Viremic – Cases in HIV

Announcer:
Welcome to Viremic–Cases in HIV, hosted by Dr. Eileen Scully and Dr. Christopher Hoffmann, both HIV specialists at Johns Hopkins, who explore quandaries in adult HIV care. Each case discussion includes medical history and diagnoses, challenges in care and treatment, and key evidence and guidelines that inform clinical decision making.

Cases are presented as a composite from the hosts’ clinical practice, with all identifying details removed to protect the privacy of patients. Case discussions are for informational purposes only and not offered as medical or clinical practice advice for patients or clinicians. Any mention of specific medications or commercially available products is a description of use only, not an endorsement.

Dr. Christopher Hoffmann:
Welcome to Viremic. I’m Chris Hoffman, and I’m joined today by my colleague, Dr. Juhi Moon. We’re both based in Baltimore at Johns Hopkins. Juhi is part of the Division of Infectious Diseases, where she is a specialist in diagnosis and management of hep C and liver-related complications of HIV.

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Juhi, I first appreciated your depth of knowledge regarding liver disease some years back when we both taught a hep C management class for primary care providers in Baltimore. It’s probably more accurate to say that you did the teaching, and the primary care providers and I did the learning. I’m so glad to have you on the podcast today so I can keep learning.

Dr. Juhi Moon:
Thank you, Chris. Thank you for having me.

Chris:
To start off, tell me a bit about what led you to the intersection of ID and liver disease for your professional work.

Juhi:
I was lucky enough to participate in a lot of the hepatitis C clinical trials before and after fellowship. Before fellowship, I was in Innova Health System in Northern Virginia, and we did some clinical trials with hep C, and then I completed fellowship and was lucky to work with Dr. Mark Sulkowski and Dr. Dave Thomas in doing hepatitis C clinical trials. I learned about FibroScan; I learned about liver disease. That has evolved over time. Now we’re doing hepatitis B trials, and I’ve learned a lot about how HIV patients are now being recognized to have metabolic-associated liver diseases. So that’s how I started, with clinical trials.

Chris:
I’d like to get help from you with a recent case I saw—an amalgam of multiple patients I’ve recently seen. This was a 41-year-old man diagnosed with HIV about 15 years ago, who was started on antiretroviral therapy soon thereafter. He has generally maintained an undetectable viral load and was switched to BIC/TAF/FTC, or Biktarvy, from a PI-based regimen about 6 years ago for an improved metabolic profile. He has consistently had an undetectable viral load for the past 6 years.

Other notable medical history includes a history of anal dysplasia, for which he’s had an ablation. He also has hypertension, for which he’s on hydrochlorothiazide. He’s been tested for both hepatitis C and hepatitis B in the past 12 months and was negative for hep C antibody and hepatitis B surface antigen and positive for hep B surface antibody. Notably, he has been vaccinated in the past for hep B. He has no known other medical conditions.

On exam, his heart rate is in the 70s, blood pressure 132/76, and his BMI is 34. Laboratory studies of note include an undetectable viral load, CD4 count of 621, normal kidney function, an ALT of 72, AST of 63 and alk phos of 52. Reviewing his labs for the past 4 years, these liver enzyme results are consistent with a fluctuation between normal and 1X to 2X the upper limit of normal during that time period.

In the U.S., Europe, and Australia, chronic liver enzyme elevation is common among people with HIV who are receiving antiretroviral therapy. In fact, about 10% of people in a number of cohort studies have fluctuations in liver enzyme elevations between 1- to 3-fold the upper limit of normal. The downstream impact is fibrosis, cirrhosis, and hepatocellular carcinoma. In addition, there’s some associations with liver enzyme elevations and coronary artery disease diagnosis and major adverse cardiovascular events.

When I see this, it’s of concern, but I’m not always sure how to manage it. What would you want to know next in building a differential and approach to a patient like this?

Juhi:
I’m wondering about his social history. Does he drink alcohol? Any drug use?

