RESUMO
Background Low birth weight (LBW) is susceptible to neonatal complications, chronic medical conditions, and neurodevelopmental disabilities. We aim to describe the determinants of very low birth weight (VLBW) in India based on the National Family Health Survey - 4 (NHFS-4). Methods Data from the NFHS 4 on birthweight and other socio-demographic characteristics for the youngest child born in the family during the five years preceding the survey were used. Data of 147,762 infant-mother pairs were included. Multiple logistic regression models were employed to delineate the independent predictors of VLBW (birth weight<1500 g) or LBW (birth weight <2500 g). Results Of the 147,762 children included in the study, VLBW and LBW were observed in 1.2% and 15.8% of children, respectively. The odds of VLBW were higher in female children (aOR: 1.36, 95% CI: 1.15-1.60), among mothers aged 13-19 years (aOR: 1.58, 95% CI: 1.22-2.07), mothers with severe or moderate anaemia (aOR: 1.61, 95% CI: 1.34-1.94), mothers without recommended antenatal care (aOR: 1.47, 95% CI: 1.31-1.90), maternal height less than 150 cm (aOR: 1.54, 95% CI: 1.29-1.85) and among mothers with multiple pregnancy (aOR: 21.34, 95% CI: 14.70-30.96) in comparison to their corresponding counterparts. In addition to the variables associated with VLBW, educational status of mothers (no education; aOR: 1.08, 95% CI: 1.02-1.15 and primary education; aOR: 1.16, 95% CI: 1.08-1.25), caste of the children (scheduled tribe; aOR: 1.13, 95% CI: 1.03-1.24), and wealthiness of the family (poorest wealth quintiles; aOR: 1.11, 95% CI: 1.03-1.19) were associated with LBW. Conclusions Interventions targeting improvements in antenatal care access, maternal health, and nutritional status may reduce the number of VLBW infants. Social determinants of LBW require further detailed study to understand the high propensity of low birth-weight phenotypes in the disadvantaged communities in India.
RESUMO
Kawasaki disease (KD) is the most common vasculitis in childhood that affects medium-sized arteries, particularly coronary arteries. The etiology remains unknown; however, many studies suggest that specific genetic factors and/or some infectious agents underlie the onset. Here, we report a set of identical twin boys who simultaneously developed KD, emphasizing the genetic component of etiology. The patients were 4-year-old twin boys who previously had been healthy and had no family history of KD. Twin A, on admission, met four of five diagnostic criteria for KD. Echocardiogram ruled out coronary artery lesion, and he was treated with 2 g/kg IVIG and aspirin, to which he responded well. Twin B, unlike his brother, met only three of the diagnostic criteria, so was diagnosed as incomplete KD. However, due to the history and shared genetic potential for KD, laboratory investigations and echocardiogram were done. His echocardiogram revealed coronary artery lesion. He was also treated with IVIG and aspirin.