Hepatology
Expert perspectives on liver disease, viral hepatitis, cirrhosis management, and liver transplantation.
Recent Discussions
In what scenario do you obtain ammonia levels in a patient with cirrhosis?
Very few people check ammonia levels now in patients with cirrhosis. It turns out that it’s not a really accurate measure, and it’s also difficult to draw and get to the laboratory. I think we need to use clinical judgment to diagnose encephalopathy and, of course, the opinion of close relatives.
For suspected drug-induced autoimmune-like hepatitis after the culprit drug is stopped and there is no advanced fibrosis, how do you decide immunosuppression duration and the relapse-free follow-up interval needed to confidently label it DI-ALH rather than classic AIH?
In cases of possible medication-induced AIH, I typically do not start a steroid-sparing agent and attempt to manage alone with corticosteroids. The duration of steroid use is individualized. If there are no steroid side effects or use concerns (i.e., in an older, diabetic patient), we pursue a slowe...
What is your approach in deciding when to start (or briefly defer) anticoagulation in newly diagnosed Budd–Chiari syndrome with large esophageal varices and very recent banding?
Generally, we start IV heparin immediately, even if recent banding performed. Bleeding from varices is caused by transmural pressure, not anticoagulation. So interventions to address portal pressure should be prioritized, including anticoagulation and TIPS as soon as feasible.
What would you your approach to evaluation and monitoring of a patient with elevated AMA and increased immunoglobulins with a low alkaline phosphatase?
The diagnosis of PBC requires 2 of the 3 following elements: Positive AMA, Elevated ALP, and Biopsy consistent with PBC. It is quite possible this person will develop an elevated ALP in time. I would follow liver enzymes yearly, but would not diagnose PBC until the ALP increases. I would start UDC...
How do you differentiate primary from secondary iron overload?
Medical history helps- transfusion history, chronic hemolytic anemias, ESRD on HD, and inflammatory conditions increase the risk of secondary iron. In my practice, I use MRI to help distinguish between primary and secondary iron overload. In primary iron overload, the iron will only be seen in the l...
What is your approach to the inclusion of simultaneous bariatric surgery at time of liver transplant, especially in MASLD/MASH cirrhotics?
Typically, a combined approach with liver transplantation and simultaneous weight loss surgery has been proposed for patients with a BMI above 30 and etiology of liver disease MASH. The workup is very similar to the usual workup of patients with ESLD requiring LT. The procedure of choice has been th...
What is your approach to discussions with patients about the MELD score, its use for prognostication of outcomes and decompensation?
l stress to patients the importance of MELD in predicting pre-transplant survival, and a lot of education is undertaken to apprise the patient and their family about the predictiveness of MELD. I also emphasize to patients that small increases or decreases in MELD may indeed not be indicative of a w...
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 ...
How would you manage a patient who presents with hair loss that began after they started a GLP-1 inhibitor?
If it fits with telogen effluvium, I recommend monitoring. Many patients will improve after this initial shedding and will not have long-term shedding or long-term thinning. If there is any underlying androgenetic alopecia or pattern hair loss, then starting treatment as you normally would is also r...
If a patient has a low ceruloplasmin with normal 24 hours urine copper excretion, how would you go about an approach to evaluation of other disorders of copper metabolism as a cause of liver disease?
It depends on how low the ceruloplasmin is. If the level is undetectable, I would be worried that the 24hr urine result is spurious. In this case, I would repeat the studies, evaluate for KF rings, and consider genetic testing based on how concerned you are for Wilson disease (i.e., family history, ...