Gestational Diabetes Mellitus - Assignment Example

Running Head: GESTATIONAL DIABETES MELLITUS Gestational Diabetes Mellitus [The Writer’s Name] [The Name of the Institution] Gestational Diabetes Mellitus Background/Introduction Gestational diabetes (GDM) is defined as glucose intolerance of variable degree with onset or first recognition during the present pregnancy. It can be screened by drawing a 1-hour glucose level following a 50-g glucose load, but is definitively diagnosed only by an abnormal 3-hour OGTT following a 100-g glucose load. GDM is a form of hyperglycemia. In general, hyperglycemia results from an insulin supply that is inadequate to meet tissue demands for normal blood glucose regulation. Studies conducted during late pregnancy, when, as discussed below, insulin requirements are high and differ only slightly between normal and gestational diabetic women, consistently reveal reduced insulin responses to nutrients in women with GDM (Xiang, 1999, 848-54: Kautzky, 1997, 1717-23). Studies conducted before or after pregnancy, when women with prior GDM are usually more insulin resistant than normal women, often reveal insulin responses that are similar in the 2 groups or reduced only slightly in women with prior GDM (Catalano, 1999, 903-16; Homko, 2001, 568-73; Osei, 1998, 1250-57). However, when insulin levels and responses are expressed relative to each individual’s degree of insulin resistance, a large defect in pancreatic β cell function is a consistent finding in women with prior GDM (Kautzky, 1997, 1717-23; Ryan, 1995, 506-12; Buchanan, 2001, 989-93). Etiology of Diabetes Mellitus For insulin dependent diabetes, the cumulative risk for siblings of diabetic patient is 6-10 per cent versus 0.6 per cent for the general population. Regarding the effect of parental genes, the offspring of women with type 1 diabetes have a lower risk of disease (21%) than the off-springs of men with type I diabetes (6.1%). The reason for this disparity is unknown. The incidence of IDDM peaks at about 11-13 years of age. There is a striking seasonal variation in the incidence in older children and adolescents, with lowest rates in spring and summer. NIDDM: The familial clustering of non-insulin dependents suggests a strong genetic component of the disease. The cumulative risk for type II diabetes in siblings of diabetes patient is 10-33 per cent versus 5 per cent for the general population. Offspring of women with type II diabetes have a two to three-fold greater risk of developing diabetes than offspring of men with the disease. The exact mode of inheritance is not known. Investigations in a number of developing countries have shown urban-rural differences of varying degree with generally higher rates in urban area. The growth and maturation of the fetus are closely associated with the delivery of maternal nutrients, particularly glucose. This is most crucial in the third trimester and is directly related to the duration and degree of maternal glucose elevation. Thus, the negative impact is as highly diverse as the variety of carbohydrate intolerance that women bring to pregnancy. For the mother with GDM there is a higher risk of hypertension, preeclampsia, urinary tract infections, cesarean section, and future diabetes. Many of the problems associated with overt diabetic pregnancies can be seen in infants of gestational diabetic pregnancies, such as macrosomia, neural tube defects, neonatal hypoglycemia, hypocalcemia, hypomagnsemia, hyperbilirubinemia, birth trauma, prematurity syndromes, and subsequent childhood and adolescent obesity. Prevalence of Gestational Diabetes Mellitus The prevalence of GDM varies worldwide and among different racial and ethnic groups within a country. The variability is partly because of the different criteria and screening regimens (i.e., not all pregnant women are screened). Studies using a 100-g 3-hour OGTT and either the criteria of the National Diabetes Data Group (NDDG) or of Carpenter and Coustan have found prevalence rates of 1.4% to 12.3% in the United States, respectively. Gestational diabetes is pathophysiologically similar to type II diabetes. Approximately 90% of the persons identified have a deficiency of insulin receptors (prior to pregnancy) or a marked increase in weight that has been placed on the abdominal region. The other 10% have deficient insulin production and will proceed to develop mature-onset insulin-dependent diabetes. HPL blocks insulin receptors and increases in direct linear relation to the length of pregnancy. Insulin release is enhanced in an attempt to maintain glucose homeostasis. The patient experiences increased hunger due to the excess insulin release as a result of elevated glucose levels. This insulin release further decreases insulin receptors due to elevated hormonal levels. Pregnancy is characterised by several factors that act to alter the blood glucose concentration. Hormones such as human placental lactogen, progesterone, prolactin, and cortisol have diabetogenic properties; their tendency to increase maternal blood glucose is counterbalanced by an increase in insulin to almost twice the nonpregnant concentration. The rise in insulin is itself offset by increasing insulin resistance, the mechanism of which is not clearly understood. Irrespective of these changes, the vast majority of pregnant women manage to maintain their blood glucose within normal limits. In a few women, the capacity for insulin secretion is exceeded as a consequence of increasing insulin resistance, and gestational diabetes develops, usually late in the second trimester. Screening The traditional method of screening for GDM is to assess risk factors: age, prepregnancy weight, family history of diabetes in a first-degree relative, previous large baby, and previous perinatal loss. Unfortunately, screening