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Restriction to those commencing antenatal care before 16 weeks gestation resulted in the final study group of 80 SS patients and 115 AA controls. Weight and height were measured at first antenatal visit and weight at 20, 25, 30, 35 and 38 weeks gestation. Longitudinal regression used mothers'weight as the outcome, genotype as a predictor and gestational age as a random effect.
Regression analyses ofmaternal weight on childhood anthropometry were repeated in separate maternal genotypes. Neonatal indices included gestational age, birthweight, head circumference and crown-heel length.
A significant relationship occurred between birthweight and maternal weight gain at 25-30 weeks gestation in AA controls but this relationship appears delayed in SS disease. El peso y la altura se midieron en la primera visita prenatal, y el peso a las 20, 25, 30, 35 y 38 semanas de gestación.


Two features characteristic of mothers with SS disease likely to contribute to this low birthweight are the low pre-pregnancy body mass index (2, 3) and the tendency to deliver at an earlier gestational age (1, 4). The anthropometry of SS disease is characterised by a low body weight and normal or increased height so that the body mass index (BMI) is usually low. The lower gestational age at delivery in most pregnancies of SS mothers contributes to the low birthweight but compared with controls with a normal haemoglobin (AA) genotype, birthweights in SS mothers remained lower for each gestational age (1) implying that other factors must contribute to the low birthweight in SS mothers.
One possibility is that the increased metabolic rate typical of SS disease (7) competes with the metabolic demands of the fetus and delays gestational weight gain. This possibility has been explored by examining the relationship between pre-pregnancy BMI, GWG, gestational age and the longitudinal weight gain at different stages of pregnancy in mothers with SS disease and in matched controls with a normal haemoglobin genotype. Each was matched by maternal age and date of delivery to a control with an AA phenotype without known chronic disease.
The final study group was 80 SS and 115 AA controls after further restriction to women with live deliveries and who first attended antenatal clinic at or before 16 weeks gestation (ensuring baseline values which allowed calculation of pregnancy weight gain). The subjects' records were examined for maternal height and weight at the first antenatal visit and maternal weight at 20, 25, 30, 35 and 38 weeks gestation. The pre-pregnancy BMI was calculated from height and weight at the first antenatal clinic visit.
Birth data included gestational age, birthweight, head circumference, crown-heel length, calculated ponderal index and placental weight.
Maternal weight gain was examined using a longitudinal regression model with mother's weight as the outcome and with gestational age as a random effect. Weight differences between patients and controls were examined, and the interaction between genotype and gestational age explored to determine whether the weight gain trajectories differed between SS and AA women. Weights predicted from this model were used as potential predictors of birthweight, crown-heel length and head circumference. For direct comparison of weight change, the predicted weights were converted to SD scores (z-scores) with a mean of 0, and a standard deviation of 1.
Stata statistical software was used to perform all analyses (Release 10, StataCorp LP, College Station, Texas, USA). No relationships occurred between crown-heel length and gestational period in either maternal genotype.
Weight gain was similar in SS and AA mothers from 12-20 weeks, 2 kg less among SS mothers from 20-30 weeks and similar again after 30 weeks.
The relationship of gestational weight gain to final birthweight also showed genotype differences, birthweight being significantly related to gestational weight gain between 25-30 weeks in normal controls but not in SS disease whereas there was a trend for birthweight to be related to gestational weight gain between 30-35 weeks in SS mothers.
The resting metabolic rate is increased in SS disease (8) and the greater metabolic demands of the mother are not met by an increased nutritional intake (9, 10). Pregnancy imposes further metabolic demands in these women which may not be fully met because of the limited reserves.


Weight gains at later gestational ages are lower but variable because of the declining number of observations. A similar correlation may occur in SS mothers at 30-35 weeks but did not reach significance because of the smaller numbers of subjects. Whatever the responsible mechanisms and recognising the relative statistical frailty due to the smaller numbers when regressions were performed in separate maternal genotypes, these observations suggest that the lower weight gain from 25-30 weeks gestation in SS mothers may contribute to the lower birthweight in their offspring. It is tempting to postulate that the delayed weight gain in SS mothers is a consequence of SS disease, the growing fetus having to compete with the greater meta-bolic demands of the bone marrow and cardiovascular activ-ity in the mother. The first antenatal clinic visit occurred at or before 15 weeks in 63% of the initial 128 SS women compared with 88% of controls.
Part of this difference may be artefactual since at the University Hospital, women perceived to be at 'high risk' may be accepted for antenatal care at later gestational ages than normal women who may be referred to other institutions for care and delivery. However, it is important to identify the reasons for later attendance among SS women in order to improve comprehensive clinical care. A further source of bias in this study results from the selection criteria which excluded early fetal losses common in women with SS disease, (4, 19) inevitably introduces a bias towards better pregnancy outcome. It is unknown whether nutritional supplementation at this stage of pregnancy will promote greater maternal weight gain or whether such weight gain would be reflected in increased birthweight but these questions should be addressed.
In conclusion, maternal weight gain between 25-30 weeks gestation correlates positively with birthweight in children of AA mothers but this relationship may be delayed beyond 30 weeks in SS mothers. The effect of gestational weight gain by body mass index on maternal and neonatal outcomes.
Energy intake and resting metabolic rate in pre-school Jamaican children with homozygous sickle cell disease. Intrauterine growth as estimated from live born birth-weight data at 24 to 42 weeks gestation. Proceedings of the 20th study group of the Royal College of Obstetricians and Gynaecologists. Maternal pre-pregnancy weight and placental weight determine birth weight in normal Jamaican infants.
The mechanisms of low birth weight in infants of mothers with homozygous sickle cell disease.



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Comments

  1. 03.04.2014 at 19:40:41


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    Author: slide_show
  2. 03.04.2014 at 22:10:14


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