Advanced Liver Disease Case Discussions

Advanced Liver Disease Case Discussions


– Thank you again, I’m gonna finish up our
day with a couple of cases of some advanced liver
disease to talk about, and some teaching points from it. So in the first case, this was a young, relatively young, actually young yes, 39, my age, man who had jaundice, who presented developing painless jaundice and increased abdominal
girth about six weeks ago, was what he reported. Some mild right upper quadrant pain, no real fevers or chills or GI bleeding, and reported that he’d also gained a significant amount of weight, which was unusual for him, over that time frame. With respect to the medical
history, really not much, just some high blood pressure
and high cholesterol. Not taking many medications
other than some simvastatin that he’d actually been on for a couple of years by that time point. He did smoke and had smoked
for about five years. And on social history, he endorsed quite a bit
of alcohol, actually. Had been drinking about nine
16-ounce alcoholic beverages every night for years, and after losing his job
had recently increased. Pretty common story, I think, amongst the folks that
come into our clinic. Had a very significant stressor and his alcohol use had
increased significantly even beyond what he was doing. Because he was ill, he quit drinking about four weeks ago, it kind of scared him, and so he stopped. And no other IV drug use. So when we saw him, his vital
signs actually looked okay. He had no fever, pretty oriented, not out-of-it from a mental
status standpoint at all. But was jaundiced, had icterus, and had a very distended abdomen, soft, a little bit of tenderness to palpation in the right upper quadrant. Pretty prominent umbilical hernia, but very easily reducible, and a lot of lower
extremity edema as well. So on initial labs that
were done in the clinic, he had an elevated
white count to about 25, did have a neutrophilic shift on that. But hemoglobin and platelets were normal. The basic panel was pretty unremarkable except for an albumin that was on the lower end of things at 2.6, for a young man that’s actually quite low. And the liver enzymes demonstrated this classic kind of
2-to-1 AST to ALT pattern, with a markedly elevated
bilirubin of about 21.5. INR was elevated as well at 1.5, and on an ultrasound, he had
this finding that we often see, diffuse hepatocellular disease,
and quite a bit of ascites. But the vessels were all patent, the vasculature was patent, both hepatic veins and portal vein. And on paracentesis, which was performed once we sent him kind of down to the emergency department for further evaluation and admission, they got out about four liters. The SAAG was elevated, consistent
with portal hypertension. And there was no SBP. So on further initial workup on admission, the acute hep-A IgM was negative, again Dr. Fontana had
highlighted how important that is for us to check in all of our patients, given that we’re in the middle of an epidemic here in Michigan. Acute hep-C, or excuse me,
acute hep-B was negative, the antibody for hep-C was negative. Tylenol, which should always,
always, always be checked in these kinds of patients,
was also negative. And the blood alcohol level was negative. An MRI/MRCP was performed given the right upper quadrant pain and concern that there
might be a biliary process going on there to exclude that, and it showed that the liver
was enlarged and was fatty. Again, vessels were open, but the biliary system was normal and there was no significant
mass in the liver. So in thinking about the diagnosis, what’s going on with this patient, we came to the conclusion that we thought this was
acute alcoholic hepatitis. So when we think about
alcoholic liver disease just in general, it’s a
spectrum of liver disease. So it starts with fat in the
liver as its most basic form, almost everybody who
uses alcohol to a degree, three to four drinks a day,
will have fat in the liver. And that fat will go away
if they stop drinking. But then you get a percentage of people who develop fibrosis, so they
get scarring on top of that. Not everybody does, I know we’ve all probably seen and heard of patients who drink heavily. And you say, “How can
you not have cirrhosis?” But they don’t. So not everybody develops
that element of fibrosis. And certain factors, including comorbid liver disease, race, certain genetic markers like PNPLA3, which we see as indicative
of increased risk for both NASH and
alcohol-related fibrosis, can result in progression of fibrosis. And then of those folks, some will go on to progress to cirrhosis, and then have some of
the feared complications of that HCC and end-stage liver disease. Chronic alcohol use for women, anywhere from 20 to 50 grams a day, and 60 to 80 grams a day
in men, will produce this. So what does that mean? There’s about 14 grams
of alcohol in a drink. So women can’t drink as much as men. More alcohol in us tends to produce more advanced liver disease more quickly. And one more point to realize
