Test your medicine knowledge with the MKSAP challenge, in partnership with the American College of Physicians.

A 66-year-old man is evaluated in the office after being treated in the emergency department for an exacerbation of chronic obstructive pulmonary disease. While in the emergency department, he was noted to have a random blood glucose level of 211 mg/dL (11.7 mmol/L). His HbA1c was 7.8% at the time. A repeat random fingerstick blood glucose level in office is 204 mg/dL (11.3 mmol/L).

The patient reports recent polyuria and polydipsia. He has lost 6 kg (13.2 lb) over the last 3 months. He has chronic epigastric pain associated with loose, oily stools due to chronic pancreatitis.

He has a 20-pack-year history of tobacco use and prior alcohol use, however, he does not currently use alcohol. Current medications are enteric-coated pancreatic enzymes, vitamins, tiotropium inhaler, and an albuterol inhaler as needed.

On physical examination, temperature is 37.1 °C (98.8 °F), blood pressure is 130/75 mm Hg, and pulse rate is 90/min. BMI is 22. He has mild epigastric pain on palpation without rebound tenderness or guarding. The rest of his examination is unremarkable.

Which of the following is the most appropriate treatment for his diabetes?

A. Exenatide
B. Glipizide
C. Insulin
D. Metformin

MKSAP Answer and Critique

The correct answer is C. Insulin.

This patient has an acquired form of type 1 diabetes mellitus caused by chronic pancreatitis (pancreoprivic diabetes), which necessitates the use of insulin for treatment of the hyperglycemia. Chronic pancreatitis results in permanent destruction of the pancreas and may impair both the endocrine and exocrine functions of the pancreas. The pancreatic exocrine abnormalities arise from loss of the pancreatic enzymes required for digestion and absorption of food. The pancreatic endocrine abnormalities can present in a similar manner as type 1 diabetes with hyperglycemia from insulin deficiency secondary to destruction of beta cells. Therefore insulin is the recommended treatment. Unlike autoimmune type 1 diabetes, chronic pancreatitis also destroys the pancreatic alpha cells causing a glucagon deficiency that increases the risk of spontaneous hypoglycemia. Glucagon acts on the liver to increase glucose production through glycogenolysis and gluconeogenesis. The recovery from hypoglycemia is also impaired with alpha cell destruction. Early recognition of hypoglycemic symptoms and strategic hypoglycemic treatment plans should be emphasized with patients with pancreoprivic diabetes.

Exenatide, a glucagon-like protein-1 (GLP-1) mimetic, suppresses glucagon and promotes insulin secretion. The pancreatic beta cell and alpha cell destruction associated with chronic pancreatitis precludes this treatment option. Postmarketing reports of pancreatitis are also cause for concern for the use of this class of medication in patients with a history of pancreatitis.

The sulfonylurea glipizide increases insulin secretion. The effect would likely be minimal to nonexistent in this patient with hyperglycemia resulting from substantial beta cell destruction from chronic pancreatitis.

Metformin decreases hepatic glucose output by inhibiting gluconeogenesis and increases insulin-mediated glucose utilization in peripheral tissues. Metformin is a first-line agent for initial treatment of type 2 diabetes; however, this patient has an insulin deficiency from pancreatic beta cell destruction and should be treated as a patient with type 1 diabetes.

Key Point

• Hyperglycemia caused by chronic pancreatitis is an acquired form of type 1 diabetes mellitus and should be treated with insulin.

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