[Activation and significance of the PI3K/Akt pathway in endometrium with polycystic ovary syndrome patients].

OBJECTIVE: To investigate activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway in the endometrium of women with polycystic ovary syndrome (PCOS) and its role in endometrium hyperplasia and carcinogenesis, and the factors affecting the activation of the PI3K/Akt pathway. METHODS: From Jan 2007 to Jun 2008, 52 patients with PCOS who underwent dilatation and curettage were selected as experimental group matched with 32 non-PCOS patients as control group. Serous hormonal parameters, fasting blood glucose and insulin, body mass index (BMI), and endometrium pathology were measured and evaluated in all patients. The PCOS patients were divided into insulin resistance and non-insulin resistance group according to homeostasis model assessment-insulin resistance index (HOMA-IR). Meanwhile, the PCOS patients were grouped as normal, endometrial hyperplasia and carcinoma depending on outcome of pathology. The expression of Akt and phosphorylated Akt (p-Akt) were determined by western blot. RESULTS: (1) The expression of p-Akt was significantly higher in PCOS group [(46 ± 18)%] than that in control [(33 ± 9)%, P < 0.01)]. (2) The expression of p-Akt was significantly higher in group of endometrial hyperplasia and carcinoma [(56 ± 19)%] when compared with those in normal endometria group [(31 ± 12)%, P < 0.05]; the expression of p-Akt was significantly higher in group of insulin resistance [(50 ± 19)%] compared with that in non-insulin resistance group [(34 ± 10)%, P < 0.01]. (3) There was a positive correlation between the expression level of p-Akt in endometrium with PCOS and HOMA-IR and BMI respectively (r = 0.400, 0.326, both P < 0.05). CONCLUSIONS: The PI3K/Akt pathway was over activated in endometrium with PCOS which may be associated with the formation of endometrial hyperplasia and carcinoma in PCOS patients. Insulin resistance and obesity may be high risk factors for over-activation of the PI3K/Akt pathway in endometrium with PCOS.

Virologic and clinical characteristics of HBV genotypes/subgenotypes in 487 Chinese pediatric patients with CHB.

BACKGROUND: The association of hepatitis B virus (HBV) genotypes/subgenotypes with clinical characteristics is increasingly recognized. However, the virologic and clinical features of HBV genotypes/subgenotypes in pediatric patients remain largely unknown. METHODS: Four hundred and eighty-seven pediatric inpatients with CHB were investigated, including 217 nucleos(t)ide analog-experienced patients. HBV genotypes/subgenotypes and reverse transcriptase (RT) mutations were determined by direct sequencing. The stage of fibrosis and degree of inflammatory activity were evaluated by the Metavir score system. RESULTS: Among 487 enrolled pediatric patients, HBV genotype C2 and B2 were the most two prevalent (73.7% and 21.1%). Comparing with HBV/B2 infected patients, no significant difference was observed in the incidence rate and mutant patterns of lamivudine- or adefovir-resistant mutations in HBV/C2 infected patients (P > 0.05). Importantly, we found that the degree of hepatic inflammation degree, fibrosis stage and ALT level were significantly higher in HBV/C2-infected HBeAg positive patients than it was in HBV/B2-infected ones. CONCLUSIONS: The pediatric patients with HBV/C2 infection might be more susceptible to develop severe liver pathogenesis.

[Extracellular signal-regulated protein kinase activation in endometrium with polycystic ovary syndrome and its significance].

