Prashant chotalia

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Prashant chotalia

Prashant chotalia

@Drpvc

Rheumatologist. Cricket and Movie fan.

Surat, India Katılım Nisan 2010
493 Takip Edilen489 Takipçiler
Prashant chotalia retweetledi
Dr.Mukesh , MD , DM
Dr.Mukesh , MD , DM@dr_immuno29·
🩸 HES (Hypereosinophilic Syndrome) — Must-Know Points • Define: AEC ≥1.5×10⁹/L (×2) + organ damage • Biggest gap → Delayed diagnosis = preventable morbidity • First rule: Exclude secondary causes (parasites, drugs/DRESS, allergy, cancer) • Classify fast: 👉 Reactive 👉 Clonal/neoplastic 👉 Lymphocytic 👉 Idiopathic / Familial • Core work-up: ✔ CBC + smear ✔ Tryp­tase / Vit B12 ✔ FIP1L1-PDGFRA (priority) ✔ PDGFRB / FGFR1 / JAK2 ✔ Flow cytometry (L-HES) • Organs at risk (screen ALL): 🫀 Heart (ECG + Echo mandatory) 🫁 Lung (HRCT ± BAL) 🧴 Skin (most common presentation) 🍽 GI (biopsies if suspected) • Cardiac HES = necrosis → thrombosis → fibrosis Often silent early → image even if asymptomatic • Treat early to prevent fibrosis & thrombosis 1️⃣ Steroids = first line 2️⃣ Imatinib (PDGFRA/B+) 3️⃣ Anti-IL5 biologics (e.g. mepolizumab) → Precision > blanket therapy • GI eosinophilia alone = possible organ-restricted HES → close follow-up • Principle: Phenotype + genotype + organ burden = therapy 🎯 Goal: shorten diagnostic delay + personalize treatment + protect organs. 📄 Cells 2024;13:1180 DOI: 10.3390/cells13141180
Dr.Mukesh , MD , DM tweet mediaDr.Mukesh , MD , DM tweet mediaDr.Mukesh , MD , DM tweet mediaDr.Mukesh , MD , DM tweet media
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Ravisutanjani
Ravisutanjani@Ravisutanjani·
@Padhi_hui_ladki Unlikely, try RailOne though Slightly better than the old app, also login at 9:57-9:58 and hit the refresh button at sharp 10:00 and use the Master list.
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Nishi Maheshwari
Nishi Maheshwari@Padhi_hui_ladki·
The day IRCTC does not fail at Tatkal time, is when I will consider India to be Viksit desh.
Nishi Maheshwari tweet media
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Prashant chotalia retweetledi
Dr Abhilasha Manwatkar (AIIMS Nagpur)
Oral ulcers in patients with autoimmune rheumatic diseases (AIRD): a practical clinical approach 1️⃣ What exactly is an aphtha? Aphthae are true ulcers there is complete loss of epithelial continuity, often extending into underlying connective tissue. This differentiates them from superficial erosions. They may be painful or painless and are often self-limiting. 2️⃣ Typical sites of involvement Most aphthous ulcers occur on non-keratinized mucosa: • Buccal mucosa • Inner lips • Soft palate • Ventral tongue • Floor of mouth However, involvement of keratinized mucosa (gingiva, hard palate) or dorsal tongue should prompt evaluation for systemic disease. 3️⃣ Recurrent Oral Aphthosis (ROA) • Affects ~20% of the general population • More common in women • Often begins in childhood or early adulthood • Frequency and severity decrease with age • Familial clustering is common When no systemic cause is identified, the condition is labeled ROA or recurrent aphthous stomatitis. Chronicity (>6 weeks) or frequent recurrence warrants further work-up. When oral ulcers are a rheumatology clue In AIRD patients, oral ulcers may be a presenting feature, a diagnostic criterion, or a marker of disease activity. Systemic diseases where oral ulcers are diagnostically relevant • Systemic lupus erythematosus – Oral or nasopharyngeal ulcers – Often painless and physician-observed • Behçet’s disease – Recurrent oral ulcers (minor, major, or herpetiform) – ≥3 episodes in 12 months • Granulomatosis with polyangiitis (GPA) – Oral or nasal inflammation – Painful or painless ulcers, often with nasal discharge • Crohn’s disease – Multiple aphthous ulcers in upper or lower GI tract – Often persistent and associated with granulomas • PFAPA syndrome – Periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis Other rheumatologic or systemic associations Oral ulcers may be present but are not part of diagnostic criteria: • Reactive arthritis (usually painless) • Sjögren’s syndrome (secondary to xerostomia) • Sweet syndrome • Ulcerative colitis (larger, persistent ulcers) 8️⃣ Important clinical observation Painless oral ulcers are particularly relevant in rheumatology, as they are less likely to be reported by patients and may reflect ongoing systemic inflammation. Coming to our case: the perforated palatal ulcer Other Differentials (Non-neoplastic, Non-congenital). 1. Recreational Drug–Induced (Most common worldwide) Classically: Cocaine Clues •Middle-aged adults •History of nasal sniffing (often denied) •Hard palate, midline •Well-defined circular perforation •Surrounding necrosis ± candidiasis Important mimic •Cocaine-induced midline destructive lesion (CIMDL) can mimic GPA 2. Fungal Infections (Very important in India ) a) Mucormycosis (Second most common overall; very common in India) Strongly associated with: •Uncontrolled diabetes mellitus •Post-COVID states •Immunosuppression Clues •Rapidly progressive ulcer → necrosis → perforation •Blackish or caseous necrotic base •Often starts as palatal ulcer before perforation •May have sinus, orbital, nasal involvement b) Other fungal causes (rare) •Aspergillosis •Paracoccidioidomycosis (South America) •Rhinoentomophthoromycosis (tropical regions) 3. Bacterial Infections a) Syphilis •Especially tertiary or malignant syphilis •Punched-out ulcer → perforation •Consider in HIV-positive patients b) Tuberculosis •Rare but reported •Associated nasal, laryngeal disease c) Leprosy •Advanced lepromatous disease ⚠️ Always exclude infection and cocaine before labeling autoimmune cause. 6. Key Geographic Thinking (Very important clinically) India - Mucormycosis USA / Europe - Cocaine-induced Immunocompromised / HIV- Syphilis, TB, fungal Post surgery / ICU- Traumatic perforation in our case …the diagnosis was NK/T-cell lymphoma.🕵🏽‍♀️ 👉 “Your differential diagnosis reveals where you practice.”
Dr Abhilasha Manwatkar (AIIMS Nagpur) tweet media
Dr Abhilasha Manwatkar (AIIMS Nagpur)@Abhilasha21822

