Video Viral Hepatitis I (HAV, HEV, HCV) Play Pause Volume Quality 1080P 768P 720P Fullscreen Captions Transcript Chapters Slides Viral Hepatitis I (HAV, HEV, HCV) Overview Review of Viral Hepatitis I (HAV, HEV, HCV) via a case-based lecture with Boards-style questions and answers enough. Hi, my name is Alan Weisberg and I'm a hepatology ist at that time. I bet there's zero Morningside in West and today I'm going to help you aced the boards by reviewing hepatitis A C. And D. Uh huh. So let's begin with hepatitis A. We'll start with a little bit of epidemiology. So hepatitis A acute infections can occur sporadically or in large outbreaks. And as most of you are aware, this is typically transmitted by the fecal oil route, which really means either direct person to person contacts such as sexual exposure, household contacts, especially day care workers who might be changing young Children's diapers and then most importantly individuals who cohabitate such as uh soldiers in the military prisoners and increasingly homeless people living in shelters and in on the street. The other way that people can be exposed to hepatitis A is by consuming food that has been irrigated with contaminated water. And there have been some very important multistate outbreaks due to imported food from other countries that have led to widespread hepatitis A here in the United States. So the incidence of acute hepatitis A in the United States is really an interesting story. So hepatitis A has been declining in all age groups since the last couple of decades owing in part to the fact that we have improved sanitation. So there once was a time when most adults have been exposed to hepatitis A as a child. So by the time they reached adulthood they had immunity but that is very much change and is no longer the case. And in addition we now have widespread vaccination of all Children since 2006. So almost all Children are given protective immunity a very young age and are therefore not susceptible to hepatitis egg. The interesting flip side of this though is that because we now have an adult population that has not been exposed to help a in childhood Um and who are not vaccinated because they were born before 2006. We now have a large population of adults at risk of developing acute hep. And we have seen some big outbreaks, particularly in 2017. There was a large outbreak in California among homeless and I. V. drug using individuals. Uh there over 400 hospitalizations and 21 deaths associated with this outbreak. And that's why on this table, you're seeing an uptick in acute hep in older demographics, but not in the younger kids. Hepatitis a clinically has an incubation period of about 28 days. So people will start to have symptoms about a month after they're exposed. The vast majority of people exposed to help will become symptomatic. So over 70 and symptoms include nausea, vomiting, malaise, anorexia, fever, abdominal pain, diarrhea. So really it is like an esoteric diarrheal Hepatitis syndrome joined us and peratis develop about two weeks after um uh peak, about two weeks after the onset of symptoms. And a few patients will even report some extra extra Paddick manifestations, but they tend to be rare. The most common ones are rational through algebra and then extremely rare are immune complex diseases and vasculitis. The labs and hepatitis A are very typically those of an acute viral hepatitis. You'll see market elevations in the L. T. N. A. S. T to the thousands. These peak about one month after the HEPA infection is established and then will decline rapidly at about 75% per week. Billy Rubin often goes up but is usually under 10 and the outline phosphates will rise as well but is usually around 3-400 despite being very sick and dramatic. The good news is is that hepatitis A is a self limited limited infection. There is no treatment and really it's just about supportive care. You obviously want to counsel your patients to avoid any additional help. A toxic medications or meds that are heavily metabolized by the liver. But the truth is, there's no treatment except supporting them through their illness and you can reassure them that full biochemical recovery will be achieved in 85% of patients by three months And in nearly 100% by six months of time. Having said that there are four important complications of acute hepatitis A that you should be aware of in clinical practice and also because they're very testable on the boards. The first is fulminate hepatic failure. So patients with acute hub can develop pulmonary hepatic failure. This is very rare. It occurs in about .1%, much less than 1% of cases and it's the severe acute liver injury that is associated with encephalopathy kogel apathy and patients must be referred urgently to a liver transplant center. The risk factors for fulminate hepatic failure, which are very testable our age over 50 and having an underlying liver disease, especially hepatitis C. So, a chronic heP C patients with acute hep has probably the highest risk of fulminate hepatic