based solely on risk factors will only identify approximately 50% of women with GDM. Glucosuria is a common finding in pregnancy due to increased glomerular filtration and is therefore unreliable as a diagnostic finding. The ADA(American Diabetes Association, 2003, S5-S20) recommend that all pregnant women, who have not been identified with glucose intolerance earlier in pregnancy, be screened with a 50-g 1-hour GCT between 24 and 28 weeks of pregnancy. Such test can be performed at anytime of the day and with disregard to previous meal ingestion. A value equal to or above 140mg/dL should be used as the threshold level and indicates the need for a 100-g 3-hour OGTT. For the OGTT, the patient is fasting and receives 100-g of glucose after a fasting glucose level is obtained. A blood sample is taken every hour for 3 hours. The patient is advised to sit quietly during the test to minimize the impact of exercise on glucose levels. The screening 1-hour glucose tolerance test was ordered because of the woman’s history of a stillborn infant. In a woman with a history of unexplained fetal death, there should be a high index of suspicion of diabetes. Although the 1-hour test result results were abnormal, a diagnosis of gestational diabetes cannot be made on that value alone; therefore, there is no immediate need for dietary control or postprandial blood sugar monitoring. However, the abnormal 1-hour test results should be followed up by a standard 3-hour glucose tolerance test. If two or more of the four results are abnormal, the patient is diagnosed as having gestational diabetes. In addition, even if the patient is diagnosed as diabetic, the degree of glucosuria in a patient with diabetes does not reflect plasma glucose values.( Fajans, 2001, 971-80) The glucose values used to detect gestational diabetes were first determined in a retrospective study designed to detect risk of developing type II diabetes in the future. (Kousta, 2001, 683-84) The values were set using venous whole blood and required 2 values reaching or exceeding the value to be positive. Subsequent information has led to alteration. For example: when methods for blood glucose determination changed from the use of whole blood to venous plasma samples, the criteria for GDM were also changed once whole blood glucose values are lower than plasma levels due to glucose uptake by haemoglobin. Screening policies must be well defined, easily administered, inexpensive, and reproducible; it should also have a high sensitivity to identify most individuals with the disorder. Many alternatives including a fasting or random blood glucose and 50g, 75g, or 100g OGTT, have been suggested, but without universal agreement. In the UK, most centres use a 75g OGTT as the final measure, but the blood glucose values recommended as a diagnostic by WHO have not yet been validated against any outcome of pregnancy. (Paternoster, 1997, 277-78) In predominantly white populations, screening policies for gestational diabetes may not be seen as the best allocation of obstetric resources because the number of white/Europid women likely to be affected is small. However, the benefits of screening ethnic groups with a high prevalence of both impaired glucose tolerance and NIDDM are clear. The implications of gestational diabetes extend far beyond pregnancy; for this reason, the potential benefits of a structured screening system during and after pregnancy should be reassessed to take account of both public health and obstetric outcomes. Corticosteroids are known to affect all inflammatory processes by decreasing the action of T-helper cells, and reducing T cell proliferation with reduced macrophage function and reduced production of inflammatory mediators such as cytokines and prostaglandins (Paternoster, 1997, 277-78). Immunosuppressive agents such as cyclosporine have been used as third-line treatments for very severe cases of PG that are unresponsive to corticosteroid medication (Schatz, 2003, 804-807) Treatment If one abnormal value is seen during the 100-g 3-hour OGTT it is recommended that the test be repeated approximately 1 month later. There is growing evidence that 1 abnormal value is sufficient to make an impact on the health of the fetus and is now the criterion used by most clinicians to initiate treatment. In a study of 106 women with one abnormal value on the OGTT, 34% were diagnosed with GDM when the test was repeated 1 month later, emphasizing the importance of repeat testing when only one abnormal value is found. The reason for lowering the glucose level to a normoglycemic one is to prevent diabetic complications. The goal of medical management of women with GDM, therefore, is to prevent perinatal morbidity and mortality by normalizing the level of glycaemia and other metabolites (i.e., lipids and amino acids) to the levels of nondiabetic pregnant individuals. Nutritional counselling is the mainstay of therapy for the gestational diabetic woman. (Retnakaran, 2003, 3507-12) The optimal dietary prescription would be one that provides the calories and nutrients necessary for maternal and fetal health, results in normoglycemia, prevents ketosis, and results in appropriate weight gain. One of the difficulties with dietary prescription for women with GDM is the difference between lean and obese women. Obese women with GDM may benefit from a low calorie diet and weight reduction to reverse the metabolic disturbances, but proper nutrition is needed to assure fetal growth and development. Jovanovic and Peterson found the following diet to result in euglycemia: 30kcal/kg/24h present pregnant weight for normal-weight women, 24kcal/kg/24h for overweight women (120%-150% ideal body weight), and 12 to 15 kcal/kg/24 h for morbidly obese women (>150% ideal body weight), and 40kcal/kg/24h for underweight women ( Read More