Abstract

T.R., an obese 40-year-old African-American man with a medical history significant for hypertension, presented to the emergency department complaining of 5 days of weakness, abdominal pain, and upper respiratory symptoms. On further questioning, he also reported ∼ 1 month of polyuria, polydipsia, and polyphagia accompanied by a 5-lb weight loss. No visual symptoms were noted. His medical history included hypertension with antihypertensive noncompliance, an exploratory laparotomy for a gunshot wound, and a remote appendectomy. He denied the use of alcohol, tobacco, or illicit drugs. His family history was strongly positive for adult-onset diabetes, including one sibling who died of related complications. On initial physical examination, he was afebrile, with a blood pressure of 140/90 mmHg and a heart rate in the 120 bpm range. Physical findings were remarkable for abdominal obesity and acanthosis nigricans. Arterial blood gas revealed a pH of 7.31 and partial pressure of carbon dioxide of 22 and bicarbonate of 3. Serum chemistries revealed the following: serum sodium 144 mEq/l, potassium 6.9 mEq/l, bicarbonate 7 mEq/l, blood urea nitrogen 50 mg/dl, and creatinine 3.5 mg/dl. Serum glucose was 1,200 mg/dl. Serum acetone was detectable in moderate quantity. C-peptide was nondetectable. Urinalysis demonstrated glycosuria with moderate ketones and negative protein. Complete blood count was consistent with hemoconcentration and otherwise unremarkable. Amylase, lipase, and thyroidstimulating hormone were within normal limits. Hemoglobin A1c (A1C) was 13.6%, and antibodies to GAD-65 were not detected. Myocardial ischemia and infectious processes were excluded. T.R. was initially admitted to the …

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