Both obesity and gestational diabetes mellitus are increasing in prevalence, being a major health problem in pregnancy with independent and additive impact on obstetrics outcomes. It is recognized that inadequate gestational weight gain is an independent risk factor for pregnancy-related morbidity. The aim of this study was to evaluate the effect of gestational weight gain on obstetric and neonatal outcomes in obese women with gestational diabetes. Retrospective multicenter study of obese women with gestational diabetes. The assessed group was divided into three categories: women who gained below (9 kg) the 2009 Institute of Medicine recommendations. Maternal and neonatal outcomes were compared and adjusted odds ratios calculated controlling for confounders. Only 35,1 % of obese women with gestational diabetes (n = 634) achieved the recommended gestational weight gain; 27,8 % (n = 502) gained below and 37,1 % (n = 670) above the recommendations. There was a positive correlation between gestational weight gain and neonatal birthweight (r = 0,225; p < 0,001). Gestational weight gain below recommendations was associated with lower odds for cesarean section, even adjusting for birthweight [aOR = 0,67 (0,54–0,85); p < 0,001]; lower odds for large for gestational age neonates [aOR = 0,39 (0,28–0,57); p < 0,001] and macrosomia [aOR = 0,34 (0,21–0,55); p < 0,001]. Excessive weight gain, even adjusting for birthweight, was associated with higher odds for cesarean section [aOR = 1,31 (1,07–1,61); p = 0,009], low Apgar score [aOR = 4,79 (1,19–19,21); p = 0,027], large for gestational age neonates [aOR = 2,32 (1,76–3,04); p < 0,001] and macrosomia [aOR = 2,39 (1,68–3,38); p < 0,001]. In obese women with gestational diabetes, a reduced gestational weight gain (<5 kg) is associated with better obstetric and neonatal outcomes than an excessive or even an adequate weight gain. Therefore, specific recommendations should be created since gestational weight gain could be a modifiable risk factor for adverse obstetric outcomes.

1. Insulin resistance is associated with hypertension but the underlying mechanism is unclear. We tested the hypothesis that insulin-induced vasodilatation is impaired in insulin-resistant obese Zucker rats. We studied mesenteric artery (≈ 220 μm diameter) function before the development of hypertension in 3-month old obese Zucker rats and age-matched lean rats. 2. In vessels from lean rats, insulin at concentrations of 50, 500 and 5000 m-units/l attenuated the constriction in response to noradrenaline (50 m-units/l: 8 ± 3%, P < 0.05; 500 m-units/l: 13 ± 3%, P < 0.02; 5000 m-units/l: 13 ± 2%, P < 0.02). 3. Vessels from obese rats failed to show any such response to insulin (2 ± 6% increase in maximal tension with 5000 m-units/l; not significant), both in the presence and absence of l-arginine (3 mmol/l). 4. Vessels from obese rats showed slight but significant impairment in the vasodilator response to acetylcholine (5 × 10⁻⁸−10⁻⁴ mol/l) (obese: 64.1 ± 3.7% relaxation; lean: 77.3 ± 3.7% relaxation; P < 0.05); however, relaxation in response to A23187 was not significantly different between the phenotypes (obese: 81.3 ± 10.6% relaxation; lean: 79.1 ± 9.7% relaxation; not significant). 5. Systolic blood pressure was not significantly different in lean (126 ± 8 mmHg) and obese (127 ± 7 mmHg) rats at the time of study (not significant). 6. We conclude that insulin-induced attenuation of noradrenaline-mediated vasoconstriction is impaired in the obese Zucker rat and that this defect precedes and therefore could contribute to the development of hypertension in this insulin-resistant model. The defect in insulin action could reside in the endothelial generation of nitric oxide, as endothelial function is also abnormal.

Fetal goiter is a rare disorder not expected to be found during a healthy woman’s pregnancy. It can be a prenatal manifestation of congenital hypothyroidism due to thyroid dyshormonogenesis and it can lead to serious perinatal complications. A vascularized fetal neck mass was detected at 29 weeks’ gestation of a healthy primigravida. Magnetic resonance was suggestive of goiter causing airway deviation without polyhydramnios. Maternal thyroid function was normal and thyroid antibodies were negative. Two intra-amniotic levothyroxine infusions were performed at 32 and 33 weeks. Serial imaging control showed no progression of the mass. Elective caesarean section was performed at 38 weeks. The male newborn was admitted to the intensive care unit due to cardiorespiratory insufficiency with pulmonary hypertension. Hormonal assays revealed primary congenital hypothyroidism and ultrasonography confirmed diffuse goiter. Levothyroxine was started. Currently, he is 6 years old with adequate growth and normal psychomotor development. Genetic study found a heterozygous mutation in the TPO gene.