IM Board Review

A 48-year-old man with uncontrolled diabetes

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A 48-year-old white man who has had diabetes mellitus for 6 years presents to the outpatient clinic because his blood sugar levels have been rising for the past week.

Both his parents had diabetes, and at the time of his diagnosis he weighed 278 pounds, all of which supported a diagnosis of type 2 diabetes mellitus. His disease was initially managed with diet, exercise, and metformin (Glucophage). Four months later, with weight loss and exercise, his blood sugar levels were consistently under 100 mg/dL, and metformin was discontinued.

He did well until 1 week ago, when he noted polyuria, polydipsia, and rising fingerstick glucose values, higher than 200 mg/dL. He has been eating well, with no nausea, vomiting, or symptoms of dehydration. He denies having any fever, chills, cough, nasal congestion, chest pain, abdominal pain, or dysuria.

In addition to his type 2 diabetes, he has hypertension, for which he takes losartan (Cozaar); hyperlipidemia, for which he takes atorvastatin (Lipitor); and gout, for which he takes allopurinol (Zyloprim).

His blood pressure is 148/70 mm Hg, pulse 100, and weight 273 pounds, and he is afebrile. On examination, his skin, head, eyes, ears, nose, throat, lungs, heart, and abdomen are normal. Urinalysis in the clinic shows large amounts of glucose and ketones.


1. Which of the following is the least likely cause of his poorly controlled diabetes?

  • Occult infection
  • Poor adherence to diet and exercise
  • Diabetic ketoacidosis
  • Pancreatitis

Until 1 week ago, this patient’s diabetes had been well controlled for several years. Pancreatitis is the least likely cause of his uncontrolled diabetes, because he has no history of pancreatitis and has none of the symptoms of acute pancreatitis (fever, vomiting, or severe midepigastric pain radiating into the back).

Poor adherence to medication and lifestyle issues are very common in patients with poorly controlled diabetes and should always be included in the differential diagnosis.

Occult infection should also be considered in a patient with uncontrolled diabetes. Although this patient had no symptoms or signs of infection, urinalysis was done to look for an occult urinary tract infection and, surprisingly, it showed a large amount of ketones.

Case continued: He is treated for diabetic ketoacidosis

Additional testing (Table 1) confirms he has a high serum ketone level and acidosis with a high anion gap, consistent with diabetic ketoacidosis. Blood cultures are negative. He is admitted to the hospital and treated with intravenous fluids and an insulin drip at 6 units/hour. Within 48 hours his anion gap normalizes, and he is discharged on a regimen of insulin glargine (Lantus) and insulin lispro (Humalog). A fasting C-peptide level drawn 7 days after his presentation is 1.9 ng/dL (normal 0.8–3.2 ng/dL).

Diabetic ketoacidosis in ‘atypical diabetes’

Diabetic ketoacidosis is one of the most serious complications of diabetes. Many patients present with nausea, vomiting, and abdominal pain. Dehydration is often present because hyperglycemia leads to glucosuria and volume depletion. Interestingly, our patient showed none of these symptoms or signs.

Diabetic ketoacidosis is increasingly being recognized as a complication in patients with type 2 diabetes mellitus.1–4 Since the mid-1990s, clinicians have become increasingly aware of a condition variably termed “atypical diabetes,” “Flatbush diabetes,” “diabetes type 1B,” and “ketosis-prone type 2 diabetes mellitus,” in which patients, usually obese, present with diabetic ketoacidosis as their first manifestation, but are subsequently found to have type 2 diabetes mellitus. These patients typically are African American or of African, Hispanic, or Caribbean descent.

Ketoacidosis results from transient suppression of beta-cell function, the cause of which is unknown. A recent study comparing patients who have type 2 diabetes mellitus with and without diabetic ketoacidosis presenting with decompensated diabetes suggested insulinopenia was the predominant mechanism.5 For many of these patients, insulinopenia is transient: as the ketoacidosis resolves, betacell function improves and, with adequate insulin, lipolysis is reduced.

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