Cristina Medina

💜🩺🌿 𝚁𝚎𝚞𝚖𝚊𝚝ó𝚕𝚘𝚐𝚊 ・𝚄𝚕𝚝𝚛𝚊𝚜𝚘𝚗𝚒𝚍𝚘 𝚎𝚗 𝚁𝚎𝚞𝚖𝚊𝚝𝚘𝚕𝚘𝚐í𝚊

[Cristina Medina @xtyme]

Im your Tyler Durden 😎

[Cristina Macía @reumacia]

Si te interesan los JAKinibs 💊 aquí tienes la súper revisión ✍️

Acceso abierto 🔑 https://t.co/jbGd8kzjmQ

[Ravi Kumar @RheumattDoc]

🧠 EULAR 2025 Recommendations – Behçet���s Syndrome

🚦 Step 1: Assess severity

•Not organ/life-threatening → start with:
•csDMARDs (AZA ± cyclosporine*)
•± glucocorticoids

👉 If response → continue
👉 If NO response → escalate to biologics

⚠️ Organ / Life-Threatening Disease

➡️ Always start high-dose glucocorticoids

Then phenotype-based treatment:

👁️ Uveitis
•Monoclonal TNFi (adalimumab/infliximab) + csDMARDs
•Early biologic use emphasized ⭐

🩸 Venous disease
•TNF inhibitors
•± anticoagulation (case-by-case)

🫀 Arterial disease
•Infliximab (IFX) > Cyclophosphamide (CYC)
•Interventions if needed (aneurysm, occlusion)

🧠 Parenchymal CNS
•IFX preferred over other immunosuppressives
•(Shift from older AZA-first approach)

🍽️ Gastrointestinal
•Monoclonal TNFi

🟢 2. Mucocutaneous + Joint Disease

🪜 Stepwise approach

Step 1: Local + baseline therapy
•Topical treatments
•Colchicine (cornerstone)

Step 2: Response check

✅ If controlled → continue

❌ If NOT controlled:
🔸 Mucocutaneous disease
•Apremilast or TNFi ⭐ (new stronger positioning)

🔸 Arthritis
•Azathioprine or TNFi

⭐ Key Takeaways

•Phenotype-driven treatment is central
•TNF inhibitors moved earlier across domains
•Infliximab preferred in severe vascular & CNS disease
•Apremilast upgraded for mucocutaneous disease
•Steroid-sparing strategy emphasized
•Anticoagulation = adjunct, not primary therapy

#RheumattDoc #MedTwitter #RheumTwitter #Medicine #rheumatology @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1 @docakx

[Samuel Hume @DrSamuelBHume]

I just found out we don't use the suffix 'mab' for new monoclonal antibodies anymore — now it's -tug/-bart/-mig/-ment

So, for the new amyloid antibody, Remternetug

'Remter–' is a random prefix; '–ne' is for neurology and '–tug' because it's unmodified and monospecific

[Cristina Medina @xtyme]

@SwitchedOnPop you guys please do an episode on ROSALIAs LUX 🤍🤍🤍🤍🤍

[vasculitides @vasculitides]

Access our new review on diagnosis, classification, and prognosis of ANCA-associated vasculitis in Nat Rev Rheum for free at https://t.co/t9dmuJRr9b

[Cristina Medina @xtyme]

@f_solorzano Ojalá pronto! Platican todo lo que contaste en misterios de la sala oscura, saludos!

[William A. Wallace, Ph.D. @WilliamWallace]

3 types of hunger explained "simply"

Hunger isn’t just about an empty stomach. Your brain receives signals from body composition, hormones, emotions, and even gut microbes. Here’s how the three major types work:

1️⃣ Homeostatic Hunger (Energy Balance Hunger)
This is your body’s “fuel gauge.” It rises and falls based on energy needs and metabolic signals.
What drives it: Ghrelin from the stomach stimulates hunger; leptin from fat cells and incretin hormones (GLP-1, PYY, CCK) reduce it.

What it does: Ensures your intake matches your energy needs for exercise, growth, and tissue repair.

🟢 Example: After a long run, homeostatic hunger pushes you to replace calories and glycogen.

2️⃣ Hedonic Hunger (Reward-Driven Hunger)
This is your “food pleasure” system. It’s triggered by sight, smell, habits, and emotions, not by actual energy needs.
What drives it: Brain reward circuits activated by highly palatable foods (sugar, fat, salt).

What it does: Encourages eating even when you’re not truly hungry. Weak satiety signals make it harder to stop.

🟢 Example: Craving dessert after dinner even though you’re full.

