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J Hepatol. 2005 May;42(5):752-9.

Hepatic phospholipids in alcoholic liver disease assessed by proton-decoupled 31P magnetic resonance spectroscopy.

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  • 1Department of Diagnostic Radiology, University Hospital, Eberhard-Karls University, Tübingen, Germany.



Alteration of the phospholipid composition of hepatic biomembranes may be one mechanism of alcoholic liver disease (ALD). We applied proton-decoupled (31)P magnetic resonance spectroscopic imaging ({(1)H}-(31)P MRSI) to 40 patients with ALD and to 13 healthy controls to confirm that metabolic alterations in hepatic phospholipid intermediates could be detected non-invasively.


All patients underwent liver biopsy. Specimens were scored in non-cirrhosis [fatty liver (n=3), alcoholic hepatitis (n=2), fibrosis (n=4), alcoholic hepatitis plus fibrosis (n=16)], and cirrhosis (n=15). {(1)H}-(31)P spectra were collected on a clinical 1.5-Tesla MR system and were evaluated by calculating signal intensity ratios of hepatic phosphomonoester (PME), phosphodiester (PDE), phosphoethanolamine (PE), phosphocholine (PC), glycerophosphorylethanolamine (GPE), and glycerophosphorylcholine (GPC) resonances.


The signal intensity ratio GPE/GPC was significantly elevated in cirrhotic (1.19+/-0.22; P=0.002) and non-cirrhotic ALD patients (1.01+/-0.13; P=0.006) compared to healthy controls (0.68+/-0.04), while PE/PC and PME/PDE were significantly elevated in cirrhotic ALD patients compared to controls (1.68+/-0.60 vs. 0.97+/-0.31; P=0.02, and 0.38+/-0.02 vs. 0.25+/-0.01; P=0.002, respectively) and non-cirrhotic patients.


The data support that {(1)H}-(31)P MRSI appears to distinguish cirrhotic from non-cirrhotic ALD patients and confirms changes in hepatic phospholipid metabolism observed in an animal model.

[PubMed - indexed for MEDLINE]
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