Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation

Research output: Contribution to journalJournal articleResearchpeer-review

  1. Telemedicine in headache care: A systematic review

    Research output: Contribution to journalReviewpeer-review

  2. A history of International Headache Society grants and their impact on headache careers

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Guidelines of the International Headache Society for Clinic-Based Headache Registries, 1st edition

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Intravenous fosphenytoin as treatment for acute exacerbation of trigeminal neuralgia: A prospective systematic study of 15 patients

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. Debate: Are cluster headache and migraine distinct headache disorders?

    Research output: Contribution to journalComment/debateResearchpeer-review

  2. CGRP-induced migraine-like headache in persistent post-traumatic headache attributed to mild traumatic brain injury

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

BACKGROUND: Pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) and vasoactive intestinal polypeptide can provoke cluster headache attacks in up to half of cluster headache patients in their active phase. At present, it is unknown whether provoked attacks are mediated via calcitonin gene-related peptide or mast cell activation.

METHODS: All enrolled patients with cluster headache were randomly allocated to receive a continuous infusion of either PACAP38 (10 pmol/kg/min) or vasoactive intestinal polypeptide (8 pmol/kg/min) over 20 min. We collected clinical data and measured plasma levels of calcitonin gene-related peptide and markers of mast cell activation (tryptase and histamine) at fixed time points: at baseline (T0), at the end of the infusion (T20), 10 min after the infusion (T30), and 70 min after the infusion (T90).

RESULTS: Blood was collected from episodic cluster headache patients in active phase (n = 14), episodic cluster headache patients in remission (n = 15), and chronic cluster headache patients (n = 15). At baseline, plasma levels of calcitonin gene-related peptide, tryptase, and histamine were not different among the three study groups. Plasma levels of calcitonin gene-related peptide (p = 0.7074), tryptase (p = 0.6673), or histamine (p = 0.4792) remained unchanged during provoked attacks compared to attack-free patients.

CONCLUSION: Cluster headache attacks provoked by either PACAP38 or vasoactive intestinal polypeptide were not accompanied by alterations of plasma calcitonin gene-related peptide, tryptase or histamine. The provoked attacks may not be mediated by calcitonin gene-related peptide or mast cell activation.Trial Registration: The study is registered at ClinicalTrials.gov (NCT03814226).

Original languageEnglish
JournalCephalalgia : an international journal of headache
Volume42
Issue number8
Pages (from-to)687-695
Number of pages9
ISSN0333-1024
DOIs
Publication statusPublished - Jul 2022

    Research areas

  • CGRP, cluster headache, histamine, PACAP, tryptase

ID: 70268812