Peroral galactose torelance test with and without peroral ethanol loading : Special reference to evaluation of serum galactose value and lactate/pyruvate ratio as a index of redox state of hepatocytes

To elucidate relationship between galactose metabolism, ethanol metabolism and hepatic NAD/NADH ratio (redox state in hepatocytes), peroral galactose tolerance test (GAL 1) using 40g galactose were performed on 40 normal subjects and on 139 patients with various liver diseases including fatty liver, chronic hepatitis (inactive stage), alcoholic liver disease, chronic hepatitis (active stage) and liver cirrhosis. The test revealed that severe liver diseases such as liver cirrhosis and chronic hepatitis (active stage) had deminished galactose elimination and usefulness of this test as a diagnostic tool was confirmed. Although there was no correlation between lactate/pyruvate ratio (L/P ratio) and serum galactose, changes of L/P ratio and serum galactose concentration after galactose loading must reflect redox state of hepatocytes, respectively. Within 2 days from performance of GAL 1, second peroral galactose test with simultaneous oral ethanol loading (GAL 2) were done on randomly selected 33 normal subjects and 74 patients with various liver diseases. The GAL 2 demonstrated further elevation of serum galactose concentration in normal subjects and patients with various liver diseases except for patients with liver cirrhosis in whom further elimination of galactose was attenuated. The reason for this unexpected result was explained by poor capacity of hepatic redox state in advanced liver diseases. L/P ratio during GAL 2 also demonstrated further elevation in normal subjects and patients with various liver diseases, paticularly in patients with alcoholic liver diseases suggesting disturbed hepatic redox state was the most reliable candidate of cause of this illness. During peroral galactose test with ethanol, blood acetaldehyde concentration were determined. There was no demonstrable elevation of blood acetaldehyde concentration in patients with alcoholic liver diseases so that hypothesis insisting acetaldehyde as a cause of this illness was uncertain.