Literature DB >> 22823064

CYP1A2 polymorphisms in slow melatonin metabolisers: a possible relationship with autism spectrum disorder?

W Braam1, H Keijzer, H Struijker Boudier, R Didden, M Smits, L Curfs.   

Abstract

BACKGROUND: In some of our patients with intellectual disabilities (ID) and sleep problems, the initial good response to melatonin disappeared within a few weeks after starting treatment. In these patients melatonin levels at noon were extremely high (>50 pg/ml). We hypothesise that the disappearing effectiveness is associated with slow metabolisation of melatonin because of a single nucleotide polymorphism (SNP) of CYP1A2.
METHOD: In this pilot study we analysed DNA extracted from saliva samples of 15 consecutive patients with disappearing effectiveness of melatonin. Saliva was collected at noon and 4 pm for measuring melatonin levels.
RESULTS: In all patients' salivary melatonin levels at noon were >50 or melatonin half time was > 5 h. A SNP was found in eight of 15 patients. The allele 1C was found in two patients and in six patients the 1F allele was found.
CONCLUSIONS: Of 15 patients with disappearing effectiveness of melatonin, seven were diagnosed with autism spectrum disorder, and in four of them a SNP was found. The other eight patients were known with a genetic syndrome. In six of them behaviour was considered to be autistic-type and in three of them a SNP was found. This finding may give a new direction for research into the genetic background of autism.
© 2012 The Authors. Journal of Intellectual Disability Research © 2012 John Wiley & Sons Ltd, MENCAP & IASSID.

Entities:  

Keywords:  CYP1A2; autism; melatonin; polymorphism; poor metaboliser

Mesh:

Substances:

Year:  2012        PMID: 22823064     DOI: 10.1111/j.1365-2788.2012.01595.x

Source DB:  PubMed          Journal:  J Intellect Disabil Res        ISSN: 0964-2633


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