failure from this infection. And that's one of the reasons why all patients with chronic liver disease, especially those with Pepsi must be vaccinated against hepatitis A. The second complication that you should be aware of is cola static Hepatitis A. This is a very protracted period of johN dis which can last more than three months rather than the timeline. I just told you about. This occurs in less than 5% of cases and its associated with jaundice, politis fever, weight loss malaise for months after the infection And here the Billy Rubin typically goes above 10 and will remain that way for several months. But it also resolves spontaneously and there's no treatment you can rest assured the patients will recover. You might want to treat them with polystyrene for their itching. But there's no specific hepatitis a therapy that's needed for this cola static hep, a complication. The next complication of acute hepatic that's important to be aware of is relapsing acute hepatitis A And this occurs in approximately 10% of patients where you'll see resolution of the acute infection and symptoms and then a relapse of biochemical changes in the labs as well as in the symptoms. We really have no idea what causes this and there are no known risk factors. But there I. G. M. Will remain positive throughout the course of these relapses. They will remain infectious and we know this because hepatitis A can be recovered in their stool. Each successive relapse tends to be milder than the preceding one and on average, patients will have about two or three relapses before they finally recover. But complete recovery is expected with supportive care alone. And then lastly, the final complication of you have to be aware of is that it can rarely be a trigger for developing chronic autoimmune hepatitis. So how should you diagnose acute hep? Well, certainly anyone who has an abrupt onset of the typical symptoms should prompt awareness of this infection. You should detect the infection by checking for hepatitis A. I. G. M. In the serum and that essentially establishes the diagnosis. The serum hepatitis A. I. G. Will arise early in the course of the infection. It persists for decades and confers lifelong immunity. So here is an area that is definitely an update and might be slightly new information from what you've heard in the past. So hepatitis A prevention prevention really refers to either vaccinating people before they've been exposed or giving them hepatitis A. In McGavin before they've been exposed. Um and so pay attention because there's a couple important changes from what you might have known. So pre exposure vaccination is really the best way to go. So anyone one year of age and older is eligible for the vaccine and you should basically give this vaccine to all Children one year and older. Anyone who has a risk of developing HEPA infection. So as I mentioned, M. S. M. Patients who are homeless who live in shelters, people who inject drugs, anyone with an occupational risk like a daycare worker, anyone traveling to an area where help is endemic, you should vaccinate them for happy. Also anyone at risk of a severe complication like forming a liver failure should be vaccinated. So here we're talking about our HEP C patients and by extension, anyone with chronic liver disease should be vaccinated and immunized against today. And then lastly anyone who wants to have the vaccine should be given one for people who are about to travel and don't necessarily have time to get the full vaccination series. Um and they're going to an area that's high risk, perhaps exposure. You can consider giving them. Um also pre exposure prophylaxis. So here is where there's some changes if they are less than 40 of age, just vaccinate them. And that's enough and we think that that vaccine even in close proximity to their travel is sufficient to protect them. If they're over 40 then you're going to give them the dose of the vaccine as well as immune globulin. And then if there's a traveler who has a country indication the vaccination, then you can give them the immune globulin alone. But the rationale for these changes that have been globulin is expensive, it's difficult to come by And the reality is in a very large multi center study showed that the vaccine was probably especially in people under 40, equally as efficacious as immune globulin. Post exposure prophylaxis has also changed and this is something that's probably different as well. So who should get post exposure prophylaxis. So if close household contact or sexual contact of someone help um someone who shares needles with someone who has acute hepatitis A or any unvaccinated staff or food handlers who might have been exposed to pay should be considered for a post exposure prophylaxis and this must be given within two weeks of exposure or it's particularly fruitless. And in 2000 and 18, the advisory Committee on immunization practice updated the guidelines. So whereas we used to use immune globulin for many different categories of patients, you can