Alcohol Use Disorder (AUD) and cirrhosis are common medical conditions with significant morbidity and mortality. Join host, Geoff Wall, as he evaluates the new American College of Gastroenterology guidelines.
The GameChanger
The MELD score is now preferred over the Madrey score for assessing mortality. Baclofen is the primary treatment for reducing consumption and craving in alcohol use disorder.
Host
Geoff Wall, PharmD, BCPS, FCCP, BCGP
Professor of Pharmacy Practice, Drake University
Internal Medicine/Critical Care, UnityPoint Health
Reference
Jophlin LL, Singal AK, Bataller R, Wong RJ, Sauer BG, Terrault NA, Shah VH. ACG Clinical Guideline: Alcohol-Associated Liver Disease. Am J Gastroenterol. 2024 Jan 1;119(1):30-54. doi: 10.14309/ajg.0000000000002572. Epub 2023 Sep 1. PMID: 38174913.
https://journals.lww.com/ajg/fulltext/2024/01000/acg_clinical_guideline__alcohol_associated_liver.13.aspx?context=featuredarticles&collectionid=5
Pharmacist Members, REDEEM YOUR CPE HERE!
Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)
CPE Information
Learning Objectives
Upon successful completion of this knowledge-based activity, participants should be able to:
1. Discuss the initial treatment of a patient admitted with acute alcoholic hepatitis
2. Describe a pharmacotherapeutic plan for adjunctive treatment of alcohol use disorder
0.05 CEU/0.5 Hr
UAN: 0107-0000-24-042-H01-P
Initial release date: 1/22/2024
Expiration date: 1/22/2025
Additional CPE details can be found here.
Alcohol Use Disorder (AUD) and cirrhosis are common medical conditions with significant morbidity and mortality. Join host, Geoff Wall, as he evaluates the new American College of Gastroenterology guidelines.
The GameChanger
The MELD score is now preferred over the Madrey score for assessing mortality. Baclofen is the primary treatment for reducing consumption and craving in alcohol use disorder.
Host
Geoff Wall, PharmD, BCPS, FCCP, BCGP
Professor of Pharmacy Practice, Drake University
Internal Medicine/Critical Care, UnityPoint Health
Reference
Jophlin LL, Singal AK, Bataller R, Wong RJ, Sauer BG, Terrault NA, Shah VH. ACG Clinical Guideline: Alcohol-Associated Liver Disease. Am J Gastroenterol. 2024 Jan 1;119(1):30-54. doi: 10.14309/ajg.0000000000002572. Epub 2023 Sep 1. PMID: 38174913.
https://journals.lww.com/ajg/fulltext/2024/01000/acg_clinical_guideline__alcohol_associated_liver.13.aspx?context=featuredarticles&collectionid=5
Pharmacist Members, REDEEM YOUR CPE HERE!
Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)
CPE Information
Learning Objectives
Upon successful completion of this knowledge-based activity, participants should be able to:
1. Discuss the initial treatment of a patient admitted with acute alcoholic hepatitis
2. Describe a pharmacotherapeutic plan for adjunctive treatment of alcohol use disorder
0.05 CEU/0.5 Hr
UAN: 0107-0000-24-042-H01-P
Initial release date: 1/22/2024
Expiration date: 1/22/2025
Additional CPE details can be found here.
Hi and welcome to this week's episode of Level Up, where we discuss the most current and relevant best practices, new technologies and staffing resources to truly level up your pharmacy career and your practice. And now get ready to level up.
Speaker 2:Hello and welcome to Game Changers Clinical Conversations. I am your host, jeff Wall, professor of Pharmacy Practice at Drake University. Welcome to our podcast. So today we are going to talk about a brand new set of guidelines from the Van College of Gastroenterology on alcohol use disorder and alcoholism.
Speaker 2:And at first, when I started to read through this at the very first, I was kind of like, well, you know big deal. I mean, there's not, probably not a whole lot out there. And after I started reading through the guideline I was like, wow, there are some huge changes in the treatment of alcoholism and alcoholic hepatitis that are recommended by these guidelines, that are, I mean, really really will change, I think, especially a lot of inpatient management of alcoholic hepatitis and some of the stuff. I'm not going to lie and I treat this all the time in my medicine service. I'd never heard of some of these things and had to do some research and so like, yeah, I was pretty gobsmacked when I read this and thought, yeah, we better get this out ASAP. I've even mentioned it some of my own team members and some of my attendings and there's like really.