3️⃣ Microbiota-Driven Hunger (Gut Microbe Hunger)
Your gut bacteria also shape hunger signals by producing metabolites that influence hormones and the brain.

What drives it: Microbes generate compounds that mimic hunger or satiety signals, affect insulin, and modulate ghrelin, GLP-1, and PYY.

What it does: Links gut health to appetite regulation and metabolic control.

🟢 Example: Certain bacterial imbalances may increase cravings or weaken satiety, nudging overeating.

[Ravi Kumar @RheumattDoc]

�� IVIG (Intravenous Immunoglobulin)

🔹 What It Is 🧪

A sterile preparation of pooled IgG antibodies derived from the plasma of thousands of donors.
→ Acts as immune support or immune modulator, depending on indication.

🔹 Mechanism of Action ⚙️

💭 Depends on indication:
•🛡️ Immunodeficiency: Provides passive immunity (antibody replacement).
•🔄 Autoimmune / Inflammatory:
• 🧩 Fc receptor blockade → ↓ phagocytosis of autoantibody-coated cells
• 🎯 Neutralization of pathogenic autoantibodies
• 🔥 Suppression of proinflammatory cytokines
• 🌿 Expansion of regulatory T cells (Tregs)
• 🧊 Inhibition of complement activation

🔹 Common Clinical Uses 🏥

🧬 Immunodeficiency:
•CVID
•X-linked agammaglobulinemia

⚡️ Neurology:
•Guillain–Barré syndrome
•Myasthenia gravis crisis
•Multifocal motor neuropathy
•Autoimmune encephalitis

❤️ Rheumatology:
•Systemic lupus erythematosus (SLE) – esp. refractory cytopenias or neuropsychiatric lupus
•Dermatomyositis / Polymyositis – steroid-sparing or rescue therapy
•Antisynthetase syndrome
•Vasculitis (e.g., ANCA-negative or refractory cases)
•Catastrophic antiphospholipid syndrome (CAPS)
•Systemic sclerosis overlap syndromes

👶 Other:
•Kawasaki disease
•Immune thrombocytopenia (ITP)

🔹 Dosing 💊
•Induction: 1–2 g/kg total (over 2–5 days)
•Maintenance: 400–600 mg/kg every 3–4 weeks (replacement therapy)

🔹 Adverse Effects ⚠️
•😣 Mild: Headache, fever, chills, fatigue
•⚡ Moderate: Aseptic meningitis, thrombosis, hemolysis
•🚨 Severe: Renal failure (esp. sucrose-containing IVIG), anaphylaxis (IgA deficiency)

🔹 Monitoring 🧾
•💧 Baseline renal function
•🧫 Serum IgG levels (for replacement therapy)
•👀 Monitor for thrombosis or hemolysis

#RheumatDocX #MedTwitter #RheumTwitter #rheumatology @IhabFathiSulima @DrAkhilX @CelestinoGutirr @Janetbirdope

[Dr sthanu subramanian @drsthanus]

"Antibiotics Cheat Sheet"

https://t.co/Q1jNSJTCkE

[Oren Gottfried, MD @OGdukeneurosurg]

Liver Functional Tests

[Cristina Medina @xtyme]

No había twiteado (xteado) en un rato pero esto es importante, @StarbucksMex regresa el biscuit de arándanos y la felicidad a mi vida #JuntosPorElBiscuitDeArandanos @aurixm

[Cristina Medina @xtyme]

@mauri8a Ayyy quiero este secretooo

[Cristina Medina @xtyme]

@MeDicenBorbon x2

[Cristina Medina @xtyme]

@RelatocuriosoK @threadreaderapp unroll

[Cristina Medina @xtyme]

@PopBase Bella Baxter vibes

[Cristina Medina @xtyme]

👀 ⁦@techsantos⁩ https://t.co/9qo7nPcG2c

[Cristina Medina @xtyme]

🐶🐻

[The Associated Press @AP]

Mexican president defends disclosing a reporter's phone number, saying the law doesn't apply to him https://t.co/P2x7ASNVZv

[Sᴡɪss Uʟᴛʀᴀsᴏᴜɴᴅ Cᴇɴᴛᴇʀ - UZR @Rheumatology]

Not every trigger finger is caused by A1 annular ligament thickening with consecutive tenosynovitis.
In this case, we have just seen today, rheumatoid arthritis is characterized by tenosynovitis of the flexor pollicis longus tendon and submuscular impingement due to proliferative pannus-like tenosynovitis, typical in rheumatoid arthritis