Biomedical subjects
U Peters
Publications and source records attributed to U Peters.
[Fibromatosis of the breast].
Fibromatosis of the breast is a rare benign mesenchymal transformation of the connective tissue, the origin of which is probably situated in the fascia of the pectoral muscle and the Cooper's ligaments. In the clinical and radiological examination, it is difficult to differentiate between a mammary carcinoma or other malignant tumours of the breast. Only histological examination can lead to the final diagnosis. Large-scale excision of these tumours, which have a tendency to relapse, is the therapy of choice. The diagnostic problems are shown in a case of a 26-year old patient.
[Claims and reality of public health expert assessment using legal public health guidelines].
The following article deals with the discrepancy between legal pretension and the practice of medical expertise in examinations for engagement, fitness for service or courses of medical treatment. To avoid injustice to the patients and conflicts for the experts, clear-cut general directions for the practice of medical expertise are demanded.
[Reduction-plasty of the breast in symmastia].
Medial confluence of the breasts, known as symmastia, has received little attention in plastic surgery literature. By reporting on one case, we present our surgical technique. The chosen method of the reduction mammoplasty is considered to be particularly important. Liposuction is integrated into the surgical procedure. Suggestions made by other authors are discussed.
Diethyldithiocarbamate delays gastric emptying and increases gastric acidity in rats in vivo.
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MHC class II antigens on lung epithelial of human fetuses and neonates. Ontogeny and expression in lungs with histologic evidence of infection.
An immunohistochemical study with anti-HLA-DP, anti-HLA-DQ and anti-HLA-DR monoclonal antibodies was carried out on lung tissue from 29 fetuses and 19 infants that died within the 1st year of life. The aim of the study was to verify the influence of lung maturation and lung inflammation, caused by intrauterine infection, on the expression of MHC class II antigens on lung epithelia. No positive reaction of lung epithelia was noticed in 6 fetuses of less than 21 weeks' gestation. In fetuses of more than 21 weeks' gestation, lung inflammation strongly correlated with the expression of MHC class II subregion products on lung epithelia. All 4 fetuses with histopathologic evidence of lung infection but only 4 out of 23 fetuses without lung inflammation bore HLA-DR antigens on their immature cuboidal alveolar epithelium. Within the bronchial epithelial layers only scattered MHC class II positive epithelia were found. After birth, MHC class II antigens were almost constantly detected on cuboidal type II pneumocytes of inflamed and noninflamed lung tissue as well. Only 3 infants that died within the 1st week of life did not show any MHC class II antigen expression on their lung epithelia.
Influence of flunarizine on postischemic flow and energy metabolism in the isolated rat brain.
Isolated perfused rat brains were subjected to complete ischemia. Reperfusion was started 10 min after the negative DC-shift. In control brains, recovery of flow was retarded and, after 10 min of reperfusion, a delayed hypoperfusion developed. In flunarizine-treated brains, recovery of flow was considerably steeper, complete and without reduction during the further course of reperfusion. Additionally, restoration of energy metabolism and mitochondrial function was significantly improved. The effect on the energetic state of the brains was at least partly independent of the improvement of flow. This could be concluded from experiments in which reperfusion was commenced simultaneously with DC-negativation. In these experiments, flow recovery was prompt and complete in control as well as in treated brains. Nevertheless, treated brains exhibited after reperfusion significantly better ratios of ATP to ADP and normalized levels of lactate and succinate.
[Interaction of quinidine and digoxin in humans (author's transl)].
After full digitalisation, 11 healthy subjects received 0.375 mg digoxin daily as maintenance dose. Under steady-state conditions and determination of serum concentration and renal clearance of digoxin, they were then given 500 or 1000 mg quinidine daily in addition to the digoxin. While serum concentration of digoxin rose significantly from 0.75 +/- 0.2 ng/ml after one week on 500 mg quinidine, and to 1.8 +/- 0.6 ng/ml after 1000 mg of quinidine, renal digoxin clearance fell from 186.2 +/- 67.4 to 125.4 +/- 61.8 ml/min after 500 mg of quinidine. Raising quinidine dosage to 1000 mg daily caused no further digoxin clearance reduction. During the total experimental period endogenous creatinine clearance remained unchanged. The results indicate that the rise in serum digoxin concentration on simultaneous quinidine administration is largely due to reduction in renal digoxin clearance. A clinical observation confirms the considerable practical importance of this interaction.
[Anticoagulant therapy: consideration of use and costs].
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[Gynecomastia caused by digitalis?].
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Quantitative studies on acid hydrolysis of digitoxin.