Chris:
He does drink alcohol, what he describes as socially, usually a couple of beers on Friday and Saturday night. During the week he usually does not drink at all. He has used marijuana in the past, but no injection drugs, and is not currently reporting any other drug use.

Juhi:
And his only medication is HCTZ.

Chris:
Right, Biktarvy and hydrochlorothiazide.

Juhi:
This is probably a patient that a lot of us see—the patient seems to be doing pretty well, and you’re seeing these nagging LFTs that are fluctuating and even can sometimes be normal in HIV patients and still have underlying liver disease.

I think the differential is broad, but we could go through some of the things that are coming to mind for me. The first all of us would look at is the medication list. We’re always trying to find a medication that we can pin this on. I would look for the things that are classically hepatotoxic, like statins, Tylenol toxicity, Bactrim, any antifungal therapy, or TB medications, which your patient doesn’t have. Then I would look at their ART because some classes specifically are associated with hepatotoxicity more than others. I think we all know NNRTIs, efavirenz, and nevirapine have a lot of hepatotoxicity, and PIs also have a moderate to high risk.

Lovely that this patient was switched from a PI 6 years ago to now Biktarvy, because the integrase inhibitors are probably the safest, and the new NRTIs also not so much having issues with liver toxicity. The problem is the classes themselves. Integrase inhibitors can cause weight gain, and weight gain is a risk factor for developing metabolic-associated liver disease, also called “MASLD.” PIs also independently can cause fat accumulation in the liver through various mechanisms.

The 2 together place this patient into my second category, which is the metabolic dysfunction-associated steatotic liver disease, again known as MASLD. People with HIV have a higher prevalence, of MASLD, about 30 to 50% compared to the general population, which is about 25 to 30%. That’s of concern for this patient who’s otherwise doing really well.

Other things I would think about is viral hepatitis. You pointed out this patient doesn’t have hep B and hep C, but again, we still see hepatitis B and C in this population.

Then I would think about alcohol use as well. This patient does drink socially on the weekends, which can be of concern if they’re binge drinking, but alcohol can definitely have its own brand of causing fat accumulation in the liver as well as liver fibrosis.

Then I would look at HIV itself—chronic inflammation from HIV for a long time. The length of time of having HIV can cause the inflammation to lead to insulin resistance. So, they have a lot of other issues which we can go into on their own for causing and leading to MASLD—the chronic inflammation itself can cause elevated LFTs. Then I would look at other HIV-related things, like opportunistic infections, like disseminated infections.

Finally I would think about other things they can get that the general population also gets—autoimmune disease, biliary pathology; that could be considered as you do your further workup.

Chris:
That’s a helpful starting point.

Getting right into the further workup. First, where would you direct that workup? Is there a specific condition after we’ve reviewed his meds, and as you’ve pointed out, probably not candidates for causing his low-level liver enzyme elevations? Then some of the other conditions like OIs—unlikely with his robust CD4 count. So, which cause on your differential would you prioritize, and how would you start your next steps of an assessment?

Juhi:
We have hepatitis B and C serologies, which we should get on everybody. Then I think we can look at the labs that we already have; an AST; an ALT; we have the person’s age; and I’m assuming you may also have a platelet count because we could get a FIB-4. FIB-4 is a measurement that we can do using labs we already have to see if we think patients may be at risk of having fibrosis. Do you have a FIB-4 four for this patient?

Chris:
I have calculated that, and that was 1.16.

Juhi:
The cutoff generally that’s used is 1.3. If <1.3, it’s considered a low likelihood of advanced fibrosis. The problem we have in [the] HIV population is they can be misclassified. There was a great study that came out this year by Cinque, et al., it was a multinational study published in hepatology that looked at 5,000 HIV patients and found the FIB-4 misclassified—36% of fibrosis cases as low risk. There was particularly poor performance in those with MASLD, so we have to be careful with the FIB-4 and HIV, because this low score that you’ve calculated may not be entirely accurate.

Chris:
Juhi, when you calculate the FIB-4, do you find it most useful if it is more than 1.3 to point to fibrosis? And if it’s less than that, that that you’re really unsure of the meaning of the result, at least among people with HIV, or what is your approach?

