Short-chain fatty acids cause reversible coma in animals and may contribute to the pathogenesis of the hepatic coma in humans. The concentrations of short-chain fatty acids in peripheral venous blood were significantly elevated in 15 patients with hepatic encephalopathy caused by cirrhosis (362 ± 83 μmol/L; mean ± S.E.M.) compared with 17 cirrhotic patients without encephalopathy (178 ± 57 μmol/L) and 11 normal individuals (60 ± 8 μmol/L). However, no correlation between the depth of coma and the level of short-chain fatty acids was found after repetitive measurements in the coma group. Compared with normal individuals, all short-chain fatty acids, except valerate, were elevated in patients with hepatic encephalopathy, whereas only the concentrations of isobutyrate and isovalerate were significantly elevated in cirrhotic patients without encephalopathy.
The concentrations of short-chain fatty acids in 21 nonencephalopathic cirrhotic patients who underwent catheterization were equally distributed in the aorta (187 ± 56 μmol/L), the hepatic vein (212 ± 75 μmol/L), the azygos vein (140 ± 37 μmol/L) and the renal vein (135 ± 43 μmol/L) compared with peripheral venous blood (178 ± 57 μmol/L).
This study does not support the idea that short-chain fatty acids are of major importance in the pathogenesis of hepatic coma in patients with cirrhosis. (HEPATOLOGY 1991;14:1040–1045.)