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Is pharmacologic intervention needed to prevent type 2 after gestational diabetes?
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Type 2 definition needs reexamination
 Robert E. Ratner |
Gestational diabetes mellitus was initially defined as having two values on a 100-g oral glucose tolerance test, exceeding two standard deviations above the mean for an unselected population. This definition was validated by the increased morbidity (development of frank diabetes) and mortality in those women meeting the criteria.
The high rate of ultimate conversion from this prediabetic state to diabetes emphasizes the difficulty in describing categorical definitions to a continuous variable. Does prediabetes really become diabetes at a fasting glucose of 126 mg/dL? Given the continuous nature of glucose with development of complications, as described by several trials, why wait to begin therapy?
The sympathetic observer would say, “to avoid stigmatizing the individual with a chronic disease and to avoid the potential side effects of drug therapy.” The cynic would respond, “because it will cost too much to treat all those individuals with prediabetes.”
The newest treatment algorithm for the therapy of type 2 diabetes makes a remarkable admission. The ADA and the EASD now recommend drug therapy with metformin at the time of diagnosis of diabetes, in part because of the paucity of data showing durability of lifestyle changes in this population. Furthermore, they recommend acceleration of pharmacologic therapy if HbA1c exceeds 7%. Unfortunately, this latter position perpetuates the “treat-to-failure” concept long held in diabetes care.
Should we not be treating individuals to prevent complications and preserve health? Meta-analyses have shown a 50% increase in the risk of cardiovascular events at two-hour post-glucose load plasma glucose levels of 150 mg/dL.
We need to reexamine our categorical definition of type 2 diabetes and initiate effective and safe pharmacologic therapy at a point in time to preserve beta cell function and prevent micro- and macrovascular complications of diabetes.
Robert E. Ratner, MD, is Vice President for Scientific Affairs at MedStar Research Institute, Hyattsville, Md.
Before intervening, consider these two steps
 Thomas Buchanen |
Gestational diabetes results from the entire spectrum of beta cell defects that occur in relatively young women. Some defects are transient, some are stable, but most are progressive and lead to diabetes within 10 years after the index pregnancy. A minority of patients have islet-directed autoimmunity or monogeneic disorders such as maturity onset diabetes of the young (MODY). The majority have chronic insulin resistance.
It is only progressive cases that are relevant to diabetes prevention. It is only cases that occur with chronic insulin resistance for which we have interventions that can delay or prevent diabetes.
Given this heterogeneity, practitioners should take two steps before considering an intervention. First, ascribe an etiology to the gestational diabetes by either eliciting a family history for MODY or testing for antiglumatic acid decarboxylase antibodies in relatively lean patients. Second, determine whether the patient already has diabetes. For women without diabetes but clinical characteristics suggesting a risk of type 2 diabetes, prevention should be pursued.
Type 2 diabetes prevention trials revealed that treatments that reduce body fat or ameliorate its metabolic effects give the best evidence for slowing or stopping progression to diabetes, and treatment can slow or stabilize the disease in prediabetics and in people with very early and mild diabetes. These facts support a stepped-care approach that starts with a lifestyle intervention to reduce body fat, combined quickly with pharmacological treatment if lifestyle fails to prevent diabetes.
Rising HbA1c or fasting glucose indicates continued loss of beta cell function and an inadequate response to lifestyle changes. Pharmacological therapy can then be implemented, particularly if the HbA1c has risen to a level consistent with early diabetes.
Thomas A. Buchanen, MD, is Professor of Medicine, Obstetrics and Gynecology, Keck School of Medicine, Los Angeles.