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Biomedical subjects

E Walter

Publications and source records attributed to E Walter.

At least 127 records · Page 7Linked to original sources
PubMed1984

Induction of neutrophilic differentiation of human promyelocytic leukemic cells by branched-chain carboxylic acid anticonvulsant drugs.

The anticonvulsant drug 1-methyl-1-cyclohexanecarboxylic acid ( MCCA ) has been shown to cause maturation of murine neuroblastoma cells in vitro at concentrations that are pharmacologically achievable. HL-60 human promyelocytic leukemia cells cultured with this drug underwent a dose-dependent decrease in growth. Similarly, neutrophilic differentiation, based on morphologic criteria and the acquisition of the ability to reduce nitroblue tetrazolium and phagocytose yeast, was observed. Valproic acid, a clinically available anticonvulsant that is chemically related to MCCA , likewise inhibited growth and promoted maturation of HL-60 cells, although only at concentrations above the recommended therapeutic blood levels. MCCA was additive in its ability to induce differentiation of HL-60 with retinoic acid, another compound that induces differentiation at pharmacologic concentrations. MCCA , or similar branched-chain fatty acids, may be useful in the treatment of human leukemia, particularly in combination with other differentiation-inducing drugs.

Anticonvulsants↗
PubMed1984

Effect of the thromboxane synthetase inhibitor Dazoxiben (UK 37-248) on the metabolism of antipyrine in patients with enhanced platelet aggregation.

The effect of the imidazole derivative Dazoxiben (400 mg daily for 1 week) on antipyrine metabolism was examined in six patients with enhanced platelet aggregation. No significant change in antipyrine saliva pharmacokinetics occurred before or after Dazoxiben treatment. The rate of formation of the three main oxidative antipyrine metabolites was similar before and after Dazoxiben. Although Dazoxiben belongs chemically to the imidazole derivatives, which exhibit inhibitory activity on drug metabolism, no influence on antipyrine disposition could be detected.

Aged↗
PubMed1983

Effect of single and multiple doses of sulphinpyrazone on antipyrine metabolism and urinary excretion of 6-beta-hydroxycortisol.

Sulphinpyrazone decreases the plasma clearance of tolbutamide and S-warfarin and increases the clearance of R-warfarin, theophylline and antipyrine. In order to determine whether sulphinpyrazone is an inducer or inhibitor or both of oxidative drug metabolism, antipyrine and its metabolites as well as 6-beta-hydroxycortisol were measured in urine before, 24 h and after 23 days of chronic administration of sulphinpyrazone (4 X 200 mg/day). During chronic treatment sulphinpyrazone increased the ratio of 6-beta-hydroxycortisol to the 17-hydroxycorticosteroids by 70% (p less than 0.02). The renal clearance of the main oxidative metabolites of antipyrine (4-hydroxyantipyrine, 3-hydroxymethylantipyrine and norantipyrine) were increased after sulphinpyrazone (p less than 0.02). Except for norantipyrine, no change in total excretion of antipyrine and its metabolites occurred after 24 h or after 23 days. It is concluded that sulphinpyrazone induces the enzymes which metabolize antipyrine and cortisol.

Adult↗
PubMed1983

[Computer tomographic and sonographic diagnosis of diaphragmatic hernias].

The diagnosis of supra diaphragmatic masses, particularly Morgagni's, Larrey's or Bochdalek's hernia was rarely possible by conventional methods. By using sonography and, more particularly, computed tomography, these hernias can be distinguished from other masses in the region of the diaphragms. Their characteristic appearances and the diagnostic procedures are described. Invasive procedures, such as diagnostic pneumoperitoneum, are no longer necessary.

Diagnosis, Differential↗
PubMed1983

[Performance of a field test as proof of automatic cell analysis].

The screening by an automatic cell analyser (A) is justified, only if the false negative rate beta (A) is less than the false negative rate beta (M) of the manual method (M). A design is considered to get the numbers of ill persons who are "positive" by the manual method and "negative" by the automatic one, and vice versa "negative" by the manual and "positive" by the automatic. The sign test can be used to test the difference beta (A) - beta (M). Formulas for the necessary number n are given.

Autoanalysis↗
PubMed1983

[Compression syndrome of the celiac trunk].

Compression syndrome of the celiac trunk or Dunbar's syndrome is usually caused by an overly large medial arcuate ligament of the diaphragm. Symptoms are postprandial periumbilical pain, the pathogenesis of which, in spite of abundant collateralization of the celiac trunk, has not yet been clarified. The diagnosis should be established by elimination via lateral aortography. Therapy consists of incision of the ligament, creation of a aorto-celiac bypass, or reinsertion of the celiac trunk. Treatment, however, is successful in only 41% of the operated patients.

