Incidence and prevalence:

Approximately 3% of all pregnancies are affected by diabetes mellitus. Overall there has been a significant increase in the prevalence of type 2 as well as gestational diabetes, especially among Asian women.

Gestational diabetes accounts for about 90% of all cases of diabetes in pregnancy, while the remaining 10% are due to pre-gestational diabetes (This refers to women who are diagnosed to have diabetes prior to pregnancy).

Gestational diabetes refers to the onset of diabetes for the first time during pregnancy.

History of Diabetes in pregnancy

Insulin was introduced in 1921. Prior to the introduction of insulin 40% of diabetic women who became pregnant died during the pregnancy, mainly due to diabetic ketoacidosis. Prior to the introduction of insulin fetal loss was also very high (about 50%), mainly due to miscarriage ,premature labour, late intrauterine and neonatal death. As soon as insulin was introduced maternal mortality fell to between 2 and 3%. However the decline in the perinatal mortality rate was much slower, mainly due to late intrauterine death among diabetic women. This led to the policy of early induction of labour in diabetic pregnant women.

Pathophysiology of diabetes in pregnancy

Pregnancy is “an insulin resistance state”.

There is increased levels of blood insulin, glucose as well as triglycerides. The insulin resistance state is caused by high levels of circulating insulin antagonists such as cortisol,oestrogens, progesterones and other hormones produced in the placenta such as placental lactogen.

Insulin regulates the release and storage of glucose, fat and amino acids.

Diabetes complicating pregnancy (weather gestational or pre-existing), leads to an increase in the circulating concentration of all metabolic substrates that are available to the fetus (Glucose crosses by facilitated diffusion, free fatty acids cross by simple diffusion and amino acids by active transfer).

Insulin (plus other polypeptide hormones such as glucagons) cannot cross the placenta, therefore the high levels of glucose and amino acids in the fetal circulation stimulates the fetal pancreatic islets of Langerhans leading to beta-cell hyperplasia and fetal hyperinsulinaemia.

Insulin , being a major fetal growth factor can lead to fetal macrosomia (especially if the diabetes is not controlled). The combination of fetal hyperinsulinaemia (high concentration of circulating insulin) and fetal hypoxia stimulates fetal medullary and extramedullary erythropoiesis (formation of red blood cells) causing polycythaemia (high levels of circulating red blood cells) possibly due to increased erythropoietin levels.

Other complications caused in the neonate due to fetal hyperinsulinaemia include hypoglycemia, respiratory distress syndrome and jaundice.

References:

Page 776 to 777 Chapter 18 Obstetrics by William R Crombleholme MD- 2006 Current Medical Diagnosis and Treatment. Edited by Lawrence M Tierney,Jr ,Stephen J McPhee and Maxine A. Papadakis. 45th Edition

Page 197 to 207 Chapter 17 Diabetes and Endocrine Disorders in Pregnancy by M.D.G Gillmer and P.A. Hurley- Dewhurst’s Textbook of Obstetrics and Gynaecology for Postgraduates -Sixth edition .Edited by D. Keith Edmonds.

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