You see a perforated palatal ulcer in clinic. No history given. No labs yet. 🧠 What is the FIRST diagnosis that comes to your mind? Your answer is shaped by where you practice…🌍 #Rheumatology #ClinicalReasoning #MedX #DiagnosticThinking

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Prashant chotalia retweetledi
Aravind Palraj
Aravind Palraj@Rheumat_Aravind·
Low complement ≠ Lupus. 🔴 Isolated low C4 is not typical SLE 🦠 Think infective endocarditis, shunt nephritis 🧊 Think cryoglobulinemia (HCV!) 🩸 Don’t miss cholesterol emboli Always interpret C3 & C4 together. Never diagnose lupus on labs alone. #Rheumatology #MedEd #Lupus @DrAkhilX @IhabFathiSulima #ClinicalReasoning #InternalMedicine
Aravind Palraj tweet media
Aravind Palraj@Rheumat_Aravind

🧵 Complement (C3 & C4) in Rheumatology: Tweet 1: “C3 & C4: two small proteins, big role in lupus care. But when are they truly helpful — and when do they mislead? A quick guide to understanding complement in rheumatology 👇” @IhabFathiSulima #MedTwitter #Rheumatology

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Jasmine Sethi
Jasmine Sethi@JasmineNephro·
🩸 Dark, cola-colored urine every morning 😳🌅 Hb keeps falling 📉 LDH 🔥 sky-high Direct Coombs: NEGATIVE ❌ Pancytopenia 😶‍🌫️ Then suddenly— Patient comes with severe abdominal pain ⚡😖-CT: Thrombosis in hepatic vein 😱 What is the diagnosis ⁉️❓
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Dr.Mukesh , MD , DM
Dr.Mukesh , MD , DM@dr_immuno29·
🔹 Peripheral Neuropathy — What Everyone Must Know (JAMA 2025) • Starts quietly in the toes, creeps upward. • Numbness, burning, tingling, pain = early warning signs. • Diabetes = #1 cause (≥50% cases). • Other culprits: B12 deficiency, alcohol, chemo drugs, monoclonal proteins, genetics. • 27% remain idiopathic even after full evaluation. • Essential tests: HbA1c, B12 + MMA, SPEP + immunofixation. • Best pain options: Gabapentin, Pregabalin, Duloxetine, Amitriptyline. • Pain control limited — only ~38% get ≥50% relief. • Opioids don’t work. • Early detection matters — but nerve damage rarely fully reverses. DOI: 10.1001/jama.2025.19400 #PeripheralNeuropathy #Neurology #Diabetes #MedicalTwitter #MedEd #JAMA #Clinicians #MedFacts #MedResearch
Dr.Mukesh , MD , DM tweet mediaDr.Mukesh , MD , DM tweet media
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ILLIASUL IBAD
ILLIASUL IBAD@IlliasulK·
He came to us in a wheelchair. A 65-year-old man. Diabetic. On dialysis four days a week. Weak. Thin. Tired. His right ankle was swollen and hurting so much that he could barely speak. He held it like something precious, something broken. His daughter stood beside him. She was young, but her face looked older from worry. She had done everything she could—carried his reports, his medicines, his hope. He had gout before. Years ago, in the left ankle. This looked the same. At least that’s what everyone thought. They had already tried steroids. He had taken them for three days. But the pain didn’t stop. It only grew. His uric acid was high — 9 mg/dL. That fit the story. Or so we thought. We examined him. He was weak from CKD. But all we could see was “gout” again. We did an ultrasound of the ankle. It showed fluid — an effusion. So we thought: Could it be infection? Could it be crystals again? We