Plasma levels of VIP are not elevated during PACAP- and VIP-induced cluster headache attacks: an exploratory study

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Dokumenter

  • Fulltext

    Forlagets udgivne version, 0,99 MB, PDF-dokument

Background: Pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) provoked cluster headache attacks in individuals with episodic cluster headache during their active phase and individuals with chronic cluster headache. In this study, we investigated whether infusions of PACAP and VIP caused alterations in plasma levels of VIP and their potential contribution to induced cluster headache attacks. Methods: Participants received either PACAP or VIP infusion for 20 min on 2 separate days with an interval of at least 7 days in between. Blood collection was performed at T0, T20, T30, and T90. Plasma levels of VIP were measured using a validated radioimmunoassay method. Results: Blood samples were collected from participants with episodic cluster headache in the active phase (eCHA, n = 14), remission (eCHR, n = 15), and from participants with chronic cluster headache (cCH, n = 15). Baseline levels of VIP did not differ among the three groups (p = 0.1161). During PACAP infusion, mixed-effects analysis revealed a significant increase in plasma levels of VIP in eCHA (p = 0.0300) and eCHR (p = 0.0058) but not in cCH (p = 0.2930). We found no difference in the increase of plasma VIP levels between patients who developed PACAP38- or VIP-induced attacks. Conclusion: Cluster headache attacks induced by PACAP38 or VIP infusion are not associated with changes in plasma levels of VIP. Further studies are needed to investigate the role of VIP and the parasympathetic system in cluster headache. Clinical trial registration: The parent study is registered at ClinicalTrials.gov (NCT03814226).

OriginalsprogEngelsk
Artikelnummer1135246
TidsskriftFrontiers in Neurology
Vol/bind14
Antal sider8
ISSN1664-2295
DOI
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
The study was funded by grants from Lundbeckfonden (grant R252-2017-1317) and the Research Foundation of Rigshospitalet. CD was supported by an IHS research fellowship grant. MA was supported by the Lundbeck Foundation Professor Grant (R310-2018–3711). Funding sources had no influence on study design, patient inclusion, or data interpretation. JH is supported by the Danish Biotechnology Center for Cellular Communication.

Funding Information:
MA reported receiving personal fees from AbbVie, Allergan, Amgen, Eli Lilly, Lundbeck, Novartis, Pfizer and Teva Pharmaceuticals during the conduct of the study. MA reported serving as Associate Editor of Cephalalgia, Associate Editor of The Journal of Headache and Pain, and Associate Editor of Brain. AS and LP are currently employed at Lundbeck. The opinions expressed in this manuscript are solely their own and do not express the views or opinions of Lundbeck. RJ reported fees from lectures for Pfizer, Eli-Lilly, Merck, TEVA, Novartis, Lundbeck and Allergan and that she has been or is investigator in clinical trials with Eli-Lilly, Novartis and Lundbeck. She is also director of Danish Headache Center, Lifting The Global Burden of Headache and director of Master of Headache Disorders at University of Copenhagen. She has received research funding from the University of Copenhagen, Rigshospitalet, Lundbeck Foundation, The Medical Society in Copenhagen, NovoNordisk Foundation, and Tryg Foundation. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher Copyright:
Copyright © 2023 Deligianni, Pellesi, Chaudhry, Haulund Vollesen, Snoer, Hannibal, Jensen and Ashina.

ID: 364549098