Objectives: To demonstrate the overlap of the hepatic and bile phosphorus ((31)P) magnetic resonance (MR) spectra and provide evidence of phosphatidylcholine (PtdC) contribution to the in vivo hepatic (31)P MRS phosphodiester (PDE) signal, suggested in previous reports to be phosphoenolpyruvate (PEP).
Methods: Phantom measurements to assess the chemical shifts of PEP and PtdC signals were performed at 7 T. A retrospective analysis of hepatic 3D (31)P MR spectroscopic imaging (MRSI) data from 18 and five volunteers at 3 T and 7 T, respectively, was performed. Axial images were inspected for the presence of gallbladder, and PDE signals in representative spectra were quantified.
Results: Phantom experiments demonstrated the strong pH-dependence of the PEP chemical shift and proved the overlap of PtdC and PEP (~2 ppm relative to phosphocreatine) at hepatic pH. Gallbladder was covered in seven of 23 in vivo 3D-MRSI datasets. The PDE(gall)/γ-ATP(liver) ratio was 4.8-fold higher (p = 0.001) in the gallbladder (PDE(gall)/γ-ATP(liver) = 3.61 ± 0.79) than in the liver (PDE(liver)/γ-ATP(liver) = 0.75 ± 0.15). In vivo 7 T (31)P MRSI allowed good separation of PDE components. The gallbladder is a strong source of contamination in adjacent (31)P MR hepatic spectra due to biliary phosphatidylcholine.
Conclusions: In vivo (31)P MR hepatic signal at 2.06 ppm may represent both phosphatidylcholine and phosphoenolpyruvate, with a higher phosphatidylcholine contribution due to its higher concentration.
Key points: • In vivo (31)P MRS from the gallbladder shows a dominant biliary phosphatidylcholine signal at 2.06 ppm. • Intrahepatic (31)P MRS signal at 2.06 ppm may represent both intrahepatic phosphatidylcholine and phosphoenolpyruvate. • In vivo (31)P MRS has the potential to monitor hepatic phosphatidylcholine.