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Conclusion

Charles M. Clark, Jr., MD

There was general agreement among the conference participants that reducing the HbA_1c of patients with type 2 diabetes results in benefits in microvascular disease and neuropathy similar to those that have been convincingly demonstrated in type 1 diabetes. This consensus was subsequently confirmed by the U.K. Prospective Diabetes Study (UKPDS), the results of which were released after the conference reported here. The group also felt that the goals of treatment for type 2 diabetes should not categorically differ from the goals of treatment for type 1 diabetes. Obviously, treatment of diabetes must take into account the individual patient's circumstances; i.e., what is the likely clinical course of the individual patient. The metabolic goal of someone who is 70 years old will clearly differ from that of someone who is 18. Nevertheless, the American Diabetes Association's goal of an HbA_1c of 7% appears to be a reasonable one based on the clinical trial and epidemiological data available.

There was also general agreement that insulin is nearly always effective in lowering HbA_1c and that there is no substantial evidence that its use is detrimental as regards macrovascular disease. Indeed, some data, such as the Diabetes Mellitus Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) Study, suggest a favorable role for insulin in type 2 patients with cardiovascular disease. The conferees also expressed great skepticism as to any theoretical or practical benefit of equal metabolic control with fewer units of insulin.

The group felt that reducing HbA_1c is the treatment goal in type 2 diabetes, as in type 1 diabetes, and that it is unlikely that any single agent or combination of agents will demonstrate any unique benefit independent of reducing hyperglycemia. The feeling was that too many providers treat either with insulin or with oral agents, whereas, in truth, the judicious mix of both may actually be very important. The consensus ultimately was that encouraging a patient to improve his or her HbA_1c is more important than how it is done. The UKPDS appears to confirm this consensus.

The participants at the conference also agreed that whereas the benefit of the treatment of diabetes per se in the prevention of macrovascular disease in type 2 diabetes has not been proved, there is a reasonable body of evidence suggesting that it is beneficial. Additionally, the benefit of treating type 2 diabetes in preventing microvascular and neurological complications is sufficient to warrant more intensive management, whether or not treating hyperglycemia prevents macrovascular disease.

Another important conclusion of the conference is that to reduce macrovascular events, the treatment of type 2 diabetes requires more than the treatment of hyperglycemia. Rather, it requires treating all the cardiovascular risk factors and abnormalities seen in patients with type 2 diabetes. There was a strong feeling that the evidence to date supports the conclusion that the focus should be on nonglycemic parameters as well as on hyperglycemia. The treatment of diabetes per se is unlikely to completely normalize cardiovascular risk. Indeed, the common practice of focusing solely on glycemic control in the hope that the other nonglycemic risk factors will improve needs to stop. What is needed is concurrent therapy rather than sequential therapy.

Finally, because the majority of diabetes care throughout the world is carried out in the primary care environment, there is a great challenge for the diabetes community to effectively communicate to the primary care practitioners the importance of metabolic control in type 2 diabetes. Something that we certainly need to eliminate is insulin being used as a threat in an attempt to improve patient compliance. The UKPDS clearly demonstrated that the natural course of type 2 diabetes is gradual pancreatic failure. Thus, every patient with type 2 diabetes will likely need to receive insulin, either alone or in combination, to attain tight glycemic control. An intriguing issue raised by Dr. Stern is whether insulin should be the first pharmacological agent used to improve glucose in patients with type 2 diabetes.

Both patients and practitioners need to recognize that the treatment of type 2 diabetes represents a journey. The journey generally begins with lifestyle modification and ends with insulin treatment, either alone or in combination with oral agents. Insulin treatment does not represent a personal or medical failure, but rather a means to the goal of improving metabolic control. In the final analysis, treatment of type 2 diabetes will require combination treatments to reduce the metabolic and cardiovascular risk factor abnormalities. Only a comprehensive approach to type 2 diabetes, which includes the use of insulin, is likely to significantly reduce the microvascular and macrovascular morbidity and mortality associated with this disease.

From the Regenstrief Institute, Indianapolis, Indiana.

Address correspondence and reprint requests to Charles M. Clark, Jr., MD, Diabetes Care Editorial Office, Regenstrief Institute, 6th Floor, 1001 W. 10th St., Indianapolis, IN 46202-2859.

Received for publication 28 December 1998 and accepted 5 January 1999.

C.M.C. has received honoraria from Eli Lilly.

Abbreviations: UKPDS, U.K. Prospective Diabetes Study.

A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

This article is based on presentations at a conference organized by the Indiana University Diabetes Research and Training Center. The conference and the publication of this article were made possible by an unrestricted educational grant from Eli Lilly and Company.

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