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Following a one-month prospective study of antimicrobial drug use in surgical departments, new guidelines were implemented. The review was repeated after two years. In both study periods, one third of patients were prescribed antimicrobial drugs. Prophylactic antibiotic consumption decreased from 0.75 to 0.53 defined daily doses/operation. Compliance with guidelines improved from 32% to 79%. Duration of prophylaxis > 24 h decreased from 21 % to 8%. Single dose prophylaxis increased from 34% to 80%. Quality of the prophylactic courses improved, as evaluated by experts using established criteria. For prophylaxis, cost savings amounted to 57%. Better quality of therapeutic courses was associated with a cost increase of 15%. Indicators of satisfactory outcome with the new policy were a stable median length of stay (5.5 days in the first review and 5.0 days after intervention) and a reduction in the number of nosocomial infections treated with antimicrobial drugs/100 bed days (1.0 before intervention vs 0.77 after intervention).

Stress urinary incontinence (SUI) can be due to different anatomic aberrations such as loss of the posterior urethrovesical angle, loss of the appropriate urethral axis and stability, urethral funneling and telescoping. Usually more than one of these aberrations play a part in the development of genuine SUI. The surgical procedure which results in repair of all the anatomical aberrations which contribute to stress urinary continence will be the most successful. Only a thorough preoperative investigation will disclose the underlying pathology and result in a proper diagnosis and an adequate therapy.

Aromatase inhibition by delta 1-testolactone [(17 oxa-D-homo 1,4 androstanediene-3,17 dione) 500 mg twice daily for 10 days] in nine normal men lowered circulating estradiol (E2) levels by about 25%, enhanced the secretion of FSH, 17-hydroxyprogesterone (17-OHP), and to a lesser degree testosterone (T), but did not affect serum LH levels. Despite E2 lowering there was greater accumulation of 17-OHP than of T after 7 days of treatment, suggesting 17,20-lyase inhibition. Unexpectedly, administration of delta 1-testolactone almost halved the T response to hCG (Pregnyl, 1500 IU), but did not affect the 17-OHP response. Thus, E2 lowering by testolactone aggravated the hCG-induced 17,20-lyase block present before testolactone administration. Although the present data might suggest that estrogens do not play a role in the genesis of the hCG-induced late steroidogenic block, the results suggest that testolactone per se, in addition to its reported antiestrogenic action, inhibits 17,20 lyase.