see now that vaccine has replaced that for almost everyone. So if your age 1-40, you should just get windows the first dose of the vaccine and obviously complete the series. If you are over 40, you should also get the first dose of the vaccine and consider giving a immune globulin based on the provider's assessment for the risk of severe infection, which really just means someone who is immunocompromised or is chronic liver disease. Those patients should get happy vaccine and immune globulin. So in a nutshell, the vast majority of patients who are who you're treating for a post exposure prevention are really just going to be treated with vaccine, not with immune globulin unless they're immune compromise of chronic liver disease. So just some high yield help points. It's self limited infection that's caused by the virus. Humans are the only known reservoir prominent failure is very rare. Less than one point less than 1% of probably around 10.1 it's vaccine, preventable and vaccine really should be offered to everyone over the age of one. Now the incidents overall is going down through the vaccination and improve sanitation. But outbreaks continue and there are updated pre imposed exposure recommendations that you should be aware of. Question number one, a 25 year old male graduate student develops mild victories, nausea, vomiting and diarrhea. Two weeks after eating a raw shellfish meal on lab testing his hep A I G. M. Is positive. His three roommates, none of whom ate at the restaurant are all unvaccinated and asymptomatic after reporting these findings to the health department, what other interventions are appropriate? So again, we have Three roommates in their 20's unvaccinated with an exposure. Should we give them happy immune globulin? Should we offer them ribavirin prophylaxis. Should they be vaccinated should be quarantined. The index patient where no intervention necessary. So a few years ago, the answer might have been to give them immune globulin. But since the 2018 updated recommendations, the answer is now to vaccinate all the roommate. Okay, let's switch gears now to Hepatitis E. Hepatitis E is, believe it or not, one of the most common causes yet least considered ideology of acute viral hepatitis. It is estimated that it accounts for 20 million infections per year in the world and up to 70,000 deaths per year. What's really fascinating to me about Hepatitis E is that it's really two distinct diseases that you can think of really. One is a disease of genotype one and two, which is the infection that most of us are more familiar with. It occurs in resource limited countries like Asia India africa and Mexico. And it is a waterborne infection due to the ingestion of water that's been contaminated with fecal matter and in these parts of the world there's a baseline endemic rate of infection but it's punctuated by explosive sporadic epidemics and a lot of times this is in times of extreme flooding when the water supply is further compromised, such as during monsoon seasons. Hepatitis E gina types one and two only infect humans and again associated with sanitation and contaminated drinking water and really it's only seen in resource rich countries in the point of a travelers illness when someone travels to one of these parts of the world and then comes back to the United States. In contrast, Genotype three and 4 is a totally different story. Genotype three is particularly found in europe north and south America. Japan genotype four in asia especially china. And this is a zoonotic infection with autochthonous infection which means that it's locally acquired. It's not a traveler's diarrhea and this occurs at a baseline and demonstrate in resource rich countries. And unlike genotype one and two, this is due to the ingestion of undercooked meat of infected animals and really it's pork and swine, they're really the main culprits other animals that have been implicated include deer, rabbits, wild boar camel, but really it's predominantly from game meats and pork and slime that's been undercooked. Um There is a possibility some infections occur because food that's irrigated with contaminated water near pig farms that have a high burden of hepatitis E can then be a source. Um We know that there's a high prevalence among slaughterhouse workers, veterinarians and also there is clearly hepatitis E and the blood supply and there have been cases of transfusion related happy infections. Um And unlike hepatitis E one and two, which is really an acute illness Hepatitis three and four. The concern is that it can lead to chronic infection, especially in immunocompromised patients who underwent solid organ transplant. So again John Type one and 2 is a resource limited country. The patients uh can get acute liver failure, especially pregnancy. That's when we're all familiar with in medical school, there's about a 25% risk of mortality and pregnancy. We think this probably has something to do with the nutritional status of a lot of the patients during their pregnancy. Um And in