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OBJECTIVE: To describe the causes of maternal death in a population-based cohort in six low- and middle-income countries using a standardised, hierarchical, algorithmic cause of death (COD) methodology. DESIGN: A population-based, prospective observational study. SETTING: Seven sites in six low- to middle-income countries including the Democratic Republic of the Congo (DRC), Guatemala, India (two sites), Kenya, Pakistan and Zambia. POPULATION: All deaths among pregnant women resident in the study sites from 2014 to December 2016. METHODS: For women who died, we used a standardised questionnaire to collect clinical data regarding maternal conditions present during pregnancy and delivery. These data were analysed using a computer-based algorithm to assign cause of maternal death based on the International Classification of Disease-Maternal Mortality system (trauma, termination of pregnancy-related, eclampsia, haemorrhage, pregnancy-related infection and medical conditions). We also compared the COD results to healthcare-provider-assigned maternal COD. MAIN OUTCOME MEASURES: Assigned causes of maternal mortality. RESULTS: Among 158 205 women, there were 221 maternal deaths. The most common algorithm-assigned maternal COD were obstetric haemorrhage (38.6%), pregnancy-related infection (26.4%) and pre-eclampsia/eclampsia (18.2%). Agreement between algorithm-assigned COD and COD assigned by healthcare providers ranged from 75% for haemorrhage to 25% for medical causes coincident to pregnancy. CONCLUSIONS: The major maternal COD in the Global Network sites were haemorrhage, pregnancy-related infection and pre-eclampsia/eclampsia. This system could allow public health programmes in low- and middle-income countries to generate transparent and comparable data for maternal COD across time or regions. TWEETABLE ABSTRACT: An algorithmic system for determining maternal cause of death in low-resource settings is described.

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OBJECTIVE: We sought to classify causes of stillbirth for six low-middle-income countries using a prospectively defined algorithm. DESIGN: Prospective, observational study. SETTING: Communities in India, Pakistan, Guatemala, Democratic Republic of Congo, Zambia and Kenya. POPULATION: Pregnant women residing in defined study regions. METHODS: Basic data regarding conditions present during pregnancy and delivery were collected. Using these data, a computer-based hierarchal algorithm assigned cause of stillbirth. Causes included birth trauma, congenital anomaly, infection, asphyxia, and preterm birth, based on existing cause of death classifications and included contributing maternal conditions. MAIN OUTCOME MEASURES: Primary cause of stillbirth. RESULTS: Of 109 911 women who were enrolled and delivered (99% of those screened in pregnancy), 2847 had a stillbirth (a rate of 27.2 per 1000 births). Asphyxia was the cause of 46.6% of the stillbirths, followed by infection (20.8%), congenital anomalies (8.4%) and prematurity (6.6%). Among those caused by asphyxia, 38% had prolonged or obstructed labour, 19% antepartum haemorrhage and 18% pre-eclampsia/eclampsia. About two-thirds (67.4%) of the stillbirths did not have signs of maceration. CONCLUSIONS: Our algorithm determined cause of stillbirth from basic data obtained from lay-health providers. The major cause of stillbirth was fetal asphyxia associated with prolonged or obstructed labour, pre-eclampsia and antepartum haemorrhage. In the African sites, infection also was an important contributor to stillbirth. Using this algorithm, we documented cause of stillbirth and its trends to inform public health programs, using consistency, transparency, and comparability across time or regions with minimal burden on the healthcare system. TWEETABLE ABSTRACT: Major causes of stillbirth are asphyxia, pre-eclampsia and haemorrhage. Infections are important in Africa.