OBJECTIVE: to investigate the activation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) signaling pathway in the endometrium of women with polycystic ovary syndrome (PCOS) and its effect and significance in the cause of hyperplasia and carcinoma; and investigate the factors which affect the activation of the MAPK/ERK signaling pathway. METHODS: collected 52 patients diagnosed as PCOS who were taken dilation and curettage of uterus as study, while 32 non-PCOS patients matched as control group. Serum hormonal parameters, fasting blood glucose and insulin were measured in all patients. The PCOS patients were sub-group as insulin resistance group and non-insulin resistance group; all the patients were carried out pathology inspection of endometria, and the PCOS patients were sub-group as endometrial hyperplasia and carcinoma group and normal endometrium group based on the outcome of pathology inspection. Western blot were performed to detect the expressions of ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2), the activation of ERK1/2. RESULTS: (1) the expression of p-ERK1/2 [(61 ± 13)%] in the endometrium in PCOS group was higher than that in the control [(44 ± 10)%, P < 0.01]. (2) The expression of p-ERK1/2 was significantly increased in group of endometrial hyperplasia and carcinoma [(70 ± 11)%] compared to that in group of normal endometrium [(55 ± 10)%, P < 0.01], while there were significant difference between group of insulin resistance [(63 ± 13)%] and group of non-insulin resistance [(55 ± 7)%, P < 0.01]. (3)Fasting insulin level, insulin area under the curve and body mass index were related to the expression of p-ERK1/2 in endometrium with PCOS, the correlation coefficient were 0.447, 0.456 and 0.381, respectively (all P < 0.01). CONCLUSIONS: the MAPK/ERK signaling pathway in endometrium with PCOS was overactivation, which was related to the endometrial hyperplasia and carcinoma; while the activation of MAPK/ERK signaling pathway were effected by insulin resistance and hyperinsulinemia.

[Clinical significance of dynamic pressure-volume curve in neonatal mechanical ventilation].

OBJECTIVE: To study the characteristics and role of dynamic pressure-volume curve (P-V curve) in neonatal mechanical ventilation. METHODS: A dynamic P-V curve was automatically drawn by the Stephanie ventilator. The slope rate of dynamic P-V curve was measured in 25 neonates who received mechanical ventilation 1, 24, 48 and 72 hrs after ventilation and before weaning from ventilation. Minute-ventilation (MV), mean airway pressure (Pmean), and fraction of inspired oxygen (FiO2) were recorded. The patterns of dynamic P-V curve during abnormal ventilation (resistance to ventilator, part or complete airway obstruction, airway leaking and tracheal catheter exodus) were observed. RESULTS: With the improvement of pulmonary disease, the slope rate of P-V curve and MV increased, Pmean and FiO2 decreased, and the P-V curve shifted to the volume axle. The slope rate of curve 48 and 72 hrs after ventilation and before weaning from ventilation (1.05+/-0.48, 1.10+/-0.42 and 1.13+/-0.37 mL/cmH2O respectively) increased significantly compared with that 1 hr after ventilation (0.76+/-0.53 mL/cmH2O) (p<0.05 or 0.01). Abnormal ventilation led to abnormal appearance of dynamic P-V curve. CONCLUSIONS: The increasing slope rate of dynamic P-V curve and the curve shifting to volume axle in neonatal mechanical ventilation may be associated with the improvement of pulmonary disease. The appearance changes of the curve may be of value in the assessment of abnormal ventilation.

[Value of blood apoH gene expression and urinary NAG and RBP in early diagnosis of renal function damage in neonates].

OBJECTIVE: To study the value of apolipoprotein H (apoH) gene expression in peripheral blood mononuclear cell (PBMC) and urinary N-Acetyl-beta-D-Glucosaminidase (NAG) and retinal-binding protein (RBP) in the early diagnosis of renal function damage in neonates. METHODS: Sixty sick neonates who renal function damage probably occurred were enrolled. The blood and urinary samples were collected twice within 48 hrs following admission, with an interval of 12-24 hrs. Expression of apoH gene in PBMC was determined with RT-PCR. The levels of blood urea nitrogen (BUN) and creatinine, and urinary activities of NAG and RBP were measured with enzymatic reaction. RESULTS: The abnormal rates of blood apoH and urinary NAG and RBP were 73.3%, 83.3% and 76.7%, respectively in the first detection. The second detection for blood apoH and urinary NAG and RBP showed abnormal rates of 70.0%, 66.7% and 76.7%, respectively. There were no significant differences in the abnormal rates between the three markers either in the first or the second detection (P>0.05). Beside there were no significant significances in the abnormal rates between urinary NAG and blood BUN in the second detection, the abnormal rates of blood apoH and urinary NAG and RBP in both detections were significantly higher than those of BUN or creatinine (P<0.01 or 0.05). CONCLUSIONS: There are identical values of blood apoH gene expression and urinary NAG and RBP in the early diagnosis of renal function damage in neonates. The above three markers are more sensitive to early renal function damage than blood BUN and creatinine.

