Acute necrotizing pancreatitis and severe hepatic failure: description of three cases.

INTRODUCTION: Acute pancreatitis is not uncommon in fulminant hepatic failure (FHF) as confirmed by histology or serology. A few reports exist of symptomatic pancreatitis in the setting of acute viral hepatitis; the diagnosis is usually made intraoperatively or postmortem. We report three cases of liver transplant (OLT) recipients with severe acute liver failure and severe acute pancreatitis as an intraoperative finding. METHODS: We undertook a retrospective review among a large cohort of liver transplant recipients to define the impact of this problem. RESULTS: Between 1999 and 2007, 293. LTs were performed including 15 (5%) who had severe acute liver failure (nine with FHF and six with an emergency retransplantation [ER]). Among this group, three patients were diagnosed intraoperatively with acute necrotizing pancreatitis (ANP): two patients with associated FHF and one with an ER due to ABO incompatibility. None of the patients had symptoms of pancreatitis. In all, ANP was classified as Balthazar CT grade D-E, which determined the outcome. All the patients developed a pseudocyst and abscess, which required surgical drains. CONCLUSION: ANP was diagnosed as an intraoperative finding in patients with FHF. The mechanism of pancreatitis in patients with FHF is unknown. It may be multifactorial (virus, acute liver failure, hypotension, infection, drug-induced lesion,). This association leads to a worse outcome due to the complications.

[Effect of indomethacin on the secretion of pepsinogen in isolated human cells in vitro]. / Efecto de la indometacina sobre la secreción de pepsinógeno en células humanas aisladas in vitro.

The effects of indomethacin on pepsinogen secretion were studied in isolated human peptic cells prepared from endoscopically obtained biopsies after collagenase digestion, mechanical disruption and percoll gradient centrifugation. Low concentrations of indomethacin (10(-8)-10(-10) M) stimulated basal pepsinogen secretion. Higher doses of indomethacin (10(-5)-10(-6) M) potentiated histamine (10(-4) M) and db-cAMP (10(-4) M)-stimulated pepsinogen secretion without affecting acetylcholine (10(-6) M) and CCK-8-stimulated pepsinogen secretion or cell vitality. Increase of pepsinogen secretion was dependent on extracellular calcium because potentiation was abolished by calcium depletion of the medium. We conclude that indomethacin potentiates basal and secretagogue-stimulated pepsinogen secretion by dispersed human peptic cells and this might be an additional mechanism of NSAID-induced gastric injury. This potentiation effect is regulated by calcium and independent of endogenous prostaglandin inhibition.