[Relationship between the pre-pregnancy BMI, gestational weight gain, and risk of preeclampsia and its subtypes].

Objective: To explore the effects of maternal pre-pregnancy body mass index (BMI) and gestational weight gain and its subtypes on the risk of preeclampsia. Methods: Pregnant women delivered in the Department of Obstetrics and Gynecology of the First Affiliated Hospital of Shanxi Medical University from March 2012 to September 2016 were selected as the research subjects. According to the inclusion and exclusion criteria, 9 274 pregnant women were included. 901 preeclampsia pregnant women were selected as the case group, and 8 373 non-preeclampsia pregnant women were selected as the control group. General demographic characteristics, pre-pregnancy weight, height, lifestyle during pregnancy, reproductive history, and disease history of pregnant women were collected, and pre-pregnancy BMI and gestational weight gain were calculated. Unconditional logistic regression was used to analyze the relationship between pre-pregnancy BMI and weight gain during pregnancy and PE and its clinical subtypes. Results: Among the 901 preeclampsia after inclusion and exclusion, 401 cases were diagnosed as early-onset PE (EOPE), 500 cases were late-onset PE (LOPE), 178 cases were Mild PE (MPE), and 723 cases were severe PE (SPE). There were statistically significant differences between PE and non-PE pregnant women in terms of maternal age, residence, parity, family history of gestational diabetes and hypertension (P<0.05). After adjusting for the above factors, the logistic regression analysis results showed that pre-pregnancy BMI<18.5 kg/m2 and inadequate gestational weight gain were protective factors for PE (OR=0.74, 95%CI: 0.56-0.98; OR=0.78, 95%CI: 0.62-0.99), while pre-pregnancy BMI≥24.0 kg/m2 and excessive gestational weight gain were risk factors for PE (OR=1.82, 95%CI: 1.54-2.14; OR=1.82, 95%CI: 1.54-2.15). After subtype analysis on PE, the results showed that pre-pregnancy BMI<18.5 kg/m2 was a protective factor for EOPE and MPE (OR=0.52, 95%CI: 0.32-0.83; OR=0.47, 95%CI: 0.23-0.97), while pre-pregnancy BMI≥24.0 kg/m2 and excessive gestational weight gain were risk factors for clinical subtypes of PE. After stratification according to pre-pregnancy BMI, excessive gestational weight gain was the risk factor for PE (OR=1.86, 95%CI: 1.51-2.30; OR=1.90, 95%CI: 1.39-2.60) in pregnant women 18.5 kg/m2≤BMI<24.0 kg/m2 and ≥24.0 kg/m2. Inadequate gestational weight gain (OR=0.55, 95%CI: 0.34-0.89) was a protective factor for PE in pregnant women with pre-pregnancy BMI≥24.0 kg/m2. Excessive gestational weight gain (OR=4.05, 95%CI: 1.20-13.69) was a risk factor for EOPE in pregnant women with pre-pregnancy BMI<18.5 kg/m2. Excessive gestational weight gain was a risk factor for the clinical subtype of PE in pregnant women 18.5 kg/m2≤BMI<24.0 kg/m2 before pregnancy. Inadequate gestational weight gain was a protective factor for EOPE and MPE (OR=0.39, 95%CI: 0.19-0.80; OR=0.29, 95%CI: 0.11-0.77) in pregnant women with pre-pregnancy BMI≥24.0 kg/m2. Excessive weight gain was a risk factor for EOPE, LOPE and SPE (OR=1.60, 95%CI: 1.06-2.42;OR=2.20, 95%CI: 1.44-3.37;OR=2.28, 95%CI: 1.58-3.29). Conclusions: Pre-pregnancy BMI and gestational weight gain affect the risk of preeclampsia and its clinical subtypes. In contrast, the influence of gestational weight gain on preeclampsia varies among different pre-pregnancy BMI groups. Therefore, it is recommended to pay attention to the changes in pre-pregnancy BMI and gestational weight gain simultaneously to reduce preeclampsia.

[Folic acid supplementation before and during pregnancy and the risk of preeclampsia].

