Gestational diabetes is also known as gestational diabetes mellitus (GDM), is a medical condition that arises in women who have never experienced diabetes before but have high glucose level in their blood in their gestational period. Diabetes mellitus affects 19% of most pregnancies, it is on the rise given the present lifestyles in which a lot of sugar is taken, and the body exhibits insulin resistance. In this case, the body fails to produce enough insulin and uses the produced insulin for pregnancy leaving the body devoid of insulin-making the level of glucose in the blood exceptionally high (hyperglycemia).
There are a number of foetal tests that can be useful in the determination of the foetal activity during mid pregnancy. Foetal testing methods like the biophysical profile, NST and arterial-wave- form velocities is the basic for the determination of problematic pregnancy in the foetal development in the first 11 weeks of pregnancy. The methods may be time consuming, but are useful in the determination of the problem in the development of the foetus and making of proper decisions during pregnancy. Foetal responses to external stimuli such as sound are the main enablers of this success of these experiments.
Ross, M. G., Ervin, M. G., Novak, D. (2007). Chapter 2 fatal physiology. In S. Gabbie, J. Niebyl, & J. Simpson (Eds.), Obstetrics: Normal and problem pregnancies (pp. 26-33). Philadelphia, PA: Churchill Livingstone Elsevie
There are a number of factors that control the transfer of glucose from the maternal blood to the foetus. In steady, the metabolically consumption of the human placenta is responsible for division of the glucose between the two main membranes in the microvillus and the absolute diffusion in the placenta. The most influential factors in this diffusion in the glucose transfer between the mother and the foetus is the facilitated diffusion process. This process is mainly at the basal membranes.
The permeability of the basal membrane and the density of GLUT 1 (fluid) is extremely valuable. The gradient between the foetal and the maternal glucose concentration is particularly serious just like the metabolic consumption of the placenta. Diffusion inside the placenta and the key conditions that exist at the apical microvillus plasma membrane are not terrifically significant. The Intrasyncytial concentration of glucose is almost the same as that of the maternal blood. Adjustments in the foetal glucose concentration due to the abrupt changes in the environment are minimal meaning the foetal is living in a steady state
Barta, E., & Drugan, A. (2010). Glucose transport from mother to foetus— A theoretical study. Journal of Theoretical Biology, 263, 295-302. doi: 10.1016/j.jtbi.2009.12.010
Maternal is hypoglycaemia is claimed to be severe than the diabetes mellitus associated with the increasing risks of adverse pregnancy result. The results of the research indicated a number of disparities. There is significant and continuous relationship between maternal f=glucose levels bellow diagnosis of diabetes and an increased weight at birth and increased cord blood serum C-peptides level.
The results of the research indicated a number of disparities. There is significant and continuous relationship between maternal glucose levels bellow diagnosis of diabetes and an increased weight at birth and increased cord blood serum C-peptides level. While this level is strongly associated with the maternal glycaemia, it is also attributed to physiological consequences of maternal glycaemia. The primary caesarean delivery and clinical and clinical neonatal hypoglycaemia, premature delivery, birth injury, preeclampsia and hyperbilirubinemia are linear to high plasma glucose and high foetal plasma glucose level which are both resulting from maternal glycaemia. All these are complications that arise out of pregnancies in those mothers with gestational diabetes. Our results indicate strong, continuous associations of maternal glucose levels below those diagnostic of diabetes with increased birth weight and increased cord-blood serum C-peptide levels.
Lawlor, D. A., Fraser, A., Lindsay, R.S., Ness, A., Dabelea, D., Catalano, P., Nelson, S. M. (2010). Association of existing diabetes, gestational diabetes and glycosuria in pregnancy with macrosomia and offspring body mass index, waist and fat mass in later childhood: Findings from a prospective pregnancy cohort. Diabetologia, 53, 89-97. doi: 10.1007/s00125-009-1560-z
Pregnancy obesity is strongly correlated to increased risk factor in pregnancy. This association makes gestational pregnancy a serious public health issue. It is necessary to note those adverse pregnancy outcomes like GDM (Gestational diabetes mellitus) gestational hypertension and foetal macrosomia and other complications. Those women with a high body mass index are at high risk for developing gestational diabetes mellitus (GDM). This results into foetal disorders. Gestational obesity is a key issue.
