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Am J Physiol Gastrointest Liver Physiol (February 5, 2004). doi:10.1152/ajpgi.00418.2003
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Submitted on September 25, 2003
Accepted on January 26, 2004

Quantitative Hepatic Phosphorus-31 Magnetic Resonance Spectroscopy in Compensated and Decompensated Cirrhosis

I R Corbin1, L N Ryner2, H Singh3, and G Y Minuk1*

1 Liver Diseases Unit, Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; Liver Diseases Unit, Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada
2 Institute for Biodiagnostics, National Research Council of Canada, Winnipeg, Manitoba, Canada
3 Liver Diseases Unit, Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

* To whom correspondence should be addressed. E-mail: gminuk{at}cc.umanitoba.ca.

Background/Aims: Few studies have examined the physiological/biochemical status of hepatocytes in patients with compensated and decompensated cirrhosis in situ. Phosphorus-31 magnetic resonance spectroscopy (31P MRS) is a non-invasive technique which permits direct assessments of tissue bioenergetics and phospholipid metabolism. Methods: Quantitative 31P MRS was employed to document differences in the hepatic metabolite concentrations among patients with compensated and decompensated cirrhosis as well as healthy controls. All MRS examinations were performed on a 1.5 T General Electric Signa whole body scanner. Results: The concentration of hepatic phosphorylated metabolites among patients with compensated cirrhosis (n=7) was similar to those of healthy controls (n=8). However, patients with decompensated cirrhosis (n=6) had significantly lower levels of hepatic ATP compared to patients with compensated cirrhosis and healthy controls (P<0.02 and P<0.009, respectively), and a higher PME/PDE ratio than controls (P<0.003). Conclusions: The results of this study indicate that metabolic disturbances in hepatic energy and phospholipid metabolism exist in patients with decompensated cirrhosis that are not present in patients with compensated cirrhosis or healthy controls. These findings provide new insights into the pathophysiology of hepatic decompensation.




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