Gestational diabetes

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Description

Gestational diabetes mellitus 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  and is increasing  more common among older women, obese women and certain ethnic groups. It usually presents after the beginning of the second trimester.

Pathological Process

In pregnancy, some women develop insulin resistance, which may stem 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 progress, the insulin demands increase, and thus, 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 a normal pregnancy blood glucose level changes are small compared to the large changes in insulin resistance. Women who present with gestational diabetes mellitus have less of a degree of compensation at the Beta cell than women who do not present with gestational diabetes . Less than 10% of women who present with gestational diabetes have been shown to have antibodies to pancreatic islets of Beta cells in their circulation. It has been postulated that their gestational diabetes may stem from autoimmune damage to Beta cells . Some gestational diabetes mellitus cases have been shown to be due to genetic defects in Beta cells . Others may be chronic hyperglycaemia first detected at pregnancy, which may explain why most women who develop gestational diabetes mellitus go on to develop type II diabetes mellitus. The exact mechanism for increased insulin resistance is still largely unclear. Maternal obesity may contribute as up-regulation of cytokines and adipokines impacts insulin pathways and skeletal muscle insulin signalling is impaired .

Consequences of Gestational Diabetes Mellitus

For Mother

Gestational diabetes mellitus is related to higher rates of:

<span style="line-height: 1.5em;" />Pre-eclampsia

Caesarean section

Gestational diabetes mellitus in subsequent pregnancies

Gestational diabetes mellitus typically resolves after birth. However, there have been many studies detailing the significantly increased risk of developing type II diabetes mellitus after having gestational diabetes mellitus, particularly in the first 5 years postpartum .

For Baby

• Macrosomnia: leading to higher rates of injury to mother and baby , and higher rates of childhood overweight and obesity 
• Fetal hyperglycaemia and hyperinsulinimia
• Preterm delivery
• Intensive neonatal care
• High neonatal body fat percentage
• Clinical neonatal hypoglycaemia 

Diagnositc Procedures

Risk Factors

Several factors have been identified which increase the risk of women developing gestational diabetes mellitus. 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 episode of gestational diabetes mellitus
• Multigravid women
• Excessive weight gain during pregnancy
• Short stature
• Smoking

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

Gestational diabetes mellitus can only be confirmed by an abnormal glucose tolerance test. The World Health Organization classify gestational diabetes mellitus as:

• A fasting blood glucose level of >7mmol/l
• A blood glucose level of >7.8mmol/l 2 hours after a 75g glucose drink

Medical Management / Interventions

Diet

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 .

Medication

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 .

References

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