Gestational diabetes: Difference between revisions
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== Description == | == Description == | ||
<div>Gestational Diabetes Mellitus (GDM) is characterised by hyperglycaemia first recognised in pregnancy. Its prevalence varies widely in the literature, but is thought to effect 4-7.5% of all pregnancies <ref name=" | <div>Gestational Diabetes Mellitus (GDM) is characterised by hyperglycaemia first recognised in pregnancy. Its prevalence varies widely in the literature, but is thought to effect 4-7.5% of all pregnancies <ref name="p1" /><ref name="p2">Lawreance, J.M., Contereras, R., Chen, W. and Sacks, D.A. (2008) 'Trends in the prevelance of preexisting diabetes mellitus and GDM among a racially/ethnically diverse population of pregnant women, 1999-2005', Diabetes Care, 31(5), 899-904.</ref> and is increasing <ref name="p1">Dabelea, D., Snell-Bergeon, J.K., Hartsfield, C.L., Bischoff, K.J., Hamman, R.F., McDuffie, R.S. (2005) 'Increasing Prevelance of Gestational Diabetes Mellitus (GDM) Over Time and by Birth Cohort', Diabetes Care, 28(3), 579-584.</ref> more common among older women, obese women and certain ethnic groups<ref name="p2" />. It usually presents after the beginning of the second trimester<ref name="p4">Alwan, N., Tuffnell,D.J., West, J. (2009) 'Treatments for Gestational Diabetes', The Cochrane Library, Issue 3.</ref>.<br></div> | ||
== Pathological Process<br> == | == Pathological Process<br> == | ||
In pregnancy, women develop insulin resistance, which stems from increased maternal adiposity and several hormones produced during pregnancy block the action of insulin at a cellular level, i.e. Tumor Necrosis Factor Alpha, human placental lactogen and placental growth hormone. As a result, blood glucose levels rise and more insulin is produced in response. As the pregnancy develops, the insulin demands increase further, and insulin resistance also increases due to rising levels of pregnancy hormones. However, this is a normal physiological change in pregnancy. Beta cells in the pancreas increase insulin production to compensate for this, and so in normal pregnancy blood glucose level changes are small compared to the large changes in insulin resistance. In GDM, women have been shown to have less of a degree of compensation at the Beta cell than non-GDM women <ref name=" | In pregnancy, women develop insulin resistance, which stems from increased maternal adiposity and several hormones produced during pregnancy block the action of insulin at a cellular level, i.e. Tumor Necrosis Factor Alpha, human placental lactogen and placental growth hormone. As a result, blood glucose levels rise and more insulin is produced in response. As the pregnancy develops, the insulin demands increase further, and insulin resistance also increases due to rising levels of pregnancy hormones. However, this is a normal physiological change in pregnancy. Beta cells in the pancreas increase insulin production to compensate for this, and so in normal pregnancy blood glucose level changes are small compared to the large changes in insulin resistance. In GDM, women have been shown to have less of a degree of compensation at the Beta cell than non-GDM women <ref name="p6">Bergman, R.N.(1989) 'Toward a physiological un derstanding of glucose tolerance: minimal model approach', Diabetes, 51, 2207-2213.</ref>. <10% of GDM women have been shown to have antibodies to pancreatic islets of Beta cells in their circulation. It has been postulated thaqt their GDM may stem from autoimmune damage to Beta cells <ref name="p7">Kim, C. and Ferrera, S. (eds.) (2010) Gestational Diabetes During and After Pregnancy, London: Springer-Verlag.</ref>. Some GDM cases have been shown to be due to genetic defects in Beta cells <ref name="p7" />. Others may be chronic hyperglycaemia first detected at pregnancy, which may explain why most GDM women go on to develop Diabetes Mellitus (DM). The exact mechanism for increased insulin resistance is still largely unclear. Maternal obesity may contribute as upregulation of cytokines and adipokines impacts insulin pathways and skeletal muscle insulin sigalling is impaired <ref name="p7" />. | ||
== Consequences of Gestational Diabetes Mellitus == | == Consequences of Gestational Diabetes Mellitus == | ||
