Continuous Use of NSAIDs Increases Hypertension Risk in AS Patients, Study Suggests

Continuous Use of NSAIDs Increases Hypertension Risk in AS Patients, Study Suggests

Continuous use of non-steroidal anti-inflammatory drugs (NSAIDs) increases the risk of hypertension by 12% in people with ankylosing spondylitis (AS), a prospective study suggests.

The study, “Nonsteroidal Anti-inflammatory Drug use is Associated with Incident Hypertension in Ankylosing Spondylitis,” was published in the journal Arthritis Care & Research.

NSAIDs are a first line treatment to manage AS, but analyses of clinical trials reported that these medications are linked to increased blood pressure in healthy and hypertensive individuals. This raised a concern that NSAIDs may increase the risk of cardiovascular events in AS patients, a population with a high prevalence of cardiovascular risk factors.

Yet, population-based studies suggest that NSAIDs may be cardioprotective for people with AS, by reducing chronic inflammation and thereby help prevent cardiovascular disease.

To better assess the association between NSAIDs and hypertension in these patients, researchers at the University of Washington and colleagues analyzed data from 628 adults who did not have hypertension from the Prospective Study of Outcomes in AS (PSOAS) group, and who also had at least one-year of follow-up. Five study sites participated in PSOAS, four in the U.S. and one in Australia.

The mean age of the patients was 39 years, and the majority (72%) were men. AS symptoms lasted for 16 years on average with a mean Ankylosing Spondylitis Disease Activity Score of 2, which is in the upper limit of low disease activity.

As for treatment, 43% of patients were taking biologic medications, mostly TNF inhibitors (TNFi), which included Enbrel (etanercept), Humira (adalimumab), and infliximab (brand names Remsima and Remicade).

Hypertension was defined as a systolic blood pressure equal or above 140 mm Hg and a diastolic pressure equal or above 90 mm Hg. Patients who reported the use of anti-hypertensive medication were also considered to have hypertension.

Results showed that 200 patients were on continuous use of NSAIDs, while the remaining 428 used these therapies in low doses or not at all.

Also, 2% of the patients had cardiovascular disease, 1% had diabetes and 3% were taking statins, a cholesterol-lowering treatment.

During a median period of seven years, 129 patients developed hypertension. Among this group, 52 (40%) participants were using NSAIDs continuously, while 60 were on TNFi (47%). Twenty-one (16%) were on both medications.

Further analysis revealed that continuous use of NSAIDs was associated with a 12% increased likelihood of hypertension compared with the non-continuous or non-use of these therapies.

Older age, TNFi use, and disease activity were also significant predictors of hypertension, although they carried a smaller risk than NSAIDs.

“Our findings support the hypothesis that NSAID use has negative effects on an important CV [cardiovascular] risk factor in a population that is known to be at-risk for CVD [cardiovascular disease],” the researchers wrote.

“[F]urther studies can inform the revision of guidelines to address the management of CV risk factors and CVD in AS,” they added.

Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.

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