is that alcoholic hepatitis, which is this systemic inflammation that comes about as a consequence of a very severe hepatic inflammation from very heavy alcohol use, often on the order of six to eight to 10 drinks a day leading into it, can occur at any time
point on this spectrum. Biopsy studies that are usually, that are most frequently
done in Europe actually, where they’ve done a lot of
large-scale studies of this, show that a high
proportion of these people have cirrhosis underlying
the alcoholic hepatitis. So even though they have alc hep, on top of it they also have
cirrhosis to keep in mind. So what is a standard drink? This is from the NIAAA. I often present this data, and people sometimes get
a little uncomfortable. Because they’re like, “Wow, so maybe when I’m
having my wine at night, “maybe I’m having a little bit more “than I should be having.” But these are relatively accurate in terms of the pictorial
representation of what that is. So one can of beer, a
not-quite-full pint of alcohol. A glass of wine that
covers just about half, not one of those like,
gigantic Bordeaux glasses that has about, you always see it on TV. It’s like people relax with this, half a bottle of wine in
this glass, effectively. And then one shot of liquor. That’s one drink. And when I talk to my
patients about alcohol, people if you ask them
how much do you drink, they’ll almost always minimize,
or have one to two drinks. If that one to two drinks they’re having is pouring a lot of
vodka into a mixed drink and having a couple of those, they could easily be getting
well over the recommended, well over safe doses of alcohol. So that’s an important point to remember. So for alcoholic hepatitis, this is by far the most severe form of alcoholic liver disease. It is by far the form of
alcoholic liver disease that gets the most research attention. And this is because of its mortality. So in-hospital, up to 15% mortality. Three-month mortality,
anywhere from 30 to 50%. So one in every two people, dead at three months with this condition. And 2/3 go back to heavy
drinking after discharge. And as we’ll show you, this is actually one of
the biggest predictors. When you’re thinking about
alcoholic hepatitis patients, you’re seeing them in either your clinic, or probably most
frequently in the hospital, there are a few prognostic
models that we use. The Maddrey’s discriminate function is a score that over 32
is considered severe, and that reflects that
high one-month mortality, that as high as 1/3 of the
patients dead in a month. The MELD score is also
used to predict mortality. Again, a 21 is about roughly equivalent to a 32 on the Maddrey’s. And the Lille Score is
a score that is used if you’re going to start prednisolone. So we’ll talk about
prednisolone in a moment. But we use this after about
a week on prednisolone to see if you’re responding. And if you are not responding, meaning if your score’s over .45, then your survival is
very low at six months, and then it isn’t to their benefit in terms of infection
risk to stay on that drug. So we typically stop it
if we’re going to use it at day seven if their
Lille Score is too high. So talking about management
of a patient like this who’s come into the hospital, what do we do with these people? So this is a seminal study that was published a couple of years ago in the New England Journal
called the STOPAH Trial. A very large trial, two-by-two randomized. You had four groups, 1,100 patients with alcoholic hepatitis. They did this in Europe
and the United Kingdom, where almost all the liver disease they see is alcohol-related. So they were able to
accumulate 1,200 patients, which is really really hard
to do for a study like this, and this probably will never
be replicated or done again. But they had a placebo-placebo group, prednisolone-placebo,
pentoxifylline-placebo, and then pentoxifylline and prednisolone in those four groups equally. And what they found at
their primary endpoint of 28-day mortality was
essentially no difference. Maybe a slight trend, but they did not meet
that primary endpoint of improvement at essentially
one-month mortality, everybody being treated for one month. Pentoxifylline was absolutely ineffective, so that was certainly not used
very much anymore for this. And when they looked out to about a year, again there was really little
benefit for any regimen. These lines really start to converge, and so not a lot of benefit. But it certainly doesn’t knock
out the use of prednisolone, we do still sometimes use it. Since the STOPAH Trial, what’s come out? So there was a network meta-analysis that attempted to overcome
some of the limitations of these trials with small sizes, because it’s a relatively rare condition even in the scope of things. And they used a statistical technique called network meta-analysis to compare these different
treatments across these trials. And again what they found was that maybe there was some short-term
benefit for prednisolone, but long-term there really wasn’t a lot of benefit for these patients. And we’ll talk about why in a moment. The takeaways from those studies, that there’s generally less
enthusiasm for prednisolone, we certainly use it less than
we did after the STOPAH Trial. But it still can be the right