Speaker 2:Where did all this come from? So? So hopefully we can talk a little bit about this as we go along. So again, just released last week the Marine College of Gastroenterology guidelines on alcohol use disorder and hepatitis. They note, and I'm sure most listeners are well aware, it's one of the leading causes of alcoholic liver disease and what leading causes of death in the United States. It is the leading cause of preventable liver related morbidity and mortality worldwide, including the United States. They define harmful drinking as a person who drinks go to three drinks a day in a man and 21 drinks a week, or two drinks and 14 drinks a week and in two drinks a day, or 14 drinks away in women a week in women, and that has been a known risk factor for liver damage and alcoholic liver disease. It often occurs in the setting of alcohol use disorder, which they do touch on here, but they don't go into as much detail as I think other guidelines do, like the American Academy of Addiction Medicine, which I think they, they, they. They obviously just go into that a little bit more. They do talk about this a little bit in the guideline, but not as much. They also note that the patients who already have what was supposedly formerly called nonalcoholic fatty liver disease but apparently is now called metabolic dysfunction associated ketotic liver disease or MASLD. You know, it's one of those things where first we call this NASH, then we called it NAFLD and now we're calling it MASLD. I don't know why we keep changing the name of this, but the bottom line is that it's it's cirrhosis, not caused by alcoholism, but actually caused by, usually obesity and metabolic derangements like diabetes and stuff like that. And so someone who has that and you might imagine many patients have, by broadening disease due to this MASLD, as we're calling it now, who are completely unaware of it because they have no symptoms. And if you have that, and then you're also a heavy drinker on top of it, that greatly accelerates the development of cirrhosis. So, because we're of the obesity epidemic, we're actually starting to see more and more patients who have the combination of fatty liver disease caused by metabolic derangements as well as by alcoholism.
Speaker 2:Globally, they note that 3 million people die a year worldwide to alcohol use and that accounts for actually 13.5% of deaths in people ages 20 to 39, which that number kind of surprised me.
Speaker 2:This, of course, is true in the United States, where, in fact, cirrhosis was the 11th leading cause of death in 2019.
Speaker 2:It had about half of those a little more related to alcohol.
Speaker 2:And the problem, of course, as we are all, I think, pretty well aware, is that the pandemic greatly increased the development of alcoholic liver disease and alcohol use disorder and in fact, they know that there was a 14% rise in admissions to the hospital for alcoholic liver disease during the pandemic years and right after it, and they also noted that there was a big increase in mortality due to alcoholic liver disease, a big increase in the number of transplant listings right after the pandemic and during the pandemic, and they noted that alcohol use disorder, even that doesn't lead to severe cirrhosis, has gone up around 22% from 2021 to compared to 2019.
Speaker 2:So the pandemic, as I've said before in this podcast, is going to have effects long, long after it becomes endemic and we don't have the terrible years of 2020 and 2021. We're still gonna see a lot of fallout from the pandemic and I think this is one of those things where coping was very difficult and still is very difficult for a lot of people and again, turning to alcohol and leading to cirrhosis, I think was one of the things that we've definitely seen and will continue to see.
Speaker 2:They note that, as we, I think are all aware, there's kind of a timeline where you start off with steatosis, whether it's again due to alcohol, hepatitis, viral hepatitis or non-alcoholic fatty liver disease or, I'm sorry, m-a-s-l-b, and then it eventually turns into fibrosis and then cirrhosis and then often, especially with viral hepatitis, we'll go on to develop a Paticellular Carcinoma which is even in patients who have compensated cirrhosis, especially those who have viral hepatitis, develop cirrhosis. Many of them will end up developing the Paticellular Carcinoma which is unfortunately lethal on those patients and patients who have alcoholic liver disease when they have acute episodes of alcoholic hepatitis. That actually greatly accelerates the development from fibrosis and cirrhosis. So not only is alcoholic hepatitis associated with short-term mortality, multiple episodes of alcoholic hepatitis accelerate the development of cirrhosis and, of course, all the problems associated with the chronic liver disease. So that gets us to the guidelines.
