ABSTRACT
INTRODUCTION AND PRESENTATION OF CASE: Eight days after being diagnosed with multiple small strokes a 71year old male patient is readmitted with suspicion of a petit mal seizure also complained of diarrhoea and abdominal pain. The patient was stable, not febrile and neurologically intact with a slight tenderness in the left lower quadrant. An ultrasound revealed presence of air in the hepatic portal venous system and a suspicion for sigmoid diverticulitis. A CT-scan confirmed both diagnoses. We proceeded with a conservative regimen under close observation. The clinical course and laboratory results were unremarkable. DISCUSSION: The review of the literature (PubMed database) triggered 685 items with only one clinical trial establishing a scoring system to detect adult individuals, which need operation. CONCLUSION: A pneumoportogram (hepatic portal venous gas, HPVG) is a very rare and usually associated with bowel ischemia and from poor prognosis. The last decades saw the emergence of numerous other aetiologies (also benign) with a shift of paradigm from systematic emergency laparotomies to individual patient selection.
ABSTRACT
Inappropriate activation of the mineralocorticoid receptor (MR) results in renal sodium retention and potassium loss in patients with liver cirrhosis. Recent evidence suggested that this MR activation is, at least in part, a result of bile acid-dependent reduction in 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD2) activity, an enzyme preventing cortisol-dependent activation of MR by converting cortisol to cortisone. Here, we investigated the molecular mechanisms underlying bile acid-mediated MR activation. Analysis of urinary bile acids from 12 patients with biliary obstruction revealed highly elevated concentrations of chenodeoxycholic acid (CDCA), cholic acid (CA), and deoxycholic acid (DCA), with average concentrations of 50-80 microm. Although CDCA and DCA both mediated nuclear translocation of MR in the absence of 11 beta HSD2 and steroids in transiently expressing HEK-293 cells, the transcriptional activity of MR was not stimulated. In contrast, CDCA and DCA both inhibited 11 beta HSD2 with IC(50) values of 22 and 38 microm, respectively and caused cortisol-dependent nuclear translocation and increased transcriptional activity of MR. LCA, the bile acid that most efficiently inhibited 11 beta HSD2, was present at very low concentrations in cholestatic patients, whereas the weak inhibitor CA did not cause MR activation. In conclusion, these findings indicate that CDCA, and to a lesser extent DCA, by inhibiting 11 beta HSD2, mediate cortisol-dependent nuclear translocation and transcriptional activation of MR and are responsible at least for a part of the sodium retention and potassium excretion observed in patients with biliary obstruction.
