We illustrate a case of giant placental chorioangioma presenting at 20 weeks of gestation. Subsequent monitoring revealed enlargement of the lesion, associated with fetal anemia and cardiac failure, prompting in utero intervention. Amnioreduction followed by percutaneous embolization of the tumour with enbucrilate:Lipiodol Ultra-Fluid™ at a dilution of 1:5 was successfully performed. No repeat intervention or additional supportive measures were required throughout pregnancy and the baby was delivered at 36 weeks of gestation, following spontaneous labour. Due to prolonged neonatal jaundice, further investigations were undertaken, demonstrating subacute right portal vein thrombosis. Other previously reported causes of neonatal portal vein thrombosis such as umbilical vein thrombosis, neonatal umbilical vein catheterization, thrombophilia and sepsis were excluded. There was resolution of the thrombus by 6 months of life. A brief discussion of measures to minimize the risk of such an event and the long-term outcomes of neonatal portal vein thrombosis was included. Whilst the simplicity and efficacy of the procedure has been demonstrated in a handful of patients, judgment on its safety is best deferred. Counselling should be comprehensive, as even rare complications can result in significant postnatal morbidity.

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Molecular characterization of the compound heterozygous condition – ^Gγ(^Aγδβ)^o/β-thalassemia – in four families showing mild β-thalassemia intermedia was carried out using DNA amplification techniques. Using the Amplification Refractory Mutation System (ARMS) to confirm the β-mutations and DNA amplification to detect the 100-kb Chinese-specific ^Gγ(^Aγδβ)^o-deletion, two families were confirmed to possess ^Gγ(^Aγδβ)^o/β-thalassemia with the IVSII No. 654 β⁺-allele. In the third family, the ^Gγ(^Aγδβ)^o-deletion was confirmed in the father and the mother was a β-thalassemia carrier with the cd 41–42 β^o-allele. Their affected child with ^Gγ(^Aγδβ)^o/β-thalassemia was found to be transfusion dependent. The same ^Gγ(^Aγδβ)^o-deletion and β-thalassemia (cd 41–42) was also confirmed in a fourth family. In addition, the mother was also diagnosed with Hb H disease (genotype -α^3.7/–^SEA). Both the children were found to possess ^Gγ(^Aγδβ)^o/β-thalassemia but they were not transfusion dependent and this could be due to co-inheritance of α-thalassemia-2 (genotype-α^3.7/αα) in the children together with their compound heterozygous condition.

IntroductionUndernutrition in young children is a significant public health problem globally. We determined the prevalence of and factors predisposing to stunting and underweight in children aged 1 to 5 years in Malaysia.Materials and methodsData were extracted from a cross-sectional nationwide campaign involving healthy children aged 1–5 years conducted over a 4-month period in 2019. We obtained information on demography, parental height and risk factors of undernutrition and anthropometric measurements (height and weight) of children enrolled. Age and sex-specific z-score for length/height-for-age (HAZ), weight-for-age (WAZ), body mass index (BMI) z-score (BAZ) and weight-for-height/length (WFH) z-score (WFHZ) were obtained using World Health Organization growth standards. The following definitions were used: (a) HAZ < −2 SD as stunted and −2 to −1 SD as at risk of stunting; (b) WFHZ < −3 SD as severe, −3 to < −2 SD as moderate wasting, and −2 to < +1 SD as normal; (c) WAZ −2 to −1 as at risk of underweight; (d) BAZ +1 to < +2 SD as at risk of and > +2 SD as overweight.ResultsOf the 15,331 children surveyed, prevalence of stunting and at risk of stunting were 16.1 and 20.0%, severe and moderate wasting were 4.0 and 6.1%, while 21.1% was at risk of underweight. Prevalence of at risk of and overweight 14.2 and 7.3%, respectively. One in fifth (25.0%) children had at least one form of undernutrition (stunting and/or underweight/wasting). Of the 1,412 (13.2%) children reported to have risk factors of undernutrition, 47.2% had feeding difficulties, 44.8% had poor dietary intake and 8.0% had both. Boys, paternal height < 156 cm and poor dietary intake were significantly associated with stunting and/or wasting. Compared with children with no risk factors, children with feeding difficulties were more likely to be wasted (AOR: 1.48, 95% CI: 1.18–1.85), and had at least one form of undernutrition (AOR: 1.45, 95% CI: 1.25–1.69).ConclusionsIn Malaysian children aged 1 to 5 years, dual burden of under- and overnutrition are common. Poor dietary intake and feeding difficulties were risk factors for undernutrition.