Liver, Pancreas, and Biliary TractSplanchnic and leg exchange of amino acids and ammonia in acute liver failure☆,☆☆
Section snippets
Patients
The study included 4 groups (Table 1). Group A (n = 8) consisted of healthy male controls. Group B (n = 5) included patients with chronic liver disease without hepatic encephalopathy (4 with alcoholic cirrhosis, 1 with primary biliary cirrhosis). Group C (n = 7) consisted of patients with AOCLD. The cause of acute exacerbation was alcoholic hepatitis in 4, upper gastrointestinal bleeding in 2 (bleeding was not present at the time of the study), and unknown in 1 patient. Group D (n = 22)
Arterial amino acid concentrations
In the ALF group, arterial concentrations of the individual amino acids were statistically significantly different from respective values in healthy controls, except those of HO-proline and tryptophan (Table 2). Arterial concentrations of most amino acids were higher in ALF than in the control group, but the BCAA and glutamic acid levels were lower (Table 2). Arterial concentrations of BCAAs (in μmol/L) were lower in cirrhotic (268 ± 48), AOCLD (193 ± 59 ), and ALF (272 ± 75) patients than in
Discussion
This is the first study to describe the splanchnic and leg exchange rates of amino acids in patients with ALF. ALF was associated with a net splanchnic uptake of glutamine and a net release of several amino acids, in particular alanine. Ammonia was also released in quantitatively important amounts in ALF. The finding that splanchnic exchange rates of ammonia and alanine were related to outcome indicates that the disturbance in ammonia metabolism may be a key pathological event in ALF. The leg
Acknowledgements
The authors thank L. Hansen, M. Poulsen, and N. Scherling for technical assistance with the analyses.
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2020, Neurochemistry InternationalCitation Excerpt :Selective deletion of Glul in the murine skeletal muscle suggests that the maximal capacity of ammonia absorption in skeletal muscle is approximately 10% (He et al., 2010b). Although this estimate is much lower than what was proposed in the past (50%; Hod et al., 1982; Lockwood et al., 1979), it should be kept in mind that skeletal muscle can upregulate Glul activity and therefore increase ammonia metabolism during liver failure (Hod et al., 1982; Desjardins et al., 1999; Clemmesen et al., 2000; Chatauret et al., 2006). The kidneys also adapt to the consequences of a failing liver by reducing ammonia release into the systemic circulation by slowing down ammonia production and by increasing ammonium (NH4+) excretion in the urine (Dejong et al., 1993; Jalan and Kapoor, 2003).
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Address requests for reprints to: Otto Clemmesen, M.D., Department of Hepatology, A-2121 Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. e-mail: [email protected]; fax: (45) 3545-2913.
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Supported by grants from the Danish Research Council (28809/96); Danish Medical Association Research Foundation (086.51/96); Medical Research Foundation for Copenhagen, Faeroe Islands, and Greenland (16/96); Danish Foundation for the Advancement of Medical Science (29/96 and 33/98); and Savaerksejer Jeppe Juhl & Hustru Ovita Juhls Mindelegat.