Gestational diabetes is a condition in which a woman without diabetes develops high blood sugar levels during pregnancy. Gestational diabetes generally produces several symptoms; However, it increases the risk of preeclampsia, depression, and requires caesarean section. Babies born to mothers with untreated gestational diabetes are at greater risk, have lower blood sugar after birth, and jaundice. If left untreated, it can also cause stillbirth. Long term, children are at higher risk of overweight and developing type 2 diabetes.
Gestational diabetes is caused by insufficient insulin in the regulation of insulin resistance. Risk factors include being overweight, previously having gestational diabetes, family history of type 2 diabetes, and having polycystic ovary syndrome. Diagnosis is done by blood test. For those who perform normal risk screening is recommended between 24 and 28 weeks of pregnancy. For those at high risk testing may occur at the first prenatal visit.
Prevention is to maintain a healthy weight and exercise before pregnancy. Gestational diabetes is treated with a diabetic diet, exercise, and possibly insulin injections. Most women are able to manage their blood sugar with diet and exercise. Blood sugar tests among those affected are often recommended four times a day. Breastfeeding is recommended as soon as possible after birth.
Gestational diabetes affects 3-9% of pregnancies, depending on the population under study. This is very common during the last three months of pregnancy. It affects 1% of those under the age of 20 and 13% of those over 44 years of age. A number of ethnic groups including Asians, Indian Americans, Indigenous Australians, and Pacific Islanders have a higher risk. In 90% of gestational diabetes patients will improve after the baby is born. Women, however, are at an increased risk of developing type 2 diabetes.
Video Gestational diabetes
Classification
Gestational diabetes is formally defined as "any degree of glucose intolerance with the first onset or recognition during pregnancy". This definition recognizes the possibility that a woman may have previously undiagnosed diabetes mellitus, or may have developed diabetes by chance with pregnancy. Whether the symptoms subside after pregnancy is also irrelevant to the diagnosis. A woman is diagnosed with gestational diabetes when glucose intolerance continues beyond 24 to 28 weeks' gestation.
The White Classification, named after Priscilla White, which pioneered research on the effect of type of diabetes on perinatal outcomes, is widely used to assess maternal and fetal risk. It distinguishes between gestational diabetes (type A) and pregestational diabetes (diabetes present before pregnancy). Both groups are subdivided on the basis of risk and related management.
Two subtypes of gestational diabetes under this classification system are:
- Type A1: abnormal oral glucose tolerance test (OGTT), but normal blood glucose levels during fasting and two hours after meals; dietary modification is enough to control glucose levels
- Type A2: Abnormal OGTT exacerbated by abnormal glucose levels during fasting and/or after meals; Additional therapy with insulin or other drugs is required
Pre-pregnancy diabetes is also divided into subtypes under this system:
- Type B: onset at age 20 or older and duration less than 10 years.
- Type C: onset at age 10-19 or duration 10-19 years.
- Type D: onset before age 10 or duration more than 20 years.
- Type E: Clear diabetes mellitus with calcified pelvic vessels.
- Type F: diabetic nephropathy.
- Type R: proliferative retinopathy.
- Type RF: retinopathy and nephropathy.
- Type H: ischemic heart disease.
- Type T: previous renal transplant.
The initial age of onset or illness comes with a greater risk, the first three subtypes.
Two other sets of criteria are available for the diagnosis of gestational diabetes, both based on blood sugar levels.
Criteria for the diagnosis of gestational diabetes, using the 100 gram Glucose Tolerance Test, according to Carpenter and Coustan:
- Fasting 95Ã, mg/dl
- 1 hour 180Ã, mg/dl
- 2 hours 155Ã, mg/dl
- 3 hours 140Ã, mg/dl
Criteria for gestational diabetes diagnosis by National Diabetes Data Group:
- Fasting 105Ã, mg/dl
- 1 hour 190Ã, mg/dl
- 2 hours 165Ã, mg/dl
- 3 hours 145Ã, mg/dl
Maps Gestational diabetes
Risk factors
The classic risk factors for developing gestational diabetes are:
- Polycystic Ovary Syndrome
- Previous diagnosis of gestational diabetes or prediabetes, impaired glucose tolerance, or fasting glycemia disorder
- Family history reveals relative first rate with type 2 diabetes
- Mother's age - the risk factor for women increases with age (especially for women over 35).