Speaker 2:The guidelines were as standard guidelines are. They got a bunch of experts together, they asked the questions in the PICO format to try and take a look at the evidence. They pulled the evidence, they distributed that evidence among the experts and then they used the grade analysis, which again almost everybody's using now for a guideline analysis. And then they divided things into recommend, which is we recommend this and that's got the highest level of evidence with the strongest benefit.
Speaker 2:And then they have suggest, which is a benefit but doesn't quite have the evidence that recommend does or not recommend it. That's how they kind of basically give you the recommendation. So it is a huge document and we're only gonna hit the highlights here. I really wanted to hit the big differences, that and big recommendations. I think that's different from the standard of care, at least in my neck of the woods, as far as dealing with alcoholic liver disease and alcohol use disorder. So one of the first ones is they have a very detailed section where they talk about the risk factors associated with cirrhosis. And again, as I noted before, they know that patients with obesity or diabetes in particular, already probably have some degree of fatty liver disease and that's gonna be greatly accelerated when patients are become heavy drinkers. And so with their big recommendation which I have no idea how this is gonna get followed is gonna be in patients with obesity, which they notice someone who has a BMI of greater than 30, they recommend avoiding consumption of all alcohol. And that's a strong recommendation with moderate level of evidence. And again, the reason they do this is, again, they know that patients who are obese probably already have some degree of fatty liver disease and that's gonna greatly get accelerated with heavy drinking. So they avoid all alcohol.
Speaker 2:I don't think that is likely to happen in most people. I think that the best we can probably hope is harm reduction in these patients and saying, look, we're trying to get your weight under control, we're trying to get your diabetes under control. I would really try to minimize alcohol intake. The occasional glass of wine with dinner's fine, but going on a binge drinking every day is probably not a very good idea for a variety of reasons, but in particular because you're at even higher risk and in fact they have an estimate suggesting 1.5 fold higher risk for liver disease and a 2.2 fold higher risk for death. And I think that's the key that I think we need to tell patients who are obese, because I don't think they're gonna listen to us and we say, yeah, sorry, you can never have alcohol again. But I think, if you can say, look, we need to minimize as much as possible alcohol and certainly binge drinking and things like that, something we really kind of need to avoid.
Speaker 2:As I mentioned before, they don't go into a lot of detail about the treatment of alcohol use disorder but there are some sections about that. Really, what they talk about most is screening and they know that every time a patient interacts with healthcare professionals is an opportunity to screen patients for alcohol use disorder. There's a number of screening tests out there and they actually recommend the AUD identification test or audit, which is a 10 item patient self-reported questionnaire. It's been shown to be accurate and validated towards screening of visual surround call use disorder and its severity and it's relatively easy to administer in a clinic setting. But if you're short on time or there's logistics, why it's difficult to do that. They note that there's a shorter version that is only three questions. That is also a reasonable use in clinical practice with a similar accuracy to the full audit tool. So they then go into the pharmacologic treatment of alcohol use disorder and of course, pharmacologic treatment is, of course, only an adjunct to psychological counseling things like alcoholics, anonymous I mean, whatever there's a lot of non-pharmacologic tools out there to help people stay off alcohol. But they note that as far as medications to decrease cravings and decrease amount of alcohol ingested and this is one of the first big changes they actually recommend not suggest recommend the use of backlifon as an option for treating alcohol use disorder. Again, a strong recommendation of moderate level of evidence. I'm not going to lie, I've never heard of that. I had never seen backlifon or heard of backlifon being used for alcohol use disorder. Very surprising Now. Their rationale for that is that backlifon is cleared almost entirely renally, which is true, and that it has been studied in patients with compensated alcoholic liver disease, whereas most of the other pharmacotherapies out there for outstorted have not been studied in that particular population. And so I think that's one of the big kind of asterisks with this is that compensated alcohol liver disease is really maybe where backlifon could be an option, whereas some other therapies, such as Naltrexone, which is something I've now been using for several years in patients who get admitted to the hospital with alcohol use disorder and they are interested in quitting, and then, in conjunction with some sort of non-promptologic program, we will go and prescribe Naltrexone to them. And again, the data about Naltrexone is pretty good and it shows that it decreases cravings, decreases total number of drinks a day, things along those lines. But the big problem with Naltrexone, of course, is that in patients who have a child puke. Class B or C in particular it's contraindicated, and so I think that may be kind of the pivot that you may consider backlifon in is particularly in patients with compensated alcoholic liver disease.
