for Health Care Providers
2: The role of alcohol: What are the acute and chronic effects in alcoholic hepatitis vs hepatitis C?
A 58-year-old man initially presented with new onset jaundice, ascites, cachexia, edema, and encephalopathy. He has been a heavy alcohol user on and off for approximately 20 years, and 2 years ago he started drinking between a pint and a quart of vodka daily. He required hospitalizations 3 times over the course of 3 months for medical management of encephalopathy and ascites, including large-volume paracenteses. He was treated with spironolactone, furosemide, prophylactic ciprofloxacin, lactulose, folic acid, thiamine, and multivitamin. He was noncompliant with medications between hospitalizations. He then stopped alcohol for 10 months and improved his medical compliance. He was able to increase his albumin and decrease his international normalized ratio (INR) to the normal ranges, increase healthy eating and regain weight, and resolve the edema and ascites. Six months after his last hospitalization, he was able to discontinue all diuretics and lactulose.
Question: Does anybody have suggestions about how to manage this patient?
Speaker 1: This case exemplifies how totally decompensated cirrhosis can be returned to a compensated state. When you see a patient with alcoholic hepatitis, more likely than not, cirrhosis is an underlying element. The condition is usually acute and chronic, and patients come in with every type of complication, but if they can stop drinking alcohol, they will be able to go back to a compensated state. So, the main issue is how to make them stop drinking. Alcohol cessation is itself a therapy, and we have resources at the VA to help them, including a whole toolkit for alcohol cessation. For any patient with cirrhosis, having two active processes working against the liver, such as drinking plus hepatitis C, or hepatitis C plus hepatitis B, is going to make the cirrhosis worse. Thus, any patient with cirrhosis of any etiology has to stop drinking.
Now, does that mean complete abstinence? How much alcohol can these patients drink, if any? Does abstinence mean never drinking even a drop? Or can they drink one drop here and there? Stopping alcohol use is the mainstay of treatment for alcoholic hepatitis and alcoholic cirrhosis. But what is the amount of alcohol that we should stop?
Speaker 2: This patient cannot drink. Ever. An alcoholic cirrhotic cannot drink at all.
Speaker 1: Exactly! This patient cannot drink at all. His main problem is alcoholism. If he were to start drinking a little bit, he would just drink more and more. So, for this patient, you want alcohol complete cessation.
Now, in patients with hepatitis C, what do you recommend if they come to you and say, "Oh, doctor, can I drink a glass of wine every now and then?"
Speaker 2: Anybody with any type of cirrhosis should avoid drinking completely.
Speaker 1: Really? I'm a little more lenient.
Speaker 2: Drinking very little--once a week or something along those lines--probably does not have a huge impact on accelerating liver disease. But I think we should distinguish between the problem drinkers and people who are actually very light, social drinkers.
We have found that very light, social drinking does not really accelerate liver disease, or it has only minor effects. Some alcohol drinking on a population level even has survival benefits, if you consider the lowered risk of hypertension in men and increased levels of high-density lipoprotein. But in general, a patient with hepatitis C probably should not drink, because you do not know how much the patient is really drinking. I think it makes sense to tell patients with hepatitis C that, in general, they should not drink. You cannot show that patients who truly drink very, very small amounts are going to have more liver disease over time. If there is any question about how much a patient is drinking, it is best to advise the patient not to drink at all. And there is no doubt in my mind that cirrhotic patients should not drink at all.
Speaker 1: How did you define "light drinking" in your study?
Speaker 2: The literature that quantitates alcohol use has shown that 50 grams per day (approximately 5 drinks per day) is a clearly harmful level.
Speaker 1: That is a huge amount.
Speaker 2: In our study, we similarly found that drinking approximately 50 grams daily can cause harm. Alcohol use at lesser amounts--for example, 1 or 2 drinks once or twice a week--has not been demonstrated to worsen liver disease. It is possible that even these lower levels of alcohol are harmful, but it has yet to be proven.
