³¹P-MRS provides unique information about human liver metabolism in vivo. Alterations of cell membrane precursors (phosphomonoesters [PME]) and cell membrane degradation product (phosphodiesters [PDE]) levels have been associated with alcoholic, viral and cholestatic etiologies¹. Main contributors to PDE signal are glycerophosphocholine (GPC) and glycerophosphoetanolamine (GPE). An additional resonance at 2.06 ppm was recently assigned to phosphatidylcholine (PtdC, part of lecithin) which is the dominant metabolite in bile^2,3. Both indipendent studies retrospectively analyzed ³¹P MRS data and noticed elevated PtdC signal arising from the gallbladder. However the limited penetration of surface coils used in these studies did not cover the gallbladder entirely in all acquired data. An extended ³¹P-MRS coverage of abdomen may be achieved using an 8 channel receive array at 3T⁴. The purpose of this study was to acquire ³¹P MRSI data with extended coverage of the hepatobiliary system using a 2 loops transmit and 8 channel receive array at 3T This protocol should enable prospective phosphatidylcholine assessment in the gallbladder. As the bile amount in the gallbladder changes according to dietary condition, the protocol was tested pre- and post-meal to observe potential variations in PtdC signal levels.

All data were acquired on a 3T MR system (Siemens Healthcare, Erlangen, Germany) using a double-tuned coil (¹H/³¹P) with a 2 loops transmit and a 8 channel receive array (Stark MRI Contrast, Erlangen, Germany)⁴.

Five male volunteers (age=29.2±3.5) underwent in vivo hepato-biliary ³¹P 3D MRSI at 3T in supine position (12x12x8, TR 1s, TA=17min, FOV=30x20x20cm³, weighted acquisition; NA=12, 1ms block excitation pulse) after overnight fasting. Prone part of the coil was placed slightly asymmetric for better coverage of the liver (Fig.1). 6 OVS slabs were used to minimize contamination from skeletal muscle and signals from each channel were combined by whitened singular value decomposition (WSVD) algorithm⁵. Coil positioning and measurement planning geometry are displayed in Figure 1. T₂ weighted reference images were acquired for the detection of the gallbladder position and standard shimming procedure was performed prior ³¹P MRSI scan. Two of the volunteers were re-scanned using the same protocol two hours after a meal with a high fat content (i.e., 150g of cheese with 60% fat). PDE region of MR spectra from gall bladder and from liver tissue were fitted via the Syngo MR spectroscopy tool (Siemens Healthcare, Erlangen, Germany) and metabolic maps were created.

All in vivo examinations provided ³¹P 3D MRSI data covering whole liver with negligible PCr contamination, sufficient SNR and narrow linewidths in clinically acceptable measurement time (Fig.2). After overnight fasting all volunteers had gallbladder filled with the bile (Fig.3. panel A). This was visible in both ³¹P-MRSI data as strong PtdC signal at 2ppm and in T₂ weighted reference images as hyperintense region. A reduced PtdC signal and volume of the bile in the gallbladder were visible in both volunteers after digestion of the meal with high fat content (Fig.3. panel B). The presented in vivo ³¹P 3D MRSI protocol in combination with using a 8 channel receive array at 3T provided improved coverage of the hepatobiliary system. ³¹P MRS data from gall bladder confirmed findings from previous retrospective studies^2,3. Prospective studies of phosphatidylcholine metabolism are feasible and should investigate the potential use of the PtdC for metabolic studies of the liver, gallbladder, and bile ducts. Stimulation of biliary PtdC excretion, and its possible monitoring by ³¹P MRS, may represent an interesting therapeutic approach to hepatobiliary disorders, and the use of several drugs (e.g., fibrates, ursodeoxycholic acid), which have been shown to enhance PtdC concentration in bile⁶. Further on it should be noted, that all findings and conclusions of altered PDE signals, especially when not ideally resolved, should take into account possible MRS contamination by bile in the gall bladder.