Speaker 2:They do also suggest that a campersite can be used. I'll be honest, I have almost never seen a campersite being used for alcohol use disorder because the data supporting it isn't that great. And B, you have to take basically a handful of pills three times a day and so the pill burden and the frequency of use just makes it almost impossible to use real work. So it's one of those nice ideas but probably it doesn't ever get used or rarely get used. They know that a whole bunch of other drugs, gabapentin to pyramid have all been studied, but they don't recommend those just because there's very little level of evidence and they recommend against the use of disulfuram or anantibuse. I haven't seen anantibuse used in over a decade in these patients because, a it doesn't work. And B I think we've kind of turned away from punishing patients for bad behavior, which is essentially what disulfuram does. So what does the data for backlifon? Because, again, I've never heard of this, I've never used backlifon for alcohol use disorder. They know that there actually is more evidence for backlifon than even the FDA approved drugs such as naltrexone and a campersate, and they know that in several studies the backlifon is much more beneficial. And they point out a particular study where a six-month course of backlifon was successfully reduced alcohol significantly in patients and these were patients who had compensated alcoholic liver disease and it's increased complete abstinence rates as well. The dose they used because again, I had never seen this before was five milligrams CID, so relatively low dose. And if the patient tolerates that you can escalate it up to 15 milligrams three times a day. And so that's if you were to use this. That's how you started it.
Speaker 2:I'll be honest, I've always been kind about backlifing the elist outside of its use as as a spasticity agent. I have used it for kind of unusual things like intractable hiccups and cough and stuff like that. But you know I see it way overused in the radial world for back spasms or skeletal muscle spasms that don't, and it not only doesn't work but it's actually, you know, dangerous a lot of the types of those patients. And so you know I've always been a little bit nervous about backlifing. Plus, I've seen some pretty bad overdoses with backlifing. So you know, I have to admit I'm a little nervous about this. I think there's some concerns about the average story of actions and especially if patients develop acute kidney injury, the drug builds up very quickly and they can can get really goofy and sometimes even require intubation because of mental status changes. So you know something to kind of keep in mind. I guess I'm gonna maybe start recommending this over now TREXON, patients with compensated alcohol, a serotic disease, and and see how we do. And you know it'll be very, very interesting to see. You know what my experience, what my attendings experience of this will be. But again, big, big change that Bacildon is now recommended over now TREXON in patients particularly with compensated alcoholic liver disease, for alcohol use disorder. So kind of a big one there.
Speaker 2:As far as treatment of withdrawal, they still recommend benzodiazepines first line. They go into some detail talking about, you know, diazepam versus lauraezepam. There are some experts out there who recommend diazepam just because for its longer half life compared to some of the shorter agents like oxazepam and lauraezepam. But then there are others who know that that diazepam and chloridae is epoxide. Both have active metabolites that can build up in patients with liver disease, which is kind of what I was taught to try and avoid those. They go into some detail about that and I think they basically note that, especially in patients who might have a history of apatica encephalopathy, the shorter agents, like again lauraezepam, might be beneficial, you know, as compared to the longer agents. But again, you know, you can certainly, you know, take a look at their discussion and of course we're going to put the link to the guidelines on our show notes. You know you can certainly read their discussion about that, but that's something that's, I think, been discussed back and forth for at least 20 years, so something to kind of talk about. They note that other drugs can be used as adjunctive agents. Baclyphan, phonidine, gabapentin, topiramide, dexametatomidine, persevere withdrawal, especially in the ICU, can all maybe be used as adjuncts. But again, they don't have a high recommendation on that because lack of perspective ran in my studies.
