劉亚鹏

愿君多采撷 此物最想思

[วท ขอเล่า @drwit117]

มะเร็งปอดระยะ 4
มียีนส์กลายพันธุ์ EGFR
เคสนี้รักษาด้วย osimertinib ผ่านไป 6 สัปดาห์ ตอบสนองดีเลย

[无羁😎 @heijix86]

คู่มือป้องกันการหกล้มในผู้สูงอายุ
https://t.co/DvtDDKpIRQ

[Alí Sebastian Meza @AliSMV7]

Sepsis in Frail Older Adults: Tailored Antimicrobial Stewardship and Individualized Care Approach

https://t.co/MOxCEHnjkD

[无羁😎 @heijix86]

Eisai Neuro Tutorial 2026 🩵
Day1 stroke, pain
Day2 dementia, sleep disorder
Day3 movement, epilepsy
Day4 neuroimmuno, neuromuscular
https://t.co/nL02S36Xxp

[无羁😎 @heijix86]

สไลด์งานประชุมโรคลมชัก 2568
https://t.co/XcScxEjX80

[无羁😎 @heijix86]

คู่มือการประเมินความพิการ 2568
https://t.co/HHc4uQdbS5

[无羁😎 @heijix86]

ประชุมออนไลน์ ฟรี
11 กค 69 >>> https://t.co/CJoeJMCfrQ

[劉亚鹏 @Jamespraschya]

@heijix86 สุขสันต์วันเกิดนะครับพี่เฮง มีความสุขมากๆนะคับ

[Internal Medicine @pgMedicine]

New 2025 TB Guidelines: 🩺

Old: 6 months (2HRZE/4HR)

New: 4 months (2HPZM/2HPM)

Major Changes:
❌ Ethambutol REMOVED
✅ Moxifloxacin ADDED
🔄 Rifampicin ➡️ Rifapentine
⌛ Duration: 6mo ➡️ 4mo

[Dr. FEVI🫀🩺 @javier20ch]

Terapia de Resincronización Cardíaca. 🫀⚡️
🔴La disincronía eléctrica (BRIHH) está presente en 20–30% de los pacientes con IC-FEVI reducida, y acelera la progresión de la enfermedad. La TRC restaura la activación ventricular sincrónica, algo que el tratamiento farmacológico no puede lograr. ⚡️♻️
🔴Indicaciones clave: IC sintomática pese a tratamiento óptimo + FEVI ≤35% + QRS ≥130 ms (particularmente BRIHH). También considerar en pacientes que requerirán estimulación ventricular crónica, ya que el pacing del VD puede inducir disfunción sistólica. ✍️🏻🧐⚡️
🔴Beneficio clínico sólido: ⤵️mortalidad (HR 0.66) y ⤵️hospitalizaciones por IC.
🔴Estrategias:
✔️Estimulación biventricular (estándar): efectiva, pero ~30% no responden.
✔️Estimulación del sistema de conducción (His/rama izquierda): más fisiológica, ligero ⤴️ de FEVI y ⤵️ hospitalizaciones.
🔴La referencia tardía se asocia a peores desenlaces. Complicaciones: 5–8%, principalmente relacionadas a electrodos. ⚠️💥

📜🆓️⤵️ Review 2026 @JAMANetwork
doi: 10.1001/jama.2026.4893
https://t.co/98cPKBO1N1

[Medicina Interna HCSBA @MHcsba]

JAMA 2026: Terapia de resincronización cardiaca

doi:10.1001/jama.2026.4893
#MedEd #MedTwitter #MedX

[CME INDIA @CMEINDIA1]

“Semaglutide shifts MASH therapy from glycemic control to multi-organ disease modification—but fibrosis still demands time and combination strategy.”

Semaglutide in MASH with F2–F3 Fibrosis (ESSENCE Trial Perspective)
🔬

MASH with F2–F3 fibrosis represents a critical therapeutic window, where timely intervention can prevent progression to cirrhosis, HCC, and liver-related mortality.

💉 Semaglutide: Disease-Modifying Potential

Once-weekly semaglutide 2.4 mg demonstrates true disease-modifying signals, not just metabolic improvement.

🧠 Histological Efficacy (Key Takeaway)

Semaglutide significantly increases:

Resolution of steatohepatitis without worsening fibrosis (~2/3 vs ~1/3 placebo)

≥1-stage fibrosis improvement (~1/3 vs ~1/5 placebo)
👉 Number needed to treat (NNT):

~3–4 for MASH resolution

~6–8 for fibrosis improvement

⚖️ Weight Loss: The Central Driver

Semaglutide induces ~10–11% weight loss vs ~2% with placebo, a threshold strongly linked to:

MASH resolution

Fibrosis regression

👉 ≥10% weight loss remains a biological pivot point in MASLD management.

❤️ Cardiometabolic Amplification

Semaglutide delivers multi-organ protection, including:

HbA1c reduction

Blood pressure lowering

Improved lipid profile

Reduced inflammatory markers (hs-CRP)

👉 Important: Cardiovascular disease remains the leading cause of mortality in MASLD.

