Acute fatty liver of pregnancy (AFLP) is a rare disorder which is fatal if not recognized and treated early. Delivery of the feto-placental unit results in dramatic improvement in maternal liver function, suggesting a role for the placenta. However, the mechanisms by which defects in the fetus or placenta lead to maternal liver damage are not well understood and form the focus of this study. Placenta and serum were obtained at delivery from patients with AFLP, and placental mitochondria and peroxisomes were isolated. Placental mitochondrial function, oxidative stress, and fatty acid composition as well as serum antioxidants, oxidative and nitrosative stress markers, and fatty acid analysis were carried out. Hepatocytes in culture were used to evaluate cell death, mitochondrial function, and lipid accumulation on exposure to fatty acids. Oxidative stress was evident in placental mitochondria and peroxisomes of patients with AFLP, accompanied by compromised mitochondrial function. Increased levels of arachidonic acid were also seen in AFLP placenta when compared to control. Patients with AFLP also had a significant increase in oxidative and nitrosative stress markers in serum, along with decreased antioxidant levels and elevated levels of arachidonic acid. These levels of arachidonic acid were capable of inducing oxidative stress in hepatocyte mitochondria accompanied by induction of apoptosis. Exposure to arachidonic acid also resulted in increased lipid deposition in hepatocytes. A cute fatty liver of pregnancy (AFLP) is an example of a primary mitochondrial hepatopathy 1 characterized by hepatic microvesicular steatosis, hepatic failure, and encephalopathy developing in the last trimester of pregnancy. 2,3 Although the majority of primary mitochondrial hepatopathies present in childhood, AFLP presents in a previously asymptomatic woman in late pregnancy. The disease is associated with defects in ␤-oxidation of fatty acids in mitochondria 4 especially the mitochondrial long-chain acyl coenzyme A dehydrogenase (LCHAD) 5,6 in the fetus, but it is now recognized that AFLP can occur without a mutation in LCHAD. 7,8 This suggests that the metabolic basis of AFLP is more heterogeneous than believed earlier, but the mechanism by which a fetal defect in lipid metabolism causes maternal liver damage is not well understood. Interestingly, it has been observed that patients with AFLP generally recover from liver dysfunction subsequent to delivery of the fetus, 9 suggesting a causative role for the placenta, which is expelled during delivery.During gestation, the placenta is essential for fetal development and utilizes fatty acids as a significant metabolic fuel. 10 The genetic composition of the placenta is identical to that of the fetus, and all enzymes of the mitochondrial fatty acid ␤-oxidation pathway are expressed and active in human placenta, 11 with activities being maximum in the second trimester and decreasing with gesta-AFLP, acute fatty liver of pregnancy; EDTA, ethylene diamine tetraacetic acid; LCHAD, long-cha...

A community-based, cross-sectional study was conducted to determine the prevalence of anaemia among unmarried, adolescent south Indian girls in an urban slum setting. A total of 100 apparently healthy girls between the ages of 11 and 18 years were recruited. Their socioeconomic, dietary and anthropometric information was collected, and blood haemoglobin (Hb) was estimated. The prevalence of anaemia (Hb < 12 g%) was 29%. Most had mild anaemia; severe anaemia was not seen. Two-thirds of those with anaemia had low serum ferritin (<12 microg/L). Significant associations were observed between anaemia and low socioeconomic status, religion and reporting infrequent/non-consumption of meat (heme iron). Only meat consumption was related to haemoglobin by multiple regression analysis. Anaemia is a common problem among adolescent girls in this setting, though severe anaemia is rare. There is a need to improve their haemoglobin status through dietary modification along with preventive supplementation and nutrition education.

BackgroundBirth weight centile curves are commonly used as a screening tool and to assess the position of a newborn on a given reference distribution. Birth weight of twins are known to be less than those of comparable singletons and twin-specific birth weight centile curves are recommended for use. In this study, we aim to construct gestational age specific birth weight centile curves for twins born in south India.MethodsThe study was conducted at the Christian Medical College, Vellore, south India. The birth records of all consecutive pregnancies resulting in twin births between 1991 and 2005 were reviewed. Only live twin births between 24 and 42 weeks of gestation were included. Birth weight centiles for gestational age were obtained using the methodology of generalized additive models for location, scale and shape (GAMLSS). Centiles curves were obtained separately for monochorionic and dichorionic twins.ResultsOf 1530 twin pregnancies delivered during the study period (1991–2005), 1304 were included in the analysis. The median gestational age at birth was 36 weeks (1st quartile 34, 3rd quartile 38 weeks). Smoothed percentile curves for birth weight by gestational age increased progressively till 38 weeks and levels off thereafter. Compared with dichorionic twins, monochorionic twins had lower birth weight for gestational age from after 27 weeks.ConclusionsWe provide centile values of birth weight at 24 to 42 completed weeks of gestation for twins born in south India. These charts could be used both in routine clinical assessments and epidemiological studies.

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