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<span style="line-height: 1.5em;" />Pre-eclampsia | <span style="line-height: 1.5em;" />Pre-eclampsia | ||
<span style="line-height: 1.5em;">Caesarean section</span><ref name=" | <span style="line-height: 1.5em;">Caesarean section</span><ref name="p8">HAPO Study Cooperative Research Group (2009) 'Hyperglycaemia and Pregnancy Outcome Study: Associations with neonatal anthropometrics', Diabetes, 58, 453-459.</ref> | ||
<span style="line-height: 1.5em;">GDM in subsequent pregnancies<ref name=" | <span style="line-height: 1.5em;">GDM in subsequent pregnancies<ref name="p9">Catalano, P.M., Kirwen, T.P., Hougel-de Mouzon, S., King, J. (2003) 'Gestational Diabetes and Insulin Resistance: rolein short- and long-term implications for mother and fetus', J Nutr, 133, 1674S-1683S.</ref></span> | ||
GDM typically resolves after birth. However, there have been many studies detailing the significantly increased risk of developing DM Type II after having GDM, particularly in the first 5 years postpartum <ref name=" | GDM typically resolves after birth. However, there have been many studies detailing the significantly increased risk of developing DM Type II after having GDM, particularly in the first 5 years postpartum <ref name="p6">Kim, C., Newton, K.M., Knopp, R.H. (2002) 'Gestational Diabetes and the incidence of Type 2 Diabetes: a systematic review', Diabetes Care, 25(10), 1862-1868.</ref>. | ||
<br> | <br> | ||
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=== For Baby === | === For Baby === | ||
*Macrosomnia: leading to higher rates of injury to mother and baby <ref name=" | *Macrosomnia: leading to higher rates of injury to mother and baby <ref name="p9" />, and higher rates of childhood overweight and obesity <ref name="p0">Hillier, T.A., Pedula, K.L., Schmidt, M.M., Mullen, J.A., Charles, M., Pettit, D.J. (2007) 'Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycaemia', Diabetes Care, 30, 2287-2292.</ref> | ||
*Fetal hyperglycaemia and hyperinsulinimia | *Fetal hyperglycaemia and hyperinsulinimia | ||
*Preterm delivery | *Preterm delivery | ||
*Intensive neonatal care | *Intensive neonatal care | ||
*High neonatal body fat percentage | *High neonatal body fat percentage | ||
*Clinical neonatal hypoglycaemia <ref name=" | *Clinical neonatal hypoglycaemia <ref name="p8" /> | ||
== Diagnositc Procedures == | == Diagnositc Procedures == | ||
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Short stature | Short stature | ||
Smoking<ref name=" | Smoking<ref name="p6">Di Cianni, G., Volpe, L., Lencioni, C., Miccoli, R., Cuccuru, I., Ghio, A., (2003) 'Prevalence and risk factors for gestational diabetes assessed by universal screening', Diabetes ResearchfckLRand Clinical Practice,62(2), 131–137.</ref><ref name="p7">Tieu, J., Middleton, P., McPhee, A.J., Crowther, C.A. (2010) 'Screening for Gestational Diabetesand subsequent management for improving maternal and infant health', The Cochrane Library, Issue 7.</ref> | ||
<br> | <br> | ||
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*A fasting blood glucose level of >7mmol/l | *A fasting blood glucose level of >7mmol/l | ||
*A blood glucose level of >7.8mmol/l 2 hours after a 75g glucose drink<ref name=" | *A blood glucose level of >7.8mmol/l 2 hours after a 75g glucose drink<ref name="p4" /> | ||
<br> | <br> | ||
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=== Diet === | === Diet === | ||
Dietary interventions<span style="line-height: 1.5em;"> have long been a cornerstone of treatement for GDM. Women diagnosed with GDM are routinely referred to a dietician. The challenge of GDM management for dieticians is striking the delicate balance between keeping maternal insulin low without restricting fetal growth. A Cochrane review in 2008 examined 3 trials investigating the effects of diet on preventing GDM, found inconclusive results <ref name=" | Dietary interventions<span style="line-height: 1.5em;"> have long been a cornerstone of treatement for GDM. Women diagnosed with GDM are routinely referred to a dietician. The challenge of GDM management for dieticians is striking the delicate balance between keeping maternal insulin low without restricting fetal growth. A Cochrane review in 2008 examined 3 trials investigating the effects of diet on preventing GDM, found inconclusive results <ref name="p9"><ref name=9> Tieu J, Crowther CA, Middleton P. Dietary advice in pregnancy for preventing gestational diabetes mellitus. Cochrane Database Syst Rev 2008;2.</ref>.</span> | ||
