Gestational diabetes overview: Difference between revisions
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== Overview == | == Overview == | ||
Gestational diabetes (GDM) is a form of [[diabetes]] which affects [[pregnant]] women who have never had diabetes before. There is no known specific cause, but it's believed that the hormones produced during pregnancy reduce a woman's receptivity to [[insulin]] resulting in high [[blood sugar | Gestational diabetes (GDM) is a form of [[diabetes]] which affects [[pregnant]] women in second or third trimester who have never had diabetes before. There is no known specific cause, but it's believed that the hormones produced during pregnancy reduce a woman's receptivity to [[insulin]] resulting in high [[blood sugar]]. | ||
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs approximately 7.5 of all [[pregnancy|pregnancies]] in the United States and may improve or disappear after delivery. | |||
Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include [[macrosomia]] (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal [[surfactant]] production and cause [[Infant respiratory distress syndrome|respiratory distress syndrome]]. [[Hyperbilirubinemia]] may result from red blood cell destruction. | |||
==Historical Perspective== | ==Historical Perspective== | ||
*Diabetes mellitus is an ancient term first found in Egyptian Eberes papyrus around 1500 BC. Hyperglycemia in pregnancy, first described by Bennewitz, a German physician in 1824. In 1950 GDM term was accepted.<ref name="pmid23634949">{{cite journal |vauthors=Negrato CA, Gomes MB |title=Historical facts of screening and diagnosing diabetes in pregnancy |journal=Diabetol Metab Syndr |volume=5 |issue=1 |pages=22 |year=2013 |pmid=23634949 |pmc=3644500 |doi=10.1186/1758-5996-5-22 |url=}}</ref> | |||
*John B. O’Sullivan, Wilkerson and Remein in 1957 proposed offering a 3-hour oral glucose tolerance test (OGTT) for patients presenting risk factors for diabetes such as family history of diabetes, gestational glycosuria and overdeveloped infants at birth.<ref name="pmid13447761">{{cite journal |vauthors=WILKERSON HL, REMEIN QR |title=Studies of abnormal carbohydrate metabolism in pregnancy; the significance of impaired glucose tolerance |journal=Diabetes |volume=6 |issue=4 |pages=324–9 |year=1957 |pmid=13447761 |doi= |url=}}</ref> | |||
==Classification== | ==Classification== | ||
Gestational diabetes refers to hyperglycemia during second or third trimester of pregnancy.<ref name="pmid26696680">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2016: Summary of Revisions |journal=Diabetes Care |volume=39 Suppl 1 |issue= |pages=S4–5 |year=2016 |pmid=26696680 |doi=10.2337/dc16-S003 |url=}}</ref> | |||
Diagnosis of diabetes in the second or third trimester of pregnancy that is not clearly either type 1 or type 2 diabetes.<ref name="pmid26696680">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2016: Summary of Revisions |journal=Diabetes Care |volume=39 Suppl 1 |issue= |pages=S4–5 |year=2016 |pmid=26696680 |doi=10.2337/dc16-S003 |url=}}</ref> | |||
==Pathophysiology== | |||
===Insulin insensitivity=== | |||
Insulin sensitivity reduces slightly during first and second trimesters but it decreases 40-60% during third trimester.<ref name="pmid8430789">{{cite journal |vauthors=Catalano PM, Tyzbir ED, Wolfe RR, Calles J, Roman NM, Amini SB, Sims EA |title=Carbohydrate metabolism during pregnancy in control subjects and women with gestational diabetes |journal=Am. J. Physiol. |volume=264 |issue=1 Pt 1 |pages=E60–7 |year=1993 |pmid=8430789 |doi= |url=}}</ref><ref name="pmid2183610">{{cite journal |vauthors=Buchanan TA, Metzger BE, Freinkel N, Bergman RN |title=Insulin sensitivity and B-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes |journal=Am. J. Obstet. Gynecol. |volume=162 |issue=4 |pages=1008–14 |year=1990 |pmid=2183610 |doi= |url=}}</ref><ref name="pmid1750458">{{cite journal |vauthors=Catalano PM, Tyzbir ED, Roman NM, Amini SB, Sims EA |title=Longitudinal changes in insulin release and insulin resistance in nonobese pregnant women |journal=Am. J. Obstet. Gynecol. |volume=165 |issue=6 Pt 1 |pages=1667–72 |year=1991 |pmid=1750458 |doi= |url=}}</ref> | |||
