Aneurysmal subarachnoid haemorrhage: effect of CRHR1 genotype on fatigue and depression.


Journal

BMC neurology
ISSN: 1471-2377
Titre abrégé: BMC Neurol
Pays: England
ID NLM: 100968555

Informations de publication

Date de publication:
18 Apr 2020
Historique:
received: 31 07 2019
accepted: 14 04 2020
entrez: 20 4 2020
pubmed: 20 4 2020
medline: 12 9 2020
Statut: epublish

Résumé

Emotional health disturbances are common after aneurysmal subarachnoid hemorrhage (aSAH) and their causes are largely unexplored. Corticotropin-releasing hormone receptor 1 (CRHR1) is a key factor in stress reactivity and development of mental health disturbances after adverse life-events. We explore the effect of CRHR1 genotype on mental health after aSAH in a retrospective cohort study. One hundred twenty-five patients have been assessed using EST-Q mental health questionnaire. Genotyping of CRHR1 single nucleotide polymorphisms (SNP-s) was performed (Rs7209436, Rs110402, Rs242924). Fatigue was present in almost half of aSAH patients, depression and anxiety in one-third. There was a high prevalence of insomnia and panic complaints. Rs110402 minor allele decreased the risk of depression (OR = 0.25, p = 0.027 for homozygotes). Depression was present in 14% vs 41% in minor and major allele homozygotes, respectively. Rs110402, Rs242924 and Rs7209436 minor alleles and TAT-haplotype, formed by them, were protective against fatigue. After Bonferroni correction only the association of Rs110402 with fatigue remained statistically significant (OR = 0.21, p = 0.006 for minor allele homozygotes). Results remained statistically significant when adjusted for gender, admission state, age and time from aSAH. In multiple regression analysis occurrence of fatigue was dependent on anxiety, modified Rankin score and Rs110402 genotype (R CRHR1 minor genotype was associated with a lower risk of fatigue and depression after aSAH. Genetic predisposition to mental health disturbances associated with negative life-events could be a risk factor for fatigue and depression after aSAH and selected patients might benefit from advanced counselling in the recovery phase.

Sections du résumé

BACKGROUND BACKGROUND
Emotional health disturbances are common after aneurysmal subarachnoid hemorrhage (aSAH) and their causes are largely unexplored. Corticotropin-releasing hormone receptor 1 (CRHR1) is a key factor in stress reactivity and development of mental health disturbances after adverse life-events.
METHODS METHODS
We explore the effect of CRHR1 genotype on mental health after aSAH in a retrospective cohort study. One hundred twenty-five patients have been assessed using EST-Q mental health questionnaire. Genotyping of CRHR1 single nucleotide polymorphisms (SNP-s) was performed (Rs7209436, Rs110402, Rs242924).
RESULTS RESULTS
Fatigue was present in almost half of aSAH patients, depression and anxiety in one-third. There was a high prevalence of insomnia and panic complaints. Rs110402 minor allele decreased the risk of depression (OR = 0.25, p = 0.027 for homozygotes). Depression was present in 14% vs 41% in minor and major allele homozygotes, respectively. Rs110402, Rs242924 and Rs7209436 minor alleles and TAT-haplotype, formed by them, were protective against fatigue. After Bonferroni correction only the association of Rs110402 with fatigue remained statistically significant (OR = 0.21, p = 0.006 for minor allele homozygotes). Results remained statistically significant when adjusted for gender, admission state, age and time from aSAH. In multiple regression analysis occurrence of fatigue was dependent on anxiety, modified Rankin score and Rs110402 genotype (R
CONCLUSIONS CONCLUSIONS
CRHR1 minor genotype was associated with a lower risk of fatigue and depression after aSAH. Genetic predisposition to mental health disturbances associated with negative life-events could be a risk factor for fatigue and depression after aSAH and selected patients might benefit from advanced counselling in the recovery phase.

Identifiants

pubmed: 32305063
doi: 10.1186/s12883-020-01727-y
pii: 10.1186/s12883-020-01727-y
pmc: PMC7165373
doi:

Substances chimiques

Receptors, Corticotropin-Releasing Hormone 0
CRF receptor type 1 5CLY6W2H1M

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

142

Subventions

Organisme : Eesti Teadusagentuur
ID : IUT20-46
Organisme : Eesti Teadusagentuur
ID : IUT20-46
Organisme : Eesti Teadusagentuur
ID : IUT2-4

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Auteurs

Artur Vetkas (A)

Tartu University Hospital, Tartu, Estonia. Artur.Vetkas@gmail.com.
Tartu University, Tartu, Estonia. Artur.Vetkas@gmail.com.

Ele Prans (E)

Tartu University, Tartu, Estonia.

Sulev Kõks (S)

Centre for Molecular Medicine and Innovative Therapeutics, Murdoch University, Perth, WA, Australia.
The Perron Institute for Neurological and Translational Science, Perth, WA, Australia.

Tõnu Rätsep (T)

Tartu University Hospital, Tartu, Estonia.
Tartu University, Tartu, Estonia.

Toomas Asser (T)

Tartu University Hospital, Tartu, Estonia.
Tartu University, Tartu, Estonia.

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Classifications MeSH