=== Medication === | === Medication === | ||
<div>When dietary management fails, insulin is considered the safest treatment, as free insulin cannot cross the placenta. Alpha-glucosidase inhibitors (acarbose) and biguanides (metformin) cross placenta but are still used increasingly. However, there are insufficient data to determine the long term effects of these on mother and baby <ref name=" | <div>When dietary management fails, insulin is considered the safest treatment, as free insulin cannot cross the placenta. Alpha-glucosidase inhibitors (acarbose) and biguanides (metformin) cross placenta but are still used increasingly. However, there are insufficient data to determine the long term effects of these on mother and baby <ref name="p5" />.</div> | ||
=== Weight Management === | === Weight Management === | ||
Revision as of 12:43, 6 June 2017
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Description[edit | edit source]
Gestational Diabetes Mellitus (GDM) is characterised by hyperglycaemia first recognised in pregnancy. Its prevalence varies widely in the literature, but is thought to effect 4-7.5% of all pregnancies [1][2] and is increasing [1] more common among older women, obese women and certain ethnic groups[2]. It usually presents after the beginning of the second trimester[3].
Pathological Process
[edit | edit source]
In pregnancy, women develop insulin resistance, which stems from increased maternal adiposity and several hormones produced during pregnancy block the action of insulin at a cellular level, i.e. Tumor Necrosis Factor Alpha, human placental lactogen and placental growth hormone. As a result, blood glucose levels rise and more insulin is produced in response. As the pregnancy develops, the insulin demands increase further, and insulin resistance also increases due to rising levels of pregnancy hormones. However, this is a normal physiological change in pregnancy. Beta cells in the pancreas increase insulin production to compensate for this, and so in normal pregnancy blood glucose level changes are small compared to the large changes in insulin resistance. In GDM, women have been shown to have less of a degree of compensation at the Beta cell than non-GDM women [4]. <10% of GDM women have been shown to have antibodies to pancreatic islets of Beta cells in their circulation. It has been postulated thaqt their GDM may stem from autoimmune damage to Beta cells [5]. Some GDM cases have been shown to be due to genetic defects in Beta cells [5]. Others may be chronic hyperglycaemia first detected at pregnancy, which may explain why most GDM women go on to develop Diabetes Mellitus (DM). The exact mechanism for increased insulin resistance is still largely unclear. Maternal obesity may contribute as upregulation of cytokines and adipokines impacts insulin pathways and skeletal muscle insulin sigalling is impaired [5].
Consequences of Gestational Diabetes Mellitus[edit | edit source]
For Mother[edit | edit source]
GDM is related to higher rates of:
<span style="line-height: 1.5em;" />Pre-eclampsia
Caesarean section[6]
GDM in subsequent pregnancies[7]
GDM typically resolves after birth. However, there have been many studies detailing the significantly increased risk of developing DM Type II after having GDM, particularly in the first 5 years postpartum [4].
For Baby[edit | edit source]
- Macrosomnia: leading to higher rates of injury to mother and baby [7], and higher rates of childhood overweight and obesity [8]
- Fetal hyperglycaemia and hyperinsulinimia
- Preterm delivery
- Intensive neonatal care
- High neonatal body fat percentage
- Clinical neonatal hypoglycaemia [6]
Diagnositc Procedures[edit | edit source]
Risk Factors[edit | edit source]
Several factors have been identified which increase the risk of women developing GDM. These include:
Older age
Ethnicity, namely black, Native American, Pacific Islander, Hispanic, South or East Asian and Indigenous Australian
High pre-pregnancy BMI
Family history of diabetes
Previous GDM
Multigravid women
Excessive weight gain during pregnancy
Short stature
Local regimens use various screening tools in conjunction with these risk factors to identify women in need of further testing.