planned to aspirate the joint. That’s what the textbooks say. That’s what we do every day. But something felt off. He was in too much pain. Pain out of proportion. Pain that did not behave like gout. Pain that steroids did not touch. And then one simple thought came: “Did anyone do an X-ray?” We ordered it. Just a plain X-ray. Quick. Cheap. Basic. And there it was. A fracture. The medial malleolus was broken. No fall. No trauma. No accident. Just weak bones from CKD. Bones that could break with normal walking. Bones that told us the truth when we finally bothered to look. This was not a gout flare. This was a fracture that we almost missed. His daughter cried. But this time, it was not fear. It was relief. “Someone finally found the real reason,” her eyes said. And that mattered more than any medicine. What this man taught us: •Do not jump to conclusions. •Even in advanced cases, always start with basics. •X-rays are powerful, even in a world of MRI and ultrasound. •CKD doesn’t just damage kidneys — it weakens bones too. •When treatment doesn’t work, stop. Think again. Look again. Medicine isn’t only about knowledge. It is also about pausing. About asking simple questions. About seeing what we almost missed. Never treat just the disease you expect. Treat the reality in front of you. One week later — he returned. This time, on crutches. Leg in a plaster cast. Pain finally under control. And on his face — a smile brighter than the sun. He looked at me and said softly: “Thank you, doctor… .” Dr Illiasul Ibad #ClinicalPearl #ListenToPain #XraySavesLives #Rheumatology #Immunology #Sullysrounds #MedX #Medtwitter #Mnemonics #Medicine #History @DrAkhilX @IhabFathiSulima @Janetbirdope #MedTwitter #rheumtwitter @CelestinoGutirr @Urchilla01 @JasmineNephro @DurgaPrasannaM1
ILLIASUL IBAD tweet media
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Ravisutanjani
Ravisutanjani@Ravisutanjani·
🚨 Indian Railway's First AC is Addictive Can't Go Back To Lower Class After Experiencing The Comfort and Privacy are Unmatchable Good Upgrade Once You Have Disposable Income
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rajamouli ss
rajamouli ss@ssrajamouli·
THANK YOU EVERYONE for all the love, accolades and applause for the #Varanasi Announcement Video. Our whole @VaranasiMovie team is grateful to all of you. 🙏🏻🙏🏻🙏🏻🙏🏻🙏🏻🙏🏻🙏🏻
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Neil Borate
Neil Borate@ActusDei·
Paying 20% more for an overseas ETFs is madness! In LRS, & even after 1% currency cost, you get the same funf for 19% less. TCS is adjusted vs advance tax. Nice story by @SanketD_ET share.google/mBwFs7Vy3xs615…. Comment global to join our community - we will help you navigate this
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Prashant chotalia
Prashant chotalia@Drpvc·
@Rheumat_Aravind Sir , i start with HCQs only but many a times the episodes are not decreased so add MTX Still not sure what works wonder for these patients.
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Aravind Palraj
Aravind Palraj@Rheumat_Aravind·
8/ 💊 Treatment options 🎯 Hydroxychloroquine = first-line 🎯 NSAIDs for acute relief 🎯 MTX if high-risk (CCP+) or evolving RA 📌 HCQ may delay RA onset and reduce flares
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