How could this be? The history and exam did not jibe with this at all. He looked and acted like an alcoholic. Yet if his story were true, how could I explain his current condition? I wanted to believe him, but his persistent liver dysfunction, diabetes, and new arrhythmia argued against it. I looked at him. He was a gnarled, emphysematous shell of a man. At least he had a nice tan. I commented on this, mentioning that he must spend some time out of the garage to keep his melanocytes so primed. He looked at me quizzically. He said he never went outside, unless it was to get the newspaper; he hated sitting in the sun.
A light bulb lit in my head, then exploded into a million pieces. What if he really hadn’t been drinking? What else could explain this clinical picture? I was sure I knew the answer now, and a lab test quickly confirmed it. To my chagrin, his ferritin was more than 2,000. Bronze diabetes: his liver abnormalities, diabetes, pseudo-tan, and cardiac arrhythmia were due to iron deposition. He had hemochromatosis!
Several years later, Mr. Q died of complications of COPD. His son found him sitting in a lounge chair in his garage, with the old black and white tuned to his favorite station. He did not die from the diagnosis I had missed. Would his clinical outcome have been any different if the diagnosis had been made earlier? Probably not. Further, if his wife had known he wasn’t drinking, he might have lost his place of refuge. I promised myself that the next time a patient told me how much they drank that I would try to be less cynical in my response.
The day he died I went home and opened a fine merlot and poured myself a glass—then didn’t drink it. TH
Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.