Juhi:
I think that’s a good way to look at it. We usually use these markers to help us rule out cirrhosis, so if it’s low, we usually feel comfortable that the patient probably doesn’t have advanced fibrosis. But now that we have some of this newer data coming out, it makes us suspect a little that this may not be the best approach, and maybe we need to go straight to FibroScan or elastography to get a better look at HIV patients.

Chris:
So, is that the next step?

Juhi:
I think so. The only other thing I would ask is did you get a hemoglobin A1c lipid panel to look for other metabolic risk factors for MASLD?

Chris:
He’s had an A1c a few years ago, which was below the cutoff for prediabetes. It’s been at least a year since he’s had a lipid panel, so something to repeat at this time.

Juhi:
I think we should definitely screen this patient for metabolic risk factors. Screening is variable according to different guidelines.

Currently, the AASLD, which is the American Association of Liver Diseases, uses 2-tier testing—a FIB-4 to a FibroScan. They recommend screening for high-risk individuals—patients with the metabolic risk factors that we’ve been talking about—diabetes, obesity, hyperlipidemia, hypertension, low HDL. If the patients meet one of those risk factors, then get a FIB-4. As we’ve talked about, it’s not the best in HIV patients, but if they do meet the clinically significant cutoff of >1.3, then move to actual liver staging. In liver staging, you can also get a measure of fat content in fibrosis. That’s the AASLD.

EASL guidelines, which are the European Association of Liver Diseases, have interesting wording: they call it “active case finding.” This approach is different. They want primary care doctors to look at the entire patient and see if they have anything that could contribute to fat or fibrosis. That includes, beyond traditional metabolic risk factors, hypothyroidism, poor diet, physical inactivity, obstructive sleep apnea, PCOS. They want primary care doctors to find these patients, and if they do, put them through a FIB-4 and then some sort of elastography. It’s interesting how they want you to find the patients before anything bad happens, before you find the elevated LFTs.

[The] Infectious Disease Society of America has a different approach, which is when you see high liver function tests, then go down the route of getting imaging first, meaning ultrasound, CT, or MRI. If you see something like steatosis on those, then get FIB-4 and FibroScan. They have an extra imaging component that the other guidelines don’t.

So, they’re not all on the same page, which can be confusing for a lot of people.

Chris:
Probably because of somewhat inadequate evidence to have clear evidence-based recommendations.

Juhi:
Yeah, even the American Association of Clinical Endocrinologists says screen for risk factors, regardless of LFTs. They don’t even care what the LFTs are. They just say look for the risk factors and then everybody says, move to FIB-4. So, it’s interesting.

Chris:
Before we move forward, perhaps you can define MASLD and metabolic associated steatohepatitis, or “MASH,” and differentiate them also.

Juhi:
MASLD includes hepatic steatosis. Patients usually have to have at least one or more metabolic risk factors— diabetes, hypertension, high cholesterol, hypertriglyceridemia, low HDL, and obesity.

MASH is a metabolic-associated steatohepatitis that includes not only the steatosis, but significant damage happening. These patients also have fibrosis. The fibrosis is of most concern because you don’t want your MASLD patient who now just has steatosis to develop so much inflammation from the fatty infiltration that they are now causing damage to their liver, which then moves them into MASH.

We used to use liver biopsy a lot to find out how much fibrosis people have and to make the diagnosis of steatohepatitis. That was the gold standard. But now we have imaging and indirect ways of separating people between the two camps.

Chris:
How does the liver enzyme elevation help, if at all, in distinguishing between MASLD and MASH?

Juhi:
If they are late-stage MASH, they can actually have normal LFTs, so it’s not always clear, and people with steatosis can also have normal LFTs. So, sometimes the fact that we wait for these LFTs to increase can confuse thin gs because you can’t really pin all your diagnosis on just rise of LFTs and saying this person has MASLD versus MASH.

Chris:
And can somebody with MASLD have elevated ALT AST?