🧪 Non-Invasive Markers Align with Histology

Consistent improvements seen in:

ELF score

VCTE (FibroScan stiffness)

PRO-C3

FAST score

ALT/AST

👉 This supports a future biopsy-sparing strategy in MASH monitoring.

⚙️ Mechanistic Insight (Very Important)

Semaglutide works via dual pathways:

Weight-dependent effects (dominant)

Reduced caloric intake

Improved insulin sensitivity

Reduced adipose inflammation

Weight-independent (partial)

Anti-inflammatory pathways

Gut–liver axis modulation

👉 However:
GLP-1 receptors are not expressed in hepatocytes, suggesting indirect hepatic benefits.

⚠️ Fibrosis: The Hard Endpoint

Fibrosis improvement is:

Slower and less weight-dependent

Likely requires longer duration and targeted antifibrotic pathways

👉 Cirrhosis (F4) shows limited reversibility with semaglutide alone.

🛡️ Safety Profile

GI side effects (nausea, vomiting) are common but transient

No major hepatotoxicity signal

Similar serious adverse events vs placebo

👉 Caution:

Gallbladder disease

Rare pancreatitis

🔄 Therapeutic Positioning

Semaglutide is best suited for:

Obese / T2DM phenotype MASH (commonest in India)

High cardiometabolic risk patients

🔬 Future Strategy: Combination Therapy

Semaglutide (systemic metabolic drug) + Resmetirom (liver-directed THR-β agonist) offers:

Upstream metabolic unloading + direct hepatic antifibrotic action

👉 Likely future paradigm:
Multi-target therapy for MASLD

❗ Clinical Gaps

Long-term outcomes (cirrhosis, HCC, mortality) not yet confirmed

Limited data in:

Lean MASH

Diverse ethnic populations

Need for omics-based patient stratification

🔴 CME INDIA key point

“Semaglutide shifts MASH therapy from glycemic control to multi-organ disease modification—but fibrosis still demands time and combination strategy.”

📚 Key Reference

Pirola CJ, Sookoian S. Semaglutide in MASH with F2–F3 fibrosis: ESSENCE phase 3 perspective. Metab Target Organ Damage. 2026.

https://t.co/KG024CiBtF

[CME INDIA @CMEINDIA1]

MASLD in elderly is not just fatty liver—it is a frailty–metabolic–cardiovascular syndrome where fibrosis and function matter more than fat.

Ageing Liver & MASLD (BMJ Frontline Gastroenterology 2026)

MASLD now affects ~25% adults, and burden is rising sharply in ≥65 years, with distinct phenotype compared to younger patients.

Elderly MASLD is a “multimorbidity disease”—frequently coexists with CVD, T2DM, sarcopenia, frailty, making outcomes more severe despite slower disease kinetics.

Pathophysiology is age-driven:
Telomere shortening, mitochondrial dysfunction, impaired autophagy, epigenetic drift → accelerated fibrosis and HCC risk.

Sarcopenia + visceral adiposity (sarcopenic obesity) is a key driver of adverse outcomes—not BMI alone.

Diagnosis is tricky in elderly:
Normal ALT is common even in advanced disease → do not rely on transaminases.

FIB-4 overestimates fibrosis in elderly → use age-adjusted cut-off (<2.0 = low risk in ≥65 yrs).

Best practical approach (Primary care):
FIB-4 → Elastography → Hepatology referral if high risk.

Fibrosis stage—not steatosis—is the strongest predictor of mortality, with exponential rise in risk from F2 onwards.

CVD is the leading cause of death in MASLD, exceeding liver-related mortality.

HCC risk increases with age, even without cirrhosis in selected patients—questioning current surveillance thresholds.

Lifestyle remains cornerstone, but in elderly:
Avoid aggressive weight loss → risk of malnutrition + muscle loss.

Target strategy in elderly MASLD:
Moderate weight loss + high-protein diet + resistance training to preserve lean mass.

Exercise is disease-modifying:
+2500 steps/day → ~47% reduction in MASLD risk.

Emerging therapies:
Resmetirom and GLP-1 RAs show promise, but elderly underrepresented in trials → evidence gap.

Key Clinical Insight:

“Younger patients lose more life-years, but elderly patients have higher event severity due to frailty and comorbidity load.”
@C_V_Schneider @schattenbergJ

@PhilSmithIsBack @OTavabie @dr_aditi_kumar @TrevorTabone @eathar_s @IrenePerezMD @KGananandan @zare_benjamin @medicalreg @dtleiberman @BASLedu @BSGtrainees @ulstergastro #GITwitter #GIX

https://t.co/cgH6vTJFUH

[Dr. Chokri Ben Lamine @abouabdrahman0]

📊 FibroScan Interpretation — Quick Pearls

🟢 Liver Stiffness (kPa) = Fibrosis Stage
➡️ F0–F1 🟢 → No / Mild fibrosis
➡️ F2 🟡 → Moderate fibrosis
➡️ F3 🟠 → Advanced fibrosis
➡️ F4 🔴 → Cirrhosis

