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A previously well 24-year-old man complained of persistent epigastric pain after a session of intensive muscle building exercise especially of the abdominal muscles. The abdomen was diffusely tender without guarding. There was an increased concentration of bilirubin (64.7 mumol/l), GOT (117 U/l), GPT (529 U/l) and alkaline phosphatase (150 U/l). Ultrasound examination showed a widening of the choledochal duct to 11 mm without signs of gallstones. Endoscopic retrograde cholangiography additionally revealed contrast-medium extravasation from the left hepatic duct. Computed tomography, performed immediately afterwards, confirmed the extravasation, while liver and pancreas were unremarkable. Laparoscopy revealed a 5 mm tear in the left hepatic duct, close to the hepatic duct bifurcation with bile effusion into the peritoneal cavity. The latter was rinsed endoscopically with Ringer's solution and drains were placed in the omental bursa and subhepatically in the region of the bile leak. To relax the sphincter Oddi glycerol trinitrate was administered postoperatively, for the first five days 72 mg/24 h intravenously, then for nine days twice daily 20 mg by month. No more bile drained as early as the second postoperative day and the patient was free of symptoms 2 weeks later.

In a 40-year-old patient unexplained recurrent attacks of epigastric colic with transient cholestatic icterus occurred over a 9-year period. When the patient was again hospitalised because of progressive pain-free icterus associated with mild pruritus (alkaline phosphatase 900 U/l, direct bilirubin 305 mumol/l, GOT 187 U/l, GPT 103 U/l) sonography revealed liver enlargement to 17 cm, extended intrahepatic bile ducts and an echodense area of about 1 cm size in the region of the bifurcation of the common hepatic duct. Fine-needle puncture did not yield clear cytological findings. Endoscopic retrograde cholangiopancreatography pointed to sclerosing cholangitis. This diagnosis was confirmed by liver punch biopsy. Since the patient did not agree to a liver transplantation, he was treated with 450 mg ursodeoxycholic acid twice daily, resulting in marked reduction of the liver parameters until severe cholangiosepsis and acute renal failure occurred about 4 months later. The septic condition and its complications could not be managed despite thorough intensive-care measures so that a liver transplant had to be performed after all. Histology of the explantate revealed a cholangiocarcinoma in the region of the bifurcation of the common hepatic duct. At first the patient's condition improved markedly but one and half months later the transplant was rejected and the patient died.

During two treatment periods (4 weeks each), serum immunoreactive trypsin (IRT), immunoreactive human lipase in stool (IRL), and chymotrypsin (CT) activity in stool were determined in 16 cystic fibrosis patients and compared with fecal fat excretion (72-h sampling). Fecal fat estimation revealed mild to severe steatorrhea in all 16 patients (X = 13.7 +/- 9.0 g/24 h) in at least one study period. Stool fat excretion was highest in underweight adolescents and adults. Comparison of IRT and IRL with stool fat values showed no significant statistical correlation. IRT values revealed an inverse exponential correlation with age, with a steep decline at the age of 5 years. CT levels were very high in 14 of our 16 patients during supplementation therapy, whereas 2 patients showed subnormal CT values. We conclude that since indirect parameters of pancreatic function do not correlate with stool fat excretion, stool fat remains the best indirect parameter for the assessment of pancreatic insufficiency in cystic fibrosis. Leaving pancreatic enzyme supplementation in cystic fibrosis patients on the basis of normal serum trypsin or fecal lipase values does not appear to be adequate.

In this prospective long-term study of chronic pancreatitis (n = 336) over the last 3 decades, 10 patients with advanced calcific pancreatitis developed a sepsis associated with intra-abdominal abscesses (6 pancreatic, 4 hepatic). None of the known precipitating factors were present (e.g., no pancreatic necrosis or recent surgical/endoscopic interventions, no evidence of cholangitis). Nine of 10 patients had alcoholic chronic pancreatitis. Interestingly a pancreatojejunostomy in 9 of 10 patients had been performed up to 12 years previously. Cultures from abscess aspirates and/or blood were polymicrobial, mainly a mixed enteric flora in 8 patients. All patients recovered after an appropriate antibiotic therapy with or without drainage procedures. The pathogenesis of "spontaneous" abscess formation in advanced chronic pancreatitis and its relationship to pancreatojejunostomy remain to be established.