Hydrolysis of 3H(G)-digitoxin by hydrochloric acid and human gastric juice is described. Incubation temperatures of 37 degrees C and 22 degrees C were chosen for electrolyte solutions, and 37 degrees C for the experiments with gastric juice. After dichloromethane extraction, the radioactive metabolites were separated by thin-layer chromatography, localized and quantified by a radiochromatogram scanner. The degradation products separated by TLC were digitoxigeninbis-digitoxoside, digitoxigenin-mono-digitoxoside, and digitoxigenin. After 10 min of incubation at pH 1, digitoxin amounted to 38.6% of the total radioactivity in electrolyte solution and 37.6% in gastric juice. After 60 min, the percentage of digitoxin decreased to 5.9% and 0%, respectively. After 120 min at 22 degrees C, amounts of unhydrolyzed digitoxin were: at pH 1 55%; and at pH 2 84%. After 10 min at pH 1, and 60 min at pH 2, digitoxin was hydrolyzed to such an extent that bioavailability should have been significantly reduced. Absorption of digitoxin (liquid) from the stomach was studied during gastroscopy in five patients. Among them, significant differences in absorption kinetics and bioavailability existed, as revealed by radioimmunological measurements of the digitoxin blood levels.
[Dihydrogenated metabolites of digoxin: clinical importance and identification (author's transl)].
Several methods for the determination of dihydrometabolites of digoxin are described. Dihydrometabolites of digoxin are essentially inactive. They are the most important group of metabolites of digoxin. Seven (7) percent of a group of in-patients excreted more than 35% of these metabolites. The average was 13%, with respect to total extractable digoxin and metabolites in urine. In blood up to 40%, and in urine up to 52% dihydrogenated metabolites were found. The main metabolite was dihydrodigoxin, but the hydrolytic metabolites of digoxin exist also in reduced form. Neither the dose of digoxin, impaired renal function, nor an increased body content of digoxin seems to affect the rate of formation of these dihydrometabolites.
Digoxin metabolism in patients.
In 100 patients receiving digoxin to control heart disease, metabolic reduction of the lactone ring of digoxin was investigated. An average of 12.4% +/- 11% (range 2.2% to 52%) of the lipid-extractable cardenolides in a 24-hour urine sample contained the reduced lactone ring. Fifty-three excreted more than 10% while seven excreted more than 35% of these metabolic products. Reduction was not influenced by age, sex, dose, or blood level of digoxin. One patient who excreted 52% reduced products in the urine had 40% reduced digoxin-metabolites in the blood; the main metabolite was dihydrodigoxin. We found no influence of other drug therapy or concurrent disease on reduction of digoxin in this group.
[Pharmacokinetics of digitoxin in patients with liver cirrhosis].
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[Pharmacokinetics of digitoxin in chronic renal failure (author's transl)].
Digitoxin concentration, measured by radio-immunoassay, was significantly lower in 51 patients in chronic renal failure (23.2 +/- 7.8 mug/l) than in 29 patients in heart failure (26.5 +/- 7.3 mug/l), although both groups were on the same maintenance dose of 0.1 mg daily. Despite a normal serum albumin concentration, digitoxin protein binding was less in uraemic patients than in those with normal renal function. Renal failure did not affect intestinal digitoxin absorption. In patients in chronic renal failure elimination half-time was significantly shorter (5.7 +/- 0.9 days) than in healthy controls (7.6 +/- 1.6 days). There was no significant difference in the excretion of water-soluble ("cardioinactive") digitoxin metabolites in urine between patients in chronic renal and those in heart failure. In patients with normal renal function, of dichloromethane-soluble (cardioactive) metabolites only digitoxin could be demonstrated by thin-layer chromatography. The results indicate that patients in chronic renal failure can safely be given the same dose as those with normal renal function, without danger of over- or underdosage.
[Digitoxin level in terminal renal insufficiency].
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[Catamnestic findings in patients following gastric resection].
A radomized study was done in 2 groups of male patients operated upon 3-17 years ago either by partial gastrectomy (Billroth II type) or hermiotomy. The inquiries covered eating, drinking and smoking habits, occupation, body weight, subjective complaints, and use of drugs. Body weight and professional activity after operation were not different in both groups. Gastrectomized patients avoided milk or foods with milk, sweets and legumes more often. Feeling of fullness, vomiting and diarrhea occurred more frequently in gastrectomized subjects, as well as statements about good or even ravenous appetite and thirst. Gastrectomized men, besides, had a higher consumption of alcoholic drinks, preferably of beer.
[Influence of rifampicin on the metabolism of digitoxin].
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