RESUMEN
OBJECTIVES: To evaluate the effect of incorporating calcium advice into early pregnancy counseling on calcium intake during pregnancy in the Netherlands. METHODS: A multicenter prospective before-after cohort study was conducted introducing risk-based care including calculating individual pre-eclampsia risk. Part of the intervention was to incorporate calcium advice into routine counseling. We calculated individual daily calcium intake and adequacy of calcium intake (≥1,000 mg/day) at 16, 24 and 34 weeks of pregnancy. We performed a multiple logistic regression adjusting for covariates to identify any differences in the risk of inadequate calcium intake between RC and CAC. RESULTS: In regular care (RC, 2013-2015, n=2,477) 60% had inadequate calcium intake, compared to 49% during calcium advice care (CAC, 2017-2018, n=774) (aOR 0.75, 95% CI 0.64-0.88). Specific calcium supplements were used by 2% and 29% in RC and CAC, respectively (OR 25.1, 95% CI 17.8-36.0). Determinants of an inadequate calcium intake were lower age (aOR per additional year 0.96, 95% CI: 0.94-0.98), nulliparity (aOR 1.22, 95% CI: 1.03-1.45) and non-Caucasian origin (aOR 1.83, 95% CI 1.09-3.09). In CAC, risk of inadequate intake decreased with increasing predicted pre-eclampsia risk, which was a trend reversal compared to RC. CONCLUSIONS: Incorporating calcium advice into early pregnancy counseling was shown to lead to a decrease in the risk of inadequate calcium intake during pregnancy, but still inadequate intake in half of the women suggesting the need for further study on improving implementation. Awareness of individual increased PE risk had positive effect on calcium intake.
Asunto(s)
Calcio , Preeclampsia , Femenino , Embarazo , Humanos , Preeclampsia/epidemiología , Preeclampsia/prevención & control , Mujeres Embarazadas , Estudios de Cohortes , Estudios Prospectivos , Calcio de la Dieta , Paridad , ConsejoRESUMEN
BACKGROUND: Gestational diabetes mellitus (GDM) complicates 1-14% of pregnancies and relates to increased risk of adverse obstetric outcomes. Currently GDM is diagnosed using an oral glucose tolerance test (OGTT), which is burdensome and time intensive. OBJECTIVE: To compare current literature on whether the homeostatic model assessment beta cell function (HOMA-ß) is an accurate predictor of an abnormal OGTT in pregnant women. METHODS: Pubmed, Cochrane and Embase were searched. Included studies evaluated pregnant women at risk for GDM using the homeostatic model assessment of beta cell function (HOMA-ß) for the assessment of beta cell function and the OGTT. Studies with animals, non-pregnant women, women with type 2 diabetes and post-partum diabetes were excluded. The QUADAS-2 criteria were used to assess the methodological quality of studies. RESULTS: A total of 12 studies were included, reporting on 7292 women. Seven studies showed a difference in beta cell function between women with impaired glucose tolerance compared to healthy pregnant women. HOMA-ß is significantly lower in impaired glucose tolerance (p < 0.001). CONCLUSIONS: Although HOMA-ß is lower in women with abnormal OGTT in pregnancy, given the high degree of heterogeneity of studies, we do not propagate HOMA-ß as a sole diagnostic tool replacing OGTT to diagnose GDM.
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Glucemia , Diabetes Gestacional/diagnóstico , Insulina/sangre , Diabetes Gestacional/sangre , Femenino , Prueba de Tolerancia a la Glucosa , Homeostasis , Humanos , EmbarazoRESUMEN
Background: Gestational diabetes mellitus (GDM) increases the risk of type 2 diabetes mellitus and cardiovascular disease (CVD) in women in later life. In the general population, metabolic syndrome (MetS) shows identical associations. The aim of this study was to evaluate the association between GDM, constituents of MetS and pregnancy outcomes. Methods: Of 2041 pregnant women undergoing an oral glucose tolerance test (OGTT) between 22 and 30 weeks of gestation, data were collected to evaluate the constituents of MetS. Odds ratios (ORs) were calculated to determine the associations between MetS and pregnancy outcomes. Results: GDM and obesity did not affect the risk of fetal growth abnormalities (SGA/LGA), preterm birth or preeclampsia (PE). Hypertension significantly increased the risk of SGA (OR1.59), PE (OR3.14), and preterm birth <37 weeks (OR2.17) and <34 weeks (OR2.96) and reduced the occurrence of LGA (OR0.46). Dyslipidemia increased the risk of PE (OR2.25), while proteinuria increased the risk of PE (OR12.64) and preterm birth (OR4.72). Having ≥2 constituents increased the risk of PE and preterm birth. Conclusions: Constituents of metabolic syndrome, rather than treating impaired glucose handling, increased the risk of preeclampsia, altered fetal growth and preterm birth. Obesity was not related to adverse outcomes.
Asunto(s)
Diabetes Mellitus Tipo 2 , Diabetes Gestacional , Síndrome Metabólico , Preeclampsia , Nacimiento Prematuro , Estudios de Cohortes , Diabetes Gestacional/epidemiología , Femenino , Humanos , Recién Nacido , Síndrome Metabólico/epidemiología , Obesidad , Preeclampsia/epidemiología , Embarazo , Resultado del Embarazo/epidemiología , Segundo Trimestre del Embarazo , Nacimiento Prematuro/epidemiología , Factores de RiesgoRESUMEN
BACKGROUND: Gestational diabetes mellitus (GDM) is a pregnancy complication characterized by second trimester hyperglycemia. Untreated, GDM is related to an increased risk for adverse pregnancy outcomes. Both beta cell dysfunction and insulin resistance underlie impaired glucose tolerance. Understanding the dominant mechanism predisposing to GDM may be important to provide effective treatment in order to improve perinatal outcomes. We hypothesize that insulin resistance rather that beta cell dysfunction predisposes to GDM. METHODS: A 75g oral glucose tolerance test (OGTT) was performed on 2112 second-trimester pregnant women to determine the relationship between insulin resistance (HOMA-IR), beta cell function (HOMA-ß), and the prevalence of abnormal glucose handling. RESULTS: High insulin resistance raised the risk of GDM (relative risk (RR) 6.1, 95% confidence interval (CI) (4.4-8.5)), as did beta cell dysfunction (RR 3.8, 95% CI (2.7-5.4)). High insulin resistance, but not beta cell function, enhances the necessity for additional glucose lowering medication on top of a low carbohydrate diet in women diagnosed with GDM. CONCLUSIONS: Both high insulin resistance and beta cell dysfunction increase the risk of GDM. As increased insulin resistance, rather than beta cell function, is related to an insufficient response to a low carbohydrate diet, we speculate that insulin sensitizers rather than insulin therapy may be the most targeted therapeutic modality in diet-insensitive GDM.