choice in the right patient. If you have a patient
who has no infections, and particularly who’s going to have good follow-up with you. You don’t ever want to send
someone home from the hospital on 40 of prednisolone with no follow-up, not knowing if they’re gonna come back, because they’ll get infected and they could die at home
without you knowing about it. Even within the STOPAH Trial, great care, excellent study trial design, a high mortality rate, half at a year, and only three underwent transplant. So this is often what we
see in these patients. To know a high infection rate. So again this was 25%, and it
was worse with prednisolone. So something to think about when you’re thinking about using it, that risk-benefit calculation. And as we talked about, just make sure that you’re
really monitoring these patients if you’re going to choose
prednisolone for them. Calculate that Lille Score at seven days. Because if you find that
they’re not improving, you can just stop it. You don’t have to taper it, just stop the prednisolone at seven days if you find that they’re not improving. Just a quick cartoon about
this idea of infection risk. Keep always in the back of your mind that when patients with alc hep die, they die of infection
and bleeding, most often. And that infection risk
is not just because of the possibility of using corticosteroids, though that certainly
does increase it here. And particularly, opportunistic
infections will go up if you put someone on prednisolone. But the nature and the pathophysiology of the way alcohol works in the body chronically over a long period of time, even before you begin developing
significant liver disease, it’s starting to drop
your immune cell function. So you’re starting to get some
relative immunosuppression with chronic long-term alcohol use. And then as you develop alcohol-related cirrhosis and alc hep, even before you think
about adding prednisolone, you have an increased infection risk. So that’s all of which just to say, just have your antenna up
for infection in these folks. I definitely check them
relatively quickly for infection. If they’re on lactulose, don’t forget the checks for C. diff, because we often forget
to do that thinking, “Oh, their stools are always
loose, they’re on lactulose.” If they’re starting to do worse, you’re not sure why, you’re concerned that they’re infected, you wanna cast a wide net
to look for that infection. But the single most important predictor for these patients long-term
is alcohol abstinence. And this is often the point at which many of us find a little
bit of frustration, or a sense of, what do I do? What do I do with these folks? We know that they need to stop drinking, but beyond telling them,
you need to stop drinking, and making a referral
to addiction treatment that they often never follow up on, what do we do? How do we help our patients? So we’ll talk about that in a moment. But this was a great study that came out in Hepatology just in the last month, and again the French group looking long-term at over six months, what kills these patients? And what kills them is alcohol use. So in the short term, they survive if they
respond to prednisolone. So the way that we interpret
this is if they’re so sick, if they’re sick enough but
they respond to prednisolone, that will be the biggest predictor of their survival in that short term. But if you get them to that six-month time
frame or out longer, what’s gonna keep them
alive is alcohol cessation. And this was a pretty
significant hazard ratio. So any relapse above about
a couple of drinks a day resulted in a four-fold
greater risk of death at that six-month time frame. And it didn’t matter how much you drank. That risk went up even if
you just had one drink. So here they’ve stratified with none being the reference point, out to one to two, three to four, four to five, or higher. And as you might expect, the more alcohol you’re
using, the greater your risk. But look at how it went up, it doubled. Even with just one to two drinks. So it’s important to
have that in our mind, that in the addiction treatment community there’s a couple of different
ways of looking at it. They think about harm reduction
versus total abstinence. But for our patient population, the message is absolutely
total abstinence. That’s what will save the
lives of these patients and also alcoholic cirrhosis patients who maybe don’t have alc hep. Alcohol use is rising dramatically, I mentioned this in my previous talk. When we think about alcohol use, there’s alcohol misuse, and then there’s alcohol use disorders, which are the more severe form
of alcohol misuse problems. And those, the more severe form, alcohol use disorders, are going up. They’ve gone up by 50%
over the past 10 years. And again this was from that large-scale epidemiologic survey that the NIAAA does about every 10 years. And this is more pronounced in women. And women tend to get
more severe liver disease more quickly with less alcohol than men. So more women are drinking heavily. In some of my studies where we’ve done qualitative interviews of
women and done surveys, they are less likely to recognize it. Even when we’ve diagnosed
