Hepatology
Expert perspectives on liver disease, viral hepatitis, cirrhosis management, and liver transplantation.
Recent Discussions
In patients with a MetALD phenotype and intermittent or underreported drinking, what triggers you to initiate medications for alcohol use disorder versus intensify fibrosis risk stratification (e.g., elastography or serum fibrosis testing) in routine practice?
GLPs have some benefits in AUD, so I default to that choice. Note: if they have an AUD, they are not metALD; they are ALD with metabolic risk. The AUD is addressed per addiction practice. None of the other AUD drugs would benefit if the patient has not “bought in,” as they won’t take them.
How do you prioritize and time post–liver transplant MASLD surveillance (biopsy vs MRI-based fat quantification vs VCTE/CAP) in recipients at high metabolic risk when recipient factors appear to drive early recurrence risk?
Patients transplanted for Mash have 80-100% recurrence of steatosis (without aggressive weight management), so starting at 1 year and on a 2-3 basis depending on results. This can be VCTE or MRE (what you have access to). Once steatohepatitis is confirmed, depending on stage, it may be q1-2 years. B...
How do you decide between delisting versus keeping a patient inactive (Status 7) when MELD-Na improves meaningfully over time but portal-hypertension complications persist (e.g., intermittent large-volume paracenteses and episodic hepatic encephalopathy)?
The clinical scenario reveals a patient with a condition resulting in ascites requiring paracentesis, which means clinically significant portal hypertension is still present. If the etiology is alcohol, abstinence may result in laboratory improvement, explaining the MELD score improvement. Additiona...
When reassessing PBC (primary biliary cholangitis) as early as 6 months to decide on escalation, what minimum dataset do you need in routine practice (labs, liver stiffness measurement, prognostic score, symptom assessment), and which missing elements most often lead to incorrect escalation decisions?
I encourage you to take a look at the new PBC (primary biliary cholangitis) guidelines, which were just published online. 4. In people with PBC who have inadequate response or are intolerant of UDCA, the societies suggest the use of PPAR agonists (elafibranor, seladelpar) either as add-on therapy to...
How do you decide when to use acid-suppressive medications for GI prophylaxis when patients are on prolonged corticosteroid therapy?
We only use acid-suppressive medications for GI prophylaxis in patients treated with corticosteroids when they have additional risk factors for upper GI bleeding. Risk factors include concomitant NSAID or antiplatelet therapy, history of GI bleeding or peptic ulcer, age over 60 years, prednisone dos...
How do you decide whether to offer acetaminophen to patients with mild and/or resolving acute liver injury?
This is an interesting question, as we often need to turn to something to help with fever or pain, while our inpatients often have a contraindication to NSAIDs, and we typically want to avoid opioids when we can, especially in our liver patients who carry risks of bleeding and encephalopathy. For ac...
How do you decide whether to use pharmacologic VTE prophylaxis in hospitalized patients with decompensated cirrhosis?
For all patients, I begin by using a standard risk prediction tool to determine if the patient is appropriate for pharmacologic VTE prophylaxis. At our institution, the Padua risk prediction tool is embedded in our electronic health record/admission set. Clinical guidelines- including those from the...
In suspected PBC–autoimmune hepatitis overlap, how do you sequence immunosuppression versus escalation of PBC-directed therapy when ALP remains elevated at 6 months but bilirubin is normal?
Assuming the autoimmune hepatitis is under control with normal ALT and AST, if the ALP is still elevated and maybe the GGT as well, then it would be time to add a PPAR. Personally, I start with seladelpar but Elafibranor works just as well and both continue to work for many months continuously norma...
In cirrhosis with suspected HRS-AKI and baseline CKD or chronically elevated creatinine, how do you define a clinically meaningful ‘improvement’ during an albumin trial (over 24–48 hours) to distinguish HRS-AKI from volume-responsive AKI?
The guidelines define it as drop in serum creatinine within to 0.3 mg/dl of baseline creatinine.
When a liver transplant recipient is frail at 12 months, which downstream complications do you monitor more proactively (e.g., falls/fractures, cardiovascular events, infections, renal decline, cognitive decline), and what follow-up cadence do you use in the subsequent year?
There are several reasons why a patient is frail at 12 months post-transplant. One needs to take the reasons and specific treatments into account (rejections, biliary complications and interventions, recurrence of original disease) and also whether frailty was a pre-transplant condition. Certainly, ...