- Ethnicity (those with high risk factors including African-Americans, Afro-Caribbean, Native Americans, Hispanics, Pacific Islanders and people from South Asia)
- Overweight, obesity or severe obesity raises each risk by factors 2.1, 3.6 and 8.6.
- Previous pregnancy resulting in a child with macrosomia (high birth weight: & gt; 90 centil or & gt; 4000 g (8 pounds 12.8 oz))
- Bad previous obstetric history
- Other genetic risk factors: There are at least 10 genes in which certain polymorphisms are associated with an increased risk of gestational diabetes, especially TCF7L2.
In addition, statistics show a double risk of GDM in smokers. Polycystic ovary syndrome is also a risk factor, although the relevant evidence remains controversial. Several studies have looked at potential risk factors that are more controversial, such as short stature.
Approximately 40-60% of women with GDM do not have proven risk factors; for this reason many supporters to screen all women. Normally, women with GDM show no symptoms (other reasons for universal screening), but some women may show increased thirst, increased urination, fatigue, nausea and vomiting, bladder infections, fungal infections and blurred vision.
Pathophysiology
The exact mechanisms underlying gestational diabetes remain unknown. Characteristic of GDM is increased insulin resistance. Pregnancy hormones and other factors are thought to interfere with insulin work because it binds to insulin receptors. Disorders may occur at the level of the cell signaling pathway beyond the insulin receptor. Because insulin pushes the entry of glucose into most cells, insulin resistance prevents glucose from entering the cells properly. As a result, glucose remains in the bloodstream, where glucose levels rise. More insulin is needed to overcome this resistance; about 1.5 to 2.5 times more insulin is produced than in normal pregnancy.
Insulin resistance is a normal phenomenon that occurs in the second trimester of pregnancy, which in the case of GDM develops afterwards to levels seen in people who are not pregnant with type 2 diabetes. It is estimated to secure the supply of glucose to the growing fetus. Women with GDM have insulin resistance that they can not keep pace with increased production in pancreatic cells. Placental hormones, and to a lesser extent, increased fat deposits during pregnancy, seem to mediate insulin resistance during pregnancy. Cortisol and progesterone are the main causes, but human placental lactogen, prolactin and estradiol also contribute. Multivariate gradual regression analysis revealed that, in combination with other placental hormones, leptin, tumor necrosis factor alpha, and resistin are involved in decreased insulin sensitivity that occurs during pregnancy, with tumor necrosis factor alpha is called the strongest independent predictor of insulin sensitivity in pregnancy Inverted correlation with changes in insulin sensitivity from the time before conception through late pregnancy accounted for about half of the variance in decreased insulin sensitivity during pregnancy: in other words, low levels or alpha TNF factor changes correspond to greater opportunities. from, or tendency to, insulin resistance or sensitivity. GABBE, STEVEN G; page Sixth Edition 890.
It is unclear why some women can not balance insulin requirements and develop GDM; However, a number of explanations have been given, similar to those in type 2 diabetes: autoimmunity, single gene mutations, obesity, along with other mechanisms.
Although the clinical presentation of gestational diabetes is well characterized, the biochemical mechanisms behind the disease are not well known. One of the proposed biochemical mechanisms involves producing insulin-cell-adaptation controlled by HGF/c-MET signal pathways. ? adaptation refers to changes made to pancreatic islet cells during pregnancy in response to maternal hormones to offset the increased physiological needs of mother and baby. These deep changes-this increase leads to increased insulin secretion as a result of increased cell proliferation. HGF/c-MET has also been involved in cell regeneration-suggesting that HGF/c-MET can help increase cell mass to compensate for insulin requirements during pregnancy. Recent studies support the loss of HGF/c-MET signaling results in the adaptation of aberrant cells.
c-MET is a receptor of tyrosine kinase (RTK) activated by ligand, hepatocyte growth factor (HGF), and is involved in the activation of some cellular processes. When HGF binds to c-MET, the receptors make a homodimerization and phosphorylate themselves to form the SH2 recognition domain. Activated downstream pathways include common signal molecules such as RAS and MAPK, which affect cell motility, cell motility, and cell cycle evolution.
