Low-Dose Hydrochlorothiazide-Induced Podagra Triggered by Seasonal Environmental Factors: A Case Report

Abstract

Aim: To highlight a rare case of thiazide-induced podagra at a low dose of hydrochlorothiazide in the context of seasonal and environmental influences. Presentation of Case: A 52-year-old male with ischemic heart disease and hypertension, on long-term hydrochlorothiazide (12.5 mg) for 10 years, presented in early summer with acute pain, swelling, and redness of the left great toe. Laboratory investigations revealed slightly elevated serum uric acid (7.4 mg/dL). Hydrochlorothiazide was identified as the potential culprit drug and subsequently discontinued, while antihypertensive therapy was continued with telmisartan. The patient responded to treatment with prednisolone after NSAIDs were stopped due to drug interactions with anticoagulation therapy. He improved clinically and was discharged hemodynamically stable. Discussion: Although thiazide-induced hyperuricemia and gout are typically associated with higher doses, this case demonstrates that long-term use of even a low dose (12.5 mg) may precipitate podagra, particularly in the setting of seasonal and climatic risk factors. Temperature and humidity variations during early summer may exacerbate uric acid crystallization and trigger gout flares, especially in predisposed individuals. Thiazides promote hyperuricemia via altered renal urate handling, an effect amplified by genetic and environmental contributors. The case underscores the need to balance thiazide efficacy in hypertension against its metabolic side effects and consider alternative antihypertensives, such as losartan, in high-risk patients. Conclusion: This report reinforces that hydrochlorothiazide can induce podagra even at low doses after long-term use, with seasonal and environmental factors serving as additional triggers. Careful monitoring of serum uric acid and consideration of alternative therapies are essential in the long-term management of hypertensive patients on thiazides.