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1 H and 31 P NMR studies indicate reduced bile constituents in patients with biliary obstruction and infection
Author(s) -
Bala Lakshmi,
Tripathi Pratima,
Bhatt Ganesh,
Das Kshaunish,
Roy Raja,
Choudhuri Gourdas,
Khetrapal C. L.
Publication year - 2009
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.1308
Subject(s) - jaundice , gastroenterology , medicine , bilirubin , cholestasis , biliary tract , cholesterol
Patients with extrahepatic biliary obstruction present with impairment of the normal bile flow, with jaundice and cholangitis as common complications. 1 H and 31 P NMR quantitative analysis of bile specimens from patients with extrahepatic biliary obstruction (n = 80) (with/without jaundice and cholangitis separately and together) was carried out for the chief biliary constituents to determine the relationship between biliary constituents and jaundice (serum bilirubin concentration ≥1.0 mg/dL) and cholangitis (total leucocyte count >11 000 cells/mm 3 and/or fever >38.5°C with/without bile culture positivity). Compared with controls (patients without jaundice and cholangitis), median indices of the chief biliary constituents (total bile acids, cholesterol, phosphatidylcholine and inorganic phosphate) were significantly suppressed in patients with cholangitis and/or jaundice. Quantities of total bile acids, cholesterol and phosphatidylcholine correlated negatively with the quantity of bilirubin and with cholangitis, i.e. total leucocyte count. Suppression of biliary constituents correlated significantly with the severity of jaundice and cholangitis. The decrease in biliary constituents in the presence of jaundice and cholangitis is possibly the result of downregulation of the function of transporters located at the canalicular side of hepatocytes, leading to their suppressed indices in bile. This information may have implications in the examination of bile for clinical studies. Copyright © 2008 John Wiley & Sons, Ltd.