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Pregestational diabetes, based on literature, appears to be present in approximately 1% of all pregnancies.1 Type 1 diabetes mellitus tends to occur early in human life and appears to be associated with an autoimmune disorder that alleviates pancreatic β cells. This generally leads to a requirement for insulin replacement. Type 2 pregestational diabetes mellitus is associated with obesity, insulin deficiency, insulin resistance, and development of certain complications, such as neurologic, renal, and vascular issues. Type 2 diabetes has increased significantly in number due to the obesity epidemic in the United States.2 Of diabetic cases in pregnancy, 90% are related to gestational diabetes mellitus. Over 50% of such patients will eventually develop type 2 pregestational diabetes. Obesity, along with diabetes, has many negative consequences during pregnancy, to the mother, to the fetus, to the newborn, or to all.


Type 1 diabetes mellitus accounts for about 5%–7% of diabetes in the United States. This subclass develops as a result of an autoimmune disorder that is usually directed against insulin-producing β cells in the pancreas. Destruction of such cells leads to the requirement for insulin replacement. Usually, onset occurs before age 30 and can affect about 0.5% of all pregnancies in the United States. Prior to insulin therapy, infertility was the most common consequence of diabetes mellitus for reproductive-age women. Mortality rates in neonates could have been as high as 60%.1,2,3 Advances in insulin therapy and improvements in neonatal care have decreased this mortality rate to 2%. All risks associated with diabetes are increased once obesity is factored in as well.

All of the causes of this disorder are still not clear. Some suggest that there is a general inflammatory state called insulinitis that may lead to this type of diabetes. Macrophages, B lymphocytes, and CD+ T lymphocytes may be able to infiltrate the Langerhans islets in the pancreas. A complex cycle generally leads to accumulation of CD+ lymphocytes, therefore leading to gradual destruction of insulin-producing β cells.3,4,5 Ultimately, insulin deficiency that causes hyperglycemia occurs. In general, pregnancy itself is a diabetogenic state in which postprandial glucose levels are already elevated and insulin sensitivities are decreased.4 This has been associated with an increase in hormones, including cortisol, progesterone, estrogen, prolactin, and human placental lactogen.6 Recently, there have been other molecules that have been associated with this entity as well. The literature has been supportive of the need for an overall increase in insulin requirement during advancing gestational weeks. This increase is even greater if obesity is a factor as well.

This especially has been noted to happen beginning near the second trimester and for the rest of the pregnancy. It is known that those with pregestational diabetes show increasing insulin requirements throughout pregnancy. A Danish prospective study showed an increase in C-peptide during ...

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