A chronic alcoholic patient is diagnosed with gouty arthritis. This condition involves the accumulation of urate crystals in the joints due to elevated uric acid levels in the blood. Let's explore the biochemical changes associated with alcohol consumption that could lead to this condition.
Alcohol metabolism and biochemical impact: Ethanol in alcohol is primarily metabolized in the liver through two key enzymes:
Alcohol dehydrogenase (ADH)
Aldehyde dehydrogenase (ALDH)
These enzyme-catalyzed reactions convert ethanol to acetaldehyde and then to acetate. In this process, NAD+ is reduced to NADH. Thus, chronic alcohol consumption results in an increased NADH/NAD+ ratio.
Effect on lactate and urate levels: The high NADH/NAD+ ratio favors the conversion of pyruvate to lactate, leading to lactic acidosis. This reduces kidney clearance of uric acid, thereby increasing blood urate levels.
Biochemical change
Impact
Increased NADH/NAD+ ratio
Favored conversion of pyruvate to lactate
Increased lactate levels
Reduced uric acid excretion (competition at renal tubules)
Increased urate levels
Accumulation leads to gouty arthritis
The correct option is: Increased urate and lactate levels. This scenario explains why alcohol consumption exacerbates gouty arthritis through elevated urate and lactate, driven by changes in biochemical pathways related to alcohol metabolism.