Hepatology
Expert perspectives on liver disease, viral hepatitis, cirrhosis management, and liver transplantation.
Recent Discussions
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...
For cirrhotic patients that we take care of in the community, when should be the optimal timing of referral for liver transplantation aside from the MELD score?
This is a challenging issue for all doctors, both as the referring doctor and the transplant institution. We do not want to evaluate patients who are unlikely to be transplanted, but the MELD score is not an adequate reflection of all patients' disease severity. For our referring doctors, I never ha...
In lean MASLD with sarcopenia or visceral adiposity despite normal BMI, how do you prioritize resistance training/nutrition versus pharmacologic cardiometabolic prevention, and what metrics do you track to decide if the plan is working?
I don't think this is a dichotomous choice, as resistance training and nutrition are complementary to pharmacologic cardiometabolic prevention. From a pharmacologic perspective, I would be cautious with incretin-based therapies as these may worsen sarcopenia, especially in an already lean (i.e., nor...
In patients with MASLD/MASH, do you perform any cardiac testing to create a patient's risk profile, given that cardiac complications are the top cause of morbidity and mortality in this patient population (especially those with advanced fibrosis)?
This is a very important question, particularly because the new ACC guidelines suggest the use of more advanced lipid markers, like Apolipoprotein B and Lipoprotein (a), in individuals who are deemed "high risk" for cardiac disease. Unfortunately, they didn't specifically mention MASLD/MASH as a ris...
Can fatty liver disease present with elevations in alkaline phosphatase without other liver enzyme elevations (AST and ALT)?
It is very atypical but can occur. Patients usually have elevations in aminotransferases (usually ALT higher than AST) and there can be very mild concurrent elevations in alkaline phosphatase. An isolated alkaline phosphatase elevation should however prompt a more extensive serological work up as we...
How do you evaluate and manage acute alcohol withdrawal when symptom-driven protocols are confounded/unreliable?
I developed a structured, objective approach centered on PAWSS risk stratification and standardized mMINDS plus RASS monitoring rather than relying solely on symptom-driven tools like CIWA. At intake, patients with suspected alcohol use disorder undergo PAWSS assessment, baseline mMINDS scoring, RAS...
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.
When pulmonary vasodilator therapy lowers PVR to transplant targets but causes systemic hypotension or worsening renal perfusion in decompensated cirrhosis, how do you adjust therapy (dose reduction, agent change, accepting higher PVR) while preserving both hemodynamic eligibility and overall transplant candidacy?
Fortunately, an uncommon problem, but when it does occur, careful dose reduction of the offending agent may help. Also, I would consider going from any offending oral medication to an inhaled prostacyclin to avoid/minimize systemic effects.
In patients entering AUD treatment who also have obesity/diabetes (a MetALD phenotype), how do you modify your thresholds for fibrosis assessment and for initiating AUD pharmacotherapy and metabolic therapy (e.g., GLP-1 receptor agonists) with the explicit goal of reducing future liver and cardiovascular events?
In patients with a MetALD phenotype entering AUD treatment, I do not lower fibrosis assessment thresholds but rather focus on the higher pre-test probability that they may have significant liver fibrosis; I apply standard guideline-based NIT cutoffs while ensuring timely and complete evaluation. I u...