It demands attention, structure, and respect—equal to any pharmacologic therapy.
journals.lww.com/ajg/fulltext...
It demands attention, structure, and respect—equal to any pharmacologic therapy.
journals.lww.com/ajg/fulltext...
🚪 Malnutrition continues beyond the hospital.
The guideline recommends:
• Structured outpatient follow-up
• Reassessment at every transition of care
We must ensure patients do not fall into post-discharge nutritional decline.
🚪 Malnutrition continues beyond the hospital.
The guideline recommends:
• Structured outpatient follow-up
• Reassessment at every transition of care
We must ensure patients do not fall into post-discharge nutritional decline.
⚕️ Adequate nutrition:
• Enhances immune response
• Promotes tissue repair
• Shortens hospital length of stay
• Reduces post-procedural complications
Conversely, untreated malnutrition increases morbidity and mortality—
⚕️ Adequate nutrition:
• Enhances immune response
• Promotes tissue repair
• Shortens hospital length of stay
• Reduces post-procedural complications
Conversely, untreated malnutrition increases morbidity and mortality—
🔬 Patients with the following conditions require early and individualized nutrition strategies:
• Active inflammatory bowel disease (IBD)
• Decompensated cirrhosis
• Severe pancreatitis
• Gastroparesis
• Short bowel syndrome
🔬 Patients with the following conditions require early and individualized nutrition strategies:
• Active inflammatory bowel disease (IBD)
• Decompensated cirrhosis
• Severe pancreatitis
• Gastroparesis
• Short bowel syndrome
🥣 The guideline strongly endorses enteral nutrition (EN) as the preferred method of support.
EN:
• Preserves intestinal mucosal integrity
• Reduces bacterial translocation and infection risk
• Is associated with improved survival
🥣 The guideline strongly endorses enteral nutrition (EN) as the preferred method of support.
EN:
• Preserves intestinal mucosal integrity
• Reduces bacterial translocation and infection risk
• Is associated with improved survival
✅ Use validated tools like:
• MUST (Malnutrition Universal Screening Tool)
• MST (Malnutrition Screening Tool)
• NRS-2002
Positive screens demand a formal nutritional assessment by a Registered Dietitian Nutritionist
✅ Use validated tools like:
• MUST (Malnutrition Universal Screening Tool)
• MST (Malnutrition Screening Tool)
• NRS-2002
Positive screens demand a formal nutritional assessment by a Registered Dietitian Nutritionist
⚖️ A low or high BMI tells an incomplete story.
The guideline emphasizes the GLIM framework, which combines:
• Phenotypic signs (e.g., weight loss, muscle wasting)
• Etiologic triggers (e.g., inflammation, reduced intake)
⚖️ A low or high BMI tells an incomplete story.
The guideline emphasizes the GLIM framework, which combines:
• Phenotypic signs (e.g., weight loss, muscle wasting)
• Etiologic triggers (e.g., inflammation, reduced intake)
📉 Nearly half of all hospitalized GI patients meet criteria for malnutrition.
⚠️ But less than 10% are formally diagnosed.
The guideline urges us to screen universally, not selectively. We cannot treat what we do not recognize.
📉 Nearly half of all hospitalized GI patients meet criteria for malnutrition.
⚠️ But less than 10% are formally diagnosed.
The guideline urges us to screen universally, not selectively. We cannot treat what we do not recognize.
Decompensation in cirrhosis is often viewed as an unpredictable turning point.
But this study shows that measurable systemic inflammation builds silently in the background—offering a potential window for risk stratification and early intervention, even in the compensated stage.
Decompensation in cirrhosis is often viewed as an unpredictable turning point.
But this study shows that measurable systemic inflammation builds silently in the background—offering a potential window for risk stratification and early intervention, even in the compensated stage.
