Vasodilators may have a protective effect against rosacea, results from a single-center retrospective cohort study showed.
“Our initial hypothesis was that perhaps antihypertensive agents might be associated with worsening rosacea,” one of the study authors, Jennifer G. Powers, MD, associate professor of dermatology at the University of Iowa, Iowa City, said in an interview. “What we found was exactly the opposite — that in fact their presence in a medical chart correlated with lower rates of rosacea diagnoses, as defined by ICD 9/10 codes.”
According to the researchers, who published their findings in the Journal of the American Academy of Dermatology, cases of acute vasodilator-induced rosacea have been reported, but no long-term association has been established. “In fact, many widely used antihypertensive medications modulate peripheral vascular tone,” they wrote. “Therefore, chronic use in patients with hypertension may reduce damage to peripheral vessels, and thus decrease risk of rosacea.”
To determine the correlates between vasodilator use and risk of rosacea, Powers and colleagues identified 680 hypertensive patients being treated with vasodilators or a thiazide diuretic in whom rosacea developed within 5 years of initiating therapy between June 1, 2006, and April 31, 2019.
Vasodilator therapies included angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), beta-blockers, and calcium channel blockers (CCBs). Patients on thiazide diuretics served as the control group. The researchers stratified the patients by age, gender, race, diabetes, chronic kidney disease, and coronary artery disease and calculated relative risk estimates comparing vasodilators with thiazides between strata.
Of the 680 patients, all but 40 were White; 127 were on thiazides, and the remaining 553 were on vasodilators. Overall, the researchers observed that use of vasodilators had a protective effect on the development of rosacea within 5 years, compared with thiazides (relative risk [RR], 0.56; P less than .0001). Specifically, the relative risk was 0.50 for ACE-inhibitors (P less than .0001); 0.69 for ARBs (P = .041); 0.55 for beta-blockers (P less than .0001); and 0.39 for CCBs (P less than .0001).
Powers and colleagues also observed significant inverse correlations in ACE-inhibitors, beta-blockers, and CCBs among White women aged 50 and older, but no significance was observed in non-White subgroups. The cohorts of patients with chronic kidney disease and coronary artery disease were too small for analysis.
“We were very surprised to find that many of the agents we think of as vasodilators might actually be beneficial for rosacea,” Powers said. “We would like to see these results reproduced in larger population studies. There are also potential questions about the mechanism at play. However, should these findings hold true, [it’s] all the more reason for our rosacea patients with hypertension to be managed well. They need not fear that those medications are worsening disease. Also, there might be new therapeutic options based on this data.”
The study received funding support from the National Center for Advancing Translational Sciences. The researchers reported having no financial disclosures.
One of Powers’ coauthors is her husband, Edward M. Powers, MD, a cardiology fellow at the University of Iowa. “We sometimes bounce ideas off one another and will talk about how systemic effects on the vasculature may impact skin disease,” she said, noting that they also published a report on statins and atopic dermatitis.
This article originally appeared on MDedge.com, part of the Medscape Professional Network.
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