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Activation of Pain by Sumatriptan

Authors

  • David M. Coulter MB, ChB, DTM&H,

    1. From the Intensive Medicines Monitoring Programme, Department of Preventive and Social Medicine (Drs. Coulter and Clark) and the Department of Pharmacology and Toxicology (Dr. Clark), University of Otago, Dunedin, New Zealand; and the Netherlands Pharmacovigilance Centre Lareb, ‘s-Hertogenbosch (Drs. Passier and van Puijenbroek).
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  • J. L. M. (Anneke) Passier PhD,

    1. From the Intensive Medicines Monitoring Programme, Department of Preventive and Social Medicine (Drs. Coulter and Clark) and the Department of Pharmacology and Toxicology (Dr. Clark), University of Otago, Dunedin, New Zealand; and the Netherlands Pharmacovigilance Centre Lareb, ‘s-Hertogenbosch (Drs. Passier and van Puijenbroek).
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  • David W. J. Clark PhD, MPharm, FPS,

    1. From the Intensive Medicines Monitoring Programme, Department of Preventive and Social Medicine (Drs. Coulter and Clark) and the Department of Pharmacology and Toxicology (Dr. Clark), University of Otago, Dunedin, New Zealand; and the Netherlands Pharmacovigilance Centre Lareb, ‘s-Hertogenbosch (Drs. Passier and van Puijenbroek).
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  • Eugene P. Van Puijenbroek MD, PhD

    1. From the Intensive Medicines Monitoring Programme, Department of Preventive and Social Medicine (Drs. Coulter and Clark) and the Department of Pharmacology and Toxicology (Dr. Clark), University of Otago, Dunedin, New Zealand; and the Netherlands Pharmacovigilance Centre Lareb, ‘s-Hertogenbosch (Drs. Passier and van Puijenbroek).
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Address all correspondence to Dr. David M. Coulter, IMMP, Department of Preventive and Social Medicine, University of Otago, PO Box 913, Dunedin, New Zealand.

Abstract

Objective.—To demonstrate that sumatriptan may induce activation or aggravation of pain at sites of inflammation caused by trauma or disease.

Methods.—Case reports from the national pharmacovigilance centers of 2 countries, The Netherlands and New Zealand, are presented. These reports come from programs that use 2 methodologies to monitor drugs for adverse reactions: spontaneous reporting and a prospective observational cohort study. The potential mechanisms for pain production by sumatriptan are discussed in detail.

Results.—Thirteen case reports of activation of pain by sumatriptan following injury and 8 associated with inflammatory diseases are presented. Most patients had one or more positive rechallenges. This type of reaction occurred at a higher rate with the subcutaneous formulation than with the oral preparation. Pain mostly was severe but short-lasting; pain was prolonged in some patients with inflammatory disease.

Conclusions.—A strong association has been demonstrated between the use of sumatriptan and the production of pain at sites of inflammation, and there is a plausible pharmacological mechanism for this reaction. Pain activation may be a class effect of the selective serotonergic agonists used in the treatment of migraine.

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