Studies have shown that HGF is an important signal molecule in stress-related situations where more insulin is needed. Pregnancy leads to an increase in insulin resistance and higher insulin demand. The cells must compensate for this by increasing the production of insulin or breeding. If no process occurs, then markers for gestational diabetes are observed. It has been observed that pregnancy increases HGF levels, suggesting a correlation showing the relationship between the signal pathway and an increased need for insulin. In fact, when there is no signal, gestational diabetes is more likely to occur.
The exact mechanism of HGF/c-MET is set? adaptation is unknown but there are some hypotheses about how the signaling molecule contributes to insulin levels during pregnancy. c-MET can interact with FoxM1, an important molecule in the cell cycle, when the FOXM1 level decreases when c-MET is not present. In addition, c-MET can interact with p27 as protein levels increase with c-MET absent. Another hypothesis says that c-MET can control apoptosis-cell because lack of c-MET causes an increase in cell death but the signaling mechanism has not been described.
Although the gestational diabetes HGF/c-MET control mechanism is not well understood, there is a strong correlation between the signal pathway and the inability to produce sufficient amount of insulin during pregnancy and thus may be a target for future diabetes. therapy.
Because glucose moves across the placenta (via diffusion facilitated by GLUT1 carrier), located in syncytiotrophoblast in both microvillus and basal membranes, this membrane may be a step that limits the rate in transport of placental glucose. There was a two- to threefold increase in the expression of sukarotrophoblast glucose transporter with increased gestation. Finally, the role of GLUT3/GLUT4 transport remains speculative. If untreated gestational diabetes fetuses are exposed to consistently higher glucose levels, this leads to an increase in the level of fetal insulin (insulin itself can not cross the placenta). The effect of stimulating insulin growth can lead to excessive growth and large body (macrosomia). After birth, the high glucose environment disappears, leaving this newborn with high insulin production and is susceptible to low blood glucose (hypoglycemia).
Screening
A number of screening and diagnostic tests have been used to look for high glucose levels in plasma or serum under certain circumstances. One method is a phased approach where suspicious results in screening tests are followed by diagnostic tests. Alternatively, more involved diagnostic tests may be used directly at the first prenatal visit for a woman with high-risk pregnancies. (eg in those with polycystic ovary syndrome or acanthosis nigricans).
A non-challenge blood glucose test involves measuring glucose levels in a blood sample without challenging a subject with a glucose solution. Blood glucose levels are determined at the time of fasting, 2 hours after eating, or only at random. Conversely, the challenge test involves taking a glucose solution and measuring the subsequent glucose concentration in the blood; in diabetes, they tend to remain high. Glucose solution has a very sweet taste that some women find unpleasant; sometimes, therefore, artificial flavors are added. Some women may experience nausea during the test, and more with higher glucose levels.
More research is needed to find the most effective way to screen for gestational diabetes. Regular screening of women with a glucose challenge test seems to find more women with gestational diabetes than simply screening women with risk factors. It is not clear how this screening test affects the rest of pregnancy. Future research should include how screening methods impact mother and baby.
Path
Different opinions about optimal screening and diagnostic measures, in part due to differences in population risk, cost effectiveness considerations, and lack of evidence base to support a major national screening program. The most complicated regimens require random blood glucose testing during the reservation visit, screening glucose screening tests around 24-28 weeks gestation, followed by OGTT if the test is beyond the normal range. If there is a high suspicion, a woman can be tested early.
In the United States, most obstetricians prefer universal screening with screening glucose testing. In the UK, midwifery units often rely on risk factors and random blood glucose testing. The American Diabetes Association and the Society of Obstetricians and Gynecologists of Canada recommend routine checks unless the woman is at low risk (this means women should be younger than 25 years and have a body mass index of less than 27, without personal, ethnic or family risk factors) Canadian Diabetes Association and the American College of Obstetricians and Gynecologists recommend universal screening. The US Prevention Task Force found that there was not enough evidence to recommend or challenge routine screening.