contrast unit types three and four occurs in resource resource rich countries and it can lead to chronic infection. It can lead to an acute on chronic liver failure and patients who have preexisting liver disease. And there's some important extra paddock manifestations to be aware of. So chronic hepatitis E is really defined as the detection of hepatitis C. RNA in the serum for greater than six months. And this really is something that exclusively occurs in the immunocompromised patient population, especially those who underwent a kidney or liver or other solid organ transplant. We have data that shows that if a liver transplant patient gets infected with happy, about 50% of the time that will become a chronic infection that it leads to accelerated progression to cirrhosis and it's also associated with early graft failure and loss. Um And unlike the acute happy infection that we're familiar with, which is more of that eric jOHn this story in these transplant patients, it's really an asymptomatic infection that's really only considered um when you see unexplained elevated um you know, trance phrases when other causes have been ruled out like rejection, hepatitis C or recurrence of the primary disease, You have to have a very high index of suspicion in someone who's had a liver transplant who has unexplained elevated liver numbers, think about hep C infection, acute on chronic liver failure is basically an acute hepatitis C infection and someone who has pre existing liver disease. And we know that this can lead to a paddock decompensation. Um and there's a very high mortality associated with this. So again, if you have someone coming into the hospital who has alcoholic liver disease and their labs are elevated and you just cannot figure out why, think about checking for an acute on chronic hepatitis C infection. And it's important to point out that hepatitis C genotype three and four is really a multi system infection. There are a lot of systems that have been implicated in uh infection, but importantly to know about are some of the neurologic impairments, especially neuralgic emilio trophy. So there's a lot of literature out there that says, if someone comes in with elevated liver enzymes, right upper quadrant pain and shoulder pain due to break your plexus neuropathy that you should think about. A cute happy infection that triad is so common in France and europe that basically say it's diagnostic of unhappy infection. So, again, right, upper quadrant pain, elevated liver enzymes, shoulder pain from a break your plexus neuropathy, hepatitis C infection, the diagnosis. So, any patient who has acute hepatitis that cannot be explained by another cause, or a chronic hepatitis with a superimposed elevation their liver enzymes that cannot be explained by any other cause you should be thinking about hepatitis E. So we way under diagnosed this. So again anyone who comes up with an acute hepatitis you've already ruled them out for Hep hep C. Happy. It all comes back negative thing kept it's under considered and underdiagnosed so much so that in the acute liver failure database they recognized that many cases of acute liver injury that were classified as dilly drug induced liver injury. When they went back they recognized that they were actually happy infections that were not considered by the clinicians. One of the problems is also that we don't have a standardized essay. There's no FDA approved tests for hepatitis E. So there's a lot of local essays that are used. Um But nonetheless we should check E. I. G. M. To look for an acute hepatitis infection. If it comes back positive you should consider repeating it with another asset for hepatitis E. Because there are false positives or by verifying it by saying conversion the hepatitis E. G. Or by checking for hepatitis E. R. N. A. In the blood or the stool. And those are tests that you can send specimens to the C. D. C. To have done for your patient. The good news is that hepatitis E. Is a very mild self limited disease for most patients and again requires nothing but supportive care. But obviously if someone were to develop fulminate hepatic failure such as in the genotype 12 story in pregnancy. They need to be referred urgently to a transplant center. And then in a patient who's immunocompromised here in the United States who develops a chronic hepatitis C infection, for instance, someone after liver transplant. What we need to do is really eradicate the hepatitis E. R. N. A. This is done in a stepwise process first by reducing their immuno suppression, especially to Cronus. Um Probably mmf sell step can be left on because there's a thought that it might have some antiviral properties and hepatitis C. But you should definitely reduce the reduce their tax problems. And if that doesn't achieve clearance of the hepatitis E, then the next step is to consider arrive of iron monotherapy for 12 weeks. So the key really is to prevent happy. If we have travelers go into an area that's endemic, they need to avoid drinking water of