[Efficacy of hyperbaric oxygen therapy under different pressures on neonatal hypoxic-ischemic encephalopathy].

OBJECTIVE: Some research has shown that hyperbaric oxygen (HBO) can decrease the rate of mortality and disability caused by hypoxic-ischemic encephalopathy (HIE) in neonates. However, the HBO pressure used in the clinical reports and the efficacy of HBO are different. This study was designed to investigate the efficacy of HBO therapy under different pressures by observing the changes of peroxidation, antioxidant levels and brain vasomotor regulation factors as well as the score of neonatal behavioral neurological assessment (NBNA) in neonates with HIE after HBO therapy. METHODS: Sixty neonates with HIE were randomly administered with 1.4, 1.5 or 1.6 atmosphere absolute (ATA) of HBO, once daily for seven days. Serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide (NO) and nitric oxide synthase (NOS) were measured before and after HBO therapy. Meanwhile, NBNA and eye ground examination were performed. RESULTS: Serum SOD level increased and serum levels of MDA, NO and NOS decreased significantly after HBO therapy in the three HBO therapy groups (P<0.01). Serum SOD level was significantly higher and serum levels of MDA, NO and NOS were significantly lower in the 1.6 ATA HBO group than those in the 1.4 ATA group after therapy (P<0.05). The 1.6 ATA HBO group also showed increased SOD and decreased MDA levels compared with the 1.5 ATA HBO group after therapy (P<0.05). NBNA scores in the three groups increased significantly after HBO therapy (P<0.05). None of the three HBO therapy group patients showed abnormal eye grounds after therapy. CONCLUSIONS: HBO therapy with 1.4, 1.5 or 1.6 ATA is safe and effective for neonatal HIE. The antioxidant capacity increases with the increasing HBO pressure in neonates with HIE.

[Risk factors for intracranial hemorrhage in very low birth weight infants].

OBJECTIVE: To study the risk factors for intracranial hemorrhage in very low birth weight infants. METHODS: Data from 169 very low birth weight (VLBW) infants (birth weight 1000-1500 g; gestational age 23-36 weeks) were studied retrospectively. Twenty-nine perinatal and postnatal factors were analyzed by Crosstabs Test with SPSS 12.0. A logistic regression analysis was used to identify the risk factors associated with the development of intracranial hemorrhage. RESULTS: Multivariate logistic analysis revealed that rupture of membranes (OR=0.146, 95%CI=0.22-0.964, P < 0.05), 1-minute Apgar score < or = 7 (OR=0.112, 95%CI=0.21-0.591, P < 0.01), pulmonary surfactant therapy (OR=0.110, 95%CI=0.24-0.504, P < 0.01), mechanical ventilation therapy (OR =0.076, 95%CI=0.009-0.668, P < 0.05), mechanical ventilation duration > 72 hrs(OR=0.053, 95%CI=0.007-0.410, P < 0.01), prothrombin time > 20 seconds (OR=4.186, 95%CI=1.606-10.923, P < 0.01), pH value on day 1 of life < 7.25 (OR=0.421, 95%CI=0.179-0.995, P < 0.05) and hyponatremia on day 1 (OR= 0.27, 95%CI=0.077-0.940, P < 0.05) or 2 (OR=2.480, 95%CI=1.053-5.838, P < 0.05) of life were risk factors for intracranial hemorrhage. CONCLUSIONS: 1-minute Apgar score < or =7 and mechanical ventilation treatment were leading risk factors for intracranial hemorrhage, followed by abnormal coagulation and electrolytes related to perinatal asphyxia in VLBW infants. These findings can be used to improve the surveillance and prophylaxis measures in VLBW infants at high risk.

[Risk factors for bronchopulmonary dysplasia in neonates with respiratory distress syndrome].