Adult↗
PubMed1982

Enhanced drug metabolism after sulfinpyrazone treatment in patients aged 50 to 60 years.

The induction of liver drug metabolism was investigated in five patients before and after the administration of 800 mg sulfinpyrazone daily for 4 weeks, by using antipyrine plasma-pharmacokinetics and by determining urinary excretion of 6-beta-OH-cortisol and serum gamma-glutamyl-transpeptidase (GGT) activity. Antipyrine half-life was shortened in all patients from a mean value of 12.3 +/- 3.9 h to 7.8 +/- 2.0 h and antipyrine clearance was increased from 39.0 +/- 16.0 ml/min to 57.6 +/- 13.7 ml/min. In contrast the volume of distribution of antipyrine was unaffected; the values being 38.0 +/- 8.6 liters and 37.4 +/- 5.7 liters, respectively. In all patients the excretion of 6-beta-OH-cortisol in the urine went up from 65.0 +/- 25.7 micrograms/24 h to 346.8 +/- 193.4 micrograms/24 h. The ratio 6-beta-OH-cortisol/free cortisol changed from 4.1 to 15.8. After 21 days of treatment the GGT increased from 17.4 +/- 4.9 units/liter to 32.6 +/- 12.5 units/liter The data presented confirm that sulfinpyrazone induces drug metabolism in patients of the older age group. Interactions between sulfinpyrazone and other drugs given simultaneously must be borne in mind.

Age Factors↗
PubMed1982

Determination of the anticoagulant phenprocoumon in human plasma and urine by high-performance liquid chromatography.

The determination of the anticoagulant phenprocoumon in plasma, after acidification and extraction with 1,2-dichloroethane was effected through isocratic high-performance liquid chromatography; a C18 reversed-phase column was used as stationary phase using aqueous acetonitrile as eluent and UV detection at 313 nm; p-chlorophenprocoumon was used as internal standard. A high proportion of phenprocoumon in urine is eliminated as the glucuronide and must be hydrolyzed enzymatically before extraction; the same column and detector as for plasma were used, but with gradient elution. The method was used in the range 0.1-5 mg/1, the sensitivity was 0.1 mg/1 for plasma and 0.02 mg/1 for urine, the precision was in the range 3-5% and the absence of interference due to other anticoagulants, drugs or endogenous compounds allows the specific determination of phenprocoumon in plasma and urine from patients and volunteers in clinical relevant cases, drug interaction, compliance, toxicological and pharmacokinetic studies.

4-Hydroxycoumarins↗
PubMed1982

Lack of effect of cimetidine on action of phenprocoumon.

In patients on oral warfarin, nicoumalone and phenindione an increase in the anticoagulant effect has been described during concomitant treatment with cimetidine. Therefore the effect of cimetidine on the steady state dynamics of phenprocoumon has been investigated in ten outpatients. No change in the anticoagulant effect of phenprocoumon was observed during or after two weeks on cimetidine, as measured by the thrombotest coagulation method, prothrombin time, fibrinopeptide A concentration and plasma phenprocoumon level. The data show that cimetidine does not interact with the metabolism of phenprocoumon in contrast to warfarin. Thus, phenprocoumon maintenance therapy when combined with concomitant cimetidine treatment can be considered not to carry an increased risk of haemorrhagic complications.

4-Hydroxycoumarins↗
PubMed1982

Cimetidine does not increase the anticoagulant effect of phenprocoumon.

In patients on oral warfarin, nicoumalone and phenindione an increase of the anticoagulant effect has been described during concomitant treatment with cimetidine. Therefore we have investigated the effect of cimetidine on the steady state dynamics of phenprocoumon in ten outpatients. No changes in the anticoagulant effect and the plasma phenprocoumon levels were observed during and after 2 weeks application of cimetidine. The data show that cimetidine does not interact with the metabolism of phenprocoumon in contrast to warfarin.

4-Hydroxycoumarins↗
PubMed1981

Does chronic aspirin treatment increase blood pressure in man?

In postmyocardial infarction patients longterm aspirin treatment with 1.5 g/day led to a significant increase in systolic and diastolic blood pressure after 6 months. This could not be found in the placebo- and the phenprocoumon-treated patients. After one year the blood pressure behaviour was the same in all three treatment groups. As nonsteroidal antirheumatic drugs can produce hypertension in animals, probably due to inhibition of prostaglandin synthesis, blood pressure control in longterm aspirin treatment is advisable.

Aspirin↗