Juhi:
They can, but it’s been pretty well documented that they don’t have to.

Chris:
One of the things that I always have to re-learn is the imaging and performance characteristics of FibroScan or transient elastography and other imaging modalities, including which patients it works well in and which patients it does not, and what it really tells us about either MASLD or MASH.

Juhi:
FibroScan is my favorite. In infectious disease, they don’t teach you about radiology, so I’ve learned a lot over the last 10 years about FibroScan. FibroScan is a brand name, but it’s also called vibration-controlled transient elastography. It’s non-invasive, it’s quick, it’s painless, and it uses ultrasound technology to measure liver fibrosis. It can also give you fat content in the liver.

The exam can be performed in a clinic; you do not need to send this patient to radiology. However, there is also shear wave elastography, which is done through ultrasound by radiology techs. That’s a separate one, but they both can measure fat and fibrosis.

The way the exam is performed is patients lay flat on an exam table, and we use an ultrasound probe, which is placed in the right upper quadrant on the right lobe of the liver. The probe has a tip, and when you press the button, a mechanical vibration is generated that creates a shear wave or a ripple that propagates through the liver. So, the probe delivers this small painless vibration. The speed of that shear wave it creates is measured. That speed is influenced by how readily the liver tissue deforms. Really healthy liver tissue is like a marshmallow—the shear wave is going to move and deform that marshmallow very easily. So, it’s soft, healthy tissue; it’s gonna go slowly. But if you have like a rubber ball there, there’s nothing that’s going to deform that. So, the shear wave is just going to go straight through; it’s going to go fast.

The velocity that we measure of that shear wave is then converted into a liver stiffness estimate that’s reported in kilopascals. The cutoffs are based off of fibrosis scores. What that means is the FibroScan was validated against liver biopsy. We have cutoffs that try and correlate with F0, F1, F2, F3, F4, and F4 cirrhosis.

Generally, the accepted literature is that <8 kilopascals is considered 93% sensitivity of the patient not having advanced fibrosis. So, they’re probably an F0, F1 disease. A cutoff of >12 kilopascals indicates a high likelihood of cirrhosis, that’s F4. In between 8 and 12 is where it gets a bit messy. We can’t tell you exactly if somebody is an F2 or an F3. We tell people that’s a moderate amount of fibrosis. So, that’s how we interpret the cutoffs that the FibroScan provides. A higher stiffness score correlates with cirrhosis. The test will measure 2 kilopascals all the way to 75.

The higher the score, you can actually also correlate clinically significant portal hypertension. So, someone who scores a 20 and above or 21 is the cutoff that AASLD uses. If they have low platelets, they probably have esophageal varices.

We can do something with these measurements and also tell how severe someone’s cirrhosis is. That’s how we measure fibrosis. The ultrasound also can measure fat, and we do that using a CAP score. CAP stands for controlled attenuation parameter; it measures the attenuation or the loss of the ultrasound energy as it passes through the liver. Fat will block that. The cutoffs here are even more messy, but we generally consider that a cutoff of >248 decibels per meter is an indication of some amount of fat in the liver. The higher the number, the worse it is. Many people will agree that the cutoff of 337 is severe amounts of fat. But again, because this is compared with liver biopsy, people want to know is there an S0, S1, S2, S3 result that we can correlate, and it’s not as clear with CAP scores. But generally, they do help if there’s fat and the higher the number, the worse the fat.

Chris:
Then for people who don’t have access to FibroScan, you did mention that ultrasound done by radiologists with shear wave elastography can also provide some information. Does that help both with the fibrosis and fatty infiltrate?

Juhi:
So shear wave elastography is great. There’s just many types of it, and they can all give you fibrosis as well as controlled attenuation parameter, so CAP results. There’s point shear wave, 2D shear wave, and there’s lots of different vendors who do this. Now it is an added program to many ultrasound machines. So, you can send your patient to radiology and get the same results.