Consequences related to weight gain during this period include increased risks of retaining extra weight after caesarian sections, caesarian section, postpartum obesity and increased likelihood of undesired diabetes and high blood pressure, Adverse effect in the development of the fetus, and preterm delivery. Amongst the risks, listed above, diabetes are the most adverse as it affects both the fetus and the mother. However, there are cynical measures that are instrumental in correcting such medical conditions, the main ones include physical activity and dietary measures during the gestation period
Henderson, M. Gunderson, E. P., & Ferrara, A. (2010). Gestational weight gain and risk of gestational diabetes mellitus. Obstetrics and Gynecology, 115(3), 597-604.
The researcher aimed at determining if the metabolic changes during the gestational periods are varying with the gestational glucose tolerance status. Women with GDM and mild glucose intolerance during the gestation period are at risk of type 2 diabetes in their later life. These changes in year one postpartum have varying degree of glucose tolerance
This research involved testing women for glucose challenge test and oral glucose test: GCT and ODTT respectively during postpartum months. The antepartum testing identified 4gestational glucose tolerance groups: GDM (n = 107); gestational impaired glucose tolerance (GIGT) (n = 75); abnormal GCT with normal glucose tolerance (NGT) on OGTT (abnormal GCT NGT) (n = 137); and normal GCT with NGT on OGTT (normal GCT NGT) (n = 73).
The prevalence of dysglycemia gradually increases across the set from the normal GCTNGT TO abnormal GCT NGT to GIGT to GDM at 3 months postpartum(2.7% to 10.2% to 18.7% to 34.6%, P < 0.0001) and 12 months’ postpartum (2.7% to 11.7% to 17.3% to 32.7%, P < 0.0001). However, there was no disparity between the groups between in relations to changes in waist circumference, weight, or insulin sensitivity. However, there were the difference in the changes in β-cell function (Insulin Secretion-Sensitivity Index-2 [ISSI-2]) (P = 0.0036), with ISSI-2 diminishing in both the GDM and GIGT groups. In addition, on MR analysis, both GDM (t = –3.06, P = 0.0024) and GIGT (t = –2.18, P = 0.03) was exhibited as negative predictors of the change in ISSI-2 between 3 and 12 months’ postpartum. This is the only contributor to the future cause of diabetes
Retnakaran, R., Qi, Y., Sermer, M., Connelly, P. W., Hanley, A. J. G., Zinman, B.{beta}-Cell Function Declines Within the First Year Postpartum in Women With Recent Glucose Intolerance in Pregnancy: Diabetes Care, Volume: 33, Issue: 8, Pages: 1798 to 1804
This research aimed at determining the most cost effective clinical measure for screening gestational diabetes. The cost effectiveness refereed to the risk factors associated with the methods. The two stage screening method of glucose challenge test and oral glucose tolerance test and universal OGITT with or without fasting. There were no prenatal deaths. There is remarkable reduction when treatment was administered as opposed to usual care in many secondary results, this included mean birth weight (3302 vs. 3408 g), neonatal fat mass (427 vs. 464 g), the frequency of large-for-gestational-age infants (7.1% vs. 14.5%), birth weight greater than 4000 g (5.9% vs. 14.3%), shoulder dystocia (1.5% vs. 4.0%), and caesarean delivery (26.9% vs. 33.8%). Treatment of gestational diabetes mellitus, in comparison to usual care is correlated to minimized rates of preeclampsia and gestational hypertension (combined rates for the two conditions, 8.6% vs. 13.6 (%); P=0.01).
