Hepatology
Expert perspectives on liver disease, viral hepatitis, cirrhosis management, and liver transplantation.
Recent Discussions
For post-LT patients who improve on PAH therapy, what objective criteria do you require before attempting medication withdrawal, and how do you structure a safe de-escalation plan?
At month 4 post-liver transplant, we routinely repeat a transthoracic echocardiogram to look at the right size and right ventricular function parameters and compare to pre-transplant echoes. We focus on reducing/discontinuing IV prostacyclin medications 1st. The final decision to stop IV prostacycli...
Do you use lactulose in acute liver failure, particularly in patients on continuous renal replacement therapy (CRRT) for ammonia or toxin clearance?
Generally lactulose should be avoided in the situation given limited benefit as well a tendency for ileus in ALF and potential for lactulose to cause bowel distention.
Do you anticipate added benefit of triple agonist therapy for patients with early type 2 diabetes mellitus and MASLD given evidence of glucagon resistance?
I anticipate triple agonist therapy will offer added benefits over dual agonist therapy in patients with diabetes and obesity. There are studies showing greater weight loss with triple agonist therapy with retatrutide (24 to 30%; Jastreboff et al., PMID 37366315, Triumph-4 trial data released by Lil...
What minimum workflow (repeat-testing interval, escalation thresholds, and referral triggers) do you recommend for implementing NIT-based prognostic stratification for MASLD in primary care/endocrinology so that a high-risk result reliably leads to an actionable care pathway?
Typically, I recommend following what the guidelines say, which is to get a FIB-4 score in the endocrine or primary care clinic in patients who have metabolic risk factors. If the FIB-4 score is less than 1.3, you can proceed with an annual FIB-4 score for monitoring. If it ever increases the 1.3 th...
How do you approach the diagnosis of hepatorenal syndrome in a patient with cirrhosis and AKI who has not responded to albumin resuscitation but has a recent nephrotoxic exposure that could explain the renal dysfunction?
If the nephrotoxic exposure (e.g., aminoglycoside) is known to cause ATN, then the findings of low urinary sodium/fractional excretion of sodium, a bland urinalysis, and no structural abnormalities on renal ultrasound should make one consider HRS as the etiology of the AKI. The findings of granular ...
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...
Would you consider the use of prophylactic antibiotics in patients admitted with decompensated cirrhosis with AKI with Cr>1.2, with ascitic fluid protein <1.5 without SBP and/or hyponatremia/Bili >3?
Is this in generalized cases or cases of GIB? If GIB, yes, I would consider it. In just generalized cases, there is no real role for empiric antibiotics.
In young, non-cirrhotic HBV–HDV coinfection with minimal fibrosis on elastography, do you perform lifelong 6-month HCC surveillance based on HDV status alone, or do you modulate surveillance intensity based on fibrosis trajectory and treatment response?
There are two separate issues. The frequency of liver cancer stent with used to initiate. It is not dependent on the risk of cancer. It is related to the doubling times of cancer in the ability to detect cancer when they are small, which is why a six-month interval is always chosen. While the rest ...
How do you determine whether to limit volume removal during therapeutic paracentesis in a patient without acute or chronic kidney disease?
Large volume paracentesis (LVP) can lead to complications such as post paracentesis circulatory dysfunction. In patients who have ongoing acute renal failure, patients with borderline low blood pressure, or in patients who have a history of hyponatremia, LVP should be limited to 5L.
In patients with ascites, how do you decide when carvedilol/NSBBs are still within a safe-and-effective “window”, and which specific thresholds make you hold or discontinue therapy?
I would direct readers to our accompanying editorial that was published along with this paper. Some methodological concerns with this trial including lacking of etiology of liver disease and an open-label design. We know that patients with alcohol associated liver disease can have recompensation wit...