[Postoperative pulmonary complications: prophylaxis after noncardiac surgery]. / Postoperative pulmonale Komplikationen : Prophylaxe nach nichtkardiochirurgischen Eingriffen.

Postoperative pulmonary complications are a major problem after upper abdominal or thoracoabdominal surgery. They lead to a prolonged ICU stay as well as increased costs and are one of the main causes of early postoperative mortality. Even after uncomplicated operations, postoperative hypoxemia occurs in 30-50% of patients. Acute respiratory failure involves a disturbance in gas exchange. The mortality ranges from 10 to 60% according to the severity of respiratory failure. The most important complications are interstitial and alveolar pulmonary edema, atelectasis, postoperative pneumonia, hypoventilation, and aspiration. Preoperative optimization, postoperative prophylaxis according to a stepwise approach, and early mobilization decrease the rate of complications.

N-acetylcysteine attenuates the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion in humans undergoing liver transplantation.

BACKGROUND: Oxidative stress and leukocyte-endothelial interactions contribute significantly to the reperfusion injury of the transplanted liver. Therefore, we investigated the effect of N-acetylcysteine (NAC) on reperfusion injury and circulating adhesion molecules during human liver transplantation. METHODS: In a prospective study, 10 orthotopic liver transplantation patients were treated with high-dose NAC and 10 patients were treated with 5% glucose (placebo group) immediately before and during reperfusion of the donor liver. Parameters of hepatocellular injury, cellular oxygenation, plasma cytokines, and circulating adhesion molecules were determined at various time points during the liver transplantation. RESULTS: NAC had no significant effect on the arterial lactate/pyruvate or hydroxybutyrate/acetoacetate ratio during the liver transplantation. At baseline, liver transplantation patients exhibited elevated levels of cytokines and circulating adhesion molecules compared with healthy volunteers (n=7). While no significant effect of NAC on circulating L- and P-selectin was observed, it significantly inhibited the increase in circulating ICAM-1 and VCAM-1 24 hr after reperfusion. There were no significant differences in maximal postoperative values of serum aspartate transaminase (peak AST) or alanine transaminase (peak ALT) between both groups. However, NAC significantly reduced the rise in alpha-glutathione S-transferase after reperfusion of the donor liver. CONCLUSIONS: NAC attenuated the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion of the donor liver, indicating possible cytoprotective effects of NAC.

Biliary lipids, lithogenic index and biliary drug concentrations during etofibrate and bezafibrate treatment.

Hypolipidemic drugs like etofibrate and bezafibrate may induce lithogenic bile and increase the risk of gallstone formation. In this study, biliary lipids, lithogenic index and biliary drug concentrations were investigated in 6 hyperlipidemic patients after cholecystectomy. Patients were treated once daily for 5 days with either 500 mg/day etofibrate or 400 mg/day bezafibrate. Hepatic bile was collected for 6 days via T-drainage in 4 hourly aliquots. In the patients treated with etofibrate, the range of the lithogenic index remained stable with 0.89-1.69 before and 0.78-1.51 after 5 day drug therapy. In the bezafibrate group, the range of the lithogenic index rose from 0.81-1.40 to 1.26-1.66 mainly as a result of an increase of biliary cholesterol concentrations. Biliary drug concentrations were substantially higher under bezafibrate treatment than under etofibrate treatment. In conclusion, the fibrate drugs, etofibrate and bezafibrate, are different with regard to lithogenicity of bile and extent of biliary excretion. The safety profile of etofibrate may be preferably compared to other fibrate drugs.

Plasma kinetics and biliary excretion of colchicine in patients with chronic liver disease after oral administration of a single dose and after long-term treatment.

Plasma kinetics and biliary excretion of colchicine in patients with chronic liver disease were evaluated after oral administration of a single dose and after long-term treatment. A single oral dose of 1 mg colchicine led to a mean peak concentration of 3.60 +/- 1.04 ng/ml at a peak time of 2.16 +/- 0.34 h and a mean area under the plasma concentration time curve, extrapolated from time 0 to infinity, of 24.90 +/- 8.47 ng.h/ml. Comparable values were obtained after repeated administration. Distribution half-life was 2.83 +/- 0.74 h, and terminal plasma half-life was 9.81 +/- 2.08 h; the mean apparent volume of distribution and the mean apparent plasma clearance were 1448 +/- 4061 and 175.3 +/- 47.6 1/h, respectively. Colchicine concentrations in bile (2025 +/- 1368 ng/ml) were clearly higher than in plasma. Long-term treatment with colchicine (1 mg/day) in patients with various stages of primary biliary cirrhosis (PBC) was associated with colchicine concentrations varying from < 0.15 to 2.0 ng/ml, with a slight tendency to higher concentrations in PBC stages III-IV than I-II. Although about 20% of colchicine is excreted in bile within 24 h, accumulation of colchicine may appear only in patients with advanced liver disease and cholestasis.

[Antineutrophil cytoplasmic antibodies in chronic inflammatory bowel diseases]. / Antineutrophile zytoplasmatische Antikörper bei chronisch-entzündlichen Darmerkrankungen.

Serum samples from 83 patients (42 women, 41 men, mean age 41 [19-85] years) with chronic inflammatory bowel diseases (ulcerative colitis: n = 41, Crohn's disease: n = 42) of differing degrees of activity were tested for antineutrophil cytoplasmic antibodies (ANCA) by immunofluorescence microscopy and various ELISA techniques. Seven patients with ulcerative colitis and one with Crohn's disease were suffering from associated primary sclerosing cholangitis. ANCA were detected in 18 sera, 13 from patients with ulcerative colitis (31.7%) and five from patients with Crohn's disease (11.9%). Six of the eight patients with primary sclerosing cholangitis were ANCA-positive. Nine sera showed a cytoplasmic (c-ANCA-) pattern and 9 others showed a partially atypical perinuclear (p-ANCA-) pattern. Among the ANCA-positive sera, ELISA techniques showed that two had antibodies against serine proteinase 3, two against lactoferrin, two against elastase and one against myeloperoxidase. There was no correlation between the anatomical pattern or activity of the disease and the presence of ANCA. The antineutrophil cytoplasm antibodies demonstrable in chronic inflammatory bowel disease appear to be directed against so far unknown antigens. They are particularly frequent in patients with associated primary sclerosing cholangitis.

Prospective study on the distribution of Campylobacter pylori in unselected patients of an endoscopy unit in West Germany.

In recent years a series of publications predominantly from English speaking countries have reported on the colonization of the gastric epithelium with Campylobacter pylori in association with gastritis and ulcer disease. In this prospective study we investigated the distribution of Campylobacter pylori in unselected patients undergoing routine endoscopy at the Department of Gastroenterology of the University of Heidelberg. A total of 175 patients were included in the study. Campylobacter pylori could be demonstrated by microbiological and histological methods in 17% of patients with normal gastric mucosa, in 44% with chronic active gastritis and in 48% with stomach ulcer. In our series only 6/23 patients with duodenal ulcer were Campylobacter pylori positive. Additionally intragastric acidity and concentrations of total bile acids were correlated to the colonization of Campylobacter pylori. Bile acid concentrations were found significantly (p less than 0.001) lower in patients with gastritis when Campylobacter pylori was present. These data suggest an association of Campylobacter pylori with diseases of the stomach also in West Germany and a negative correlation of these organisms to enterogastric bile reflux.