Conclusions: while the treatment for mild gestational diabetes mellitus does not remarkably reduce the frequency of composite outcomes such as still births or prenatal deaths and other neonatal complications, it also reduces the risk of foetal overgrowth shoulder dystocia, caesarean delivery, and hypertensive disorders
Landon, M. B., Sponge, C. Y., Thom, E., Carpenter, M. W., Ramin, S. M., Casey, B., Anderson, G. B. ( 2009). A multicenter, randomized trial of treatment for mild gestational ‘diabetes. The New England Journal of Medicine, 361(14), 1339-1348
Metformin is a logical treatment for women with gestational diabetes mellitus, but randomized trials to assess the efficacy and safety of its use for this condition are lacking. This experiment focuses on the women d=with gestational diabetes mellitus during the gestation period (23-33) weeks into gestation. This involved the use of metformin and insulin supplement. Then researchers realised that this form of intervention resulted into a composite of neonatal hypoglycaemia, respiratory distress, necessitating the need for phototherapy, birth trauma, 5-minute Apgar score less than 7, or prematurity. The experiment was initially designed to rule out 32% increase in the in the composite outcome in the infants of those women who received metformin. This was in comparison to those who received insulin injection during their gestation period. The main secondary result included neonatal anthropometric measurements, maternal glycemic control, maternal hypertensive complications, postpartum glucose tolerance, and acceptability of treatment.
Among the women who were treated with metformin, 92.6% were given metformin until delivery and 46.3% given supplemental insulin. The speed of the primary composite outcome was 32.0% among those women assigned to metformin and 32.2% among the insulin group; this had a relative risk of 1.00; 95% confidence interval, 0.90 to 1.10. The response was that the most women who received metformin injection preferred receiving metformin injection rather than insulin. On the other hand, they indicated they would prefer receiving the sane intervention the next time they are pregnant: 76.6% vs. 27.2 (%), P<0.001). However, the rate of acceptance of the treatment methods did not differ much between the two groups (those treated with metformin and those treated with insulin) additionally metformin did not have serious adverse effects.
Rowan, J. A., Hague, W. M., Gao, W., Battin, M. R., & Moore, M. P. (2008). Metformin versus insulin for the treatment of gestational diabetes. The New England Journal of Medicine, 358(19), 2003-2015.
When scientist tested 25,505 pregnant women at 15 centres in nine countries by giving 75-g oral glucose-tolerance testing at 24 to 32 weeks of gestation, no data was collected. Among the fastingwomen, plasma glucose level was 105 mg per deciliter (5.8 mmol per liter) or less and the 2-hour plasma glucose level was 200 mg per deciliter (11.1 mmol per liter) or less. The main outcomes at the primary level high birth weight, primary cesarean delivery, clinically diagnosed neonatal hypoglycemia, and cord-blood serum C-peptide level above the 90th percentile. Secondary outcomes included a delivery before 37 weeks of gestation, shoulder dystocia or birth injury, need for intensive neonatal care, hyperbilirubinemia, and preeclampsia.
For those women with blinded data, the adjusted odds ratios for unfavourable pregnancy outcomes related to increases in the fasting plasma glucose level of 1 SD (6.9 mg per deciliter [0.4 mmol per liter]). There was an increase in the 1-hour plasma glucose level of 1 SD (30.9 mg per deciliter [1.7 mmol per liter]). Later an increase in the 2-hour plasma glucose level of 1 SD (23.5 mg per deciliter [1.3 mmol per liter]) was conducted. For birth weight above the 90th percentile, the odds ratios were 1.38 (95% confidence interval [CI], 1.32 to 1.44), 1.46 (1.39 to 1.53), and 1.38 (1.32 to 1.44), respectively; for cord-blood serum C-peptide level above the 90th percentile, 1.55 (95% CI, 1.47 to 1.64), 1.46 (1.38 to 1.54), and 1.37 (1.30 to 1.44); for primary caesarean delivery, 1.11 (95% CI, 1.06 to 1.15), 1.10 (1.06 to 1.15), and 1.08 (1.03 to 1.12); and for neonatal hypoglycaemia, 1.08 (95% CI, 0.98 to 1.19), 1.13 (1.03 to 1.26), and 1.10 (1.00 to 1.12). It is necessary to note that there were no observable thresholds at which risks increased.