unknown purity, avoid eating raw vegetables. Obviously we need to counsel people, especially those who are immunocompromised like our transplant patients to avoid eating undercooked meats, particularly game meats and pork products. Um in southern France. Mhm dried sausage that's not cooked that's made out of dried pork meat. And because of that there's a very high rate of happy infection in southern France. So avoid air dried meats and make sure that they're cooked properly. Um And then prevention the best would be a hepatitis B vaccine. There is one that's been developed in china shown to be incredibly efficacious and safe, but it's not licensed in the United States. Okay, so question number two, A 64 year old man who has no prior medical histories are referred for evaluation of fever, malaise, nausea, mild medical quadrant pain. He is noted to have elevated liver enzymes and jaundice. He reports social alcohol intake of only 2-3 beers per week. He was recently hunting with his buddies and he and his friends hunted wild boar. There were no recent medications supplements or antibiotics. A sonogram of deliver was relatively normal. Um And you can see by his labs that he was negative for hepatitis A. I. G. M. He was negative for hepatitis B and he was negative for hepatitis C and all his autonomy markers are normal. So, in acute hepatitis with jaundice ruled out for the common causes. What should we be thinking about hepatitis E and therefore, what is the next best step to manage him and to treat him? Is that supportive care, robert Byron? A direct acting antiviral MRI. And if positive and keep correct, the answer is supportive care. He does not have underlying chronic liver disease. He has an acute hepatitis E infection from the wild board that he ate and we expect him to fully recover. Next question. A 26 year old medicine resident in her second trimester of pregnancy just returned from a trip to India four weeks ago with fatigue and scleral victories. She has no known liver disease or other prior medical history, she does not drink alcohol. She only takes a prenatal vitamin Her LT and a steering the thousands. Her Billy Rubin is seven point to her. Iron Ore is elevated to 1.8. She's been ruled out for help A. B. And C. As well as autoimmune liver disease and she has normal bile salts. Which of the following statement is true about her condition. Okay, A vaccine is available in the United States prevent this illness. She she will likely develop chronic infection. See this illness is associate with the high maternal mortality D. She most likely has genotype three or 4 infection. E. She should be treated with driving around for 12 weeks correct. The answer is c The mortality rate is up to 25% when pregnant women develop acute hepatitis infection with genotype one or two which she likely acquired while traveling to that part of the world where Jean types one and two are more prevalent. Okay, lastly, let's talk about hepatitis C, which I think is probably more familiar to most of us. So the epidemiology of hepatitis C is also quite fascinating. We saw a major decline in the early two thousands and there was a hope that we were eventually going to eradicate hepatitis C. There was even a W. H. O. Suggestion that by 2030 we would achieve that goal. But unfortunately in early 2010, we saw a major uptick in the opioid crisis in the United States. And in concert with that, we saw a rise in acute hepatitis C cases in both men and women in the last 10, 15 years. And this occurred in predominantly younger people. Whereas we used to think of hepatitis C as a infection that people acquired in the 60s and 70s. Um and we're now baby boomers. The new hepatitis C epidemic is really something we're seeing in young people in their twenties and thirties. And unfortunately even in their teens, no, I know click exit and say that I so this is the cascade of care for chronic hepatitis C. In the United States. On the left hand side of the screen, you can see what the cascade used to look like. Back in the interfere on era. We had about four million people chronically infected, only about 50% new of their diagnosis and a very smaller subset of them, about 16% were prescribed Hepatitis C treatment, Which with very poor treatments where we had a less than 50% cure meant that only about 9% of the total patient population of Pepsi was being cured of their hepatitis C. Fast forward to the right side of the slide where we have our direct acting antiviral era. And the cascade looks a little bit different. Instead of four million people at Pepsi, we're now down to about two and a half-3 million and that's because so many of the people who knew about their diagnosis were cured. However, the percentage of those who are aware of their diagnosis now has actually gone down because most of those who are diagnosed, sought out cure and so we have a greater proportion of patients with Hep C. Now who are not diagnosed, We still are doing a pretty poor job linking those patients who know of their diagnosis to