healthy male subjects. 2 Cholestyramine treatment decreased the biological half-life of plasma warfarin (from a mean value of 2 days -1.3 days) and increased the total clearance of this drug (from a mean value of 37 ml kg-1 day-1--53 ml kg--1 day--1). 3 The total anticoagulant effect per dose of warfarin, as measured by the area under the effect v time curve, was also reduced by cholestyramine (average reduction of about 25%). 4 Warfarin possibly undergoes enterohepatic recycling in man which can be interrupted by cholestyramine.

Adult↗