alcoholic liver disease, it’s tougher to get it, sometimes to get it out of
the women that they have this, and acknowledging it, and
getting them into treatment. So there seems to be some type
of a bias amongst some women, between women and men, about alcohol use problems
and addiction problems being a problem of men. But they’re not. And it’s important to note that there’s a difference between
men and women for this, and a difference between
its effect on the liver. So 80% more for women, and they’re more likely
to get liver disease, means we could be seeing a
much bigger problem in women. So this is the definition from the DSM-V of alcohol use disorders. Almost all of our patients with advanced alcoholic liver disease are going to fit into a category of a true alcohol use disorder, usually moderate to severe. These are people who are drinking more over a longer period of time. They try to cut back, but they can’t. It occupies a lot of their life, getting it, the consequences, recovering from the consequences. They have a craving or a strong desire or urge to use alcohol, and that’s important to ask them about. Because there are some medications, both FDA and non-FDA approved medications, that can help with alcohol relapse and that target craving, they target that craving aspect. They use alcohol when
it’s physically hazardous. So in transplant we really
think about this as, did they use even though they were diagnosed with alcoholic liver disease? So they were told a year ago
they had alcoholic cirrhosis, they kept drinking, now they’re presenting for transplant. These are people that
we are gonna hold off on transplanting right away, because we wanna know that people have developed insight, that they’ve developed
some of the protection against relapse
post-transplant or long-term, that we need to see. And this is just a cartoon that
shows how we diagnose this. Mild, moderate, or severe is
how we’re thinking about this. It used to be abuse and dependence, it used to be alcohol
abuse, alcohol dependence. That has changed. You can think of dependence as severe, so that’s sort of the
category that we’re in. A lot of the older studies
talk about dependence. So what can you do? First of all, you gotta find it. So in an alcoholic hepatitis patient that’s pretty straightforward, right. We typically have, they’ve told us that
they’re drinking heavily, we know that they’re drinking heavily, but what about people who
just come in to your clinic who maybe have elevated LFTs, who maybe you’re not kinda sure how much of a problem is alcohol playing? And I can tell you, it can be a challenge. This is what I do, this is what I love, I do a lot of research in this. And it can be tough to
detect this in patients. Because people don’t wanna tell you. They feel a lot of shame, they
feel a great sense of stigma. Cirrhosis itself is very stigmatizing, and on top of it when you have an alcohol use disorder
or an addiction problem, that’s very stigmatizing. And people feel bad about that,
they don’t wanna tell you. So the AUDIT-C, which is what you’re seeing
here is the full AUDIT, all 10 questions. But the AUDIT-C is kind of the short form, first three questions that get at frequency, quantity, and
frequency of heavy drinking, is actually quite
effective at picking it up. And there was a great study that was done, I believe this was in Australia, that looked at it actually
in a transplant clinic. This was a post-transplant clinic, and patients who’d been transplanted for alcoholic liver disease. So our antenna should
be really up for this, really looking at it. We as the hepatologists did the worst at
assessing the alcohol use. So if you look here, hepatologists assessed
patients as abstinent, 78% of the patients were
assessed as abstinent. Then they got a blinded AUDIT-C, that said only 63% were abstinent. And then everybody got a
blinded addiction specialist, blinded meaning the doctors
did not see the AUDIT-C before addressing the patients. The addiction specialist
assessed only 60%. So the takeaway from
this is that we’re not, not that we’re not that great, but we’re not that great at assessing these alcohol use disorders. And we’re inappropriately
assessing people as abstinent and missing 20% of people post-transplant who have returned to
some level of drinking. That’s huge, that’s a big deal. But just doing an AUDIT-C
improved that by almost 15%. So just doing that in your clinic might help you pick up a
little bit more alcohol use, and then maybe get some
candor out of the patient and direct them to treatment. The other thing that you can use to try to find
alcohol-related liver disease and find the alcohol use if you’re stuck and your patient is not telling you about what they’re using, are alcohol biomarkers. The first of which is liver enzymes. So in my practice, both
pre- and post-transplant, one of the first things that cues me in that I might need to call
my patient, talk to them, and send some of these other biomarkers, is the liver enzymes go up. I see the alk phos go up a little bit. I see the enzymes go up
in a two-to-one fashion. This happens, I’ve had listed
