Nu Cindy Chai1, Bizu Gelaye1, Gretchen E Tietjen1, Paul D Dash1, Barbara A Gower1, Linda W White1, Thomas N Ward1, Ann I Scher1, B Lee Peterlin2. 1. From the Department of Neurology (N.C.C., L.W.W., B.L.P.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Anesthesia (N.C.C.), University of California, San Francisco; Department of Epidemiology (B.G.), Harvard School of Public Health, Boston, MA; Department of Neurology (G.E.T.), University of Toledo, OH; Department of Neurology (P.D.D.), Johns Hopkins Community Physicians, Baltimore, MD; Department of Nutrition Sciences (B.A.G.), University of Alabama at Birmingham; Department of Neurology (T.N.W.), Dartmouth Hitchcock Medical Center, Lebanon, NH; and Uniformed Services University (A.I.S.), Bethesda, MD. 2. From the Department of Neurology (N.C.C., L.W.W., B.L.P.), Johns Hopkins University School of Medicine, Baltimore, MD; Department of Anesthesia (N.C.C.), University of California, San Francisco; Department of Epidemiology (B.G.), Harvard School of Public Health, Boston, MA; Department of Neurology (G.E.T.), University of Toledo, OH; Department of Neurology (P.D.D.), Johns Hopkins Community Physicians, Baltimore, MD; Department of Nutrition Sciences (B.A.G.), University of Alabama at Birmingham; Department of Neurology (T.N.W.), Dartmouth Hitchcock Medical Center, Lebanon, NH; and Uniformed Services University (A.I.S.), Bethesda, MD. lpeterlin@jhmi.edu.
Abstract
OBJECTIVE: To evaluate ictal adipokine levels in episodic migraineurs and their association with pain severity and treatment response. METHODS: This was a double-blind, placebo-controlled trial evaluating peripheral blood specimens from episodic migraineurs at acute pain onset and 30 to 120 minutes after treatment withsumatriptan/naproxen sodium vs placebo. Total adiponectin (T-ADP), ADP multimers (high molecular weight [HMW], middle molecular weight, and low molecular weight [LMW]), leptin, and resistin levels were evaluated by immunoassays. RESULTS:Thirty-four participants (17 responders, 17 nonresponders) were included. In all participants, pretreatment pain severity increased with every quartile increase in both the HMW:T-ADP ratio (coefficient of variation [CV] 0.51; 95% confidence interval [CI]: 0.08, 0.93; p = 0.019) and resistin levels (CV 0.58; 95% CI: 0.21, 0.96; p = 0.002), but was not associated with quartile changes in leptin levels. In responders, T-ADP (CV -0.98; 95% CI: -1.88, -0.08; p = 0.031) and resistin (CV -0.95; 95% CI: -1.83, -0.07; p = 0.034) levels decreased 120 minutes after treatment as compared with pretreatment. In addition, in responders, the HMW:T-ADP ratio (CV -0.04; 95% CI: -0.07, -0.01; p = 0.041) decreased and the LMW:T-ADP ratio (CV 0.04; 95% CI: 0.01, 0.07; p = 0.043) increased at 120 minutes after treatment. In nonresponders, the LMW:T-ADP ratio (CV -0.04; 95% CI: -0.07, -0.01; p = 0.018) decreased 120 minutes after treatment. Leptin was not associated with treatment response. CONCLUSIONS: Both pretreatment migraine pain severity and treatment response are associated with changes in adipokine levels. Adipokines represent potential novel migraine biomarkers and drug targets.
RCT Entities:
OBJECTIVE: To evaluate ictal adipokine levels in episodic migraineurs and their association with pain severity and treatment response. METHODS: This was a double-blind, placebo-controlled trial evaluating peripheral blood specimens from episodic migraineurs at acute pain onset and 30 to 120 minutes after treatment with sumatriptan/naproxen sodium vs placebo. Total adiponectin (T-ADP), ADP multimers (high molecular weight [HMW], middle molecular weight, and low molecular weight [LMW]), leptin, and resistin levels were evaluated by immunoassays. RESULTS: Thirty-four participants (17 responders, 17 nonresponders) were included. In all participants, pretreatment pain severity increased with every quartile increase in both the HMW:T-ADP ratio (coefficient of variation [CV] 0.51; 95% confidence interval [CI]: 0.08, 0.93; p = 0.019) and resistin levels (CV 0.58; 95% CI: 0.21, 0.96; p = 0.002), but was not associated with quartile changes in leptin levels. In responders, T-ADP (CV -0.98; 95% CI: -1.88, -0.08; p = 0.031) and resistin (CV -0.95; 95% CI: -1.83, -0.07; p = 0.034) levels decreased 120 minutes after treatment as compared with pretreatment. In addition, in responders, the HMW:T-ADP ratio (CV -0.04; 95% CI: -0.07, -0.01; p = 0.041) decreased and the LMW:T-ADP ratio (CV 0.04; 95% CI: 0.01, 0.07; p = 0.043) increased at 120 minutes after treatment. In nonresponders, the LMW:T-ADP ratio (CV -0.04; 95% CI: -0.07, -0.01; p = 0.018) decreased 120 minutes after treatment. Leptin was not associated with treatment response. CONCLUSIONS: Both pretreatment migraine pain severity and treatment response are associated with changes in adipokine levels. Adipokines represent potential novel migraine biomarkers and drug targets.
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