Speaker 2:What I thought was very interesting is they did not recommend phenobarbital at all. That's not even mentioned at all in their guidelines. One way or another and you know, phenobarbital of course is being used more and more, especially for severe withdrawal in hospitals. In fact there's a lot of places that have almost abandoned benzodiazepines and really gone to phenobarb. So that's kind of interesting. They don't even mention it. I'm not going to lie and people who know me have heard me kind of get on my soapbox about this that I am not sold on phenobarb for severe withdrawal. I think the reason being is that you know barbiturates are inherently dangerous medications. I mean, we actually invented benzodiazepines because they're less dangerous than phenobarb. You know and I have not read data, at least prospective data that shows that you get better outcomes of phenobarb compared to benzodiazepines. Again, I know that's going to irritate some listeners because, again, there are some very passionate people out there who believe that phenobarb is really the way to go.
Speaker 2:And again, it's not like I have some sort of mental block against it, it's just that I'd like to see some perspective of the data that shows that it actually has some superior outcomes. That study there are some studies looking at exactly that that are ongoing and certainly, if they do show, you know, decreased length of stay in the hospital, you know, decreased delirium rates, etc. Etc. Then yes, I will hop on the phenobarb train just like everybody else does. But until that happens I'm still kind of in the in the benzo corner more than the phenobarb corner. Plus, again, being an old man, I've seen some pretty bizarre side effects from phenobarb, even short term phenobarb. I've seen a case or two of acute liver injury. I've seen severe rashes, even leading to kind of deschlamating type skin reactions.
Speaker 2:So you know, those are rare, but they do occur, and I think until we have evidence that shows that there is some you know tangible benefit of phenobarb over over benzos for alcohol withdrawal, I'm still kind of on the fence about its use. But again, I realize there's some very passionate people out there who who really like it.
Speaker 2:So it's worth noting that again, they don't even mention that at all in the guidelines.
Speaker 2:Well, that the word phenobarb doesn't even appear in the guidelines section on withdrawal, so it's kind of interesting. As far as asymptomatic liver disease markers, they note that, you know, in patients suspected heavy alcohol use that they should be, you know, again frequently monitored, frequently canceled to decrease their liver intake. It is reasonable to consider doing fiber scans so to look for fibrosis to see if they, if we can maybe even catch these guys before they get into full cirrhosis. They don't. They don't go into a ton of detail on this, but they basically note that when someone is suspected of heavy drinking that they should be seen frequently by healthcare providers, counseled multiple times and given options to help decrease their alcohol use and at least once, if insurance pays for it, to ask a screening for fibrosis to kind of get an idea where they are on that continuum of liver disease. Then we get into the treatment of alcoholic hepatitis. Again, there are some pretty big changes here and so we're going to talk about those changes right after. A word from our sponsor, ce impact.
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Speaker 2:So we're back talking about the American College of Gastroenterology and brand-news guidelines for the treatment of alcoholism, alcohol liver disease and somewhat some stuff on alcohol-accused disorder, and we're up to talking about how to treat acute alcoholic hepatitis. This is not an unusual reason why I have patients admitted to my medicine service and you know it's something that I see pretty frequently and I was pretty surprised about some of the big, big changes that I again really have the have the potential to change how I practice and treat these patients, and now I think a lot of other people do it as well. So they know that acute alcoholic hepatitis should be suspected in any patient who has heavy alcohol use, and especially if they've gone on a binge and they've developed either nuance worse than in jaundice, that actually that simple physical exam finding has been shown to have a high sensitivity and high specificity for alcoholic hepatitis, and so those patients should be promptly evaluated and often probably admitted to the hospital, because there is actually a very high short term mentality. Usually within that first 30 to 90 days after about of acute alcoholic hepatitis. There's a significant spike in mortality due to the compensated cirrhosis and, as I mentioned before, even in patients who do fine with acute alcoholic hepatitis, though every bout of that greatly accelerates the development of cirrhosis and worsening cirrhosis in these patients.
Speaker 2:They know that many times these patients admitted one of the things that may trigger the worsening of hepatitis in addition to alcohol use is infection and it's often missed. And so it should be looked for both urinary tract infections and they know it in particular that skin infections are sometimes forgotten. And you know a physical exam should really be done. You know good physical exam to look for the potential of other infections and be good about treating those things. They unfortunately, many of these patients will present and look like they have sepsis right. They'll have the surge criteria and all that other stuff and unfortunately, even in the absence of infection, an acute bout of alcoholic hepatitis can look like sepsis for all the world to the clinicians. So kind of keep that in mind as you go along. But if you do have objective signs of infection, then treating them is something you should look for and something you should definitely do.
