The study supports the view that these bacteria continue to play a minor role in secondary peritonitis. The point has to be emphasized, however, that the patients under study were in relatively good condition (APACHE II median 9 for cephalosporins and 10 for penicillins) and that postoperative cases of peritonitis were excluded.
Roughly 70% of all patients with breast cancer can be treated by breast-preserving procedures under optimal circumstances. Risk factors for the development of local recurrences are age, angioinvasion, poor differentiation of the tumor, negative steroid hormone receptors, extensive intraductal component and positive margins. Contraindications for breast preservation are large tumors without remission after preoperative chemotherapy, multicentricity, extensive intraductal component, large ductal carcinoma in situ, inflammatory breast cancer after preoperative chemotherapy, Paget disease and local recurrence after breast-conserving surgery. Preoperative needle biopsy allows determination of nearly all of the risk factors. To further increase the rate of breast conservation, preoperative chemotherapy should be used more extensively.
Rapid gastric emptying and exaggerated plasma concentrations of the insulinotropic hormone GLP-1 precede reactive hypoglycemia after oral glucose in gastrectomy patients. We suspected that the plasma volume drop associated with rapid gastric emptying (early dumping) would be accompanied by elevated plasma concentrations of norepinephrine. In order to study any relationship between postprandial norepinephrine, the enteroinsular axis, and plasma glucose, twelve patients with dumping syndrome and nine controls were studied. The plasma concentrations of norepinephrine, GLP-1, GIP, glucagon, insulin, and glucose were measured following a 1.5 g/kg lean body mass glucose meal. The early (0-30 min) integrated norepinephrine concentration was significantly higher in dumpers (22.1 +/- 3.8 nmol/ml/min) compared to controls (14.7 +/- 3.1 nmol/ml/min; P < 0.001) and correlated closely with the postprandial hematocrit increment (r = 0.71; P < 0.05). Early immunoreactivities of GLP-1, GIP, and glucagon peaked 30 min after glucose ingestion and were significantly higher in dumpers. Insulin peaked after 60 min and correlated with early GLP-1. In 11 of the patients glucose fell below baseline after a median interval of 120 min. Glucose at 120 min, when most of the nadirs occurred was lowest in patients with high early GLP-1 concentrations (r = 0.78; P < 0.001). Gel filtration chromatography of the dumpers' plasma revealed that pancreatic glucagon was detectable at time 0 and after 20 min, but not after 120 min. It is concluded that in dumpers pancreatic glucagon is augmented in the early postprandial period, probably through stimulation by catecholamines. At 120 min, when most of the hypoglycemias are encountered, pancreatic glucagon is no longer detectable, probably through inhibition by GLP-1.
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