Splanchnic metabolism of fuel substrates in acute liver failure

Citation
Jo. Clemmesen et al., Splanchnic metabolism of fuel substrates in acute liver failure, J HEPATOL, 33(6), 2000, pp. 941-948
Citations number
54
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
JOURNAL OF HEPATOLOGY
ISSN journal
01688278 → ACNP
Volume
33
Issue
6
Year of publication
2000
Pages
941 - 948
Database
ISI
SICI code
0168-8278(200012)33:6<941:SMOFSI>2.0.ZU;2-G
Abstract
Background/Aims: This study aimed to characterize the exchange of fuel subs trates in the splanchnic circulation in acute liver failure. Methods: Liver vein catheterization was used in 22 patients with acute live r failure after development of hepatic encephalopathy grade III-IV. Healthy controls, patients with cirrhosis and patients with acute on chronic liver disease were also studied. Results: In acute liver failure there was splanchnic removal of glucose (0. 21+/-0.44 mmol/min), release of lactate (0.34+/-0.37 mmol/min), pyruvate (0 .08+/-0.06 mmol/min) and ketone bodies (0.04+/-0.02 mmol/min), while extrac tion of amino acids and free fatty acids was insignificant. In the acute li ver failure group, a normal hepatic venous oxygen saturation (0.69+/-0.12) and normal pyruvate/lactate ratio suggested absence of hypoxia even though the acetoacetate/beta -hydroxybutyrate ratio was decreased. Only in the acu te liver failure group did the measured splanchnic oxygen content differenc e exceed what could be accounted for even by hypothesizing complete oxidati on of all extracted blood-borne fuel substrates; oxidation of endogenous su bstrates may be quantitatively important in this condition. Conclusion: Acute liver failure was associated with a state of accelerated glycolysis in the splanchnic region, leading to release of lactate in the a bsence of splanchnic hypoxia.