Joined March 2020
28 Photos and videos
A single FibroScan reading has a 35.6% day-to-day coefficient of variance. A reading of 10 kPa = true range of 6.5โ€“13.5 kPa. Prof. Arun Sanyal on what non-invasive liver fibrosis tests actually tell you โ€” and what they don't.
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For resource-limited settings: If FibroScan isn't practically accessible, FIB-4 alone is sufficient to stratify risk and initiate treatment. Don't let lack of elastography delay care for a patient with FIB-4 >1.3.
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Full clip ๐Ÿ‘‡ [YouTube link] Part of a 7-clip Grand Rounds series on MASH best practices with Prof. Arun Sanyal (@VCU). #MASLD #MASH #FIB4 #FibroScan #ELFtest #Hepatology #LiverTwitter #MedTwitter #CME
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"There is no point being obsessed about the liver if the patient is going to die from a heart attack next year. And no point fixing the heart if liver cancer is coming in twelve months." โ€” Prof. Arun Sanyal This is what integrated metabolic care actually means.
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The three-axis model for every MASLD patient: 1๏ธโƒฃ End-organ axis โ€” steatosis โ†’ MASH โ†’ fibrosis โ†’ cirrhosis 2๏ธโƒฃ Aetiological axis โ€” metabolic, alcohol, or combined 3๏ธโƒฃ Competing threat axis โ€” cardiac, renal, glycaemic, cancer, neurocognitive
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The bidirectionality matters too. More metabolic syndrome features = higher liver outcome hazard ratio: 2 features โ†’ HR ~1.5 6 features โ†’ HR ~4.0 The liver drives CRM outcomes. CRM drives liver outcomes. Same biology. Same patient.
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Temporal sequence (CDC data): Obesity surge โ†’ fatty liver โ†’ diabetes The liver gets hit first. T2DM comes later, once beta-cell reserve is lost. If you're screening for diabetes and not for liver disease, you're detecting the downstream event and missing the upstream driver.
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The mechanism isn't theoretical. MASLD upregulates hepatic HMG-CoA reductase SREBP-2 โ†’ excess VLDL โ†’ LDL โ†’ coronary plaque. Most of the body's cholesterol is made in the liver. Fat in the liver = atherogenic factory running in overdrive.
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In >1M patients, MASLD is independently associated with: โ–ธ MACE: HR 1.4 ( 40%) โ–ธ T2DM: HR 2.6 ( 160%) โ–ธ CKD: HR 1.4 ( 40%) โ–ธ Alzheimer's: independently impacted All adjusted for confounders. All from hepatic steatosis alone โ€” before advanced fibrosis.
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We've been treating HTN, T2DM, CKD, HFpEF, and fatty liver as separate problems in the same patient. Prof. Arun Sanyal says they're one disease with multiple organ manifestations. The data are hard to argue with.
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Free live lecture: Management of MASH โ€” Best Practices Speaker: Prof. Arun J. Sanyal, MD (VCU) Past President, AASLD ยท Chair, NIH NASH CRN 500 publications ยท H-index 150 Sat, April 25 ยท 8:00 AM EST Register โ†’ INEDSYS.com #MASH #MASLD #Hepatology #LiverTwitter
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