Some pregnant women and care providers prefer not to perform routine checks because of the absence of risk factors, but this is not recommended because most women who have gestational diabetes although they do not have risk factors and hazards for both mother and baby if diabetic pregnancies remain untreated.
Non-challenge blood glucose test
When plasma glucose levels are found to be higher than 126 mg/dl (7.0 mmol/l) after fasting, or more than 200 mg/dl (11.1 mmol/l) at every opportunity, and if this is confirmed on the day, the diagnosis GDM is created, and no further testing is required. These tests are usually performed on the first antenatal visit. They are easy to manage and inexpensive, but have lower test performance compared to other tests, with moderate sensitivity, low specificity and high false positive rates.
Check the glucose challenge test
Screen glucose testing tests (sometimes called the O'Sullivan test) are performed between 24-28 weeks, and can be seen as a simplified version of the oral glucose tolerance test (OGTT). No previous fasting is required for this screening test, in contrast to OGTT. O'Sullivan's test involves drinking a solution containing 50 grams of glucose, and measuring blood levels 1 hour later.
If the cut-off point is set at 140Ã, mg/dl (7.8 mmol/l), 80% of women with GDM will be detected. If this threshold for further testing is reduced to 130 mg/dl, 90% of GDM cases will be detected, but there will also be more women who will undergo OGTT consequently unnecessarily.
Oral glucose tolerance test
Standard oral glucose tolerance test (OGTT) should be done in the morning after overnight fasting between 8 and 14 hours. For the previous three days, subjects had to undergo an unlimited diet (containing at least 150 g of carbohydrates per day) and unlimited physical activity. Subjects must remain seated during the test and should not smoke during the test.
This test involves drinking a solution containing a certain amount of glucose, typically 75 g or 100 g, and drawing blood to measure glucose levels at baseline and at prescribed time intervals thereafter.
Diagnostic criteria from the National Diabetes Data Group (NDDG) have been used most often, but some centers rely on Carpenter and Coustan criteria, which set the normal cutoff to lower values. Compared with the NDDG criteria, the Carpenter and Coustan criteria lead to the diagnosis of gestational diabetes in 54 percent more pregnant women, with increased costs and no convincing evidence of increased perinatal outcomes.
The following are the values ​​considered by the American Diabetes Association as abnormal for 100 g of glucose OGTT:
- Fasting blood glucose levels> = 95 mg/dl (5.33 mmol/L)
- 1 hour blood glucose>> = 180 mg/dl (10 mmol/L)
- 2 hours blood glucose>> = 155 mg/dl (8.6 mmol/L)
- 3 hours blood glucose>> = 140 mg/dl (7.8 mmol/L)
An alternative test uses a 75 g glucose load and measures blood glucose levels before and after 1 and 2 hours, using the same reference value. This test will identify fewer women at risk, and there is only a weak concordance (agreement ratio) between this test and a 100 g 3 hour test.
The glucose value used to detect gestational diabetes was first determined by O'Sullivan and Mahan (1964) in a retrospective cohort study (using 100 grams of glucose OGTT) designed to detect the risk of type 2 diabetes in the future. Values ​​are set using whole blood and two values ​​are required that reach or exceed values ​​to be positive. Subsequent information caused a change in O'Sullivan's criteria. When the method of determining blood glucose changed from the use of whole blood to venous plasma samples, the criteria for GDM also changed.
Urine glucose test
Women with GDM may have high glucose levels in urine (glucosuria). Although dipstick tests are widely practiced, it performs poorly, and stopping routine dipstick tests has not been shown to cause underdiagnosis where universal screening is performed. Increased glomerular filtration rates during pregnancy contribute to approximately 50% of women who have glucose in their urine on dipstick tests at some point during their pregnancy. The glucosuria sensitivity for GDM in the first 2 trimesters is only about 10% and the positive predictive value is about 20%.
Prevention
The 2015 review found that when performed during pregnancy, physical exercise is effective for the prevention of gestational diabetes. However, the 2014 review found no significant effect.
Theoretically, quitting smoking can reduce the risk of gestational diabetes among smokers.
Management
GDM treatment with diet and insulin reduces maternal and child health problems. GDM treatment is also accompanied by more induction of labor.