Speaker 1: I think a couple of distinctions need to be made. First, the amount of alcohol that leads to cirrhosis is different for males and for females. Women who drink 10-20 grams a day, which is 1-2 drinks a day, are at risk of developing cirrhosis. For men, the amount is 50 grams a day. The NIAAA defines "at-risk drinking" for women as "more than 1 drink a day or more than 4 drinks at a time," and for men, as "more than 2 drinks a day or more than 6 drinks at a time."
The second distinction is the source of cirrhosis. When patients with alcoholic cirrhosis ask whether they can drink, the answer is "no alcohol whatsoever." But for patients with hepatitis C cirrhosis who ask me, "Can I drink a glass of wine once a weekend? Is that going to be bad?". . . I allow them, actually.
Participant: With the case at hand, the whole issue is that we are assuming the patient has cirrhosis, but we are not sure. Does this patient have alcoholic hepatitis and portal hypertension, or is this truly alcohol-induced cirrhosis? Now that he is compensated, I think we need to investigate whether he has cirrhosis.
Speaker 1: This is a very important question. Does this patient have only alcoholic hepatitis right now, without cirrhosis? The fact that he is looking so good now means that the alcoholic hepatitis has resolved and there is no cirrhosis underlying the whole thing. A patient with pure alcoholic hepatitis can present with all of these symptoms--jaundice, encephalopathy, and ascites--without necessarily having cirrhosis. In most cases, alcoholic hepatitis is found in patients who present with underlying cirrhosis. My experience has been that alcoholic hepatitis by itself is extremely rare, so you must look carefully for signs of cirrhosis that is in the compensated state. In examining a patient with decompensated alcoholic hepatitis, we have to assume that there is underlying cirrhosis, and then look carefully when it is in the compensated state to determine whether cirrhosis is truly present. Does the patient have a nodular contour to the liver, or splenomegaly, even after the acute event has resolved? That question remains unanswered.
To summarize this discussion about the reversible states of alcoholic hepatitis: It is important to impress upon trainees and house staff how these patients with alcoholic hepatitis can actually stop drinking and return to a normal state of hepatic function. Often, the house staff does not see the patients in an outpatient setting when they have stopped drinking, and they can look like any healthy individual sitting in this room.
- Acute alcoholic hepatitis can present with severe clinical decompensation, including jaundice, ascites, variceal bleeding, and encephalopathy.
- Acute alcoholic hepatitis can be clinically reversed with cessation of alcohol intake, and can be returned to a compensated state with normal synthetic function.
- Patients with acute alcoholic hepatitis are likely to have underlying alcoholic cirrhosis, but not necessarily.
- If patients recover from the acute alcoholic hepatitis decompensation, they should be evaluated for evidence of underlying cirrhosis to stratify their need for ongoing surveillance programs and monitoring.
- Patients with alcoholic hepatitis or alcoholic cirrhosis should be advised to completely abstain from all alcohol permanently.
- Patients with chronic hepatitis C cirrhosis who have not had a history of alcohol dependency should be clearly advised to avoid heavy or daily drinking, but there is still debate among experts about whether light, occasional drinking is harmful.
- Ann Busch, Liver Transplant Clinical Nurse Specialist, Portland VAMC
- Sue Currie, Associate Director, HCRC, San Francisco VAMC
- Guadalupe Garcia-Tsao, Director, HCRC, Connecticut VAMC
- Douglas Heuman, Liver Transplant Program Director, Richmond VAMC
- Alexander Monto, Director, HCRC, San Francisco VAMC
- Roberta Ruimy, Manager, Liver/Kidney Transplant Programs, Portland VAMC
- Brenda Salvas, Health System Specialist, Manager, Liver and Kidney Transplant Program, VA Transplant Program, VA Central Office, Washington, DC
- Anna Sasaki, Staff Physician, Portland VAMC
- Kristine Stick, Nurse Practitioner for Hepatology, San Francisco VAMC
- Suchat Wongcharatrawee, Associate Director HCRC, Connecticut VAMC
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