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the patients had had pathological fractures. All patients except one had a daily calcium intake of less than 50 mg daily, and a dietary vitamin D intake ofless than 50 IU daily. One patient was taking regular supplements of vitamin D. All had plasma urea and creatinine concentrations within the normal range for our laboratory. Seventeen age and sex matched healthy volunteers were also studied as controls. All controls had body weights within 10% of the average body weight appropriate for height (Geigy Scientific Tables).A fasting venous blood sample was collected from each patient without stasis. Blood was allowed to clot and centrifuged immediately at 4°C. Serum was aliquoted and stored a -20°C for PTH, 25 OHD, and 1,25(OH)2D assays. Plasma calcium and albumin concentrations, and phosphate, and alkaline phosphatase activities were measured by a SMAC Technicon autoanalyser (Technicon, Baskingstoke, UK).Serum 25 OHD was measured by the method described by Preece et al 'and PTH was measured by a radioimmunoassay with an antibody directed against the mid molecular fragment of PTH as described by Roos et al 4; 17f estradiol was measured by a double antibody radioimmunoassay. 1,25(OH)2D was measured by the method described by Reinhardt et al.5

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Preeclampsia (PE) is a major pregnancy complication of placental origin which leads to adverse pregnancy outcome. Brain derived neurotrophic factor (BDNF) is suggested to promote trophoblast growth and regulate placental and fetal development. This study for the first time examines the levels of maternal plasma BDNF at various time points during gestation, cord plasma and placental BDNF levels and their association with birth outcome in women with PE. Normotensive control (NC) women (n=89) and women with PE (n=61) were followed at three different time points [16-20 weeks (T1), 26-30 weeks (T2) and at delivery (T3)]. Maternal blood at all time points and cord blood was collected. Results indicate that maternal BDNF levels at T1 (p=0.050) and T3 (p=0.025) were lower in women with PE than in NC women. Cord BDNF levels at delivery in women with PE were lower (p=0.032) than those in NC women. Placental BDNF gene expression was also lower (p=0.0082) in women with PE than in NC women. Our data suggests that BDNF plays an important role in the development of the materno-fetal-placental unit during pregnancy. Alteration in the levels of BDNF during pregnancy may be associated with an abnormal development of the placenta resulting in PE.

Our earlier studies in preeclampsia (PE) suggest a causal relationship between altered angiogenic factors and birth outcomes. Recent studies suggest that brain-derived neurotrophic factor (BDNF) can stimulate angiogenesis. The present study examines the levels of maternal and cord BDNF in women with PE (n = 106; full term [n = 60] and preterm [n = 46]) and normotensive women (n = 95; control) delivering at term. Maternal BDNF levels were lower (P < .05) in women with PE when compared to normotensive women. Cord BDNF levels were higher (P < .01) in women with PE delivering at term, while it was lower (P < .01) in women delivering preterm. Maternal BDNF levels were negatively associated with systolic and diastolic blood pressure (P < .01 for both). Our data for the first time suggest a possible role for BDNF in the pathophysiology of PE. Differential regulation of cord BDNF levels in preterm PE suggests a need to follow-up children to assess the neurodevelopmental effects in later life.