Hepatology
Expert perspectives on liver disease, viral hepatitis, cirrhosis management, and liver transplantation.
Recent Discussions
How do you decide between immediate liver transplant referral versus a time-limited “recompensation observation” period in patients with alcohol-related cirrhosis who present with a first decompensation and achieve early, verified abstinence?
It can be difficult to differentiate the two, so one never errs on the side of evaluating the patient for a transplant and then getting to know them and their support system a bit better. The more data and time you have to make such a decision, the better it is. Often, the natural history of the dis...
Are there clinical contexts where you would not use spleen stiffness to drive endoscopy/NSBB decisions because you suspect the SSM signal is dominated by splenic congestion/hyperdynamic circulation rather than portal pressure, and how do you identify those contexts at the bedside?
Spleen stiffness measurements have recently become available when the technology was added to the vibration-controlled transient elastography equipment that measures liver stiffness. It is not invasive, and elevated spleen stiffness has been added to the Baveno criteria and other professional societ...
How do you triage PSC patients with multifocal, predominantly intrahepatic dominant strictures and recurrent cholangitis (without advanced cirrhosis) between ERCP (targeted minimal-contrast drainage), percutaneous drainage, and early transplant evaluation?
A lot to untangle from this one question: Recurrent cholangitis is an indication for liver transplantation even in the absence of cirrhosis. Once a patient has had two episodes of cholangitis within a year, that triggers a transplant evaluation in my practice. The challenge will be in the patient's...
In severe alcohol-associated liver disease with limited documented abstinence, what prospectively measurable psychosocial signals are sufficient for you to support expedited listing (treatment engagement, insight, caregiver reliability, objective toxicology strategy), and which findings reliably predict unacceptable relapse risk in your experience?
I will give an answer that is a bit more subjective than objective. There are certainly validated scoring systems (Stanford Integrated Psychosocial Assessment for Transplantation [SIPAT], Sustained Alcohol Use Post-Liver Transplant [SALT]) that can help assess psychosocial risk in all patients, espe...
In MASLD patients with high cardiometabolic risk who already meet a clear metabolic indication for a GLP-1 receptor agonist, how much fibrosis-stage certainty do you require before treating it as liver-directed MASH therapy (and documenting/monitoring it as such), versus starting for metabolic benefit and using NIT trends to decide on subsequent biopsy or add-on liver-specific therapy?
If you have the option to get it for type 2 diabetes, it is often more likely to be approved by insurance. There would be no fibrosis requirements and no follow-up on continuing to prove fibrosis staging requirements. Whoever submits for prior authorization can mention if the patient is stage 2 to 3...
How would you treat a patient with alcoholic cirrhosis and IgA nephropathy with high risk features including nephrotic range proteinuria, microscopic hematuria, and declining eGFR?
Cirrhosis is a well-known cause of secondary IgA nephropathy. Impaired removal of IgA-containing complexes by the Kupffer cells in the liver is thought to predispose to IgA deposition in the kidney (Amore et al., PMID 8302021). As in primary IgAN, polymeric IgA1 appears to be the dominant IgA isofor...
Is there a role for nitazoxanide for treatment of norovirus gastroenteritis in immunocompromised patients?
There is no good-quality evidence supporting a role for nitazoxanide for treatment of norovirus gastroenteritis in immunocompromised patients. The efficacy of nitazoxanide in viral gastroenteritis is supported by a small manufacturer-sponsored randomized, double-blind trial in non-immunocompromised ...
For patients with mixed metabolic- and alcohol-associated liver disease (or ongoing moderate alcohol use) who otherwise meet presumed F2–F3 criteria by NITs, how do you operationalize initiation and monitoring of a GLP-1 receptor agonist, particularly how you interpret NIT trends when alcohol intake (and inflammation) may be changing during treatment?
In patients with MetALD, I’ll initiate a GLP‑1 RA once F2-F3 risk is supported by concordant NITs, but only after establishing a stable baseline that includes recent alcohol intake and inflammatory markers (e.g., GGT). For monitoring, I interpret NIT trends cautiously. Early improvements (<6M) in VC...
In routine practice where repeat biopsy and outcomes data are not available, what longitudinal NIT pattern (e.g., VCTE/ELF ± MRI-PDFF/ALT trajectory) do you consider sufficient to continue semaglutide specifically for MASH, and what trajectory would trigger a “futility” decision to stop or switch despite weight loss?
Aligned with clinical practice guidance that GLP-1 RAs primarily improve steatosis and inflammation rather than established fibrosis, I look for a concordant metabolic response, including ≥30% PDFF reduction with ALT improvement of ≥17 IU/L or ≥20%, alongside at least stability or modest improvement...
What is your approach to initiating naltrexone in patients with alcohol use disorder and co-occurring liver disease?
In patients with AUD and co-occurring liver disease, I think the hepatotoxicity concerns around naltrexone have historically been overstated relative to both the actual evidence and the hepatic risk of ongoing alcohol exposure itself. The original 1980s data that triggered the FDA hepatotoxicity war...