Hydrochlorothiazide and Gout: When Treatment Becomes the Trigger
Patient Background:
Mrs. Jim is a 68-year-old female recently diagnosed with essential hypertension. Her provider initiated hydrochlorothiazide 25 mg once daily, resulting in satisfactory blood pressure control.
Clinical Presentation:
After several months of therapy, Mrs. Jim presented with pain, redness, and swelling in her right first metatarsophalangeal joint (big toe). Laboratory investigations revealed elevated serum uric acid levels, consistent with acute gout. To manage the episode, her provider prescribed naproxen for pain and inflammation, and allopurinol to lower uric acid levels long-term.
Clinical Issue Identified:
The underlying cause of the patient’s gout was hydrochlorothiazide-induced hyperuricemia, a well-documented adverse effect of thiazide diuretics. By reducing renal excretion of uric acid, hydrochlorothiazide can precipitate gout flares, particularly in susceptible older adults.
In this scenario, the addition of allopurinol and naproxen representedA Prescribing Cascade.
“the initiation of new medications to treat an adverse effect caused by an existing drug, rather than addressing the original cause”
Pharmacist Intervention and Clinical Management:
Medication Review and Causality Assessment:
Identify hydrochlorothiazide as the likely precipitating factor for gout.
Evaluate the necessity of continuing hydrochlorothiazide, especially given the dose (25 mg daily) and the onset of adverse metabolic effects.
Therapeutic Optimization:
Option 1: Reduce the hydrochlorothiazide dose to 12.5 mg daily, as lower doses are associated with fewer uric acid elevations while maintaining antihypertensive efficacy.
Option 2: Consider alternative antihypertensives such as:
ACE inhibitors (e.g., lisinopril)
ARBs (e.g., losartan, which has mild uricosuric properties)
Calcium channel blockers (e.g., amlodipine)
Discontinue hydrochlorothiazide if blood pressure can be adequately managed with alternative agents.
Gout and Pain Management:
Continue short-term NSAID (naproxen) for acute flare control as needed, monitoring renal function and gastrointestinal tolerance.
Reassess the need for allopurinol once hydrochlorothiazide has been modified or discontinued. In many cases, uric acid levels normalize after removal of the precipitating agent.
Monitoring and Follow-Up:
Repeat serum uric acid, renal function, and electrolyte levels within 4–6 weeks after therapy adjustment.
Monitor blood pressure response after switching or lowering the thiazide dose.
Educate the patient on gout triggers, hydration, and the importance of adherence to revised therapy.
Clinical Rationale and Ramifications
This case exemplifies a prescribing cascade, where an adverse effect of one medication leads to the unnecessary addition of others. Instead of addressing the root cause—thiazide-induced hyperuricemia—the provider initiated two new medications (allopurinol and naproxen), exposing the patient to additional risks such as renal impairment, gastrointestinal bleeding, and polypharmacy.
Early recognition of drug-induced causes can prevent such cascades. By reassessing the necessity and dose of hydrochlorothiazide, and considering safer antihypertensive alternatives, the provider can simplify Mrs. Jim’s regimen, minimize medication burden, and prevent future gout flares.
This case reinforces the importance of critical medication review, dose individualization, and interprofessional collaboration in preventing avoidable adverse effects and ensuring rational, evidence-based pharmacotherapy in older adults.