Screening for Gestational Diabetes Mellitus[edit | edit source]
GDM can only be confirmed by an abnormal glucose tolerance test. The World Health Organisation classify GDM as:
- A fasting blood glucose level of >7mmol/l
- A blood glucose level of >7.8mmol/l 2 hours after a 75g glucose drink[3]
Medical Management / Interventions
[edit | edit source]
Diet[edit | edit source]
Dietary interventions have long been a cornerstone of treatement for GDM. Women diagnosed with GDM are routinely referred to a dietician. The challenge of GDM management for dieticians is striking the delicate balance between keeping maternal insulin low without restricting fetal growth. A Cochrane review in 2008 examined 3 trials investigating the effects of diet on preventing GDM, found inconclusive results [7].
Medication[edit | edit source]
When dietary management fails, insulin is considered the safest treatment, as free insulin cannot cross the placenta. Alpha-glucosidase inhibitors (acarbose) and biguanides (metformin) cross placenta but are still used increasingly. However, there are insufficient data to determine the long term effects of these on mother and baby [9].
Weight Management[edit | edit source]
The Role for Physiotherapy
[edit | edit source]
Physiotherapy in the Management of Gestational Diabetes Mellitus[edit | edit source]
Physiotherapy in the Prevention of Gestational Diabetes Mellitus[edit | edit source]
Resources
[edit | edit source]
Kim and Ferrera (2010) Gestational Diabetes During and After Pregnancy
Recent Related Research (from Pubmed)[edit | edit source]
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References[edit | edit source]
References will automatically be added here, see adding references tutorial.
- ↑ 1.0 1.1 Dabelea, D., Snell-Bergeon, J.K., Hartsfield, C.L., Bischoff, K.J., Hamman, R.F., McDuffie, R.S. (2005) 'Increasing Prevelance of Gestational Diabetes Mellitus (GDM) Over Time and by Birth Cohort', Diabetes Care, 28(3), 579-584.
- ↑ 2.0 2.1 Lawreance, J.M., Contereras, R., Chen, W. and Sacks, D.A. (2008) 'Trends in the prevelance of preexisting diabetes mellitus and GDM among a racially/ethnically diverse population of pregnant women, 1999-2005', Diabetes Care, 31(5), 899-904.
- ↑ 3.0 3.1 Alwan, N., Tuffnell,D.J., West, J. (2009) 'Treatments for Gestational Diabetes', The Cochrane Library, Issue 3.
- ↑ 4.0 4.1 4.2 Bergman, R.N.(1989) 'Toward a physiological un derstanding of glucose tolerance: minimal model approach', Diabetes, 51, 2207-2213. Cite error: Invalid
<ref>tag; name "p6" defined multiple times with different content Cite error: Invalid<ref>tag; name "p6" defined multiple times with different content - ↑ 5.0 5.1 5.2 5.3 Kim, C. and Ferrera, S. (eds.) (2010) Gestational Diabetes During and After Pregnancy, London: Springer-Verlag. Cite error: Invalid
<ref>tag; name "p7" defined multiple times with different content - ↑ 6.0 6.1 HAPO Study Cooperative Research Group (2009) 'Hyperglycaemia and Pregnancy Outcome Study: Associations with neonatal anthropometrics', Diabetes, 58, 453-459.
- ↑ 7.0 7.1 7.2 Catalano, P.M., Kirwen, T.P., Hougel-de Mouzon, S., King, J. (2003) 'Gestational Diabetes and Insulin Resistance: rolein short- and long-term implications for mother and fetus', J Nutr, 133, 1674S-1683S. Cite error: Invalid
<ref>tag; name "p9" defined multiple times with different content - ↑ Hillier, T.A., Pedula, K.L., Schmidt, M.M., Mullen, J.A., Charles, M., Pettit, D.J. (2007) 'Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycaemia', Diabetes Care, 30, 2287-2292.
- ↑ Cite error: Invalid
<ref>tag; no text was provided for refs namedp5