Recurrent OGTT should be done 6 weeks after delivery, to ensure diabetes has disappeared. After that, routine screening for type 2 diabetes is recommended.
If the diabetes diet or G.I. Diet, exercise, and oral medications are inadequate to control glucose levels, insulin therapy may be necessary.
The development of macrosomia can be evaluated during pregnancy using sonography. Women who use insulin, with a history of stillbirth, or with hypertension are managed like women with real diabetes.
Lifestyle
Pre-pregnancy counseling (eg, about folic acid supplementation prevention) and multidisciplinary management are important for good pregnancy outcomes. Most women can manage their GDM with dietary and exercise changes. Self-monitoring of blood glucose levels can guide therapy. Some women will need antidiabetic drugs, most often insulin therapy.
Every diet needs to provide enough calories for pregnancy, usually 2,000 - 2,500 kcal with the exception of simple carbohydrates. The main purpose of diet modification is to avoid peak blood sugar levels. This can be done by spreading carbohydrate intake over food and snacks throughout the day, and using a source of slow release carbohydrates - known as G.I. Diet. Because insulin resistance is highest in the morning, breakfast carbohydrates need to be more restricted. Adding more fiber in foods with whole grains, or fruits and vegetables can also reduce the risk of gestational diabetes.
Strong physical exercise is regularly recommended, although there is no consensus on the specific structure of exercise programs for GDM.
Self-monitoring can be performed using a hand-held capillary glucose dosing system. Compliance with this glucometer system can be low. Target range recommended by Australasian Diabetes in Pregnancy Society is as follows:
- fasting capillary blood glucose level & lt; 5.5 Ã, mmol/L
- 1 hour postprandial capillary blood glucose & lt; 8.0 mmol/L
- 2 hours postprandial blood glucose level & lt; 6.7 mmol/L
Regular blood samples can be used to determine HbA1c levels, which provide an overview of glucose control over a longer period of time.
Research shows the possible benefits of breastfeeding to reduce the risk of diabetes and related risks for mothers and children.
Medication
If monitoring indicates a failure to control glucose levels with these measures, or if there is evidence of complications such as excessive fetal growth, treatment with insulin may be necessary. This is a fast-acting insulin given just before eating to collect glucose after a meal. Care should be taken to avoid low blood sugar levels due to excessive insulin. Insulin therapy can be normal or very strict; more injections can lead to better control but require more effort, and no consensus has any major benefits. The 2016 Cochrane Review concludes that quality evidence is not yet available to determine the best blood sugar range to improve maternal health with GDM and their babies.
There is some evidence that certain drugs by mouth may be safe in pregnancy, or at least, less harmful to developing fetuses than uncontrolled diabetes. Metformin drugs are better than glyburide. If blood glucose can not be adequately controlled with a single agent, the combination of metformin and insulin may be better than insulin alone. Other reviews find good short-term safety for mothers and infants with metformin but long-term safety is unclear.
People may prefer metformin by mouth to insulin injections. Treatment of polycystic ovary syndrome with metformin during pregnancy has been noted to decrease GDM levels.
Nearly half of women do not achieve adequate control with metformin alone and require additional therapy with insulin; compared with those treated with insulin alone, they require less insulin, and they gain less weight. In the absence of long-term studies in girls treated with these drugs, there is still the possibility of long-term complications of metformin therapy. Infants born to women treated with metformin have been found to develop less visceral fat, making them less susceptible to insulin resistance later in life.
Prognosis
Gestational diabetes generally heals once the baby is born. Based on different studies, the possibility of developing GDM in a second pregnancy, if a woman has GDM in her first pregnancy, is between 30 and 84%, depending on ethnic background. A second pregnancy within 1 year of previous pregnancy has a high probability of GDM.
