Developing a Quality Measure for Clinical Inertia in Diabetes Care

OBJECTIVE: To develop a valid quality measure that captures clinical inertia, the failure to initiate or intensify therapy in response to medical need, in diabetes care and to link this process measure with outcomes of glycemic control. DATA SOURCES: Existing databases from 13 Department of Veterans Affairs hospitals between 1997 and 1999. STUDY DESIGN: Laboratory results, medications, and diagnoses were collected on 23,291 patients with diabetes. We modeled the decision to increase antiglycemic medications at individual visits. We then aggregated all visits for individual patients and calculated a treatment intensity score by comparing the observed number of increases to that expected based on our model. The association between treatment intensity and two measures of glycemic control, change in HbA1c during the observation period, and whether the outcome glycosylated hemoglobin (HbA1c) was greater than 8 percent, was then examined. PRINCIPAL FINDINGS: Increases in antiglycemic medications occured at only 9.8percent of visits despite 39percent of patients having an initial HbA1c level greater than 8 percent. A clinically credible model predicting increase in therapy was developed with the principal predictor being a recent HbA1c greater than 8 percent. There were considerable differences in the intensity of therapy received by patients. Those patients receiving more intensive therapy had greater improvements in control (p<.001). CONCLUSIONS: Clinical inertia can be measured in diabetes care and this process measure is linked to patient outcomes of glycemic control. This measure may be useful in efforts to improve clinicians management of patients with diabetes

Muscle-specific Pparg deletion causes insulin resistance.

Thiazolidinediones (TZDs) are insulin-sensitizing drugs and are potent agonists of the nuclear peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Although muscle is the major organ responsible for insulin-stimulated glucose disposal, PPAR-gamma is more highly expressed in adipose tissue than in muscle. To address this issue, we used the Cre-loxP system to knock out Pparg, the gene encoding PPAR-gamma, in mouse skeletal muscle. As early as 4 months of age, mice with targeted disruption of PPAR-gamma in muscle showed glucose intolerance and progressive insulin resistance. Using the hyperinsulinemic-euglycemic clamp technique, the in vivo insulin-stimulated glucose disposal rate (IS-GDR) was reduced by approximately 80% and was unchanged by 3 weeks of TZD treatment. These effects reveal a crucial role for muscle PPAR-gamma in the maintenance of skeletal muscle insulin action, the etiology of insulin resistance and the action of TZDs