Other changes in molecular level that may lead to insulin resistant include: reduced ability of insulin to phosphorylate the insulin receptor, decreased expression of insulin receptor substrate 1 (IRS-1) and increased levels of a specific kinase.<ref name="pmid17596458">{{cite journal |vauthors=Barbour LA, McCurdy CE, Hernandez TL, Kirwan JP, Catalano PM, Friedman JE |title=Cellular mechanisms for insulin resistance in normal pregnancy and gestational diabetes |journal=Diabetes Care |volume=30 Suppl 2 |issue= |pages=S112–9 |year=2007 |pmid=17596458 |doi=10.2337/dc07-s202 |url=}}</ref> | |||
== | Factors affecting insulin insensitivity include: [[Estrogen|estrogens]] and [[progesterone]]<ref name="pmid7002669">{{cite journal |vauthors=Freinkel N |title=Banting Lecture 1980. Of pregnancy and progeny |journal=Diabetes |volume=29 |issue=12 |pages=1023–35 |year=1980 |pmid=7002669 |doi= |url=}}</ref>, human chorionic somatomammotropin (hCS) or [[placental lactogen]] (HPL), [[prolactin]], placental growth hormone variant (hGH-V), [[corticotropin-releasing factor]] (CRF) and [[corticotropin]], [[leptin]]<ref name="pmid9588462">{{cite journal |vauthors=Lepercq J, Cauzac M, Lahlou N, Timsit J, Girard J, Auwerx J, Hauguel-de Mouzon S |title=Overexpression of placental leptin in diabetic pregnancy: a critical role for insulin |journal=Diabetes |volume=47 |issue=5 |pages=847–50 |year=1998 |pmid=9588462 |doi= |url=}}</ref>, [[Tumor necrosis factor-alpha|tumor necrosis factor α]] (TNF-α)<ref name="pmid12086951">{{cite journal |vauthors=Kirwan JP, Hauguel-De Mouzon S, Lepercq J, Challier JC, Huston-Presley L, Friedman JE, Kalhan SC, Catalano PM |title=TNF-alpha is a predictor of insulin resistance in human pregnancy |journal=Diabetes |volume=51 |issue=7 |pages=2207–13 |year=2002 |pmid=12086951 |doi= |url=}}</ref>, [[adiponectin]]<ref name="pmid15778860">{{cite journal |vauthors=Retnakaran R, Hanley AJ, Raif N, Hirning CR, Connelly PW, Sermer M, Kahn SE, Zinman B |title=Adiponectin and beta cell dysfunction in gestational diabetes: pathophysiological implications |journal=Diabetologia |volume=48 |issue=5 |pages=993–1001 |year=2005 |pmid=15778860 |doi=10.1007/s00125-005-1710-x |url=}}</ref>, [[resistin]], [[ghrelin]] and [[interleukin-6]]. | ||
===Maternal metabolic changes=== | |||
Basal and postprandial levels of glucose, FFAs, triglycerides, and amino acids are higher in GDM than of normal pregnancy.<ref name="pmid7190092">{{cite journal |vauthors=Metzger BE, Phelps RL, Freinkel N, Navickas IA |title=Effects of gestational diabetes on diurnal profiles of plasma glucose, lipids, and individual amino acids |journal=Diabetes Care |volume=3 |issue=3 |pages=402–9 |year=1980 |pmid=7190092 |doi= |url=}}</ref> | |||
Maternal hyperglycemia leads to fetal hyperinsulinism, which is responsible for macrosomia and neonatal morbidity. Development of macrosomia (defined as birth weight >4000 g or above the 90th percentile for gestational age) is a frequent complication of pregnancies complicated by DM and GDM.<br> | |||
Increased adiposity is the primary component of the macrosomia. Infants of diabetic mothers may have up to twice the body-fat content of infants of normal mothers. <ref name="pmid14710101">{{cite journal |vauthors=Catalano PM, Thomas A, Huston-Presley L, Amini SB |title=Increased fetal adiposity: a very sensitive marker of abnormal in utero development |journal=Am. J. Obstet. Gynecol. |volume=189 |issue=6 |pages=1698–704 |year=2003 |pmid=14710101 |doi= |url=}}</ref> | |||
==Causes== | ==Causes== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Gestational diabetes (GDM) is a form of diabetes which affects pregnant women in second or third trimester who have never had diabetes before. There is no known specific cause, but it's believed that the hormones produced during pregnancy reduce a woman's receptivity to insulin resulting in high blood sugar.