Women who are diagnosed with gestational diabetes have an increased risk of developing diabetes mellitus in the future. The highest risk in women who require insulin treatment, has antibodies associated with diabetes (such as antibodies to decarboxylase glutamate, islet cell antibody and/or antigen-2 insulinoma), women with more than two previous pregnancies, and obese women (in sequence interests). Women who need insulin to manage gestational diabetes have a 50% risk of developing diabetes within the next five years. Depending on the population under study, diagnostic criteria and length of follow-up, the risks can vary greatly. The risk seems to be the highest in the first 5 years, reaching the plateau thereafter. One of the longest studies follows a group of women from Boston, Massachusetts; half of them had diabetes after 6 years, and more than 70% had diabetes after 28 years. In a retrospective study of Navajo women, the risk of diabetes after GDM was estimated to be 50 to 70% after 11 years. Another study found the risk of diabetes after GDM was over 25% after 15 years. In low-risk populations for type 2 diabetes, in lean subjects and in women with auto-antibodies, there is a higher rate of women who develop type 1 diabetes (LADA).
Girls with GDM have an increased risk for obesity in children and adults and an increased risk of glucose intolerance and type 2 diabetes later in life. This risk is associated with an increase in the value of maternal glucose. It is not currently clear how many genetic susceptibilities and environmental factors contribute to this risk, and whether GDM treatment can affect this outcome.
There are rare statistical data about the risk of other conditions in women with GDM; in Jerusalem Perinatal studies, 410 of 37962 women reported to have GDM, and there is a tendency for more breast and pancreatic cancers, but more research is needed to confirm these findings.
Complications
GDM poses a risk to both mother and child. This risk is mostly associated with uncontrolled blood glucose levels and their consequences. The risk increases with higher blood glucose levels. Treatments that result in better control of these levels can significantly reduce some of the risk of GDM.
The two major risks GDM inflicts in infants are growth abnormalities and chemical imbalances after birth, which may require admission to the neonatal intensive care unit. Babies born to mothers with GDM are at greater risk for gestational (macrosomic) gestational age in unmanaged GDM, and are small for gestational age and intrauterine growth retardation in managed GDM. Macrosomia in turn increases the risk of instrumental delivery (eg forceps, ventouse and cesarean section) or problems during vaginal delivery (such as shoulder dystocia). Macrosomia can affect 12% of normal women compared to 20% of women with GDM. However, the evidence for each of these complications is not as strong; in studies of Hyperglycemia and Adverse Pregnancy Outcome (HAPO) for example, there is an increased risk for infants to be large but not small for gestational age in women with uncontrolled GDM. Research on complications for GDM is difficult because of many confounding factors (such as obesity). Labeling women as having GDM may increase the risk of unnecessary cesarean sections.
Neonates born to women with high blood sugar levels are consistently also at increased risk of low blood glucose (hypoglycemia), jaundice, high red blood cell mass (polycythemia) and low blood calcium (hypocalcemia) and magnesium (hypomagnesemia). Untreated GDM also interferes with maturation, causing dismatured infants to be susceptible to respiratory distress syndrome due to incomplete lung maturation and disturbed surfactant synthesis.
Unlike pre-gestational diabetes, gestational diabetes has not been clearly demonstrated as an independent risk factor for birth defects. Birth defects usually originate at any time during the first trimester (before the 13th week) of pregnancy, whereas GDM gradually develops and is the least pronounced during the first and early second trimesters. Studies have shown that female offspring with GDM have a higher risk for congenital malformations. A large case-control study found that gestational diabetes was associated with a limited group of birth defects, and that this association was generally confined to women with higher body mass index (> = 25 kg/m²). It is difficult to ensure that this is not in part due to the inclusion of women with pre-existing type 2 diabetes who are not diagnosed before pregnancy.
Because of conflicting studies, it is unclear at this point whether women with GDM have a higher risk of preeclampsia. In the HAPO study, the risk of preeclampsia was between 13% and 37% higher, although not all confounding factors may be corrected.
Epidemiology
Gestational diabetes affects 3-10% of pregnancies, depending on the population under study.
References
External links
- IDF Diabetes Atlas
- International Diabetes Federation
- National Institute of Child Health and Human Development - Am I at Risk for Gestational Diabetes?
- National Institute of Child Health and Human Development - Managing Gestational Diabetes: A Patient Guide for a Healthy Pregnancy
- Gestational Diabetes Resource Guide - American Diabetes Association
- Diabetes.co.uk: Gestational Diabetes
Source of the article : Wikipedia
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