Just so everyone knows, FibroScan is not infallible. You must interpret it knowing the patient as a whole, because it is influenced by other things. What do I mean by that? The liver isn’t solid; it is also viscous. There’s fluid in it, blood, cells, extracellular matrix, proteins. There’s other things in the liver, so when patients have a lot of inflammation, like acute hepatitis or congestion from heart failure, or a lot of edema in the liver, if they have kidney failure, all that fluid changes how the tissue functions. So, it’ll alter your measurement. I tell our technicians this:

It’s like if you put wood in a mattress. That is very stiff. That’s not going to change, but if you take the same mattress, and you throw it in a lot of water, and it’s full of water, it will also feel firm, just like the mattress with the wood in it, but it is firm because of all the fluid in it. It’s changing the tissue itself. It’s changing the mattress itself. The same thing happens in the liver. If you have a lot of congestion, it will alter how the mechanical energy tracks through the tissue.

Someone with acute hepatitis or heart failure will score very high on the FibroScan. It will indicate a high amount of stiffness, but it cannot tell you if that is fibrosis or not. So, you must interpret the FibroScan and the patient as a whole.

Chris:
Early on, I heard a lot about doing the FibroScan and the results on larger patients. Many of the people that we’re thinking about MASLD or MASH for may have a larger body habitus or higher BMI or higher abdominal girth. How does that affect the current use of FibroScan or shear wave elastography?

Juhi:
There is a higher failure rate sometimes with patients with really high BMIs, especially folks with central obesity. There may be high variability because we do multiple measurements, but that has been overcome through getting the extra-large probe, which measures deeper than the regular medium probe that we used, and that has increased a lot of our success rates.

Without the XL probe, there was a problem with fibrosis maybe being overestimated or the test failing, but now that we have these extra-large probes, it’s actually been really beneficial. We’ve had some studies concerning MASLD in our clinic, and we have used the XL probe on all these patients, which has been really great.

Chris:
How do you advise patients to come to the clinic prepared for the FibroScan? Is there anything specific they should be considering in terms of fasting or any other considerations?

Juhi:
Absolutely. Patients should be fasting at least 2 to 3 hours because meals can transiently increase liver stiffness. Patients can take their medication and drink a little bit of water with it, but no coffee, no tea, no flavored beverages. You really want that liver to be in a resting state.

Chris:
So, getting back to the patient we’re discussing, I don’t have any FibroScan results, but it sounds like that is the next step. Let’s imagine that the FibroScan points to an elevated CAP score, maybe even some fibrosis. What is your next step in discussing these results with a patient and counseling them on what they can do to reduce their risk of progression of liver disease and its complications?

Juhi:
Treatment for what we presume this patient has, which is MASLD because of the high CAP score (he does have steatosis), revolves around weight reduction, risk factor modification. We still have to get an updated lipid panel, updated hemoglobin A1c for this patient. We should treat patients and control the risk factors that we can. So, controlling their hypertension diabetes and hyperlipidemia. Then weight reduction we put as a separate category because you don’t need that much weight loss to see change. The steatosis improvement can happen in just 3% weight loss. You can resolve MASH with 7% weight loss, and you can see fibrosis regression at 10% weight loss. So, you don’t need that much weight loss to see change, which is why there’s so much emphasis placed on weight reduction.

After that, you could think about specific therapies for MASH. Before we had what we currently have, which I’ll talk about in a minute, there was off-label use of pioglitazone and vitamin E. Pioglitazone was helpful for diabetes type II, and it would decrease steatosis as well, but it had many side effects, including weight gain, which was not advantageous, fluid retention, so patients may get heart failure exacerbation. Vitamin E was the second medication that used to be used because it was an antioxidant and considered to reduce oxidative stress in the liver. But it had a ton of risks, like hemorrhagic stroke, prostate cancer. Neither one of them improved fibrosis and that’s what we want, in addition to improving steatosis. That’s why they’ve fallen out of favor.

Now we have 2 FDA-approved medications for steatosis and fibrosis. The first is semaglutide. It’s a GLP1 agonist, and it addresses many concerns—diabetes, it improves cardiovascular risk, liver disease, weight loss.