patients have this happen. And we start talking,
and we get biomarkers, and we find that they have
slipped or they have relapsed, and they haven’t called me and told me. It was found by looking at liver enzymes and sending biomarkers. So that’s one good way to do it. Blood alcohol levels
only last about 12 hours, so maybe not the greatest
at assessing longer term. Urine ethyl glucuronide, now ethyl gluc is a
breakdown product of alcohol excreted in the urine. And it picks it up to
around about three days, sometimes as far back as five days, but think of it more as
kind of a three-day pickup. And it can pick up
drinking in your patients within that three-day period. Ethyl sulfate is what we’re using as the confirmatory test at
the University of Michigan to confirm that the urine ethyl
gluc is truly from alcohol, because there can be false positives. And then the phosphatidylethanol is one of the newer biomarkers
that we’re using for this. It’s a blood test, it’s actually a finger stick,
like a glucose testing. And it actually gets it out
to about two to three weeks. So this is actually a phospholipid that’s affected by alcohol metabolism. And it’s been validated in advanced liver disease as accurate. Again, there are things that
can cause false positives. So the take-home from this slide is that alcohol biomarkers can help
you in detecting alcohol use. They are recommended by the American Society of Addiction Medicine to be used in caring for patients with alcoholic liver disease, or excuse me, caring for
patients who have addiction. But you always wanna talk
to your patient about this. So we don’t ever make decisions just based on an alcohol biomarker. It can actually expose
you to medical legal risk. So you don’t want to make
big treatment decisions, not send someone for transplant, for us take someone off a list, solely because of a biomarker. You wanna talk to your
patients, see what’s going on, maybe have them assessed
by an addiction specialist, which is typically my practice if I see something like this happening. And the patient is not being
candid with me particularly. Just to get on that a little bit more, the relationship that you have
with your patients matters. So what I frequently hear is, “What do I do, what do I
do with these patients?” If we’re not trained
in addiction medicine, and I’m not trained in addiction medicine, how do we manage this? Detection is important, can’t help them, can’t get them into treatment
if we don’t detect it. But the relationship that you have with your patients actually
can be therapeutic. And there’s a lot of literature in the psychological and
psychiatric literature and addiction literature
that the relationship that we have with our patient can help people do better or worse. And the view that our patients have of us, but even more, that we
have of our patients, can affect their outcomes. This has not been done in liver disease, but within the psychology literature, therapists or providers who have a more judgmental attitude
towards their patients that the patients are picking up on, their patients do worse. So it’s how we think of our patients, how we portray our views of
these things to our patients, that can actually affect if
they get abstinent or not. So that can be therapeutic, and our words can be therapeutic, something to remember. Assessment is holistic, this just goes back to the point that I made earlier
about using biomarkers, using validated questionnaires, history, physical exam, the
psychosocial assessment, and making sure that you talk
to your patient about this. I set the stage for all of
my patients by telling them, “I’m going to be getting alcohol
biomarkers, and here’s why. “I’m not doing this to
get you into trouble, “I’m doing this to find it
so that we can treat it.” Try to promote candor as much as you can. Just very briefly, we
are involved right now, Dr. Fontana is the PI on this study on a phase-two, blinded RCT of an investigational
medication from Gilead for treatment of alcoholic hepatitis. It’s an apoptosis-signaling
kinase inhibitor, I’m happy to talk to anybody, and Dr. Fontana is as well, afterward about this. Patients are randomized to,
everybody gets prednisolone, but then some get placebo,
some get the study drug. And then looking at outcomes one month on. So if you think you have an alcoholic hepatitis
patient who might qualify, please feel free to email either Dr. Fontana or myself for that. So moving on quickly to the
next study, or the next patient. So this was a 60-year-old
man with jaundice who, about two weeks prior to admission, had reported having flu-like symptoms, subjective fevers and chills, nausea, vomiting, all got better. And then subsequently noticed
that his stools turned light, his urine turned dark. And he actually went to
work, and everybody was like, “Dude, you look really yellow.” And so he went to his, and
that’s exactly what he said. And so he went to his local ER where they checked labs
and did a thorough workup, and he had no other risk factors. But they found that his
hepatitis A IgM was positive. So this is a case that we’ve been seeing relatively frequently, as Dr. Fontana alluded to. LFTs were quite elevated,