📌 Cutoffs (approx):
🟢 ~7 kPa → F1
🟡 ~9.5 kPa → F2
🟠 ~12.5 kPa → F3
🔴 >12.5–14+ kPa → F4 (cirrhosis range increases progressively)

⚠️ Interpretation caveats:
🔸 Inflammation ↑ → falsely ↑ stiffness
🔸 Cholestasis / congestion → falsely ↑
🔸 Post-prandial state → ↑ readings → fast ≥3h

🟡 CAP Score (dB/m) = Steatosis
➡️ 238–260 → S1 🟡 (11–33% fat)
➡️ 260–290 → S2 🟠 (34–66% fat)
➡️ >290 → S3 🔴 (≥67% fat)

📌 Clinical use:
🧠 Combine stiffness + CAP → fibrosis + steatosis phenotype
🧪 Always correlate with ALT/AST, platelets, imaging, etiology

🚨 High-risk flags:
🔴 F3–F4 → screen for portal HTN + HCC
🔴 Rapid rise → reassess cause (flare, congestion, drug)

#FibroScan #Hepatology #LiverFibrosis #NAFLD #Cirrhosis #KFSHRC

[无羁😎 @heijix86]

IMBR Berlin 2026 🩵
https://t.co/TmD1qTvv0V

[Alí Sebastian Meza @AliSMV7]

Sulbactam–Durlobactam for Carbapenem-Resistant Acinetobacter baumannii–calcoaceticus Complex

https://t.co/RecU8o0nvT

[Dr Rani Khatib FESC @DrRaniKhatib]

Resistant Hypertension
Hypertension on both sides of the Atlantic.
#ESCPrev26

[CME INDIA @CMEINDIA1]

Time to Measure

In primary aldosteronism, chasing renin may mislead—Angiotensin II tells the real story

Angiotensin II Measurement in Primary Aldosteronism Screening

Core Concept

Primary aldosteronism (PA) is a renin-suppressed, aldosterone-driven state, but Angiotensin II (Ang II) is the true proximal driver of aldosterone secretion, not renin itself.

Why Renin Alone Is Inadequate

Plasma renin is not a direct surrogate for Ang II levels due to downstream enzymatic modulation (ACE, degradation pathways).

Discordance exists:
→ Renin may be low/high, but Ang II may not parallel it

Therefore, ARR (aldosterone–renin ratio) can misclassify physiology in selected patients.

Pathophysiological Insight

Angiotensin II directly stimulates zona glomerulosa → aldosterone secretion

Additional modulators:
→ ↑ K⁺, ACTH, adipokines (positive)
→ ANP, ↓ K⁺ (negative)

Thus, aldosterone regulation is multifactorial—not renin dependent alone

Key Paradigm Shift

Traditional model:
→ Renin → Ang I → Ang II → Aldosterone

Emerging insight:
→ Measuring Ang II provides a closer estimate of aldosterone drive than renin

Clinical Implication

In suspected PA:

ARR remains first-line screening tool

But consider Ang II when:

Discordant ARR results

Atypical physiology (e.g., CKD, ACE variability, medications)

Unexplained aldosterone excess despite low/normal renin

Timing Matters (Practical Pearls)

Hormonal assays (renin, aldosterone ± Ang II):

Morning sampling preferred (8–10 AM)

Patient ambulant ≥2 hours, seated 5–15 min before sampling

Ensure:

Normal potassium

Liberal salt intake

Drug interference minimized

Why Angiotensin II Measurement Matters Now

Advances in mass spectrometry-based peptide assays allow accurate Ang II quantification

Helps distinguish:

True autonomous aldosterone secretion (PA)

vs

RAAS-driven secondary hyperaldosteronism

CME INDIA – Takeaways

Renin ≠ Ang II → do not equate physiology blindly

Ang II is the real effector hormone in aldosterone regulation

ARR is screening—not pathophysiology

Consider Ang II measurement in complex or discordant cases

Standardize timing, posture, and biochemical conditions before testing

Tagline

➡️ “In primary aldosteronism, chasing renin may mislead—Angiotensin II tells the real story.”

https://t.co/3VCJ89HNv1

[BennieRule ^w^ | #ไอศูรย์ราชัน #วรรณคดีติดเกาะ🌈 @Bennie_Rule]

ประชาสัมพันธ์ #ไอศูรย์ราชัน พีเรียดอาเซียนแฟนตาซี เรื่องราวของเจ้าชายมังสามเกียดแห่งหงสาวดี ทำสัญญากับผีนัตลี้ลับย้อนเวลากลับมาในวัยเยาว์เพื่อแก้ไขโชคชะตา ถ้าท่านใดสนใจอาเซียนศตวรรษที่16 ภูตผี อาหาร การตื่นรู้ทางวิทยาศาสตร์ ดนตรี การค้า วิถีชีวิต ขอเชิญลิ้มลองแลกทัศนาครับ✨️🙏🏻💖

[Eryy eyy @pearlyx_z]

งาน commission ปกนิยาย ค่ะ 😭💕