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs approximately 7.5 of all pregnancies in the United States and may improve or disappear after delivery. Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction.
Historical Perspective
- Diabetes mellitus is an ancient term first found in Egyptian Eberes papyrus around 1500 BC. Hyperglycemia in pregnancy, first described by Bennewitz, a German physician in 1824. In 1950 GDM term was accepted.[1]
- John B. O’Sullivan, Wilkerson and Remein in 1957 proposed offering a 3-hour oral glucose tolerance test (OGTT) for patients presenting risk factors for diabetes such as family history of diabetes, gestational glycosuria and overdeveloped infants at birth.[2]
Classification
Gestational diabetes refers to hyperglycemia during second or third trimester of pregnancy.[3] Diagnosis of diabetes in the second or third trimester of pregnancy that is not clearly either type 1 or type 2 diabetes.[3]
Pathophysiology
Insulin insensitivity
Insulin sensitivity reduces slightly during first and second trimesters but it decreases 40-60% during third trimester.[4][5][6] Other changes in molecular level that may lead to insulin resistant include: reduced ability of insulin to phosphorylate the insulin receptor, decreased expression of insulin receptor substrate 1 (IRS-1) and increased levels of a specific kinase.[7]
Factors affecting insulin insensitivity include: estrogens and progesterone[8], human chorionic somatomammotropin (hCS) or placental lactogen (HPL), prolactin, placental growth hormone variant (hGH-V), corticotropin-releasing factor (CRF) and corticotropin, leptin[9], tumor necrosis factor α (TNF-α)[10], adiponectin[11], resistin, ghrelin and interleukin-6.
Maternal metabolic changes
Basal and postprandial levels of glucose, FFAs, triglycerides, and amino acids are higher in GDM than of normal pregnancy.[12]
Maternal hyperglycemia leads to fetal hyperinsulinism, which is responsible for macrosomia and neonatal morbidity. Development of macrosomia (defined as birth weight >4000 g or above the 90th percentile for gestational age) is a frequent complication of pregnancies complicated by DM and GDM.
Increased adiposity is the primary component of the macrosomia. Infants of diabetic mothers may have up to twice the body-fat content of infants of normal mothers. [13]
Causes
Differentiating Gestational diabetes other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Generally a test for gestational diabetes is carried out between the 24th and 28th week of pregnancy. If patient is at risk for gestational diabetes (see Risk Factors) he or she could prescribe a glucose test earlier in the pregnancy.
Often, gestational diabetes can be managed through a combination of diet and exercise. If that is not possible, it is treated with insulin(usually 15% need Insulin), in a similar manner to diabetes mellitus.