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OBJECTIVE: We investigated whether previous reports of reduced bone mineral density after management for childhood acute lymphoblastic leukemia (chALL) were confirmed in a more recently treated cohort. STUDY DESIGN: In a cross-sectional study 75 subjects who were given the diagnosis of chALL between January 1, 1991, and December 31, 1997 (69% standard, 31% high risk), at Denver Children's Hospital and who were 11 to 82 months post-diagnosis with no history of relapse, secondary malignancy, or transplant underwent whole body areal bone mineral densitometry (BMD(A) expressed as age- and sex-standardized z scores), a food frequency questionnaire, and a weight-bearing activity survey. RESULTS: Overall, the mean whole body BMD(A) z score was normal (+0.22 +/- 0.96). A significant positive association was found with whole body BMD(A) z score and years elapsed since the beginning of maintenance (linear regression coefficient = +0.2 Deltaz score/year; 95% CI = 0.09 to 0.3) after adjustment was done for risk status/age category, history of cranial radiation, and total days hospitalized. No association was found with high risk/older age at diagnosis, nutrient intake, chemotherapy dosage, or weight-bearing activity. CONCLUSION: Contrary to previous reports in which cranial radiation and longer hospitalizations were prominent components of therapy, our study suggests that more recently treated patients with chALL do not have persistent abnormalities of bone mineral density after completion of therapy.

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OBJECTIVES: The purpose of this study was to examine the zinc status of young infants with cystic fibrosis before and after the initiation of pancreatic enzyme therapy. STUDY DESIGN: Cross-sectional data were obtained for infants with cystic fibrosis identified by newborn screening. Plasma zinc concentrations were measured and analyzed according to enzyme use at the time of the blood draw. On a subgroup of infants, zinc concentrations were determined again after several weeks with enzyme therapy. RESULTS: Mean (+/-SD) plasma zinc concentration for the infants studied before the initiation of enzyme therapy was 10.4 +/- 2.2 micromol/L (68.3 +/- 14.7 microgram/dL) (n = 48), which was significantly lower than the mean for those receiving enzymes for >/=2 weeks, 11.8 +/- 2. 3 micromol/L (77.1 +/- 14.9 microgram/dL) (n = 15) (P =.03). For the group not yet receiving enzymes, 29% of infants had zinc concentrations in the deficient range. Data were available before and after enzyme therapy for 30 infants and indicated a mean increase of 1.64 +/- 3.0 micromol/L (10.7 +/- 19.3 microgram/dL) (P =. 005). CONCLUSIONS: These data suggest that many of the infants were zinc deficient at the time of diagnosis. We conclude that zinc should be included among the specific micronutrients given consideration in the management of cystic fibrosis, particularly in infants.

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To investigate whether a fundamental lesion in energy metabolism is a feature of cystic fibrosis, we measured total energy expenditure using the doubly labeled water technique in 19 infants with presymptomatic cystic fibrosis (0.8 to 6.6 months of age) identified through newborn screening. Total energy expenditure data collected in a cohort of healthy infants by the same method were used for comparison. Energy balance studies were additionally performed in 10 of the infants with cystic fibrosis. Total energy expenditure levels in infants with cystic fibrosis, expressed as either kilocalories per day or kilocalories per kilogram of fat free mass per day, did not differ from control levels. When expressed on the basis of body weight (in kilocalories per kilogram per day), expenditure levels in infants with cystic fibrosis were greater (p < 0.05) than control levels. No differences in expenditure were observed between those infants who were homozygous (n = 10) for the delta F508 mutation and the heterozygous infants (n = 7), regardless of how expenditure was expressed. Assessment of energy balance indicated that infants with cystic fibrosis grow at a normal rate for metabolizable energy intakes similar to those reported for healthy infants. We conclude that there are no differences in energy expenditure between infants with presymptomatic cystic fibrosis and healthy infants, once differences in body composition are taken into account. This finding indicates that the primary cystic fibrosis defect is not an energy-requiring one.

