INTRAUTERINE GROWTH-PATTERN AND RISK OF CHILDHOOD-ONSET INSULIN-DEPENDENT (TYPE-I) DIABETES - POPULATION-BASED CASE-CONTROL STUDY

Citation
G. Dahlquist et al., INTRAUTERINE GROWTH-PATTERN AND RISK OF CHILDHOOD-ONSET INSULIN-DEPENDENT (TYPE-I) DIABETES - POPULATION-BASED CASE-CONTROL STUDY, BMJ. British medical journal, 313(7066), 1996, pp. 1174-1177
Citations number
17
Categorie Soggetti
Medicine, General & Internal
ISSN journal
09598138
Volume
313
Issue
7066
Year of publication
1996
Pages
1174 - 1177
Database
ISI
SICI code
0959-8138(1996)313:7066<1174:IGAROC>2.0.ZU;2-X
Abstract
Objective-To investigate whether prenatal growth affects the risk of d evelopment of childhood onset insulin dependent (type I) diabetes mell itus. Design-Population based case-control study. Setting-Data from a nationwide childhood diabetes case register were linked with data from the nationwide Swedish Medical Birth Registry. Subjects-Data from a t otal of 4584 diabetic children born after 1973 and diagnosed with diab etes from 1978 to 1992 were studied. For each child with insulin depen dent diabetes three control children were randomly selected from among all infants born in the same year and at the same hospital as the pro band. Main outcome measures-Birth, weight, gestation, maternal age and parity, number of previous spontaneous abortions, and sex specific bi rth weight by gestational week expressed as multiples of the standard deviation (SD). Results-There was a clear trend in the odds ratio for childhood onset diabetes according to SD of birth weight. The odds rat io (95% confidence interval) for small for gestational age after strat ification for maternal age, parity, smoking habits, and maternal diabe tes was 0.81 (0.65 to 0.99) and for large for gestational age after si milar stratification was 1.20 (1.02 to 1.42). Conclusions-Intrauterine conditions that affect prenatal growth seem also to affect the risk o f development of childhood diabetes in the way previously described fo r postnatal growth: a poor growth decreases and an excess growth incre ases the risk. The mechanism for this association is unclear.