A 62-year-old woman comes to the office for follow-up of diabetes treatment. She has had type 2 diabetes mellitus for 10 years, which is managed with oral metformin twice daily and insulin glargine at bedtime. The patient has no chest pain, dizziness, sweating, polyuria, or palpitations. She checks her blood glucose level every morning and has had values of 75-132 mg/dL over the last month. Medical history is notable for hypertension and mild intermittent asthma, for which the patient takes lisinopril, amlodipine, and albuterol as needed. Blood pressure is 128/72 mm Hg and pulse is 79/min. BMI is 41 kg/m². Laboratory results show a random glucose level of 298 mg/dL and hemoglobin A1c of 8.1%. Which of the following best explains the suboptimal glycemic control in this patient?

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11ec25c8_d3a8_93be_bc81_f99e38777a92_MD0003_00 Hemoglobin A1c reflects average glucose levels over the lifespan of hemoglobin (about 3 months). A1c is influenced by both fasting and postprandial glucose concentrations and is useful for estimating overall glycemic control in patients with diabetes mellitus. The target A1c is <7% in most patients. Very high A1c levels (>10%) suggest significant hyperglycemia throughout the day, whereas lesser abnormalities are often due to elevations in only postprandial glucose levels. This patient's hemoglobin A1c is elevated despite an acceptable morning (fasting) glucose (usual target range: 80-130 mg/dL). In association with her markedly elevated random glucose (290 mg/dL), this suggests the patient is experiencing frequent postprandial hyperglycemia leading to impaired overall glycemic control. Improving management in this patient will require better control of postprandial glucose without inducing fasting hypoglycemia. This can be achieved with a combination basal-bolus insulin regimen, continuing the long-acting basal insulin (ie, insulin glargine) to control baseline fasting glucose and adding a rapid-acting mealtime insulin (eg, insulin aspart) to control postprandial glucose excursions. (Choice A) Autoimmune pancreatitis causes diabetes due to destruction of beta cells. However, patients typically have recurrent abdominal pain and symptoms of biliary dysfunction (eg, obstructive jaundice) and often have frequent and severe hypoglycemia due to loss of glucagon-producing alpha cells. (Choice B) The dawn phenomenon is an early morning hyperglycemic surge due to the diurnal increase in growth hormone and cortisol secretion. It causes elevated fasting (not postprandial) hyperglycemia. (Choice C) This patient's fasting glucose is well controlled, suggesting an adequate basal insulin dose. Increasing the dose would likely lead to fasting hypoglycemia without a significant improvement in overall control. (Choice D) Insulin-neutralizing antibodies can cause very high insulin dose requirements, typically resulting in both fasting and nonfasting hyperglycemia. These antibodies were commonly seen in the past with bovine and porcine insulin but are rare with recombinant insulin analogues. Educational objective: Patients with diabetes mellitus who have an elevated hemoglobin A1c despite normal fasting glucose levels may have postprandial hyperglycemia. A combined regimen including a long-acting basal insulin (to control fasting glucose) and a rapid-acting mealtime insulin (to control postprandial glucose) can improve glycemic control. References: Diagnosis and management of diabetes: synopsis of the 2016 American Diabetes Association Standards of Medical Care in Diabetes. (http://www.ncbi.nlm.nih.gov/pubmed/26928912)

A 62-Year-Old Woman Comes to the Office for Follow-Up of Diabetes