The results also proved that there was a strong, continuous relationship of maternal glucose levels which was lower than those diagnostic of diabetes with increased birth weight and increased cord-blood serum C-peptide levels.
The HAPO Study Cooperative Research Group. (2008). Hyperglycaemia and adverse pregnancy outcomes. The New England Journal of Medicine, 358(19), 1991-2002.
Summary
Plasma glucose level was 105 mg per deciliter (5.8 mmol per liter) or less and the 2-hour plasma glucose level was 200 mg per deciliter (11.1 mmol per liter) or less. The main outcomes at the primary level high birth weight, primary cesarean delivery, clinically diagnosed neonatal hypoglycemia, and cord-blood serum C-peptide level above the 90th percentile. Secondary outcomes included a delivery before 37 weeks of gestation, shoulder dystocia or birth injury, need for intensive neonatal care, hyperbilirubinemia, and preeclampsia. There is a strong, continuous relationship of maternal glucose levels which was lower than those diagnostic of diabetes with increased birth weight and increased cord-blood serum C-peptide levels.
Additionally the rate of acceptance of the treatment with metformin does not differ much (those treated with metformin and those treated with insulin) additionally metformin did not have serious adverse effects
References
Landon, M. B., Sponge, C. Y., Thom, E., Carpenter, M. W., Ramin, S. M., Casey, B., Anderson,.. B. (2009). A multicenter, randomized trial of treatment for mild gestational diabetes. The New England Journal of Medicine, 361(14), 1339-1348
Retnakaran, R., Qi, Y., Sermer, M., Connelly, P. W., Hanley, A. J. G., Zinman, B.{beta}-Cell Function Declines Within the First Year Postpartum in Women With Recent Glucose Intolerance in Pregnancy: Diabetes Care, Volume: 33, Issue: 8, Pages: 1798 to 1804
Henderson, M. M., Gunderson, E. P., & Ferrara, A. (2010). Gestational weight gain and riskof gestational diabetes mellitus. Obstetrics and Gynecology, 115(3), 597-604.
Lawlor, D. A., Fraser, A., Lindsay, R.S., Ness, A., Dabelea, D., Catalano, P. Nelson, S. M. (2010). Association of existing diabetes, gestational diabetes and glycosuria in pregnancy with macrosomia and offspring body mass index, waist and fat mass in later childhood: Findings from a prospective pregnancy cohort. Diabetologia, 53, 89-97. doi: 10.1007/s00125-009-1560-z
Barta, E., & Drugan, A. (2010). Glucose transport from mother to foetus— A theoretical study. Journal of Theoretical Biology, 263, 295-302. doi: 10.1016/j.jtbi.2009.12.010
Landon, M. B., Sponge, C. Y., Thom, E., Carpenter, M. W., Ramin, S. M., Casey, B., Anderson, G. B. (2009). A multicenter, randomized trial of treatment for mild gestational diabetes. The New England Journal of Medicine, 361(14), 1339-1348
Ross, M. G., Ervin, M. G., Novak, D. (2007). Chapter 2 fatal physiology. In S. Gabbe, J. Niebyl, & J. Simpson (Eds.), Obstetrics: Normal and problem pregnancies (pp. 26-33). Philadelphia, PA: Churchill Livingstone Elsevie
Rowan, J. A., Hague, W. M., Gao, W., Battin, M. R., & Moore, M. P. (2008). Metformin versus insulin for the treatment of gestational diabetes. The New England Journal of Medicine, 358(19), 2003-2015.
The HAPO Study Cooperative Research Group. (2008). Hyperglycemia and adverse pregnancy outcomes. The New England Journal of Medicine, 358(19), 1991-2002.
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