Changani K K, Jalan R, Cox I J, Ala-Korpela M, Bhakoo K, Taylor-Robinson S D, Bell J D
Magnetic Resonance Unit, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, UK.
Gut. 2001 Oct;49(4):557-64. doi: 10.1136/gut.49.4.557.
Alterations in gluconeogenesis in the diseased liver can be assessed non-invasively using magnetic resonance spectroscopy by measuring changes in phosphomonoester resonance which contains information regarding several metabolites, including the phosphorylated intermediates of the gluconeogenic pathway.
31P magnetic resonance spectroscopy was used to determine changes in phosphomonoesters following bolus infusions of 2.8 mmol/kg L-alanine in five patients with functionally compensated cirrhosis and in five patients with functionally decompensated cirrhosis.
Compared with six healthy volunteers, baseline phosphomonoester values were elevated by 35% (p<0.05) in the compensated cirrhosis group and by 57% (p<0.01) in the decompensated cirrhosis group. Following alanine infusion, phosphomonoesters in healthy volunteers increased by 46% from baseline values (p<0.01), in patients with compensated cirrhosis by 27% (p<0.02) but those with decompensated cirrhosis showed no increase from baseline. There was a reduction in the percentage of inorganic phosphate signal in all subjects.
By analysing changes in phosphomonoester and inorganic phosphate resonances it is possible to discern clear metabolic differences between healthy volunteers and patients with cirrhosis of varying severity using magnetic resonance spectroscopy. Those patients with functionally decompensated cirrhosis have higher percentage baseline phosphomonoester values but the absence of phosphomonoester elevation following L-alanine infusion suggests that they are unable to mount a significant metabolic response with a progluconeogenic stimulus.
通过磁共振波谱测量磷酸单酯共振的变化来无创评估患病肝脏中糖异生的改变,该共振包含有关几种代谢物的信息,包括糖异生途径的磷酸化中间体。
对5例功能代偿性肝硬化患者和5例功能失代偿性肝硬化患者静脉推注2.8 mmol/kg L-丙氨酸后,采用³¹P磁共振波谱测定磷酸单酯的变化。
与6名健康志愿者相比,代偿性肝硬化组的基线磷酸单酯值升高了35%(p<0.05),失代偿性肝硬化组升高了57%(p<0.01)。静脉输注丙氨酸后,健康志愿者的磷酸单酯较基线值增加了46%(p<0.01),代偿性肝硬化患者增加了27%(p<0.02),而失代偿性肝硬化患者的磷酸单酯较基线值未增加。所有受试者的无机磷酸信号百分比均降低。
通过分析磷酸单酯和无机磷酸共振的变化,利用磁共振波谱可以明确区分健康志愿者和不同严重程度肝硬化患者之间的代谢差异。功能失代偿性肝硬化患者的基线磷酸单酯值百分比更高,但静脉输注L-丙氨酸后磷酸单酯未升高,这表明他们在糖异生刺激下无法产生显著的代谢反应。