they were up in the thousands, and his bilirubin was
high, and his INR was 1.3. So this was also kind of again, what we talked a little bit about, hmm is this person someone who’s gonna potentially be progressing
to an ALF pattern? Right upper quadrant
ultrasound looked good, again we always wanna do a thorough workup for other causes of acute hepatitis and potential acute liver
injury in these patients, and all of that was also normal. So when he presented, they evaluated him, sent him out, said he was doing okay. He was oriented, he had
no evidence of asterixis. At about a week later, or about four weeks
after his symptom onset, they repeated labs, and things had actually gotten worse. His total bilirubin had gotten worse, and his AST and ALT were not improving. And the INR inched up a tiny bit, so they actually called
us and had him come in for admission and follow-up here. So hepatitis A, as Dr. Fontana said, we are in the middle of an epidemic here in Southeast Michigan and across the US in various locales. And again as was already mentioned, we have as many cases
as California right now, with 20 deaths, and this was as of just a
couple of weeks ago here. So it is a big deal, we’ll talk about kind
of what we need to do in terms of halting it. Looking at the time course
of acute hepatitis A, our patient fit right
into this time course. They are infected, and there’s a period of
about two to four weeks before you begin to see,
before any clinical illness, if you’re going to have
symptoms, not everybody does. And in fact, most people don’t. He was probably past his viremic phase, again kind of ballpark guessing about when this might have started on the basis of when he said
his symptoms had started. And so as you can see, he should be kind of on
the downswing of his ALT, we should be kind of
starting to see this improve. IgMs can stay positive out several months if you’re taking care of these patients, IgG levels that are protective for life will continue to go up
around this time frame. And these are the clinical
symptoms, what he described, this kind of flu-like
syndrome that gets better. And then a little bit
later, about a week later, they start to develop signs of dark urine, acholic stools, and then jaundice, if they’re going to get
those clinical symptoms. So how does it spread, and who’s at risk? This is the fecal-oral route, so this is the restaurant worker that maybe doesn’t wash their hands and spreads it that way. Again, homeless patients, IV drug users, these are folks who in
these current outbreaks, particularly as you’ve been hearing about San Diego and here, these are the folks that are really being heavily affected by it. But people who have
close household contacts or are kind of intimately
caring for someone who has acute hep-A can
certainly be at risk as well. And as Dr. Fontana said, people who are healthcare
workers in these epidemics, we’re certainly at risk so
we’re vaccinating everyone. Looking at the acute liver failure, again the vast majority
of ALF is not hep-A, and hep-A is actually fairly rare. In the ALF study group of
which our center is a part, and Dr. Fontana is an
investigator on that trial, about 37 patients had
hep-A, so pretty low risk. But again, something that you want to
keep your eyes open for, because it can happen and
be fairly devastating. So if you see someone that you’re worried potentially has acute liver failure, you wanna check an INR. Because acute liver failure, as you know, is synthetic dysfunction in
the setting of liver injury with encephalopathy symptoms
starting to develop. And those can be subtle, they can be not very overt initially, and then develop quickly. So you wanna check them for asterixis, check their mental status, and if you have any concern at all, you wanna contact a transplant center for a discussion about
should they be transferred. We have M-LINE, which many
of you may be aware of, that if you have someone
that you’re worried about, call M-LINE, they can get
you in touch with any of us. We always an inpatient
hepatologist on call to address these kinds of issues if you have any concerns about that. So speaking about vaccination, so according to the CDC and ACIP, these are the vaccination
guidelines just in general. So children over one, if you’re going to a
high-hep-A rate country, you’re gonna travel there. Chronic liver disease patients, so we will get this
regularly in our clinic, are you immune or do you need to be vaccinated for hepatitis A? We’re often looking at it in conjunction with hep-B vaccination because there is a
combined vaccine, TWINRIX, that gives you hep-A and hep-B over the course of three
shots over six months. Healthcare workers now, the CDC guidelines won’t
say healthcare workers, but now we are wanting
to vaccinate everybody, particularly here, because it’s such a high-risk area for us. And then anybody who has work ongoing with high-risk populations. And anybody who wants it, it’s a safe vaccine, they can get it. People who’ve been exposed, so if you think you or one of
your patients has acute hep-A, you wanna think about
who needs to be protected after your patient has been
