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  • Abstract lecture
  • A23

Pharmacogenetic assessments of treatment response in cluster headache

Appointment

Date:
Time:
Talk time:
Discussion time:
Location / Stream:
Strauss 2-3

Session

Precision medicine

Topics

  • Cluster headache
  • Genetics genomics | RNA

Authors

Anja Sofie Petersen (Glostrup/ DK), Mads Barloese (Glostrup/ DK; Hvidovre/ DK), Nunu Lund (Glostrup/ DK), Adam Sebastian Pedersen (Glostrup/ DK), Marie Louise Kulas Søborg (Glostrup/ DK), Mona Ameri Chalmer (Glostrup/ DK), Ida Callesen (Glostrup/ DK), Bendik Slagswold Winsvold (Oslo/ NO), John-Anker Zwart (Oslo/ NO), Sisse Rye Ostrowski (Copenhagen/ DK), Ole Birger Pedersen (Køge/ DK), Finn Thorup Sellebjerg (Glostrup/ DK), Helle Bach Søndergaard (Glostrup/ DK), Malene Bredahl Hansen (Glostrup/ DK), Rigmor Højland Jensen (Glostrup/ DK), Thomas Folkmann Hansen (Glostrup/ DK)

Abstract

Abstract text (incl. figure legends and references)

Background: The response to cluster headache treatments has a high interindividual variation. To date, treatment response has only been assessed by candidate gene approach and no investigations into metabolic pathways have been performed.

Question: To investigate the association between polygenetic risk of cluster headache and treatment response to first line cluster headache treatments. Additionally we investigated known functional variants of CYP3A4 and the response to verapamil1. Further, to replicate previous single nucleotide polymorphisms found to be associated with treatment response in cluster headache and/or migraine.

Methods: 508 cluster headache patients diagnosed according International Classification of Headache Disorders ere genotyped and participated in a semi-structured interview to evaluate treatment response. Polygenetic risk score was calculated by effect retrieved from meta-analyzing the latest two GWAS on cluster headache.

Results: We confirm previous findings that inferior treatment response associates with chronicity of cluster headache no evidence for response to first-line abortive and preventive treatment was predicted by a high genetic risk of cluster headache or functional variants of CYP3A4. We did not found support of the suggested genetic variants previously reported to be associated with treatment response to triptans or verapamil.

Conclusion: The clinically relevant variation in treatment response for cluster headache is unlikely to be influenced by genetic factors and other factors should be searched.

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