The most probable diagnosis for this patient is Alcohol- related Liver disease. It is not apparent from the history but the patient must had been a hidden alcoholic and had consumed alcohol in excess during his business trip. The points in favor of the diagnosis are as follows-
1) The levels of transaminases are high
The transaminases are markers of cell necrosis, and in most cases, the serum ALT( Alanine amino transferase) is higher than the AST(Aspartateamino transferase). However, this patient’s serum AST is higher than the serumALT, and his serum GGT (Gamma Glutamyl transpeptidase) is disproportionately elevated over the serum ALP (Alkaline phosphatase). GGT is a marker of alcoholism. Both ALP and GGT rise in obstructive liver diseases.
This enzyme relationship (GGT high and normal ALP) in this patient is characteristic of alcohol-related liver disease. Alcohol is a mitochondrial poison, and AST is primarily located in the mitochondria, hence it is preferentially elevated over the ALT. Alcohol also induces the synthesis of GGT rather than of ALP. Thus, the patient has alcohol-related liver disease rather than a viral hepatitis or obstructive liver disease.
Alcohol intake also explains the patient’s hypoglycemia and memory problems. In the metabolism of alcohol, NADH is increased, which results in the reversal of all the normal NAD: NADH reactions,one of which is pyruvate to lactate. Since pyruvate is an intermediate of pathway of gluconeogenesis, its conversion to lactate reduces its concentration, so fasting hypoglycemia may occur. Recall that the brain requires glucose as a fuel; therefore, fasting hypoglycemia results in mental status abnormalities (neuroglycopenia) in these patients.
3) Hyperuricemia –
Hyperuricemia in this patient is likely due to the increase in lactic acid and Beta hydroxy butyric acid (Ketone body) formation. Both these products compete with uric acid for excretion in the proximal tubule, as they share a common transporter. Uric acid is retained while the other two products are excreted.
The synthesis of ketone bodies is increased in alcoholism owing to the increase in acetyl-CoA as the end product of alcohol metabolism and its conversion into ketone bodies by the liver. The increase in NADH produced from the metabolism of alcohol drives the reaction from acetoacetic acid to beta hydroxy butyrate.(Acetone , Acetoacetate and beta hydroxybutyrate are the three ketone bodies. Acetoacetate is the primary ketone body,acetone is produced by spontaneous decarboxylation of Acetoacetate, while beta hydroxybutyrate is produced from reduction of Acetoacetate)
Hence, people with alcoholism commonly have two causes for metabolic acidosis: lactic acidosis and ketoacidosis. Approximately 20% of patients with Hyperuricemia will develop gout.