Speaker 2:There is, you know again, there's no absolute diagnostic criteria for alcoholic hepatitis. Again, we noted that new or worsening jaundice seems to have a pretty decent sensitivity and specificity for alcoholic hepatitis. There's really no great lab that looks at that Obviously elevated ASTs and ALTs, high AST to ALT ratio, and they know that even just one AST to ALT ratio of just 1.5, with no other cause of acute hepatitis, all can suggest the development of an acute bout of alcoholic hepatitis. So then we come to the big changes, and one of the biggest ones is the abandoning of the Madri Discriminant Function Index or the Madri score for the go-no-go on treatment for acute alcoholic hepatitis with steroids. Again, I've been taught this and have done it for years and years and years. The original study by Madri showed that they developed basically a fairly simple scoring system and that if that scoring system was high and over 32, it actually found a up to 50% mortality in the 30 days following the acute bout of alcoholic hepatitis. So that's something to kind of keep in mind. And so you know again, I've calculated the Madri score a million times over the years and they're now abandoning that. They're actually now saying the meld score, which is the score that we use to look at overall mortality in a serotic patients as well as where patients can put on the transplant list. All of that is used with the meld score and they now recommend meld over the Madri score in assessing the need for steroids in patients with alcoholic hepatitis. Now why did they recommend meld over Madri?
Speaker 2:Some of the in the text they noted the advantages include that its accuracy for go-no-go on steroids is actually about the same as the Madri score, which I did not know, and they also noted that it's much better at assessing overall mortality in the long term, as well as its worldwide use for organ allocation. And the fact that it uses INR over prothrombin time, which has always been one of the confusing factors when you calculate the Madri score, is because in most hospitals and this includes my hospital there's a range of normal in the prothrombin time and it's like well, what number are you using to compare the patients prothrombin time to the prothrombin time that the lab is using? So there's always been some confusion there where you can use INR with the meld score. Also, the meld score incorporates serum pre-attaining, which has long been known as a marker for mortality patients with cirrhosis and alcoholic hepatitis. So bottom line is that I guess we don't have to calculate madri scores anymore, that belt score should be used and that a belt score of over 20 is the go-no-go about using steroids. So instead of a madri score greater than 32, a belt score greater than 20, you should consider using steroids.
Speaker 2:Pregnace alone, of course, is the drug that was studied in the madri score, because prednisone, of course, is a pro drug that has to get converted to prednisolone by the liver, and so the thought was always well, if your liver doesn't work, it's probably not going to do that. So prednisolone, I think, is what's often used. I do see some confusion among clinicians about. You know, the problem with prednisolone, at least in the United States, is it doesn't come as a tablet, where there's no tablets of prednisolone, so you have to get the liquid and the liquid tastes horrible. So it is totally reasonable to use methyl prednisolone, you know, or medrawl, you know that you can certainly use that and that would be perfectly fine, and I think that makes things easier for everybody if you just use those tablets. So you know, you know prednisolone by itself is fine to use, but in patients who don't want to drink this terrible tasting liquid, it's reasonable to use a methyl prednisolone in those patients.
Speaker 2:So they recommend not using prophylactic antibiotic stress BP prevention, unless of course the patient has some other, you know. You know they have ascites and they have high neutrophils in the ascites, which is the definition of SPP, you know, or they have a GI bleed and you're going to put them on five days of prophylaxis for that, but just in all comers not to do prophylactic antibiotics. They also note that that these patients, of course, should receive thiamine. They note that, interestingly, vitamin B12 and zinc deficiencies are far more common in patients of alcoholic hepatitis than we previously suspected, so you should replete those as well. I, in an attempt, I think, to decrease costs, I would say that really there's no need to give those individually. A really any oral vitamin mineral supplement should be fine in in getting both B12 and zinc.
