Step 1: Understanding the Question:
The patient has signs of "Beriberi": symmetrical neuropathy (Dry Beriberi) and heart failure (Wet Beriberi).
We must link this deficiency to the long-term use of diuretics like hydrochlorothiazide.
Step 2: Detailed Explanation:
Clinical Presentation: Symmetrical paresthesia and peripheral neuropathy point to neurologic involvement, while heart failure (typically high-output) points to cardiovascular involvement. This classic combination defines Thiamine (Vitamin B1) deficiency.
Mechanism of Drug-Induced Deficiency: Thiamine is a water-soluble vitamin. Chronic use of diuretics (especially loop diuretics and thiazides like hydrochlorothiazide) increases the renal excretion of thiamine.
Role of Thiamine: Thiamine pyrophosphate (TPP) is a mandatory cofactor for Pyruvate Dehydrogenase and Alpha-ketoglutarate Dehydrogenase. Without it, aerobic metabolism is impaired, particularly in the brain and heart.
Beriberi Types:
Dry Beriberi: Predominantly neurological (polyneuritis, muscle wasting).
Wet Beriberi: Predominantly cardiovascular (dilated cardiomyopathy, edema, heart failure).
Evaluating other options: While B12 (C) causes neuropathy, it does not typically cause the acute high-output heart failure associated with this presentation and diuretic use. Selenium, Zinc, and B12 are not primarily depleted by thiazide use in this manner.
Step 3: Final Answer:
Thiamine deficiency (Beriberi) is a recognized complication of long-term diuretic therapy due to increased urinary loss of the vitamin.