OBJECTIVE: To identify the risk factors for bronchopulmonary dysplasia (BPD) in neonates with respiratory distress syndrome (RDS). METHODS: Data from 72 patients with RDS (birth weight 1607 +/- 277 g; gestational age 29.47 +/- 2.54 weeks) who were hospitalized for >28 days and who received mechanical ventilation treatment between January 2001 and August 2005 were studied retrospectively. A logistic regression analysis was used to identify the risk factors associated with the development of BPD. RESULTS: Of the 72 patients, 17 developed BPD (23.6%). Uniovariate analysis revealed that in addition to a gestational age of < or = 30 weeks and a birth weight below 1250 g, the times of mechanical ventilation treatment (> or = 2 times), concurrent pulmonary infection and pneumorrhagia, prolonged mechanical ventilation (> or = 5 days), and positive sputum bacterial cultures on 2 occasions were all associated with an increase in the incidence of BPD. Multivariate logistic analysis revealed that birth weight below 1250 g, prolonged mechanical ventilation (> or = 10 days),and positive sputum cultures on 3 or more occasions were independent risk factors for BPD (OR=6.614,14.997 and 39.752 respectively). CONCLUSIONS: The risk for BPD is multifactorial. Preventing small gestational age and low birth weight prematurity, decreasing the duration of mechanical ventilation and treatment of pulmonary infection are necessary to prevent BPD.

[Clinical features of 35 cases of autoimmune hepatitis-primary biliary cirrhosis overlap syndrome].

OBJECTIVE: To realize the clinical features of autoimmune hepatitis-primary biliary cirrhosis (AIH+PBC) overlap syndrome. METHODS: We analyzed and compared the biochemistry, autoimmune antibodies, and liver biopsy results of 129 autoimmune hepatic disease cases retrospectively, using the international criteria to see which could be diagnosed as AIH/PBC overlap syndrome. RESULTS: Our 35 AIH+PBC overlap syndrome patients were mainly women, with a sex ratio of 1 female: 10 male, and a median age of 50.79+/-11.27 (20 to 70 years old). They had AIH characteristics such as flare of ALT, AST and elevated immunoglobulin G (IgG), gamma-immunoglobulin. There were also antinuclear antibodies (74.3%); moderate or severe periportal or periseptal lymphocytic infiltration, piecemeal necrosis, and florid bile duct lesions, high serum levels of ALP, presence of mitochondrial antibodies (68.6%) and M2 antibodies (45.7%), and features of PBC. CONCLUSIONS: AIH+PBC overlap syndrome is not rare. It should be diagnosed in time and to find effective treatments for it.

[To re-evaluate the clinical classification criteria of liver failure].

OBJECTIVE: To study the clinical feature and more reasonable diagnostic typing criteria for patients with liver failure. METHODS: 13/21 cases of ALF, SALF with no past liver disease, 49/72 cases of with chronic hepatitis, and 23/73 cases ALF, SALF with liver cirrhosis, were analyzed respectively. RESULTS: 1 ALF patients (1). There exist significant statistic differences in ALB, ALT, CHE in three ALF groups.(2). It had statistic differences in those patients with hepatic encephalopathy.(3). The prognosis of the patients with chronic hepatitis group (42.85 percent) was best than that of chronic cirrhosis (26.09 percent) and no past liver disease (15.38 percent). (2) In SALF patients (1). There exist significant statistic differences in ALB, GLO, ALT, AST, BDIL, GLU and CHE in three SALF groups.(2). It had statistic differences in those patients with hepatic encephalopathy in three SALF groups.(3). The prognosis of the patients with chronic hepatitis group (51.39 percent) was best than that of chronic cirrhosis (36.85 percent) and no past liver disease (33.33 percent). CONCLUSION: There are different clinic feature and prognosis in three ALF or SALF groups, so we suggest that it were clinic practicability and science in classify of liver failure at present.

[Reevaluation of the typing criteria for patients with chronic severe hepatitis].

BACKGROUND: To study the clinical features and more reasonable typing criteria for patients with chronic severe hepatitis and decompensated liver function. METHODS: Data of 106 cases of decompensated cirrhosis, 124 cases of chronic liver failure and 100 cases of chronic liver failure (chronic liver failure group I, CLF I) with decompensated cirrhosis (chronic liver failure group II, CLF II) were analyzed retrospectively. RESULTS: (1) The ages were youngest in chronic liver failure group I (about 30 years), and the oldest in decompensated cirrhosis group (about 50 years). (2) There were significant differences in albumin, globulin, ALT, AST, protruding activity, blood glucose, blood lipid and cholinesterase among the three groups. (3) There was no significant difference in upper digestive tract bleeding and hepatorenal syndrome, on the other hand, there was significant difference in ascites and hepatic encephalopathy. (4) The prognosis of the patients in decompensated cirrhosis group was better than that of chronic liver failure group I and chronic liver failure group II. CONCLUSION: The clinical feature and prognosis in three groups were different, so, it is suggested that chronic severe liver disease be divided into 2 types: one is chronic severe liver disease type I, which is associated with chronic hepatitis, and the other is chronic severe liver disease type II, which is associated with cirrhosis, and the typing criteria for decompensated cirrhosis remains unchanged.