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The objectives of this study were to examine the growth pattern of healthy infants who were fed human milk exclusively for > or = 5 months and its relationship to intakes of milk, energy, and zinc. Monthly anthropometric measurements were obtained on 71 infants through 7 months of age and on 43 through 9 months. Milk zinc concentrations were determined and milk intake was measured by 3-day test weighing. Mean (+/- SD) calculated energy intake from human milk was 106 +/- 20, 79 +/- 11, 70 +/- 10, and 57 +/- 12 kcal/kg per day at 2 weeks and 3, 5, and 7 months of age, respectively; intake from milk plus solids was 70 +/- 13 kcal/kg at 7 months. Zinc intakes from human milk were 2.3 +/- 0.68, 1.0 +/- 0.43, 0.81 +/- 0.42, and 0.52 +/- 0.31 mg/day at these points. The maximum mean weight-for-age percentile for both sexes was 62 at 2 months; the mean percentile declined to 33 by 7 months and to 25 by 9 months of age. Mean length-for-age percentile declined from 43 at 2 weeks of age to 28 and 26 by 7 and 9 months of age, respectively. Energy intake at 2 weeks of age was positively associated with the weight increment from 2 weeks to 7 months of age (p = 0.003) and with a change in weight-for-age z scores from 2 weeks to 3 months of age (p = 0.028). Mean energy intakes of healthy breast-fed infants are lower through the first 7 months of life than current recommendations. Zinc intakes of breast-fed infants are likely to be adequate, on average, through 5 months of breast-feeding but subsequently are marginal without the introduction of weaning foods. Revision of standards for growth based on observations in breast-fed infants may be appropriate, but the possibility of growth-limiting nutrient deficiencies should also be investigated.

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To evaluate the impact of early pancreatic insufficiency on growth and nutritional status in cystic fibrosis, we studied 49 infants identified by a newborn screening program. Pancreatic insufficiency, determined by increased 72-hour fecal fat excretion, was present in 59% (23/39) of infants at diagnosis (7.0 +/- 0.8 weeks; mean +/- SEM). Before initiation of pancreatic enzyme replacement, growth and nutritional status of pancreatic-insufficient (n = 16) and pancreatic-sufficient (n = 13) infants were compared. Pancreatic-insufficient infants gained less weight from birth to diagnosis (13.4 +/- 3.4 vs 22.3 +/- 4.0 gm/day; p = 0.05), had decreased triceps skin-fold thicknesses (4.5 +/- 0.3 vs 6.1 +/- 0.4 mm; p less than 0.005), and had lower blood urea nitrogen (3.07 +/- 0.42 vs 4.62 +/- 0.65 mg/dl; p = 0.02) and albumin (2.99 +/- 0.14 vs 3.54 +/- 0.14 gm/dl; p less than 0.01) levels despite higher gross calorie (154 +/- 8 vs 116 +/- 13 kcal/kg per day; p less than 0.01) and protein intakes (2.81 +/- 0.21 vs 2.14 +/- 0.33 gm/kg per day; p = 0.03). Fecal nitrogen loss was correlated with fat loss (r = 0.79; p less than 0.001). Fat malabsorption was present in 79% (30/38) and 92% (33/36) of infants tested at 6 months and 12 months of age, respectively, indicating that pancreatic insufficiency persists and increases in frequency throughout infancy. We conclude that pancreatic insufficiency is prevalent in young infants with cystic fibrosis and has a significant impact on growth and nutrition.

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Nutritional evaluations were undertaken on 102 Mexican-American preschool children who were below the 3rd percentile for height, weight, or head circumference. Serum vitamin A concentrations were low in 36 of 102 children (35%). Hair zinc concentrations were low in 28 of 96 children (29%) and plasma zinc concentrations were low in 35 of 94 children (37%). Children with only low height had a mean hair zinc level of 87.5 microgram/g, whereas those with only low weight had a mean level of 108.6 microgram/g and those with only low head circumference had a mean level of 100.1 microgram/g. There was no correlation of height percentiles with plasma zinc, hair zinc, or serum vitamin A. However, further studies are needed to determine if there is a relationship between growth retardation and zinc and/or vitamin A status in this population.

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