Fam Pract Manag. 1999 Sep;06(8):48-50.
This month's Diary is a bit of a departure from the normal format. I've patterned it after Wallace Stevens' poem “Thirteen Ways of Looking at a Blackbird,” in an attempt to demonstrate how a single disease can take on many faces.
Ginger has been my patient for 16 years. Before, in the late 1970s, she was in an aircraft accident in which her son was killed and she suffered a lacerated liver and ruptured spleen. She needed 45 units of blood to survive major surgery, as well as a tracheotomy. When she first began coming to me in 1983, I noted liver enzyme elevation on her chemistry panel. We just assumed it was the result of her liver damage, but as the years went by and the elevations persisted, it became more puzzling. Then in 1992 when the first-generation hepatitis C antibody tests came on line, it all became clear. Ginger was the first patient I ever had to tell that she had hepatitis C. She was curious as to what it all meant, and back then I really didn't know. We kept yearly tabs on her liver function, and several years ago her alanine aminotransferase (ALT) normalized and stayed low on successive exams.
This year I became curious and asked her if she didn't mind our testing for the virus directly. She agreed, so we ran the test. The polymerase chain reaction (PCR) viral RNA was negative. Today, I gave her the good news. “Ginger, it appears that although you still have antibody to hepatitis C, you no longer have the virus,” I said. “You're probably cured.”
“Cool,” she said.
I knew that a small percentage of hepatitis C patients clear the virus, and Ginger was one of the fortunate ones. Piqued, I asked, “Did you do anything differently this year?” Sheepishly, she said that she had taken milk thistle three times a day. Not being one to quarrel with success, I congratulated her, and, thinking of my 25 other patients with hep C, I asked her which brand.
Harry probably acquired hepatitis C when he was a teenager in the late 1960s, after running away from rural Iowa to come to the Haight-Ashbury district in San Francisco. There he tried drugs for the first time. He moved up to Mendocino in the mid-1970s, and, when I met him, he only used marijuana recreationally but was a heavy drinker. His chemistry panels showed marked liver enzyme elevation, so, thinking he had alcoholic hepatitis, I urged him to stop drinking long enough to allow his enzymes to normalize. It took him two years to go two months without a drink, and when I re-tested him his enzymes were even higher. (Another mystery that cleared with time.) Several years ago I referred him to a liver specialist, who did a biopsy, which showed fibrotic changes. Since then he has developed diabetes and hypertension. At his last visit, his enzymes were still in the 200 range and his platelets were decreased, but his prothrombin time and albumin were holding steady. A liver ultrasound showed no hepatoma, but his carcinoembryonic antigen (CEA) was more than 100. Another visit to the specialist and he was told he was a transplantation candidate, to get health insurance and to come back for his transplant workup.
How does someone with hepatitis C get health insurance? Harry says he will try to get share-of-cost Medicaid. His mood is upbeat, and he is taking better care of himself. A chronic worrier, he was once told that his hepatitis had “burnt itself out” as his liver became more cirrhotic. I think he believes it, but who am I to tamper with his coping mechanisms?
Sally is a health care worker who acquired hepatitis C from a needlestick injury 25 years ago. At the time, she worried about getting hepatitis B, as the patient she was doing a blood gas on was a drug addict who had just received eight units of blood for a bleeding ulcer. She took a gamma globulin shot, but two months later had a sudden onset of malaise and figured, “here it comes.” She tested her liver enzymes, which were up, and awaited the onset of jaundice and serious illness. Then, miraculously, she recovered in several days. Her take on it all was that she had acquired a minor, nonicteric case of hepatitis B. No one knew better.
Over the years, periodic testing revealed an ALT in the 60 to 70 range. Then, in the late 1980s, it shot up to the mid-hundreds, so she stopped drinking entirely, blaming it on moderate alcohol consumption. In 1992, she heard her first lecture on hepatitis C and panicked. She tested positive and proceeded to learn everything she could about the disease. When she came to see me, she already knew what she wanted done: nothing. She figured the odds. About 3.5 million Americans have the disease; 1,000 get liver transplants for it each year; and 10,000 die. “So I've got about a one in 3,500 chance of needing a new liver,” she said, “and a one in 350 chance of dying from this. I can live with that.”
