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Antihypertensive drugs and the risk of incident rosacea.

Br J Dermatol. 2014 Jan 16;

Authors: Spoendlin J, Voegel JJ, Jick SS, Meier CR

Abstract
BACKGROUND: Despite scarce evidence, use of calcium channel blockers is discouraged in rosacea patients, whereas beta-blockers are recommended as an off-label treatment for erythematotelangiectatic rosacea.
OBJECTIVES: To study the association between use of calcium channel blockers, beta-blockers, and other antihypertensive drugs and incident rosacea.
METHODS: We conducted a matched case-control study of antihiypertensive drugs and incident rosacea, using the UK-based General Practice Research Database. Cases had a first diagnosis of rosacea recorded between 1995 and 2009. Each case was matched to one control on age, sex, general practice, and years of history on the database before the index date. Drug use was stratified by timing (≤ or > 180 days before the index date) and duration (number of prescriptions) of drug exposure, in a multivariate conditional logisitic regression model.
RESULTS: Among 53,927 cases and 53,927 controls, we observed ORs around unity for calcium channel blockers across all strata, with a slightly decreased OR of 0.77 (95% CI 0.69-0.86) for current users of dihydropyridine calcium channel blockers with ≥40 prescriptions. Among beta-blockers, atenolol and bisoprolol yielded slightly decreased ORs across all exposure strata, whereas propranolol revealed ORs around 1.0, irrespective of timing and duration of exposure. Neither ACE-inhibitors nor angiotensin receptor blockers altered the relative rosacea risk.
CONCLUSIONS: Our data contradict the prevailing notion that calcium channel blockers increase the risk of rosacea. Beta-blocker use was associated with a slightly decreased risk of rosacea, but the effect may be somewhat stronger in patients with erythematotelangiectatic rosacea. This article is protected by copyright. All rights reserved.

PMID: 24428524 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/24428524?dopt=Abstract = URL to article

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