Objective: To investigate the relationship between folic acid supplementation and the risk of preeclampsia (PE). Methods: A total of 9 048 pregnant women were selected from the First Hospital of Shanxi Medical University in Taiyuan from March 2012 to September 2016. Among them, 882 pregnant women with PE were divided into case group, and 8 166 pregnant women without PE were divided into control group. Information on demographic characteristics, folic acid supplementation, maternal complications, and other factors were collected by face-to-face interviews after child birth in the hospital. Unconditional logistic regression analyses were used to investigate the relationship between folic acid supplementation and the risk of PE and the effects of pre-pregnancy BMI on the relationship of folic acid supplementation with the risk of PE. Results: Compared with nonusers, folic acid supplement users had reduced risk of PE (OR=0.79, 95%CI: 0.64-0.96). Folic acid supplementation before and during pregnancy were negatively related with the risk of PE (OR=0.63, 95%CI: 0.49-0.81). Pregnant women who used folic acid tablets only or used both folic acid tablets and multivitamin containing folic acid had reduced risk of PE (OR=0.81, 95%CI: 0.66-0.99; OR=0.64, 95%CI: 0.49-0.85). No significant relationship was observed in the multivitamin group. Supplemental folic acid doses of <400, 400, and >400 µg/d were related with reduced risk of PE (OR=0.62, 95%CI: 0.42-0.91; OR=0.81, 95%CI: 0.66-0.99; OR=0.68, 95%CI: 0.49-0.94). After stratified by pre-pregnancy BMI, pregnant women who used folic acid supplementation, those with pre-pregnancy BMI<24.0 kg/m(2) had reduced risk of PE (OR=0.75, 95%CI: 0.59-0.96). However, no significant relationship was observed in women with pre-pregnancy BMI≥24.0 kg/m(2). Conclusions: Folic acid supplementation before and during pregnancy were related with reduced risk of PE. Pre-pregnancy BMI might affect the relationship between folic acid supplementation and the risk of PE. Appropriate folic acid supplementation should be recommend for women with different pre-pregnancy BMI.

[Association of fat mass and obesity associated gene polymorphism with the risk of gestational diabetes].

Objective: The aim of this study is to investigate the relationship between fat mass and obesity associated (FTO) gene polymorphism and the risk of gestational diabetes mellitus (GDM), and provide clues and basis for the study of GDM mechanism. Methods: The case group of GDM pregnant women who delivered at the First Affiliated Hospital of Shanxi Medical University from March 1, 2012 to July 30, 2014 were selected, and matched the control group among non-GDM pregnant women by age, gestational age and residential address, and 324 cases and 318 controls were finally included. DNA was extracted and genotyped, and min P test and unconditional logistic regression model were used to estimate the relationship between FTO gene polymorphism and GDM. Results: At gene level, we did not find the association between FTO and the risk of GDM (P>0.05). After adjusted for family history of diabetes, pre-pregnancy body mass index and multiple comparisons using false discovery rate method, unconditional logistic regression analysis showed that pregnant women who carried the rs11075995 TT genotype (OR=0.59, 95%CI: 0.35-0.89), rs3826169 GG genotype (OR=0.59, 95%CI: 0.35-0.88), and rs74245270 GA genotype (OR=0.69, 95%CI: 0.49-0.98), GA or AA genotype(OR=0.70, 95%CI: 0.50-0.97) had reduced risk of GDM. However, pregnant women who carried the rs74018601 GA genotype (OR=1.51, 95%CI: 1.07-2.12), GA or AA genotype (OR=1.46, 95%CI: 1.06-2.02), rs7205009 AA genotype (OR=1.83, 95%CI: 1.18-2.86), GA or AA genotype (OR=1.53, 95%CI: 1.08-2.19), and rs9888758 AG genotype (OR=1.43, 95%CI: 1.02-2.00) had elevated risk of GDM. Conclusion: The polymorphisms of FTO gene rs11075995,rs3826169, rs74245270, rs74018601, rs7205009 and rs9888758 were associated with the risk of GDM.

[An animal experiment regarding the effect of lipopolysaccharide intervention program on Legionella pneumonia].

Objective: To explore the effect of lipopolysaccharide intervention program on Legionella pneumonia. Methods: C3H/HeN mice (6-8 weeks old) were used as experimental animals. The mice were randomly divided into lipopolysaccharide intervention, non-lipopolysaccharide intervention and control groups. Each group was again divided into three time points: 12 h, 24 h and 48 h. Mice in the lipopolysaccharide intervention group were intraperitoneally injected with E. coli lipopolysaccharide (100 ng per mice), and the rest groups were intraperitoneally injected with normal saline. After 24 hours, mice in the lipopolysaccharide intervention and the non-intervention groups mice were infected with Legionella by tracheal injection and the control group was given the same amount of saline. All the mice were killed at 12, 24 and 48 hours respectively. The mice were anatomized, lungs of the mice were separated and weighed. Organ coefficients (lung weight/body weight of mice) were calculated. 1 ml Orbital blood was collected. Toll-like receptor 4 (TLR4) levels of peripheral blood mononuclear cells were measured by flow cytometry. The contents of TNF-α and IL-1ß in the upper left lung lobe were measured by ELISA. Results: In the lung organs, the coefficients of lipopolysaccharide non-intervention group were higher than the other groups and there was no significant difference seen between the lipopolysaccharide intervention group and the controls. TLR4 peaked at 12 hours in both the lipopolysaccharide intervention and the non-intervention groups while the TLR4 level in the intervention group was higher than that in the non-intervention group. There were no significant differences appeared on the TLR4 expression levels between the two Legionella pneumonia modelled groups at 24 or 48 hours. There was no significant difference seen regarding the concentration of TNF-α and IL-1ß between the intervention and the control groups. The secretion levels of TNF-α and IL-1ß in the non-intervention group were higher than those in the intervention group at each time point. Conclusion: The lipopolysaccharide intervention program may alleviate the inflammatory symptoms of Legionella infection.