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Dietary Therapy
All women diagnosed with GDM require nutritional counseling for the appropriate amount of weight gain during pregnancy as well as dietary control. Women with a normal BMI [20-25], can consume about 30kcal/kg/d while those who are obese [BMI >25-34] should restrict their diet to 25 kcal/kg/d and those that have a BMI >34 should consume 20kcal/kg/d or less. These patients should restrict fat intake and substitute simple or refined sugars in their diet to more complex carbohydrates. Moderate amount of non-weight bearing exercise is an important adjunct to dietary advice. It is recommended that pregnant women exercise for about 20-30 minutes everyday or at least most days of the week. It is a critical point in time for changing the lifestyles of these women since they are at a high risk for development of type 2 diabetes.
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
References
- ↑ Negrato CA, Gomes MB (2013). "Historical facts of screening and diagnosing diabetes in pregnancy". Diabetol Metab Syndr. 5 (1): 22. doi:10.1186/1758-5996-5-22. PMC 3644500. PMID 23634949.
- ↑ WILKERSON HL, REMEIN QR (1957). "Studies of abnormal carbohydrate metabolism in pregnancy; the significance of impaired glucose tolerance". Diabetes. 6 (4): 324–9. PMID 13447761.
- ↑ 3.0 3.1 "Standards of Medical Care in Diabetes-2016: Summary of Revisions". Diabetes Care. 39 Suppl 1: S4–5. 2016. doi:10.2337/dc16-S003. PMID 26696680.
- ↑ Catalano PM, Tyzbir ED, Wolfe RR, Calles J, Roman NM, Amini SB, Sims EA (1993). "Carbohydrate metabolism during pregnancy in control subjects and women with gestational diabetes". Am. J. Physiol. 264 (1 Pt 1): E60–7. PMID 8430789.
- ↑ Buchanan TA, Metzger BE, Freinkel N, Bergman RN (1990). "Insulin sensitivity and B-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes". Am. J. Obstet. Gynecol. 162 (4): 1008–14. PMID 2183610.
- ↑ Catalano PM, Tyzbir ED, Roman NM, Amini SB, Sims EA (1991). "Longitudinal changes in insulin release and insulin resistance in nonobese pregnant women". Am. J. Obstet. Gynecol. 165 (6 Pt 1): 1667–72. PMID 1750458.
- ↑ Barbour LA, McCurdy CE, Hernandez TL, Kirwan JP, Catalano PM, Friedman JE (2007). "Cellular mechanisms for insulin resistance in normal pregnancy and gestational diabetes". Diabetes Care. 30 Suppl 2: S112–9. doi:10.2337/dc07-s202. PMID 17596458.
- ↑ Freinkel N (1980). "Banting Lecture 1980. Of pregnancy and progeny". Diabetes. 29 (12): 1023–35. PMID 7002669.
- ↑ Lepercq J, Cauzac M, Lahlou N, Timsit J, Girard J, Auwerx J, Hauguel-de Mouzon S (1998). "Overexpression of placental leptin in diabetic pregnancy: a critical role for insulin". Diabetes. 47 (5): 847–50. PMID 9588462.
- ↑ Kirwan JP, Hauguel-De Mouzon S, Lepercq J, Challier JC, Huston-Presley L, Friedman JE, Kalhan SC, Catalano PM (2002). "TNF-alpha is a predictor of insulin resistance in human pregnancy". Diabetes. 51 (7): 2207–13. PMID 12086951.
- ↑ Retnakaran R, Hanley AJ, Raif N, Hirning CR, Connelly PW, Sermer M, Kahn SE, Zinman B (2005). "Adiponectin and beta cell dysfunction in gestational diabetes: pathophysiological implications". Diabetologia. 48 (5): 993–1001. doi:10.1007/s00125-005-1710-x. PMID 15778860.
- ↑ Metzger BE, Phelps RL, Freinkel N, Navickas IA (1980). "Effects of gestational diabetes on diurnal profiles of plasma glucose, lipids, and individual amino acids". Diabetes Care. 3 (3): 402–9. PMID 7190092.
- ↑ Catalano PM, Thomas A, Huston-Presley L, Amini SB (2003). "Increased fetal adiposity: a very sensitive marker of abnormal in utero development". Am. J. Obstet. Gynecol. 189 (6): 1698–704. PMID 14710101.