There is strong evidence that the avoidance of hyperglycemia is essential inoptimizing pregnancy outcome in type 1 diabetes. The price to pay is a striking increase in severe hypoglycemia (SH), defined as episodes requiring help from another person. During type 1 diabetic pregnancy, occurrence rates of SH up to 15 times higher as in the intensively treated group of the Diabetes Control and Complications Trial (DCCT) are reported. Blood glucose (BG) treatment targets differ considerably between clinics; some authors advocate lower limits as low as 3.3 mmol/l. Improved glycemic control and/or recurrent hypoglycemia (i.e. BG <3.9 mmol/l) may result in impairment of glucose counterregulatory responses. Also, glucose counterregulation may be altered by pregnancy itself. Short-acting insulin analogs may help reduce hypoglycemia with preservation of good glycemic control, but their use during pregnancy has yet to be proven safe.Several clinical studies did not establish an association between maternal hypoglycemia and diabetic embryopathy. However, animal studies clearly indicate that hypoglycemia is potentially teratogenic during organogenesis. Increased rates of macrosomia continue to be observed despite near normal HbA(1c) levels. This may, at least in part, be the result of rebound hyperglycemia elicited by hypoglycemia. Exposure to hypoglycemia in utero may have long-term effects on offspring including neuropsychological defects. It is yet unclear to what extent the benefits of tight glycemic control balance with the increased risk of (severe) hypoglycemia during type 1 diabetic pregnancy. Efforts must be made to avoid low BG, i.e. <3.9 mmol/l, when tightening glycemic control.
Copyright 2002 John Wiley & Sons, Ltd.