Speaker 2:However, you do want to be careful, especially in patients with with alcoholic hepatitis, that there are high risk for warreniches and cephalopathy, and there's some recent evidence to suggest that that we really need to do a better job of assessing and treating, not just preventing, warreniches and cephalopathy. So you know I'd have a low threshold of using high dose thiamine to treat those patients, because high dose thiamine has those side effects and is too cheap. So I'm gonna keep that in mind as we go along here. So again, scortico steroid therapy at the meltscore is greater than 20. They also note, though, that that there is a a kind of window where steroids are beneficial, and in fact, the higher the meltscore, steroids by themselves don't seem to be as beneficial, and they note that there was a big study that noted that that a meltscore greater than 50, actually steroids had no benefit, and so if you have somebody who has an oh my goodness high meltscore, fun thing their mortality is is going to be sky high as well. They note that that that steroids are just probably not warranted because they're beyond the point where steroids are going to be beneficial in a meltscore greater than 50. They do still recommend using the lily score, which is a score that was validated years ago, to assess the response to steroid treatment. That's worth noting, because the original madry score found a benefit of the steroids, but every other randomized controlled study that looked at steroids and how alcoholic hepatitis did not find a benefit, and so, using the lily score either day four or seven, if the lily score is 0.45, they note that that those patients are non-responders and that steroids should probably be discontinued.
Speaker 2:Finally and this is again another big change that I had had not seen or used is they know that in high, but not extremely high meltscores so kind of 30 above up to 50, that intravenous anesthetical cystine can be used as an adjunct to prednisolone. Never seen that, never heard it before, so that was really surprising to me. Again there that we know, of course, that anesthetical cystine is the treatment of choice for acetaminophen poisoning. But there is some evidence, and there was actually a network meta analysis just published that noted that the combination five days of acetal cystine infusion plus prednisolone had the best survival benefit at 28 days with an 85% relevant risk reduction of death from alcoholic hepatitis. And so again they note that that this is only a network meta analysis, that there have been a lot of really well done randomized control trials and and they note that these studies are ongoing. But it is not unreasonable to consider IV and acetylcystine in patients with higher than 20 meltscores, particularly if they're in that kind of 30 to 50 range with a meltscore. That is probably reasonable to do, given that IV and acetylcystine is now generic, it's relatively inexpensive and is fairly relatively well tolerated as well. So again, very surprising, and I've never done that before.
Speaker 2:Something I have to think about doing Finally, and this is a little bit beyond the scope of this podcast is is the screening for transplant candidates.
Speaker 2:You know, in in my state and in a lot of other states, the kind of scenario of thumb for patients with alcoholic liver disease is that you had to be sober for at least six months before you could be put on the transplant list.
Speaker 2:They actually say in their transplant notes that and this is a quote selection for liver transplant and patients with alcohol, whereas you should not be based solely on an arbitrary decision of sobri or duration of sobriety. There should be a comprehensive psychosocial evaluation by a social worker and addition specialist to help with that decision making. And I know several other large transplant centers have really abandoned the six month rule, and so that's, I think, good to see. I've always kind of noted that you've got patients who have, I think, a pretty high chance of staying off alcohol but because they didn't meet this arbitrary six month window they just weren't candidates and they might have very, very bad cirrhosis and may not survive that six months. So again, that's that I was kind of heartened to see that the guidelines basically say you know, yes, sobriety is an important factor, but it shouldn't be the only factor in determining organ transplant listing and where on the organ transplant.
Speaker 2:So again some big big changes, things that are really, really going to, I think, change of how we treat stuff. Again, you know, back with them for decreasing alcohol use and alcohol abuse disorder, using the meld score instead of the madri score for alcoholic hepatitis IV and acetyl cysteine in patients with moderately high meld scores, and then again, not having an arbitrary limit of obesity all big, big changes from what we previously done. So that's it for this week of Game Changers. We will see you next week, but until then, remember time flies. I don't know where it's going, but the most important day is today.
Speaker 1:Jen here. Be sure to check out our education at cempackcom. You'll find it to be your one stop shop for all the CE resources you need. Become a pharmacist by design member today to access it all for free, including CE for this podcast. Thanks for listening. We'll talk to you next week on Game Changers Clinical Conversations.