Premature birth occurs in up to 10% of all pregnancies and is a major cause of mental and physical handicap and infant mortality. Half of all surviving infants born at 25 weeks or less show neurodevelopment impairment at 30 months of age, which can have devastating consequences for the patients and their families. Aside from the human cost, there is a significant economic burden on society once these very sick infants leave hospital.

Preterm delivery has a higher prevalence among unemployed, poorly educated, psychologically stressed or socially deprived mothers. The ethnic susceptibility to preterm birth is particularly disturbing and despite improvements in obstetric and neonatal care, Black infants continue to experience mortality rates two and half times higher than that for Whites. This discrepancy is largely accounted for by a higher incidence of extreme preterm birth and sepsis, that are largely associated with the social context of Black women's lives.

While the underlying pathophysiological pathways are poorly understood, there is accumulating evidence that infection and inflammation play a major role in premature birth and the associated neurocognitive defects. Recent reports, and our own preliminary observations, have implicated polymorphisms in genes encoding the cytokine IL-6 and the processing enzyme caspase-12 in sepsis and premature birth in the Black population. We are currently analyzing single (small) blood samples from preterm infants for polymorphisms and immune competence. The results will further our understanding of the aetiology of preterm birth and may suggest novel therapeutic approaches to alleviate this significant clinical problem.

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