Semiquantitative Assessment of Amniotic Fluid Among Individuals With and Without Diabetes Mellitus

Author(s):  
Matthew J. Bicocca ◽  
Emma J. Qureshey ◽  
Suneet P. Chauhan ◽  
Edgar Hernandez‐Andrade ◽  
Baha M. Sibai ◽  
...  
1982 ◽  
Vol 142 (5) ◽  
pp. 492-496 ◽  
Author(s):  
Sharon L. Dooley ◽  
Boyd E. Metzger ◽  
Richard Depp ◽  
Norbert Freinkel ◽  
Richard L. Phelps

1996 ◽  
Vol 28 (01) ◽  
pp. 39-40 ◽  
Author(s):  
R. Di Iorio ◽  
Emanuela Marinoni ◽  
Arianna Picca ◽  
C. Letizia ◽  
E. Cosmi

1969 ◽  
Vol 61 (2) ◽  
pp. 369-377 ◽  
Author(s):  
P. Berle

ABSTRACT HCG is measured in the amniotic fluid, in the plasma of the umbilical vein and of the umbilical artery. The values are as 3:1.5:1. From the 9th week of gestation onwards appears a striking rise in the HCG concentration in the amniotic fluid reaching peak values around the 13th week. This peak is followed by a substantial decrease reaching relative constant and low values, which are sustained until the 40th week. The HCG reaches the amniotic fluid by transamnial or transchorial way. Only small amounts come from the foetus. The increased HCG concentration in the amniotic fluid and in the blood of the umbilical vein in severe erythroblastosis and in diabetes mellitus could be caused by an increased production of HCG in the placenta and/or by a decreased inactivation of HCG by means of the foetus.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
H. Bakhsh ◽  
H. Alenizy ◽  
S. Alenazi ◽  
S. Alnasser ◽  
N. Alanazi ◽  
...  

Abstract Background The amniotic fluid is a protective liquid present in the amniotic sac. Two types of amniotic fluid disorders have been identified. First refers to polyhydramnios, which is an immoderate volume of amniotic fluid with an Amniotic Fluid Index (AFI) greater than 24 cm. Second includes oligohydramnios, which refers to decreased AFI i.e., less than 5 cm. This study aims to; a) identify the maternal risk factors associated with amniotic fluid disorders, b) assess the effect of amniotic fluid disorders on maternal and fetal outcome c) examine the mode of delivery in pregnancy complicated with amniotic fluid disorders. Methods A comparative retrospective cohort study design is followed. Sample of 497 pregnant women who received care at King Abdullah bin Abdul-Aziz University Hospital (KAAUH) between January 2017 to October 2019 was included. Data were collected from electronic medical reports, and was analyzed using descriptive statistics. Association of qualitative variables was conducted by Chi-square test, where p-value < 0.05 was considered statistically significant. Results Among the collected data, 2.8% of the cases had polyhydramnios and 11.7% patients had oligohydramnios. One case of still born was identified. A statically significant association was found between polyhydramnios and late term deliveries (P = 0.005) and cesarean section (CS) rates (P = 0.008). The rate of term deliveries was equal in normal AFI and oligohydramnios group (P = 0.005). Oligohydramnios was mostly associated with vaginal deliveries (P = 0.008). Oligohydramnios and polyhydramnios were found to be associated with diabetes mellitus patients (P = 0.005), and polyhydramnios with gestational diabetes patients (P = 0.052). Other maternal chronic diseases showed no effect on amniotic fluid index, although it might cause other risks on the fetus. Conclusion Diabetes mellitus and gestational diabetes are the most important maternal risk factors that can cause amniotic fluid disorders. Maternal and fetal outcome data showed that oligohydramnios associated with gestational age at term and low neonatal birth weight with high rates of vaginal deliveries, while polyhydramnios associated with gestational age at late term and high birth weight with higher rates of CS.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Daria Di Filippo ◽  
Thiyasha Wanniarachchi ◽  
Daniel Wei ◽  
Jennifer J. Yang ◽  
Aoife Mc Sweeney ◽  
...  

