Gastroenterology
Expert perspectives on IBD, liver disease, motility disorders, and GI diagnostic and therapeutic procedures.
Recent Discussions
In an infant whose mother resumes TNF inhibitor therapy (e.g., adalimumab, infliximab, certolizumab) after delivery and is breastfeeding, do you recommend delaying live vaccinations?
IgG-based biologic therapies - including TNF inhibitors - are all considered compatible with breastfeeding, since IgG passes only minimally into breast milk. Given these agents are proteins, the minimal drug that is transferred is unlikely to remain intact (or active) with passage through the infant...
What techniques do you find most effective for visualization of rectal disease with intestinal ultrasound?
I am not sure that this is the correct use of "intestinal ultrasound". There is the transabdominal ultrasound technique that is taught to gastroenterologists who can use it at point of care for their UC and CD patients to assess the small bowel and the colon. If you want to specifically look at the ...
At what BMI or waist-circumference threshold do you opt to move from Fibroscan to other NILDA for fibrosis assessment?
The XL-validation study found a liver stiffness measurement (LSM) failure of 1% for the XL and 16% for the M probe, in patients with a BMI of 28 or above. In people with a BMI of 40 or above, the XL-probe failure was 5%, and the best predictor of failure was a skin-to-capsule distance (SCD) ≥25 mm (...
How do you decide between TCAs, SSRIs, SNRIs, Pregabalin & atypical antipsychotics for neuromodulation in IBS patients?
TCAs are the first-line neuromodulator for IBS pain, with SSRIs, SNRIs, pregabalin, and atypical antipsychotics filling specific niches based on predominant symptoms and IBS subtype. TCAs - Strongest evidence for abdominal pain (NNT ~4). Slow GI transit, making them ideal for IBS-D. Start amitriptyl...
Would you consider anti-IL-5 therapy (mepolizumab or benralizumab) to either prevent or treat the more severe manifestations of eosinophilic granulomatosis with polyangiitis, such as "infiltrative" (e.g., cardiomyopathy, pulmonary infiltrates, or gastroenteritis) or "vasculitic" (e.g., neuropathy, palpable purpura, or glomerulonephritis)?
Yes, I would consider early starting biologics for infiltrative EGPA.
In patients with a peptic esophageal stricture and LA Grade D esophagitis, do you dilate at index EGD or treat first with PPI therapy and defer dilation?
In our practice, generally speaking, we prefer to dilate on the repeat endoscopy, once the patient has been on twice daily PPI therapy and once the inflammation/esophagitis is hopefully under control. Overall, inflammation is the enemy of dilation.
For patients with celiac disease confirmed on endoscopy with characteristic endoscopic findings, do you routinely repeat EGD to document healing, or just follow up with serial serologies and repeat EGD only based on the absence of clinical response?
If a patient has been able to effectively avoid gluten and there is no diarrhea, labs are normal, and tissue transglutaminase (TTG) is normal, there is no need for a follow-up endoscopy. Follow-up endoscopy is indicated if there is suspicion that villous atrophy continues.
What antibiotic prophylaxis do you recommend for a cirrhotic patient with an upper GI bleed, if any, in light of the recent meta-analysis published in JAMA Internal Medicine?
This study highlights the lack of high-quality data supporting the recommendation for antibiotic prophylaxis in cirrhosis patients with upper GI bleeding. At my institution, we usually recommend a short course of 3 to 5 days, though some clinicians extend it to 7 days. If there is ongoing bleeding, ...
How would you approach the treatment of a patient with solid food esophageal dysphagia and GERD without a detectable esophageal stricture on upper endoscopy?
I would obtain a barium esophagram followed by high-resolution esophageal manometry and 48-hour esophageal pH testing.
When patients meet criteria for more than one MASH-directed agent class, how do you sequence versus combine therapies in someone with high cardiovascular risk but borderline hepatic severity, and what surrogate-response threshold would make you comfortable escalating to dual therapy?
In a patient with high cardiovascular (CV) risk and only borderline hepatic severity, I generally prioritize a metabolically effective agent first, such as glucagon-like peptide-1 (GLP-1)-based therapy, given the dual CV and hepatic benefit, and reassess liver response before adding liver-directed t...