care only about 11%. However, once they're linked to care, because our new treatments are so effective almost universally, they're going to be cured and that's why there's really no document between the percent who are treated and the percent who are cured. So we have a lot of work to do in improving the diagnosis of patients to raise awareness and linking them to care. But once they're actually linked to care, chances are we're going to cure them. So, as I alluded in 2030 is a lofty goal for us to eradicate hepatitis B and C. In the world. This is what the W. H. O. Came out with a few years ago and the reality is we're doing a very poor job at reaching that goal despite the fact that we've got these great new wonderful treatments for hepatitis C. And we're seeing a lot of people being cured in our clinics in our offices. The cure has really only been achieved by about three million out of the total 71 million people in the United States who in the world to have hepatitis C. Excuse me. So let's talk about strategies to improve this number and get that W. H. O. Goal of eradication Even if it's not in 2030. So the first is screening and raising awareness of the diagnosis. So back in the nineties, the goal was to screen anyone with a high risk for having chronic hepatitis C. And that wasn't very effective. So in 2013 we switch gears and started screening all the baby boomers Understanding that the majority of the patients with Pepsi at the time were born between 1945 and 1965. We're still doing a terrible job at achieving high rate of diagnosis. So in August of 2019 the recognition was adjusted and now it's that all adults ages 18-80 should be screened at least one time for hepatitis C. This is a little rudimentary but this is the algorithm and there probably will be test questions on this. So you should start with the hepatitis C antibody and if it's negative then they don't have to see you don't need to do any further testing unless you think they have active risk factors. Then you should continue to test them periodically. For instance, patients on prep patients used I. V. Drugs. If the antibodies positive then they should reflects to uh an RNA test. If the RNA is positive, they have Pepsi and they should be referred to a treater. We need to know what their genotype and their fibrosis stages but they should be referred to a HEP C. Treater. If the antibodies positive but the RNA is negative, they're not infected. And this means one of several things either they were exposed and they spontaneously cleared it so they're no longer infected or they have been previously treated and cured of their hepatitis C. Or it's a false positive. It's important to remember that patients who are cured of Hep C. Will remain Hep C antibody positive for life but that does not confer protective immunity. So here's a question. We have a 36 year old woman referred for a positive antibody per hepatitis C. After routine screening by her primary care doctor. Her RNA however was undetectable. Her labs are normal including her liver panel. She has no high risk factors for having viral hepatitis. She's never had a blood transfusion. She had a normal sonogram about a half a year ago. For other reasons. What's the next best step in her management? Do you want to repeat the RNA in six months, assess her fibrosis stage with the fiber scan. No further testing screen her close contacts for Hep C. Or check Arriba test and the correct answer was no further testing here is someone who has a positive antibody with negative RNA. She has no risk factors. So this is likely to be a false positive result. So this is a little bit of editorially editorializing, but for me, hepatitis C is one of the easiest things to treat. In fact, I find it um, the easiest patients in my practice, the only thing simpler than a HEP C patient is a no show. However, despite the ease of curing patients with effective therapies, we continue to be making a very small dent in the hepatitis C epidemic. And we really need to emphasize improved detection and improved linkage to care. And these days we have treatments that honestly can offer the prospect of cure to every single patient with hepatitis C. There's a regiment appropriate for them. And the most recent additions to this circle of opportunity for curing hepatitis C now includes patients who inject drugs, Children. And we've even bringing cure to very resource limited countries. So there's not a single patient whether they have infection with HIV Hepatitis B regardless of their genotype, prior treatment experience. Um, prior fibrosis stage, including cirrhosis, renal insufficiency resistance, even there's not a single patient with Pepsi that cannot be treated and cured. So I don't believe you need to know each individual drug for the, for the boards, but it's good to know the three main classes of direct acting antivirals, all the regiments today consist of combinations of two or three of the different classes of medicines. So it's important to understand the classes, We have