Should drug therapy be used to reduce cardiometabolic risk from gestational diabetes?
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Pharmacologic therapy should be considered.
A basic principle of medicine is to provide people at risk with the most clinically and cost-effective management for their condition or risk profile. Diagnosis of gestational diabetes is well known to carry long-term maternal health risks, in particular progression to type 2 diabetes and development of clinically manifested cardiovascular disease.
Elevated CVD risk is present even in women who do not progress to overt diabetes. Overweight and obesity commonly accompany gestational diabetes and must be addressed as part of a comprehensive “whole of life cycle” approach to reducing cardiometabolic risk.
Nonpharmacologic measures, including breastfeeding, dietary modification and increased physical activity, are of proven benefit in reducing progression to type 2 diabetes following gestational diabetes, but their absolute effect is limited to an approximate 5% reduction during 4 years to 5 years, which clearly leaves room for exploration of alternative approaches.
The thiazolidinedione drugs were the first medications demonstrated to reduce progression to overt diabetes after gestational diabetes, but adverse effects preclude their use. Women with a history of gestational diabetes are at higher risk for progression to overt diabetes than other women with prediabetes, and in this group, metformin’s efficacy is equivalent to intensive lifestyle intervention, both in the short term and at 10 years of follow-up.
In many cases, management of obesity is also an important aspect of post-gestational diabetes care. Standard lifestyle interventions show limited efficacy in this area, with mean weight loss of 3 kg to 5 kg after 1 year and a tendency to regaining weight after the active intervention phase is completed. By contrast, bariatric surgery produces an average weight loss of 25 kg to 20 kg at 1 year and must be considered as a therapeutic option for women with history of gestational diabetes and marked obesity or other comorbidities.
Women with prior gestational diabetes are also at risk for developing more overt CVD and may well require medications for hypertension and hyperlipidemia. Medications for these conditions must also be considered as part of our treatment strategy.
Thus, whilst acknowledging that lifestyle modification should be a key strategy in reducing cardiometabolic risk after gestational diabetes, clinicians should include medications — and indeed surgical interventions — in their therapeutic armamentarium.
- Reference:
- Epinette JA, et al. J Arthroplasty. 2014;doi:10.1016/j.arth.2013.12.011.
- For more information:
- David McIntyre, MD, FRACP, is director of obstetric medicine at Mater Health Services and head of the Mater Clinical Unit at University of Queensland in Australia. He can be reached at david.mcintyre@mater.org.au.
Lifestyle interventions should be the focus.
Based on 20-plus years of studies we’ve done, mostly with Hispanic women with prior gestational diabetes, we know that type 2 diabetes develops slowly as pancreatic beta-cell function, measured as beta-cell compensation for insulin resistance, and declines in almost a linear fashion over time. In response, blood glucose levels rise slowly for many years, then rise quickly as patients get close to diabetes.
In our studies, weight gain and insulin resistance were the primary conditions leading to beta-cell decline, so they should be the primary targets to preserve beta-cell function and delay or prevent diabetes. This information applies to women with clinical characteristics suggesting a risk for type 2 diabetes. Less is known about mechanisms for diabetes development in other women, in particular, those who are lean. They should be tested for evidence of evolving type 1 diabetes or, if family history is suggestive, monogenic forms of diabetes.
For women with a history of gestational diabetes who have risk factors for type 2 diabetes, such as obesity or high-risk race/ethnicity, lifestyle interventions should be the first thing that clinicians prescribe, even if patients do not yet have prediabetes. Monitoring the response to treatment should include regular assessment of glucose and HbA1c levels, looking not for a particular level, but change over time. Stable levels indicate stable beta-cell function, which is the desired outcome.
The lifestyle prescription can be continued unchanged. If risk levels indicate continued loss of beta-cell function, then the patient and clinician need to discuss and decide whether they should intensify the lifestyle intervention or add medication. There is evidence that medications such as metformin and pioglitazone can slow or stop declining beta-cell function at this stage. But whether that is necessary to maintain long-term glycemic stability and/or to reduce long-term complications compared to starting medications once diabetes develops is not clear.
So, the choice is up to the patient and her provider. Personally, I suggest a focus on lifestyle in the prediabetes stage, reserving medications for when and if diabetes develops.
- For more information:
- Thomas Buchanan, MD, is professor of medicine and co-director of the Diabetes and Obesity Research Institute at Keck School of Medicine at University of Southern California. He can be reached at buchanan@usc.edu.
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