The great thing about it is it not only improves MASH, which the ESSENCE trial showed with 800 patients who had 63% resolution in MASH; it also showed about 36% improvement in at least one stage of fibrosis. So, it’s doing both; that’s where it’s been really great.

In HIV-specific patients, there have been some studies looking at this medication. In in 2026, the CNICS cohort published a paper showing that they looked at 1,800 people with HIV and noticed they had a decrease in their FIB-4 score by 0.6 points, which is big. That’s in moderate to advanced fibrosis patients. This is the first substantial HIV-specific data that shows improvement in fibrosis for this population.

The other thing we should touch upon with this drug (semaglutide) is the improvement in lipohypertrophy. Patients with HIV have loss of subcutaneous fat, and they accumulate visceral fat. Visceral fat puts them at risk of a lot of cardiovascular diseases. It’s not just general obesity. There was a Lancet paper in 2024. by Eckert et all, and they did a randomized controlled trial with just 108 patients, but it showed that patients were able to decrease their visceral fat by 30% on this drug. They had 10% weight reduction as well, and we know with 10% weight reduction, you can get fibrosis regression. So, this drug is a game changer for everyone, including HIV patients.

The second drug, resmetirom, I don’t have as much knowledge of using this drug. It came out in 2024, but it’s also approved for treating non-sclerotic MASH F2, F3 fibrosis. It is a thyroid hormone receptor beta agonist that is selective to the liver. It is not as favorably looked upon with HIV patients because it’s metabolized using cytochrome 2-C-8 and OAT; it’s an inhibitor of the OAT. Because of that, it is going to cause drug-drug interactions with HIV medications. Semaglutide has peptide-based metabolism, so it’s more favorable for our group.

Chris:
Nice to hear that we have these options. There can sometimes be a tension with any disease that is partly lifestyle-related, and partly structural, partly genetic, partly metabolic, and whether to work on lifestyle change first and how long to do that or jump right to a medication and acknowledge that there are also some important metabolic components that may or may not be outside of some lifestyle changes. How do you approach your patients? What sort of metrics and timelines do you set in terms of change?

Juhi:
One thing I do is try and refer patients to see a dietitian so they can be on the appropriate diet because a lot of patients don’t know what they should even be eating or what diet they should be following. The EASL guidelines like to say that patients should be on the Mediterranean diet. And that all has fun things in it that that patients should follow. But the weight loss strategy does take time. That’s something that you have to counsel your patients. How much time are we going to let this go? Usually, you can see changes in a year if patients are willing. What do you do with your patients?

Chris:
I start with trying to work on lifestyle changes. I may be slower to move to other things, partly because of insurance issues of getting semaglutide, partly because maybe I sometimes underappreciate the medium-term impact and give myself perhaps more time than I should.

I’m open to hearing from you, Juhi, if I should be moving with more urgency in achieving weight reduction and at reducing MASLD or MASH

Juhi:
It’s important that patients know that this takes time, which is why I think it’s important to give it a lot of time. Liver fat doesn’t begin decreasing until patients have had a minimum of 2 weeks, but people will say it can take up to 2 months to even show liver fat decreasing. And it takes 2 to 3 three months to even show that the ALT and AST are responding to the changes that patients are making.

We have seen with FibroScan that CAP scores can begin to improve. Most data say it takes 6 months before you can see an improvement in the CAP score from a FibroScan. That’s I think the point where maybe significant reductions in steatosis can occur. If we’re looking for MASH resolution, patients need to achieve some sort of meaningful weight loss, and that can take 6 to 12 months.

We have also seen that liver stiffness fibrosis measurements can improve, but it takes at least 1 year and can take up to 3 years to see fibrosis improvement and regression if patients can have a sustained 10% weight loss.

Chris:
So certainly thinking about the long range there.

