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Current Visit
When seen at the current semiannual visit, PD’s weight is 165 lbs (BMI 23.7) and she reports a 2- to 2.5-pound monthly weight loss without really trying, which is causing her concern. She has also noticed that she has been having higher blood glucose excursions, with fasting blood glucose levels increasing from their former levels of 105 mg/dL to 110 mg/dL up to the current high range of 160 mg/dL to 175 mg/dL. When she tried increasing the glimepiride dose on occasion, it seemed to have no added effect.
Q: What is the explanation for the change in PD’s
formerly stable condition?
A: The unanticipated weight loss and associated
hyperglycemia in a previously well-controlled patient suggest that the oral medications are no longer able to compensate for her progressive dysfunction in pancreatic beta cell insulin secretion.
Insulin or C-peptide levels do not need to be checked, since a clinical diagnosis can easily be made in PD. She is in a catabolic state, with loss of stored adipose tissue triglyceride and gradual loss of muscle mass resulting from her relative insulin deficiency. It was clear from her lack of response to metformin initially that beta cell dysfunction was her primary pathophysiologic defect leading to the development of diabetes with overt hyperglycemia. This development might also have been anticipated based on her known previous gestational diabetes. The loss of beta cell insulin secretion is characteristic of the natural history of type 2 diabetes when treated with a sulfonylurea, metformin, or insulin, as was demonstrated in the UKPDS.3
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