Rishika Trivedi

Honored and grateful to submit my application for GI fellowship ✅

Thank you to the mentors who saw something in me and the patients who taught me so much 🤝

Wishing everyone a great match! 💙
#GastroenterologyFellowship #WomenInGI #Match2026

Just wow. A rare cause of ascites that I honestly wouldn’t have thought of without this case.

📚 Medicine always keeps us on our toes.

#LiverSky #GastroSky #MedTwitter #Hepatology #AscitesPearls

ACG Clinical Guideline: Malnutrition and Nutritional... : Official journal of the American College of Gastroenterology | ACG arcopenia in patients with advanced liver disease. Patients with cirrhosis and/or alcohol-associated hepatitis should be assessed for malnutrition because it adversely affects patient outcomes includi...

Reading this ACG guideline was a reminder that nutrition is a form of precision medicine.
It demands attention, structure, and respect—equal to any pharmacologic therapy.

journals.lww.com/ajg/fulltext...

7 | Discharge is not the endpoint of nutritional care.
🚪 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.

6 | Nutrition is a treatment with measurable impact.
⚕️ Adequate nutrition:
• Enhances immune response
• Promotes tissue repair
• Shortens hospital length of stay
• Reduces post-procedural complications
Conversely, untreated malnutrition increases morbidity and mortality—

5 | High-risk GI populations require proactive intervention.
🔬 Patients with the following conditions require early and individualized nutrition strategies:
• Active inflammatory bowel disease (IBD)
• Decompensated cirrhosis
• Severe pancreatitis
• Gastroparesis
• Short bowel syndrome

4 | When in doubt, feed the gut.
🥣 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

3 | Nutrition screening should be systematic and team-driven.
✅ 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

2 | Nutritional assessment is more than a number on a scale.
⚖️ 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)

1 | Malnutrition is widespread—yet underdiagnosed.
📉 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.

Malnutrition is not a side issue—it is a systemic threat to patient recovery.
The 2025 ACG Guideline presents a bold redefinition of nutritional care in gastrointestinal disease.
Here is a detailed exploration of the clinical insights that resonated most with me:
🧵 #ACG2025 #Malnutrition #GI

#Cirrhosis
#LiverDisease
#PortalHypertension
#SystemicInflammation
#Biomarkers

5. Why this matters:
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.

4. 🚨 Clinical takeaway:
📈 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

3. ✔️ IL-6 and CD163 levels were even higher in those who later decompensated
✔️ LPS and FABP were elevated, pointing to early gut barrier dysfunction and bacterial translocation

3. Key findings:
✔️ Patients with CSPH (but still compensated) had higher IL-6 and CD163 levels than patients with subclinical PH and healthy controls

2. Biomarkers were measured at baseline, 1 year, and 2 years:
🧪 IL-6 (systemic inflammation)
🧪 CD163 (macrophage activation)
🧪 LPS (bacterial translocation)
🧪 FABP, haptoglobin (gut barrier integrity)

1. Cirrhosis is silent—until it isn't.
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.

🌟 New insight in compensated cirrhosis!
📌 Systemic inflammation may not just be a bystander—it might be the driver of decompensation.

🧵 Short thread on a high-impact study from JHEP Reports (Feb 2025):
"Progressive systemic inflammation precedes decompensation in compensated cirrhosis"

This really resonates.💡

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!

9/9
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

8/9
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

7/9
🔥 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.

6/9
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.

5/9
🧊 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.

4/9
🔬 They used CODEX imaging, a technique that shows:
✅ Which immune cells are in the tumor
✅ How many
✅ Where they are located

Like a tumor map, at the single-cell level 🗺️
Really helpful for studying how the immune system interacts with cancer.

3/9
🧬 The study grouped 24 iCCA tumors by mutation:
1️⃣ FGFR2 fusion
2️⃣ IDH1 mutation
3️⃣ Wild-type (no FGFR2/IDH1)

Each group had a different immune cell pattern

2/9
📖 Article:
“Deep immune profiling of intrahepatic cholangiocarcinoma with CODEX multiplexed imaging”
by Baretti et al., Hepatology Communications, 2025

It looks at how mutations in iCCA (intrahepatic cholangiocarcinoma) affect the tumor immune microenvironment (TME).
#GIOnc #MedTwitter

1/9
Just finished my inpatient GI rotation 🏥
From heavy diverticular bleeds 💥 to gallstone pancreatitis 🫨 and even a duodenal tumor accessed via EUS 🔄
But the cholangiocarcinomas... they stayed with me.

☕ This morning while enjoying Chai, I read something that pulled me in. Let’s explore. 🧵

Join ACG for a free online concert this Wednesday, 3/26 at 8pm ET!

Tune It Up: A Concert To Raise Colorectal Cancer Awareness

Blues Traveler and Adam Lambert along with an incredible array of artists!

The concert will stream free at gi.org/Concert/

#GastroSky #ColorectalCancerAwarenessMonth