Abstracts of theses and treatises
Milns N (1987) Low birthweight in the Northern Territory: relationship with neonatal and maternal immunity and identification of major risk factors. Unpublished Bachelor of Medical Science thesis, University of Queensland, Brisbane, Queensland.
Low birthweight (LBW) and intrauterine growth retardation (IUGR) were studied in 85 Aboriginal and 82 non-Aboriginal neonates born over a 9 month period in 1987 at the Royal Darwin Hospital. The prevalence of risk factors for LBW and IUGR was assessed in the mothers to identify any factors that may be contributing to the high incidence of LBW in the Aboriginal population. Maternal and neonatal cell mediated immunity (CMI) and neutrophil function was measured and their relationship with birthweight and gestational age assessed.
Preventable factors including cigarette use and possibly maternal undernutrition accounted for over one quarter of the LBW in the group and were more prevalent in the Aboriginal mothers, suggesting that these are possible major risk factors in this group. Over one half of the LBW was unable to be accounted for by any recognised risk factor.
Maternal lymphocyte subset distributions were altered in normal pregnancy through a decrease in helper/inducer and an increase in cytotoxic/suppressor T-lymphocyte numbers. This may be an expression of the CMI suppression needed to prevent rejection of the foetal allograft. Mothers with LBW infants failed to show a decrease in helper/inducer T-lymphocyte numbers suggesting that there may be a relative failure to suppress CMI and that this may be related to pregnancy outcome. Aboriginal neonates as a group showed raised numbers of suppressor/cytotoxic T-lymphocytes, and LBW Aboriginal neonates showed a decreased number of helper/inducer T-lymphocytes. These alterations in lymphocyte subset distribution in Aboriginal neonates may help explain their increased mortality and morbidity. No effect of birthweight on lymphocyte blast transformation as a measure of CMI was found in either Aboriginal or non-Aboriginal neonates.
Neutrophil chemataxis was impaired in all neonates and further reduced with decreasing birthweight. Total bactericidal capacity was related to neonatal maturity, but not birthweight. Intracellular metabolic capacity was normal in all neonates suggesting that the defective bactericidal capacity is not a result of impaired degradation of particles. The increased susceptibility of neonates, particularly LBW and growth retarded neonates, to infection may in part be explained by these defects in neutrophil function.
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