Loop diuretics remain the cornerstone of heart failure management, yet they carry an often-overlooked metabolic cost. These medications increase renal clearance of thiamine (vitamin B1), a critical cofactor for pyruvate dehydrogenase—the enzyme responsible for converting carbohydrate-derived energy into ATP. Research by Hänninen et al. reveals that 33% of hospitalized heart failure patients are thiamine deficient, nearly triple the rate observed in control populations. Despite the measurable biochemical consequences of deficiency, thiamine status is not routinely monitored in standard clinical practice. Total body thiamine stores—only 25–30 mg—can be depleted within 2–3 weeks of chronic diuretic use without supplementation. This raises an important clinical question: should routine thiamine monitoring and supplementation become standard practice for patients on chronic loop diuretic therapy?
Was this article helpful?
