A Closer Look at Thiazides as Treatment for Hypertension for Patients with Gout

Internal Medicine World ReportAugust 2014

For patients with hypertension, finding the right course of treatment can be critically important especially when other health factors are taken into consideration.

For patients with hypertension, finding the right course of treatment can be critically important especially when other health factors are taken into consideration.

Brian Mandell, MD, PhD, of the Cleveland Clinic looked at the impact taking thiazides has for patients who were being treated for hypertension and gout. He also observed what possible implications are for switching medications during treatment.

Mandell said in his own practice he works to “use a thiazide if it helps to control the blood pressure and to adjust the dose of hypouricemic therapy as needed to reduce the serum urate to the desired level.”

In his study, Mandell said thiazides are a common tool in fighting hypertension despite previous studies showing they have been known to raise serum urate levels.

When approaching strictly the patient’s hypertension condition, Mandell noted many will not reach the desired blood pressure set by their doctors.

“The reasons for failing to reach target pressures are complex and many: physicians may simply not be aggressive enough in pursuing a target blood pressure; patients cannot tolerate the drugs or cannot afford the drugs; and many patients need two or my antihypertensive drugs to control adequate control,” he noted.

It is that last category, which Mandell said thiazides prove the most popular, as he described them as “cheap and effective and work synergistically with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.”

Another problem cited by Mandell is that an alternative to thiazides like loop diuretics can also raise serum urate levels in patients. “Switching to one of them will not eliminate concern over hyperuricemia,” he noted.

When looking at patients taking hydrochlorothiazide in doses of either 12.5 or 25mg once per day, Mandell said the serum urate levels appear to increase around .8 mg/dL or possibly even less for patients with normal renal function. Citing other sources he said patients taking chlorthalidone see similar results.

For patients taking xanthine oxidase inhibitors for gout and looking to lower their serum urate to the American College of Rheumatology’s goal level of less than 6.0 mg/dL, Mandell said, “this small elevation in serum urate is unlikely to negate the clinical efficacy of these drugs when dosing is optimized.”

“When I add a thiazide to a patient’s regimen, I do not usually need to increase the dose of allopurinol significantly to keep the serum urate level below the desired target,” he said.

One treatment option Mandell’s study looked at was switching antihypertensive therapies during treatment, especially when serum urate levels rise “marginally,” above the estimated precipitation threshold of 6.7mg/dL. A drug like losartan, he said, would provide the patient a medication that would reduce serum urate levels and control their blood pressure without needing to take more than one prescription.

“This decision must be individualized, taking into consideration the efficacy and cost of the alternative antihypertensive drug, as well as the potential but as yet unproven cardiovascular and renal benefits of lowering the serum urate with a more potent hypouricemic to a degree not likely to be attained with losartan alone,” he added.

A second option he explored was leaving the patient on the thiazide medication and adjusting their gout therapy. This, he said is a viable choice for healthcare providers and patients depending on their situations. “Taking this course of action will not worsen the control of the serum urate level or gouty arthritis, and in most patients will not complicate the management of gout,” he commented.

One warning Mandell gave was that patients should not take low doses of aspirin for “cardioprotection,” if they have hyperuricemia or gout as the medication could affect serum rate level controls. He commented results have shown even the low dose can increase the levels by nearly .3 mg/dL.

“Since patients with gout have a higher risk of having cardiovascular disease, metabolic syndrome, and a chronic kidney disease, many will benefit from low-dose aspirin therapy.”

Related Videos
Video 6 - "Evaluating Safety of Novel LDL Management Mechanism"
Video 5 - "Optimizing PCSK9 Inhibitors and Analyzing Plaque Reduction Data"
Video 4 - "Innovations in Small Interfering RNA (siRNA) Therapy"
Video 3 - "Ongoing Lp(a) Trials and Clinical Approaches to Treatment"
Roger S. McIntyre, MD: GLP-1 Agonists for Psychiatry?
Payal Kohli, MD | Credit: Cherry Creek Heart
Matthew Nudy, MD | Credit: Penn State Health
Kelley Branch, MD, MSc | Credit: University of Washington Medicine
Kelley Branch, MD, MS | Credit: University of Washington Medicine
David Berg, MD, MPH | Credit: Brigham and Women's
© 2024 MJH Life Sciences

All rights reserved.