She continued to argue her case at her last visit. “I don't want interferon because it makes you feel lousy and only sustains remission in 25 percent of those taking it,” she said. “I haven't had a drink in 10 years. I don't even take Tylenol anymore. I take care of myself.”
She went on to further detail her belief that the people dying from hepatitis C probably were the ones whose initial viral insults were larger, from blood transfusions or multiple IV drug exposures.
When she was finished, I said, “Sally, you've convinced me that you don't want treatment for this disease, but have you convinced yourself?”
Matt is a new patient, a 33-year-old allied health professional in our town who was seeking a regular medical doctor. As with all my new patients, I put him through my wellness program. In taking a medical history, I learned that in 1985 at the age of 19, he had fallen while walking along a fence and impaled himself on a piece of pipe. He sustained major blunt trauma to his abdomen, lost half his liver and intussuscepted his bowel. He took 100 units of blood. On exam he had a scar that started along his mid-axillary line just below his lowest right rib, crossed over to his xiphoid and extended down to his groin; it looked like a huge skin flap had been created to give his surgeons maximum exposure to his macerated viscera. There were numerous scars from old drains. The next year, a tree limb fell on his head and herniated several cervical disks. He had chronic neck pain but refused surgery for fear that a cervical fusion would greatly reduce his mobility. While I was drawing his blood, he asked if my panel included an SGOT (serum glutamic-oxaloacetic transaminase). I told him it did, but I didn't ask why he wanted to know.
I knew the odds of Matt not having hepatitis C were almost nil but decided to wait until his follow-up visit to discuss it with him. His lab work was entirely normal except for an SGOT of 75. On his return this week, I asked why he mentioned the SGOT. “Oh, you picked up on that,” Matt said. “I just thought that with all the Tylenol and ibuprofen I take for pain, I might have some liver damage — besides the surgeons having removed nearly half of it.” Matt listened to my take with equanimity and asked for a confirmatory test. It came back negative, so I suggested a viral titer, as some hepatitis C patients do not make detectable antibody. If he is positive for the virus, Matt will almost certainly become a resource for my other similarly infected patients.
Jose and Joan are a married couple in their early 50s who got hepatitis C when they were teenagers experimenting with drugs. They stayed together, raised a family and are now expecting their first grandchild. I've known them for years. Two years ago, they came in for physicals. Jose's lab work was normal; Joan had an elevated ALT. Jose's hepatitis C antibody was positive, but his viral hepatitis PCR was nondetectable. Joan also had a positive antibody, but her viral PCR was 1.2M. Furthermore, she was symptomatic, experiencing midday fatigue on a regular basis. Very few of my hepatitis C patients have symptoms, and I have always been reluctant to ask them about fatigue, since it is an almost universal complaint. But Joan volunteered this information, so I arranged for her to call a liver specialist who was doing interferon studies. If she was selected for one of the protocols, her biopsy and medicine would be free of charge. She wasn't excited about the idea of taking an intramuscular injection three times a week, getting a needle stuck in her liver or driving to the city every month for tests. She still hasn't made the call.
Gary is my most nervous hepatitis C patient. He insists on blood work four times a year and is upset with any liver enzyme rise. He's had his hepatitis A and B immunizations and is intent on knowing where his medications are metabolized. Instead of asking about drug interactions, he queries the pharmacists about drug excretions.
Last year he saw an article about a doctor who was using amantadine for hepatitis C and asked me if he could try it. I e-mailed for the protocol and found that the study was done on a small sample of patients without a control. Nevertheless, there were some encouraging results with several patients showing no detectable virus, and the drug seemed relatively benign, even for chronic use. After two months of 200 mg of amantadine daily, Gary's viral count rose severalfold. He stopped taking the drug and now awaits the latest scientific breakthrough.
Eugene is, at age 69, my oldest hepatitis C patient and the most blasé. He's had the disease at least 50 years, from when he “skin popped” (a method for injecting heroin) as a teenager. He never remembers to come in for his yearly physical and he never mentions his disease. Last week he came in for an exam only because he has a new girlfriend and wanted to try Viagra. When I gave him his results today, he wanted to know his cholesterol but never asked about his liver function tests. “ Hello!” I want to shake him and say, “You have chronic hepatitis. Don't you even care?” Instead, I murmur something about continuing to stay away from alcohol and drugs. On the way out he turns and says to me, “By the way doc, have you got any Viagra samples?”
Copyright © 1999 by the American Academy of Family Physicians.
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