our NS five a inhibitors which all end in as veer we have our Ns five B preliminaries inhibitors which are all in in bustier with A B And all of Rns 3, 4 protease inhibitors which end in previous. And just by looking at the sub boxes of the drugs, you will know which class of medicines are being included in that regiment and these are the current preferred regimens. You can see that they're all combinations of two or three agents. The first two are genotype specific. However, the last three or all pan gina typically and the one on the bottom of the list is supposed to help atmosphere and box elop, revere. This is the only available triple regimen that includes above ear and as a beer. And a preview here and this is for patients who have previously failed direct acting antiviral therapy. I don't believe they're going to ask you individual treatment decisions. But for your own reference, you can go to the double S L D I D S A combined treatment guidelines which are online at HCV guidelines dot org and you simply choose the drop down menu that applies to your patient whether they be naive or experience their fibrosis stage and it will come up with a table highlighting the preferred regimen for that patient. But it is important and I think you will be tested on what you need to do prior to starting antiviral therapy. So you need to stage the degree of their fibrosis and know whether or not they have cirrhosis. You need to review their meds to look for other medicines they're taking. That might be important drug drug interactions. There are some important baseline labs you need to check, including blood counts, liver numbers I and our renal function, viral load genotype. And you must assess every HEP C patients for two things history of prior d compensated cirrhosis and number two prior exposure or co infection currently with hepatitis B. So co infection is defined as having a positive S. And a gym prior infection is to find us having an antibody to the surface antigen or to the core. We're both it's important because in 2016 the FDA came out with a black box warning about all of the direct acting antiviral therapies for hepatitis C, which I guarantee will be on the board, basically what they warned was that when you treat patients with chronic hepatitis C, who have current co infection with B or previous infection with hepatitis B, that there is a risk for fatal reactivation including death. So again, hepatitis B is something that's never truly cured. It remains latent inside our bodies even if it's cleared. So presence of core antibody suggesting prior exposure, there is a risk of reactivation with direct acting antiviral therapy. So question 46 year old man is started on heP C therapy for genotype, one hep C prior to his treatment, he's found out a positive core antibody to have be but he's negative for S. And again and s antibody. There's an isolated court antibody before starting him on it. Um And before starting him on treatment for his HEP C. You check and he has undetectable HBV DNA and his liver enzymes are all normal. Which is the right strategy to monitor and manage happy reactivation in this patient while on D. A. Therapy for his hepatitis C. Is it no monitoring is needed because he's dave ironic monitor his liver enzymes. And if it increases more than two times the upper limit of normal stardom on happy therapy. Is it begin antiviral prophylaxis now and continue for 12 weeks after he finishes his HEP C. D. A. Therapy or monitor Happy DNA. During and immediately after the D. A. Therapy and start happy treatment. If they if it becomes elevated and the answer is to check hepatitis B viral load. And if that rises then start him on antiviral therapy. So two points one is that viral load for heP B. Is going to elevate before the A. L. T. Does in a heavy reactivation. So if you want to monitor for happy reactivation you're going to first be looking for the DNA followed by a rise in the A. L. T. And if you wait for the L. T. You could potentially miss the opportunity to identify, manage and treat HBV reactivation. So the bottom line is that if you have somebody who has surface antigen positive and especially if they have detectable hep B. Viral load who you're going to start treating them on Pepsi their co infected. And they really should be put on HPV therapy at the prior to starting them on HEP C. Treatment if you have someone else prior exposure. So there's no Happy DNA. There? S antigens negative but their core antibody positive that someone who you should monitor during HEP C. Treatment for the rise and Happy DNA. And if it ever becomes elevated then you initiate happy therapy. One more question. 