Juhi:
I think it’s important to note, which we haven’t touched upon yet, that in the HIV population, patients can have low BMIs and still have MASLD. That’s unique to HIV patients—they can still have clinically significant fibrosis and have something that’s been called “lean MASLD,” which is low BMI MASLD. That’s interesting because for many MASLD patients, we think of all the traditional metabolic risk factors. But with HIV patients and the fact that they can get this at a low BMI, we have to think about things that they unfortunately can’t control.

The virus itself causes chronic inflammation that can lead to insulin resistance. The HIV can directly infect liver cells, causing fibrinogenesis. There’s the leaky gut that we all know of, you know, the gut barrier disruption that allows for microbial translocation into the liver that causes this pro-inflammatory cytokine release. This can happen even in patients who are virally suppressed. Their own regimens are causing weight gain and fat accumulation that they can’t control. It’s not an indication to switch therapy. I don’t know if you have switched therapy in patients because of their risk of MASLD from their ART.

Chris:
In terms of weight gain, I do not switch. I think the data suggests that although people often do gain weight when they’re switched to an INSTI or TAF, it’s often not because of those agents, but because of the agents they switched from, especially if they switched from an efavirenz/TDF-based regimen.

I have switched people who are on a protease-based regimen, especially an older protease, but even if they’re on boosted darunavir, hoping that can help with some of the metabolic issues. Other than that, I’m not sure really how to manage those lean MASLD patients, but I’m all ears to learn from you.

Juhi:
For lean MASLD, they can still have important factors that we can consider to control. One of them is you can still look for metabolic abnormalities because these patients often have visceral adiposity—the central fat distribution. They could have lipodystrophy from a prior antiretroviral therapy, and they can still also have insulin resistance. So, we can look for those. That would still be an indication for some of these neurotherapies, beyond lifestyle changes.

The other thing that’s interesting in these patients is that they should still exercise. It’s not because we want to lose weight, it’s because it can reduce liver fat. There’s been data that’s shown that aerobic exercise and resistance training in this population can reduce liver fat; that’s what we’re going for in this group. They should still do diet changes because it can improve liver and cardiometabolic health. And these folks can also be considered for semaglutide, resmetirom. And even though they don’t meet those traditional risk factors, they can still have fibrosis.

Chris:
Juhi, thanks so much. In wrap up, for my 41-year-old patient with chronic low-level liver enzyme elevations, it sounds like MASLD is a likely diagnosis, although we don’t have all the testing results back yet.

But the things that put this at the top of the differential is the commonness of this diagnosis, as well as his elevated BMI, suggesting metabolic conditions. Although I do note that there is lean MASLD in people with HIV. Then doing some sort of elastography to get a better sense of both the fatty infiltrates as well as whether he has developed fibrosis is an important staging point and diagnostic point. Finally, starting with some lifestyle modifications, not just weight loss and perhaps a healthier diet that can be guided by a dietitian, butit resistance exercises should be something I also prioritize counseling patients on.

Anything else you wanted to add to that, Juhi?

Juhi:
I think that’s a great start. I think the expectations should be well set in terms of weight loss is not going to happen easily, and it takes time, and it doesn’t take that much weight loss to make a change in the liver’s status of steatosis. I think that makes patients feel a little better because they think they have to lose a ton of weight, but they really just have to lose 3%, and you can improve the fat content in your liver. Which I think feels more achievable.

Chris:
Juhi, this has been really fun, and I have learned a lot, as I always do when you talk about liver disease among people with HIV.

Juhi:
Thank you for having me, this has been fun.

Chris:
To our listeners, thanks for joining in to another episode of Viremic. Please send any comments or questions to viremicpodcast@jh.edu, and we’ll be back in 2 weeks with updates from the AIDS Conference 2026 in Rio, Brazil.

Announcer:
Viremic is sponsored by the Clinical Guidelines Program, a collaborative effort of the New York State Department of Health AIDS Institute and the Johns Hopkins University Division of Infectious Diseases.

Visit the program’s website at: HIVguidelines.org.

Viremic’s case discussions are for informational purposes only and not offered as medical or clinical practice advice for patients or clinicians. Any mention of specific medications or commercially available products is a description of use only, not an endorsement

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