📈 Worsening inflammation preceded the first clinical decompensation
🧪 IL-6 and CD163 may serve as early biomarkers to flag patients at highest risk
👀 A potential opportunity for earlier intervention in compensated cirrhosis
📈 Worsening inflammation preceded the first clinical decompensation
🧪 IL-6 and CD163 may serve as early biomarkers to flag patients at highest risk
👀 A potential opportunity for earlier intervention in compensated cirrhosis
✔️ LPS and FABP were elevated, pointing to early gut barrier dysfunction and bacterial translocation
✔️ LPS and FABP were elevated, pointing to early gut barrier dysfunction and bacterial translocation
✔️ Patients with CSPH (but still compensated) had higher IL-6 and CD163 levels than patients with subclinical PH and healthy controls
✔️ Patients with CSPH (but still compensated) had higher IL-6 and CD163 levels than patients with subclinical PH and healthy controls
🧪 IL-6 (systemic inflammation)
🧪 CD163 (macrophage activation)
🧪 LPS (bacterial translocation)
🧪 FABP, haptoglobin (gut barrier integrity)
🧪 IL-6 (systemic inflammation)
🧪 CD163 (macrophage activation)
🧪 LPS (bacterial translocation)
🧪 FABP, haptoglobin (gut barrier integrity)
But what flips the switch from compensated to decompensated?
💡 This study followed 164 patients with clinically significant portal hypertension (CSPH)—defined as HVPG >10 mmHg—for a median of 37 months.
But what flips the switch from compensated to decompensated?
💡 This study followed 164 patients with clinically significant portal hypertension (CSPH)—defined as HVPG >10 mmHg—for a median of 37 months.
I’m training in South Texas, where cirrhosis is so common there’s a saying:
“Every thrombocytopenia is liver disease until proven otherwise.” 🫣
Thank you for highlighting this!
I’m training in South Texas, where cirrhosis is so common there’s a saying:
“Every thrombocytopenia is liver disease until proven otherwise.” 🫣
Thank you for highlighting this!
It’s humbling to go from seeing iCCA in real patients…
To reading how their tumors behave at the cellular level 🧫
This study helped me connect clinical cases to the science behind them.
📖 Baretti et al., Hepatology Communications (2025)
#GIOnc #HepOnc #IMResidency
It’s humbling to go from seeing iCCA in real patients…
To reading how their tumors behave at the cellular level 🧫
This study helped me connect clinical cases to the science behind them.
📖 Baretti et al., Hepatology Communications (2025)
#GIOnc #HepOnc #IMResidency
So what does this mean for treatment? 💭
👉 FGFR2+ tumors may need FGFR-targeted therapy first to help the immune system get in
👉 IDH1+ tumors might benefit from strategies that help immune cells work together better
So what does this mean for treatment? 💭
👉 FGFR2+ tumors may need FGFR-targeted therapy first to help the immune system get in
👉 IDH1+ tumors might benefit from strategies that help immune cells work together better
🔥 IDH1-mutant tumors:
More fibroblasts (structural/stromal cells)
CD4+ T cells were closer to tumor cells
But CD8+ and CD4+ T cells were not close to each other
So… some immune engagement, but not fully coordinated.
🔥 IDH1-mutant tumors:
More fibroblasts (structural/stromal cells)
CD4+ T cells were closer to tumor cells
But CD8+ and CD4+ T cells were not close to each other
So… some immune engagement, but not fully coordinated.
What are PMN-MDSCs? 🤔
Polymorphonuclear myeloid-derived suppressor cells
They:
🛑 Suppress T cell activity
🧪 Release nitric oxide + enzymes
🚷 Block the immune response
Tumors with lots of these cells often resist immunotherapy.
What are PMN-MDSCs? 🤔
Polymorphonuclear myeloid-derived suppressor cells
They:
🛑 Suppress T cell activity
🧪 Release nitric oxide + enzymes
🚷 Block the immune response
Tumors with lots of these cells often resist immunotherapy.
🧊 FGFR2+ tumors:
Had fewer CD8+ T cells (the “killer” T cells)
Had more PMN-MDSCs (immune-suppressive cells)
Immune cells were far from tumor cells
This pattern = “cold tumor” → harder to treat with immunotherapy.
🧊 FGFR2+ tumors:
Had fewer CD8+ T cells (the “killer” T cells)
Had more PMN-MDSCs (immune-suppressive cells)
Immune cells were far from tumor cells
This pattern = “cold tumor” → harder to treat with immunotherapy.