Physical review letters 50(20), 1619 - 1622 (1983). doi:10.1103/PhysRevLett.50.1619, Published by APS, College Park, Md.

The use of a spectrophotometric method is reported for the characterization of a beta-lactamase (EC 3.5.2.6) from Bacillus cereus. Absorption coefficients of the mercaptides of various penicillins were determined with this method. The enzyme was kinetically characterized using penicillins. Inhibition studies with Bacillus cereus beta-lactamase and various penicillins showed a substrate type of inhibition, indicating an additional binding site for substrates without catalytic activity. The dissociation constant of this binding site was determined and the influence of this binding site upon the catalytic activity is discussed. Studies with beta-lactamase-stable penicillins as inhibitors and various penicillins showed different types of inhibition, which indicated the presence of an additional catalytically inactive binding site. Experiments with clavulanic acid, a beta-lactamase inhibitor without remarkable intrinsic antibacterial activity, showed a mixed type of inhibition. Based on the hypothesis for the existence of more than one substrate binding site on the enzyme, clavulanic acid was found to be bonded to both the catalytic active and the catalytic inactive binding site.

Cefotaxime (HR 756) is a new semisynthetic parenteral cephalosporin with exceptional activity against gram-negative organisms and considerable stability against their β-lactamases. To study its pharmacokinetic properties, 0.5-, 1-, and 2-g doses were administered to each of six volunteers intravenously over 15 min, followed by a sustaining infusions of 0.5, 1, and 2 g/h, respectively, for 3 consecutive hours. The loading doses produced mean peak levels of 41, 93, and 160 μg/ml, and mean steady-state serum concentrations were 27, 64, and 138 μg/ml, respectively. The mean terminal half-life was 75 ± 7 min. The total volume of distribution averaged 0.22 ± 0.03 liters/kg of body weight. Total body and renal clearances were 232 ± 30 and 145 ± 24 ml/min per 1.73 m 2 , respectively; 63 ± 9% of the administered dose was excreted through the kidneys in 24 h. To determine the effect of cefotaxime on the renal tubules, urinary alanine aminopeptidase excretion was measured before, during, and after the infusions. It remained within the normal range in all instances; however, 48 ± 14% of the total daily alanine aminopeptidase output was recovered during the infusion period. Side effects were dose related and included fatigue, loose stools, and night sweats. No significant changes in hematology, serum chemistry, or urinalysis were recorded.

We investigated intestinal permeability in healthy adult volunteers, and in patients with Crohn's disease, ulcerative colitis, idiopathic sprue and idiopathic hyperamylasemia by oral administration of 10 g low molecular weight polyethylene glycol (PEG-400) and quantitation of its renal excretion over the subsequent 6 hours by high performance liquid chromatography (gel permeation HPLC). The mean amount of PEG-400 excreted during the first 6 hours by the 12 patients with Crohn's disease (3.1 +/- 0.3 g, mean +/- SE) and the 8 patients with ulcerative colitis (2.6 +/- 0.3 g) was not significantly different from the amount excreted by the 24 healthy volunteers (2.9 +/- 0.1 g). The 3 patients with idiopathic sprue excreted significantly less (1.4 +/- 0.3 g, p less than 0.05) and the 3 patients with idiopathic hyperamylasemia significantly more (4.0 +/- 0.4 g, p less than 0.05) than the healthy controls. In conclusion, no alteration of intestinal permeability could be demonstrated in patients with Crohn's disease or ulcerative colitis. However, intestinal permeability was decreased in patients with idiopathic sprue and increased in those with idiopathic hyperamylasemia.