rss Posted February 18, 2021 Report Share Posted February 18, 2021 J Invest Dermatol. 2021 Feb 15:S0022-202X(21)00119-6. doi: 10.1016/j.jid.2021.02.002. Online ahead of print.ABSTRACTBACKGROUND: The pathogenesis of rosacea is incompletely understood. Signaling neuropeptides including pituitary adenylate cyclase-activating polypeptide (PACAP), a regulator of vasodilation and edema, are upregulated in rosacea skin. Here, we evaluated PACAP38-induced rosacea features and examined whether a 5-HT1B/1D receptor agonist could reduce these features.METHODS: A total of 35 patients with erythematotelangiectatic rosacea received an intravenous infusion of 10 pmol/kg/min of PACAP38 followed by an intravenous infusion of 4 mg sumatriptan or placebo (saline) on two study days in a double-blind, randomized, placebo-controlled and crossover trial.RESULTS: PACAP38 increased facial skin blood flow by 90%, dilated the superficial temporal artery by 56%, and induced prolonged flushing and facial edema. Compared with placebo, sumatriptan reduced PACAP38-induced facial skin blood flow for 50 mins (p = 0.023), constricted the superficial temporal artery for 80 mins (p = 0.010) and reduced duration of flushing (p = 0.001) and facial edema (p < 0.001).CONCLUSIONS: We established a clinical experimental model of rosacea features and showed that sumatriptan was able to attenuate PACAP38-induced rosacea flushing and edema. Findings support a key role of PACAP38 in rosacea flushing pathogenesis. It remains unknown whether PACAP38 inhibition can improve rosacea.PMID:33600826 | DOI:10.1016/j.jid.2021.02.002{url} = URL to article Link to comment Share on other sites More sharing options...
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