potentially exposing folks. So post-exposure prophylaxis
is typically recommended for people who are
unvaccinated and not immune, and have not been exposed
to it in the past, in the two weeks around the time frame when the patient was infected. So you can give hep-A vaccination if they’re between the ages of one to 40. For post-exposure prophylaxis, the CDC actually recommends not TWINRIX, but HAVRIX, or there’s
another one called Vaqta. Just the hep-A vaccination only, because it actually has double
the dose than the TWINRIX, you get a slightly
lower dose with TWINRIX. If all you have is, if that’s
all you have is TWINRIX, after a shot of TWINRIX
about 95% of people will have antibody to hep-A,
so it can be protective. But if you’re doing it for
post-exposure prophylaxis, the CDC recommends that you
use the hep-A specific vaccine, just because the dose
is a little bit higher. If you have someone
outside this age range, immunosuppressed, chronic liver disease, you might consider giving passive immunity with hep-A immunoglobulin. That lasts for about three to five months. If you don’t have access to
that for whatever reason, just vaccinate. That’s okay, the CDC says that’s fine, because not everybody has
access to the immunoglobulin to give people who are in that window and require protection. It’s not a live vaccine, so you can give it to the
immunosuppressed, and that’s okay. And there’s really minimal side effects, other than if someone
is allergic to vaccines or allergic to a component of it, so that’s important to remember. So going back to our patient, we followed up with him in clinic, and his liver enzymes
got a little bit better but he just wasn’t improving
as fast as we would have liked. And in fact, his alk phos was
going in the wrong direction. So it was just kinda
inching up and up and up. His bilirubin had definitely come down, but it just wasn’t getting any better. So we assessed him further for
other causes of liver disease and some complications of hep-A, which I’ll talk about in a moment. Most notably, autoimmune
hepatitis we looked for, and he did have a positive
anti-smooth muscle and a high immunoglobulin. So complications of hep-A, which are rare, but can occur afterward. And to keep in mind, if you don’t see them getting
better or they’re not, those enzymes aren’t coming down the way that you think that they should, a cholestatic hepatitis
can happen in under 5%. Usually they get better over
time, but it can be protracted. So it can last for months, and we simply support people through this after we rule out other reasons for somebody having a
cholestatic liver disease. Relapsing hepatitis can
happen in up to 10%, so this is not what this gentleman had. Because typically what you will see is that they go back to
normal or near-normal. So they get all the way back to normal and their liver enzymes
are pretty darn close, and then you start watching and they go back up again months later, and they can be infected
in that period too. So again, something just for us to keep in the back of our mind that
we do wanna just maybe watch, follow up with these patients after they’ve recovered from acute hep-A. Particularly if it was
something severe like this. And then the final variable, this is very rare but it is
reported in the literature, was what this patient had,
was autoimmune hepatitis. And what we think happens is that on this patient’s liver biopsy, he had findings consistent
with autoimmune hepatitis, but there was some chronicity to it. We didn’t know what his liver
enzymes were coming into this. And so it’s not clear in this patient, did he have kind of underlying
autoimmune hepatitis and then it was flared up by his hep-A, which he clearly had? We think it can trigger
an autoimmune hepatitis in someone who maybe never even
had elevated liver enzymes. And so you do your usual diagnostic workup for autoimmune hepatitis. This requires a biopsy, so you don’t have to biopsy
all your acute hep-As. In fact, you shouldn’t, if you think that that’s what’s going on. But if you find yourself in a situation weeks to months down the road where things are not what
you think they should be, they’re not getting back to normal, and you think this is
on your differential, then that’s when you get a biopsy. And we did biopsy him and
it was not viral attendant, it was autoimmune. And so we treated him, treated this individual, and he did get better
with steroids and Imuran. So just some brief pearls, be aware of the current epidemic that’s going on here and elsewhere, and know kind of who’s at risk. And that now we’re kind of just vaccinating everybody in this area to try to protect as
many people as we can. If you see an acute hep-A, check that INR, check the mental status. And if you have any concern
that they might have ALF, please do call us or a transplant center, and we can talk it through with you and get them here if need be. And then good hand hygiene,
as always, wash your hands. My favorite restaurant in
Michigan had a hep-A outbreak, so it was very sad. I hadn’t eaten there in the time frame, so it was okay, but I
still haven’t been back. That’s all, thank you.