Abstract Background Gestational diabetes mellitus (GDM) is glucose intolerance first recognised during pregnancy. Both modalities and thresholds of the GDM diagnostic test, the Oral Glucose Tolerance Test (OGTT), have varied widely over time and among countries. Additionally, OGTT limitations include inconsistency, poor patient tolerability, and questionable diagnostic reliability. Many biological parameters have been reported to be modified by GDM and could potentially be used as diagnostic indicators. This study aimed to 1) systematically explore biomarkers reported in the literature as differentiating GDM from healthy pregnancies 2) screen those indicators assessed against OGTT to propose OGTT alternatives. Main body A systematic review of GDM diagnostic indicators was performed according to PRISMA guidelines (PROSPERO registration CRD42020145499). Inclusion criteria were full-text, comprehensible English-language articles published January 2009-January 2021, where a biomarker (from blood, ultrasound, amniotic fluid, placenta) was compared between GDM and normal glucose tolerance (NGT) women from the second trimester onward to immediately postpartum. GDM diagnostic method had to be clearly specified, and the number of patients per study higher than 30 in total or 15 per group. Results were synthesised by biomarkers. Results Of 13,133 studies identified in initial screening, 174 studies (135,801 participants) were included. One hundred and twenty-nine studies described blood analytes, one amniotic fluid analytes, 27 ultrasound features, 17 post-natal features. Among the biomarkers evaluated in exploratory studies, Adiponectin, AFABP, Betatrophin, CRP, Cystatin-C, Delta-Neutrophil Index, GGT, TNF-A were those demonstrating statistically and clinically significant differences in substantial cohorts of patients (> 500). Regarding biomarkers assessed versus OGTT (i.e. potential OGTT alternatives) most promising were Leptin > 48.5 ng/ml, Ficolin3/adiponectin ratio ≥ 1.06, Chemerin/FABP > 0.71, and Ultrasound Gestational Diabetes Score > 4. These all demonstrated sensitivity and specificity > 80% in adequate sample sizes (> / = 100). Conclusions Numerous biomarkers may differentiate GDM from normoglycaemic pregnancy. Given the limitations of the OGTT and the lack of a gold standard for GDM diagnosis, advanced phase studies are needed to triangulate the most promising biomarkers. Further studies are also recommended to assess the sensitivity and specificity of promising biomarkers not yet assessed against OGTT. Trial registration PROSPERO registration number CRD42020145499.


2001 ◽  
Vol 35 (7-8) ◽  
pp. 859-861 ◽  
Author(s):  
Gerald G Briggs ◽  
Michael P Nageotte

OBJECTIVE: To report a case of anhydramnios, pulmonary hypoplasia, very small placenta, and fetal death in a pregnancy complicated by chronic hypertension and diabetes mellitus that had been treated through the first 24 weeks of gestation with valsartan and atenolol. CASE SUMMARY: A 40-year-old Hispanic woman with well-controlled chronic hypertension and diet-controlled type 2 diabetes mellitus was treated with valsartan and atenolol until pregnancy was diagnosed at 24 weeks' gestation. An ultrasound examination revealed normal fetal growth and anatomy but anhydramnios (amniotic fluid index 0). Valsartan was discontinued, and amniotic fluid volume normalized within two weeks. Intrauterine fetal death was documented at 33 weeks' gestation. Labor was induced, with the delivery of a stillborn female fetus with small, hypoplastic lungs (weight 41% of expected) and an extremely small, 148-g placenta (weight 48% of the 10th percentile for gestational age). DISCUSSION: The use of valsartan, a selective angiotensin II receptor antagonist (ARA), in human pregnancy has not been reported, but this class of agents would be expected to cause fetal toxicity similar to that observed with angiotensin-converting enzyme inhibitors. This toxicity includes reduced perfusion of the fetal kidneys, resulting in anuria, oligohydramnios, and subsequent pulmonary hypoplasia. The small hypoplastic lungs and very small placenta were probably a consequence of valsartan and atenolol combination therapy. CONCLUSIONS: Resolution of anhydramnios after discontinuing valsartan is evidence for ARA-induced fetal toxicity. The pulmonary hypoplasia observed in the stillborn infant was a direct result of the severe oligohydramnios. The cause of fetal death nine weeks later is uncertain, but because the woman's chronic hypertension and diabetes were well controlled, we believe the primary cause was chronic placental insufficiency resulting from the previous combination of valsartan and atenolol.


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