Improved accuracy in the diagnosis of intrahepatic bile duct ectasia in Caroli's disease by combination of ultrasound and endoscopic retrograde cholangiography

Caroli's disease is characterized by dilatation of the intrahepatic bile ducts. Cholangitis, liver cirrhosis and development of a cholangiocarcinoma are possible complications. For optimal therapy, a correct diagnosis of the extent of the disease is mandatory. The present report demonstrates that the combination of endoscopic retrograde cholangiography and ultrasound may lead to a more reliable diagnosis of the extent of Caroli's disease. It is therefore essential to perform ultrasound in all these patients

Gallige Peritonitis bei einem alkoholkranken Mann nach traumatischer Gallenblasenperforation--Differenzialdiagnostik zur aszitisch dekompensierten Leberzirrhose. [Bile peritonitis in an alcoholic man after traumatic gallbladder perforation--differential ascitic decompensated liver cirrhosis diagnosis]

Traumatic rupture of the gallbladder is a very rare event associated with high mortality. Since clinical symptoms are nonspecific, diagnosis is difficult. We present an alcoholic with biliary ascites after traumatic perforation of the gallbladder. Initially, he was misdiagnosed to have ascites caused by liver cirrhosis. This case demonstrates, that the combination of patients history, clinical investigation and ultrasound allows the diagnosis of traumatic rupture of the gallbladder

Chloride transport-driven alveolar fluid secretion is a major contributor to cardiogenic lung edema.

Alveolar fluid clearance driven by active epithelial Na(+) and secondary Cl(-) absorption counteracts edema formation in the intact lung. Recently, we showed that impairment of alveolar fluid clearance because of inhibition of epithelial Na(+) channels (ENaCs) promotes cardiogenic lung edema. Concomitantly, we observed a reversal of alveolar fluid clearance, suggesting that reversed transepithelial ion transport may promote lung edema by driving active alveolar fluid secretion. We, therefore, hypothesized that alveolar ion and fluid secretion may constitute a pathomechanism in lung edema and aimed to identify underlying molecular pathways. In isolated perfused lungs, alveolar fluid clearance and secretion were determined by a double-indicator dilution technique. Transepithelial Cl(-) secretion and alveolar Cl(-) influx were quantified by radionuclide tracing and alveolar Cl(-) imaging, respectively. Elevated hydrostatic pressure induced ouabain-sensitive alveolar fluid secretion that coincided with transepithelial Cl(-) secretion and alveolar Cl(-) influx. Inhibition of either cystic fibrosis transmembrane conductance regulator (CFTR) or Na(+)-K(+)-Cl(-) cotransporters (NKCC) blocked alveolar fluid secretion, and lungs of CFTR(-/-) mice were protected from hydrostatic edema. Inhibition of ENaC by amiloride reproduced alveolar fluid and Cl(-) secretion that were again CFTR-, NKCC-, and Na(+)-K(+)-ATPase-dependent. Our findings show a reversal of transepithelial Cl(-) and fluid flux from absorptive to secretory mode at hydrostatic stress. Alveolar Cl(-) and fluid secretion are triggered by ENaC inhibition and mediated by NKCC and CFTR. Our results characterize an innovative mechanism of cardiogenic edema formation and identify NKCC1 as a unique therapeutic target in cardiogenic lung edema