11 Comments

  • T Boned says:

    Understood about 10% but also understood that this professional is on the mark. God Bless everyone with liver disease. My prayers are with you!

  • Andrew Lancastera says:

    So pretty much liver disease is associated with alcohol?

  • Andrew Lancastera says:

    I am about to pass from liver and pancreatic cancer, I use to drink 1 beer a day: did this mess me up?

  • Andrew Lancastera says:

    “Amongst the folks that come into our clinic” really??

  • ms21songs says:

    My sister just passed away suddenly from this gf.me/u/tdhp4r

  • Yashika Sharma says:

    My friend’s grandfather was diagnosed with liver cirrhosis and they went every possible doctor in the hope of some positive results but his condition has been deteriorating day by day. Someone told them about Planet Ayurveda and they immediately approached them and I saw his grandfather’s condition and now I couldn’t believe my eyes, He is super healthy. Now I have total faith in Ayurveda

  • Mr. clean One says:

    Been drinking straight for seven years after getting chirosis . Finally caught up. To me. Why stop now.

  • Manish Arora says:

    Ascites which is a disease of liver. It is a common problem nowadays. My friend also had this problem but Allopathic medicines shows no good results. He used Ayurvedic remedies of Planet Ayurveda and got very effective results. If you want this Use Liver Care Pack of "Planet Ayurveda". It is really very effective.

  • Alicia Page says:

    Is alcohol stores going up regularly a part of the agenda 21 plan? Not a good time to be an alcoholic, healthcare isn't what it's stacked up to be. Luckily, 3D printed organs, with livers they use fungi, are medically feasible.

  • Amritpal singh says:

    It feels very bad when such a problem occurs. Actually, I had the same problem, then I went to many hospitals. But the result was not good. Then, Someone told me about planet Ayurveda. I went to Planet Ayurveda & got his treatment started. Now I am fine. If you have this type of problem or any other type of health problem. you should go to Planet Ayurveda.

  • ronald evers says:

    How is the hell is the general public suppose to understand this …This should be something you should hear in Med school….Liver 109…..SMH…Really…?

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