Medizinische Universität Graz - Research portal

Go directly to the nagivation.
Go directly to the content.

Navigation/Search

Selected Publication:

SHR Neuro Cancer Cardio Lipid Metab Microb

Klintschar, M; Reichenpfader, B; Saternus, KS.
A functional polymorphism in the tyrosine hydroxylase gene indicates a role of noradrenalinergic signaling in sudden infant death syndrome.
J Pediatr. 2008; 153(2): 190-193. Doi: 10.1016/j.jpeds.2008.02.032
Web of Science PubMed FullText FullText_MUG

Co-authors Med Uni Graz: Reichenpfader Barbara
Altmetrics:
Dimensions Citations:
Plum Analytics:
Scite (citation analytics):
Abstract:: OBJECTIVES: Catecholamines may contribute to the cause of sudden infant death syndrome (SIDS). TH01, a tetrameric short tandem repeat marker in the tyrosine hydroxylase gene, regulates gene expression and catecholamine production. STUDY DESIGN: We investigated TH01 in 172 German Caucasian SIDS cases and 390 sex- and age-matched control subjects. RESULTS: The *9.3 alleles were more frequent in patients with SIDS than in control subjects (40.12% vs 31.15%; P = .006). For homozygotes the odds ratio was 1.83 (95% confidence interval: 1.09-3.05), for carriers 1.58 (1.09-2.28). Moreover, *9.3 alleles were significantly more frequent during the winter (47.73% vs 35.38% in the warmer seasons), and the frequency of *9.3 alleles varied significantly with the age at death (weeks 7 to 12: 49.04% vs 29.63% within the first 6 weeks). Other risk factors (sleeping position, gestation, smoking) had no significant impact on the frequency of *9.3. CONCLUSIONS: Our results indicate a relationship between SIDS and TH01 genotype, presumably caused by an impairment of breathing regulation or arousal. We propose that noradrenalinergic neuronal activity contributes to the cause of a major subset of SIDS victims. Moreover, the results further stress that SIDS is a highly heterogenic group.
Find related publications in this database (using NLM MeSH Indexing): Autopsy -; Case-Control Studies -; Catecholamines - metabolism; Female -; Gene Expression Regulation, Enzymologic -; Genetic Markers -; Genetic Predisposition to Disease -; Humans -; Infant -; Male -; Polymorphism, Genetic -; Signal Transduction -; Sudden Infant Death - genetics; Tyrosine 3-Monooxygenase - genetics