Hepatology
Expert perspectives on liver disease, viral hepatitis, cirrhosis management, and liver transplantation.
Recent Discussions
At follow-up around 72 weeks, what degree of noninvasive-test nonresponse would prompt you to stop a GLP-1 receptor agonist prescribed specifically for MASH (even if weight and aminotransferases improve), and what objective criteria do you use in the absence of validated futility rules?
When using GLP-1 as liver-directed pharmacotherapy for the treatment of MASH, liver-related endpoints to assess therapeutic efficacy include >/= 30% relative reduction in MRI-PDFF, decrease in ALT >/= 20%, decrease in VCTE >/= 30%, or MRE-LSM >/=20%. Refer to AASLD Guidance for use of semaglutide fo...
In cirrhosis patients with borderline pre-transplant PVR (≈2–3 WU), what additional findings (e.g., mPAP/TPG, pulmonary artery compliance, RV strain on echo, DLCO) prompt you to treat this as higher risk and arrange closer follow-up or PH-center referral rather than reassuring the transplant team?
Agree that recent data do suggest that pulmonary vascular resistance (PVR) 2 to 3 Wood units should be followed carefully in patients who are liver transplant candidates.Using historical data and International Liver Transplant Society (ILTS) Guidelines, mean pulmonary arterial pressure (mPAP) < 35 m...
In PSVD, what specific clinical/imaging or thrombophilia features would make you start pre- emptive anticoagulation before any documented PVT, and how do you monitor for net benefit (thrombosis prevention) versus harm (bleeding) in this population?
Porto-sinusoidal vascular disorder (PSVD) is a more recent umbrella term for a number of manifestations, e.g., nodular regenerative hyperplasia (NRH). There is no pre-emptive benefit to blood thinners. These patients can manifest the usual features of portal hypertension, including portal/splanchnic...
In patients with PBC and possible autoimmune hepatitis overlap on immunosuppression, how do you decide whether improvement in ALT/IgG after starting a PPAR agonist reflects adequate control of hepatitic activity versus nonspecific biochemical improvement, and how (if at all) does that influence immunosuppression adjustments?
It is important to establish how convincing the diagnosis of overlap is. I use several different sources of information: Histology: interface hepatitis with a rich lymphoplasmacytic infiltrate (predominant) plus bile duct injury, or bile duct injury predominant with little to no hepatitis. Serum ma...
Is there a role for use of GLP-1/GIP receptor agonists in the management of substance use disorders, whether or not they meet other inclusion criteria for their use?
Currently, we lack the RCTs to understand the full impact of GLP-1s on SUD outcomes. Most evidence is pre-clinical, observational, suggesting potential reductions in cravings and alcohol use. A recent RCT, lab study of semaglutide in non-treatment-seeking adults with AUD showed decreased alcohol con...
What are some practical tips for when a patient's consistently stated goals of care do not correlate with their actions?
First, it's important to remember that most of us have inconsistent beliefs. We both want to lose weight, and we want to eat chocolate cake; we want to get an A, and we want to go to the party. So when we see inconsistencies in others' beliefs, rather than being judgmental, we should get curious. Ou...
In hospitalized patients treated for presumed overt hepatic encephalopathy who show no meaningful improvement after 48–72 hours of adequate therapy and precipitant management, what is your highest- yield next diagnostic step and what clinical features drive that prioritization?
At this point in the clinical care pathway, I would repeat an infectious workup (blood, urine, diagnostic paracentesis; occult infections are common in our cirrhotic patients) and perform a high-quality multiphasic cross-sectional imaging test to look for portosystemic shunting that could cause refr...
What is your practical approach to monitoring pruritus severity over time in PBC to guide treatment adjustments (e.g., daily vs interval numeric rating scales), especially when follow-up intervals are long and symptom scores can be variable?
I do not use rating scales outside the context of a research protocol. I ask the patient about pruritus, I observe the patient in clinic (e.g., are they scratching), I examine the patient for excoriations, and I follow serum fractionated bile acids. I also tell them to message me if symptoms develop...
How do you choose between a PPAR agonist, obeticholic acid, or a fibrate as second-line therapy in PBC with optimized ursodeoxycholic acid when the immediate priority is clinically significant pruritus but you also want to optimize long-term biochemical risk reduction?
I would prioritize the disease-modifying treatments first for their ability to modify the course of the disease, while at the same time, they may also alleviate pruritus. Elafibranor, for example, has had some antipruritic effects.
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...