[Changes of platelet endothelial cell adhesion molecule-1, tissue type plasminogen activator and plasminogen activator inhibitor-1 expression in the lung tissue of neonatal rats after intraperitoneal injection with lipopolysaccharide].

OBJECTIVE: To further explore the pathogenesis of neonatal acute lung injury and neonatal pulmonary hemorrhage by establishing the animal model of neonatal acute lung injury (ALI) and by investigating the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1), tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in ALI. METHODS: Totally 88 neonatal rats which were divided into 8 groups randomly including one normal saline control group and 30 min, 1 h, 2 h, 4 h, 8 h, 16 h and 24 h post injection groups. The changes of lung pathology in newborn rats were observed at different time after LPS was injected intraperitoneally. The changes of PECAM-1 protein, t-PA and PAI-1 mRNA expression were measured by immunohistochemistry and RT-PCR. RESULTS: The expression of PECAM-1 protein and mRNA was decreased and the lowest level was reached at 8 h and 16 h post injection, respectively. The average values were 95.1 +/- 9.76 and 0.861 +/- 0.016, respectively, which were significantly lower than those in the control group (129.5 +/- 6.15, 1.192 +/- 0.035, P < 0.01). The expression of t-PA and PAI-1 mRNA was increased after LPS was injected. The highest level of t-PA mRNA expression was observed at 2 h after injection. The average value was 1.195 +/- 0.036, which was significantly higher than that in the control group (0.781 +/- 0.017, P < 0.01). The highest level of PAI-1 mRNA expression was observed at 2 h, 4 h and 8 h post injection. The average values were 1.178 +/- 0.069, 1.153 +/- 0.036 and 1.176 +/- 0.044, respectively, which was significantly higher than those of the control group (0.681 +/- 0.019, P < 0.01). CONCLUSIONS: The expression of PECAM-1 protein and mRNA was decreased after LPS injection, suggesting the disruption of the tissue protective mechanism; the expression of t-PA and PAI-1 mRNA was increased, indicating the presence of a hypercoagulability state. At the same time, the expression of t-PA mRNA was increased which caused the extra-cellular matrix degradation at the early phase after LPS injection. These three phenomena might be the contributory factors to pulmonary hemorrhage.

[Effect of intrauterine acute ischemic-hypoxia on the expression of lung SP-A and SP-B in neonatal rats].

OBJECTIVE: Neonatal asphyxia is one of the main causes for the acute respiratory distress syndrome (ARDS) in full-term newborns. Now it is believed that the reduced amount and abnormal function of pulmonary surfactant due to various causes is a major factor leading to acute lung injury. This study aimed at using an intrauterine acute ischemic-hypoxia rat model and investigating the effect of intrauterine acute ischemic-hypoxia on the expression of surfactant protein A (SP-A) and surfactant protein B (SP-B) in neonatal rat lungs. METHODS: The rat model of acute intrauterine ischemic-hypoxia was established by ligating the unilateral uterine horn vessels of Wistar rats at the 21st gestational day. While the rat pups from the other side of the uterus, of which the uterine horn vessel was not ligated, were the sham-operation group. Rat pups were delivered by cesarean section at the 20, 30 and 40 min following the ischemic-hypoxia insult. The rat pups delivered by cesarean section from the gestation of 21 days were the normal control group. There were 42 rat pups and 6 pups in each group in this study. The distribution of SP-B protein in the neonatal rat lungs of different period of ischemia was examined by using SABC method. The average gray value of SP-B staining in type II alveolar epithelial cells were measured by Universal Imaging Porporation with Meta Morph software. The reverse transcription polymerase chain reaction (RT-PCR) was performed to quantitate the expression of SP-A and SP-B mRNA. RESULTS: Following the intrauterine acute ischemic-hypoxia, the numbers of type II alveolar epithelial cells with the positive SP-B staining were markedly declined. The average gray values at the 20, 30 and 40 min after the ischemia were 78.89 +/- 1.08, 79.69 +/- 0.13 and 80.00 +/- 0.63, respectively, which increased significantly compared with the normal control group (76.13 +/- 0.43, P < 0.01). The expression of SP-A and SP-B mRNA was weak following the ischemic-hypoxia insult. The relative amounts of SP-A (1.16 +/- 0.06, 1.14 +/- 0.01 and 1.13 +/- 0.04, respectively) and SP-B (0.81 +/- 0.02, 0.78 +/- 0.02 and 0.79 +/- 0.04, respectively) at the 20, 30 and 40 min after the ischemia were reduced significantly compared with controls (1.27 +/- 0.09 and 0.89 +/- 0.06, respectively, P < 0.05 and < 0.01) and reduced gradually following the prolongation of the insult. There were no significant differences (P > 0.05) between the normal and sham operation control groups on the expressions of SP-B protein as well as the SP-A and SP-B mRNA. CONCLUSION: The reduced synthesis of SP-B protein and the reduced expression of SP-A and SP-B mRNA might be caused by intrauterine acute ischemic-hypoxia, which may support theoretically the early application of pulmonary surfactant including SP-A and SP-B for treating the lung injuries of asphyxia in newborns.

