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Biomedical subjects

E Wolff

Publications and source records attributed to E Wolff.

At least 55 records · Page 3Linked to original sources
PubMed1985

[Not Available].

Explore the source record for details and available documents.

Germany↗
PubMed1982

[Prednisolone reduction by benoxaprofen].

The prednisolone sparing effect of benoxaprofen has been examined in only 13 cases of rheumatoid arthritis. The examination was terminated prematurely because of an accumulation of side effects of the skin. The results of these 13 cases are not significant, but the drug seems to show a relatively high mean value of its prednisolone sparing effect but it seems to cause a high proportion of side effects, especially of the skin. This preliminary result should be reported in regard to possibly following studies with simular observations.

Anti-Inflammatory Agents↗
PubMed1980

[Fibrosarcoma of the right heart. Contribution to the problem of primary heart tumors].

Report on a fibrosarcoma of the right ventricle in a 70-year-old woman. The tumour was diagnosed by autopsy. Clinically were of importance the chronic insufficiency of the right heart, in the ECG the low voltage, a bifascicular block and a subepicardiac lesion in the area of the anterior wall. Roentgenogram of the thorax and the laboratory findings corresponded to a massive cardiac decompensation. The cytology from the effusion of the pericardium which often occurred gives a possibility of making a diagnosis intra vitam, if it is thought of a cardiac tumour.

Aged↗
PubMed1980

[Investigations on the clinical effect of the antirheumatic agent piroxicam (author's transl)].

In the glucocorticoid-sparing test, which shows certain advantages compared with other experimental procedures, the clinical efficacy of the new antirheumatic substance piroxicam (Feldene) was investigated. It was shown that a single daily dose of 20 mg piroxicam gave at least an equal, if not better, effect compared with other substances tested earlier, as far as comparison is permissible between two collectives treated with different substance. The mean saving of prednisone was 5.7 mg/day and according to another evaluation 64.7% of the previously required dose of prednisolone. It is worth noting that owing to the long half-life there is a remarkable clinical effect over at least 24 hours with a single daily dose. Tolerance was good. Pathological laboratory values which were definitely to be attributed to the preparation were not seen in a trial period of a maximum of four weeks.

Anti-Inflammatory Agents↗
PubMed1980

[Study of the dose-reducing effect of acemetacin on prednisolon (author's transl)].

The dose-reducing effect of [1-(p-chlorobenzoyl)-5-methoxy-2-methylindol-3-acetoxy[ acetic acid (acemetacin, TV 1322, Rantudil¿) on prednisolon was studied on 22 patients suffering from rheumatoid arthritis. The average prednisolon-saving was 4.33 mg; in 31.8% of the patients it was possible to dispense with prednisolon completely (in 6 cases the reduction was 5 mg and in 1 case 7.5 mg). During the short test period the medication was well tolerated. Undesired gastro-intestinal drug reactions were not recorded for any of the patients. None of the investigated laboratory parameters revealed any pathological changes which were attributable to Acemetacin, but in one patient getting a long-term treatment with gold a decrease of lymphoid cell count was observed.

Adult↗
PubMed1978

Growth and glucocorticoids in children with kidney disease.

Glucorticoid therapy inhibits statural growth. Alternate-day therapy causes less growth suppression than does daily therapy, and, in experimental animals and children with asthma, it has been associated with normal growth. Although catch-up growth may occur after cessation of steroid therapy, this is not always the case, especially when therapy has been prolonged. In children treated with steroids for glomerulonephritis or nephrotic syndrome and especially in children after renal transplantation, factors other than steroid therapy may contribute to growth retardation. Steroids may suppress growth by direct action on cell metabolism, by inhibition of growth hormone or somatomedin and/or by effects on calcium and phosphorus metabolism. Present knowledge of mechanisms of action and dose-response relationships is complete, and it is difficult to prescribe therapy which will achieve a predictable therapeutic effect without inhibiting growth.

Animals↗