50 year old man comes to review treatment options for his hep C. He has never been treated because he was always worried about interferon and ribavirin toxicity. He does have a history of heavy alcohol use in the past but has now been sober for eight years. He has a history of societies and mild encephalopathy. But they actually both improved after stopping alcohol. He did have any G. two years ago that had small viruses. They were non bleeding which of the following treatments would be an acceptable treatment for this patient. Is that Elvis here goes up revere the dip is here suppose severe like a premier paid rent is here the triple regimen abc or all of the above. Right. The key here is to understand that if you have a history of hepatic decompensation even if you have subsequently become compensated. You have a contra indication to treatment with a protease inhibitor. All the produce inhibitors are contra indicated in the history of history of the compensated liver disease or currently compensated liver disease. So again, you don't need to know the regimens but you can easily look and see which of the regiment's contains a protease inhibitor and rule them out. So the only acceptable answer here is B the dip is here. So possibly because it does not contain a pre veer medicine. And again this is something very testable and important because the FDA issued a black box warning on this when they notified physician and treaters that there is a very serious risk of worsening liver function including death in patients with d compensated cirrhosis where prior d compensated services after putting them on hep C. Protease inhibitor. Yeah. Drug drug interactions are important to consider and be mindful of. It is not possible to know every drug interaction out there in my practice. Use this great website on Helpdesk drug interactions. I enter my patients meds I enter the HEP C. Therapy I'm considering using and it spits out an algorithm of whether there are any concerning contraindications but it is important to know there are a few that you might be tested on specifically anti acids have been known to reduce the absorption of some of the Ns five S five A replication inhibitors. All the as veers. So you have to be careful about dozing them with anti acids and the anti arrhythmic, particularly amiodarone are contra indicated in with use with sofa severe because there have been some deaths related to that combination. So that's very testable on the boards. It's a question # seven, A 65 year old man with chronic hep C is being evaluated for treatment. He has a history of a fib and he's on Coumadin and amiodarone. What is the best treatment option for him? Is it the difference yourself? A severe Sevastova, Devere Bell Patti's fear, the triple regimen that has such a severe in it or none of the above. And the answer is none of the above because as I just mentioned, say facebook here is absolutely contraindicated to be used with Emilio drone because there have been fatal Breda Kartik events and this medicine can never be co administered. It's definitely gonna be on your boards. And then the last bit is the extra paddock manifestations of Pepsi, which there are many and they're very visual and easy to test. So I would make myself aware of all of these. I'm not going to have to go through each one for the sake of time, but there are a few that I think are worth highlighting. Um, but you can see that there are many different systems that can be affected by hepatitis C outside of the liver and the big ones are non hodgkin's lymphoma, PCT diabetes, potentially and mixed chronic lobular anemic syndrome. So question number eight A 52 year old man with a Hepatitis C. Infection and a new rash. He's a former I. V. Drug user but he's been sober for four years. He's never been treated. He developed a purple raised rash on his lower extremities, malaise joint pain. His exam is notable for purpura on his legs. He has a normal CBC but his renal function is elevated with the crowning of 1.6 and he has a very active urine sediment with both blood and protein. What is going to be the best most appropriate step in his management? Is it monitor the clinical course referring to nephrology. Start riTUXimab plasmapheresis or start treating his heP C. With D. A. Therapy. So this is a gentleman presenting with mixed crowd global anemic vasculitis and the treatment is best to start him on HeP C. Therapy. And the last slide is what to do after cure. Um So post SVR management is also a very important topic and one that's very testable. So if you cure someone who has advanced fibrosis or who has cirrhosis then it's important to continue surveying them lifelong for liver cancer every six months with an ultrasound or other imaging technique. It's also important that they be screened for viruses with an endoscopy and again any patient with advanced liver disease should be vaccinated for hepatitis A. And Hepatitis B. If they do not have advanced liver disease then you need to follow them the way you would. Anyone who does not have Hepatitis C or never did and continue to counsel them on diet, lifestyle and keep their livers and the rest of their bodies healthy. That is it? Good luck on your exam and thank you. Published Created by Featured Faculty Ilan S. Weisberg, MD Assistant Professor of Medicine, GastroenterologyIcahn School of Medicine at Mount Sinai View full profile