[Blood motilin concentration and enteral nutrition in premature infants].

OBJECTIVE: To study changes of plasma motilin concentration and it's effect on enteral nutrition in premature infants. METHODS: The plasma motilin concentration of 72 premature infants was measured within 12 hours after birth before enteral feeding and on day 3 and 7 of life by using radioimmunoassay. Sixteen full-term neonates were enrolled as controls. RESULTS: (1) The plasma concentrations of motilin in premature infants before enteral feeding after birth and on day 3 and 7 were 198.65 +/- 58.42 ng/L, 248.83 +/- 56.00 ng/L, and 376.77 +/- 139.46 ng/L, respectively, which were significantly lower than those in the control group (300.33 +/- 67.15 ng/L, 334.26 +/- 83.81 ng/L, 510.64 +/- 179.85 ng/L) (P < 0.001 or < 0.01). There was positive correlation between the concentration and gestational age, age in day and the volume of milk. On day 7 the level of motilin was higher than the pre-enteral feeding level of the full term control group. (2) The plasma motilin concentration in feeding un-tolerated premature infants group was lower than that in the normal group, especially on day 3 of life (P < 0.05). (3) Early enteral feeding could improve the plasma motilin levels, gastrointestinal motility and nutrition tolerance in premature infants. CONCLUSIONS: The gastrointestinal functions of premature infants are adaptable to enteral nutrition. Early enteral feeding (including minimal enteral nutrition and non-nutritive sucking) can promote adaptive rapid growth and development of intestine.

Etude des causes des infections du liquide amniotique avant l'accouchement

Au cours de ces travaux; les auteurs ont observe 115 cas de grossesses normales. L'age gestationnel est compris entre 37 et 42 semaines. Les patientes sont reparties en deux groupes: celles examinees par voie rectale (groupe rectal G.R.) et celles faisant l'objet d'un examen par voie vaginale (Groupe vaginal G.V.). Le liquide amniotique preleve par ponction trans-abdominale; a ete examine au microscope apres coloration de Gram. Ils ont pu ainsi proceder a la numeration des globules blancs necrotiques et a celles des bacteries. Le resultat de l'examen montre que le taux d'infection du liquide amniotique varie avec la methode d'examen pratiquee avant l'accouchement. Le taux d'infection est de 100 pour cent pour les patientes ayant contacte un rapport sexuel une semaine avant l'accouchement. Le taux d'injection chez les patientes presentant une perte des eaux est fonction du delai qui s'ecoule entre la rupture des membranes et l'accouchement. Il est d'un grand interet de promouvoir la pratique de l'examen rectal pour la surveillance des parturientes; afin de reduire l'incidence de l'infection iatrogene. La necessite d'un declenchement artificiel du travail aussitot que possible est a souligner pour les patientes ayant perdu les eaux. Il est interdit de contacter un rapport sexuel une semaine avant l'accouchement