Javi del Cid

✅ Happy to share that we have just published #LupusGPT... in the Lancet #Rheumatology 👍 Check the post below by @LupusEurope for the link 🔓

LANCET SEMINAR 2026: Anemia de células falciformes #MedEd #MedTwitter #MedX DOI:10.1016/S0140-6736(25)02278-0 medicina-interna.org

Polymyalgia Rheumatica by C Dejaco & E Matteson @MayoClinic @NEJM #polymyalgia nejm.org/doi/full/10.10…

Efficacy and Safety of Obinutuzumab in Active Systemic Lupus Erythematosus #SLE #Rheumatology 👇 nejm.org/doi/full/10.10…

SLE With Ascites Clinical course of SLE-related ascites. 👥 72 patients
⬇️ albumin → recurrence risk ↑
🔥 CRP ↑ → recurrence risk ↑
🔁 recurrence → 54%
💊 steroid response → high #SLE #Lupus Link: journals.lww.com/jclinrheum/abs…

Correspondence: Blinatumomab in Combined Immune Thrombocytopenia and Antiphospholipid Syndrome nejm.org/doi/full/10.10… #Hematology #Immunology

@MikeEhrenstein @SLEuroSociety @MuhammadShipa 👏👏

Here are some of the team talking about our new clinical trial STRATIFY lupus ⁦@SLEuroSociety⁩ Lisbon ⁦@MuhammadShipa⁩

Health disparities matter in SLE. 🌍 Life expectancy still varies across countries, and in Slthese gaps are amplified by social determinants of health and access to healthcare, Understanding these factors is essential to provide equitable care. #sle #sleuro #healthequity

Delighted to present my work under the mentorship of Professor Isenberg and to have been selected for the Lupus Award. Always grateful to UCLH for all the support #sle #research #uclh #autoimmune #sleeurope

Key message: Early systemic involvement and cytopenias matter. Risk stratification at diagnosis is crucial to improve long-term outcomes. #SLE #lupus #sleeuro #autoimmune

In our SLE cohort, baseline proteinuria, leuko and thrombocytopenia, serositis, rash, anti-Ro profile were independently predicted mortality. Deaths were mainly due to infection, cancer & CV, with no differences by LN, ethnicity or period. SLE Euro Conference coming. #SLE #Lupus

Independent predictors of mortality: • Proteinuria • Leukopenia • Thrombocytopenia • Serositis • Rash • Anti-Ro profile • Older age at diagnosis These reflect systemic & renal burden at baseline..

📌 TAFRO Syndrome (A variant of idiopathic Multicentric Castleman Disease – iMCD) TAFRO is an acute, aggressive inflammatory syndrome characterized by systemic inflammation, organ dysfunction, and cytokine storm features. 🧩 What Does TAFRO Stand For? T – 🩸 Thrombocytopenia A – 💧 Anasarca (massive edema, pleural effusion, ascites) F – 🔥 Fever R – 🧬 Reticulin fibrosis (bone marrow fibrosis) O – 🫁 Organomegaly (hepatosplenomegaly, lymphadenopathy) 🧠 Pathogenesis •Cytokine-driven hyperinflammatory state •↑ IL-6, VEGF •Considered a subtype of idiopathic multicentric Castleman disease (iMCD-TAFRO) 🩺 Clinical Features •Acute/subacute onset •Severe thrombocytopenia (often <50,000) •Renal dysfunction (AKI common) •Massive fluid overload •Mild lymphadenopathy (unlike typical iMCD where nodes are bulky) •Elevated CRP, ESR •Hypoalbuminemia 🧪 Lab & Histopathology Labs: •Low platelets •High CRP •Elevated IL-6 •Renal impairment •Normal or mildly elevated immunoglobulins Bone marrow: •Reticulin fibrosis •Megakaryocytic hyperplasia Lymph node biopsy: •Hyaline vascular or mixed Castleman pattern ⚠️ Differentials •Severe sepsis •HLH •SLE flare •POEMS •Malignancy (lymphoma) 💊 Treatment 1️⃣ First-line •High-dose steroids •Anti–IL-6 therapy •Tocilizumab •Siltuximab 2️⃣ Refractory cases •Rituximab •Cyclosporine •Cyclophosphamide •Combination immunosuppression Supportive: •Dialysis if needed •Fluid management •Infection surveillance #RheumattDoc #MedTwitter #RheumTwitter #Medicine #rheumatology @DrAkhilX @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1

“A Change Is Gonna Come” to Treatment of Lupus Nephritis: A Review - American Journal of Kidney Diseases. Well summarised all trials in LUPUS NEPHRITIS! 💯🔥👌🏻 #MedTwitter #ajkd #NephTwitter ajkd.org/article/S0272-…

When you submit your paper to a journal This is how reviewer 1 and reviewer 2 treat it

📌 IPAF: Classification, Controversy, and Clinical Care 📌 IPAF (Interstitial Pneumonia with Autoimmune Features) Classification Criteria - ERS/ATS 2015 ✅ Mandatory Requirements (All must be met) 1.Presence of interstitial pneumonia •By HRCT or surgical lung biopsy 2.Exclusion of alternative etiologies 3.Does NOT meet criteria for a defined CTD 4. At least ONE feature from at least TWO of the following domains: •Clinical •Serologic •Morphologic 🔹 A. Clinical Domain 1.Distal digital fissuring (“mechanic’s hands”) 2.Distal digital tip ulceration 3.Inflammatory arthritis OR morning stiffness ≥60 min 4.Palmar telangiectasia 5.Raynaud’s phenomenon 6.Unexplained digital edema 7.Unexplained fixed rash on digital extensor surfaces (Gottron’s sign) 🔹 B. Serologic Domain 1.ANA ≥1:320 (diffuse, speckled, homogeneous) OR nucleolar/centromere pattern (any titer) 2.RF ≥2× upper limit of normal 3.Anti-CCP 4.Anti-dsDNA 5.Anti-Ro (SSA) 6.Anti-La (SSB) 7.Anti-RNP 8.Anti-Smith 9.Anti-Scl-70 (topoisomerase I) 10.Anti-tRNA synthetase (Jo-1, PL-7, PL-12, EJ, OJ, KS, Zo, tRS) 11.Anti-PM-Scl 12.Anti-MDA-5 🔹 C. Morphologic Domain 1️⃣ HRCT Patterns •NSIP •OP •NSIP + OP overlap •LIP 2️⃣ Histopathology (Surgical biopsy) •NSIP •OP •NSIP + OP overlap •LIP •Interstitial lymphoid aggregates with germinal centers •Diffuse lymphoplasmacytic infiltration ± lymphoid follicles 3️⃣ Multicompartment involvement •Unexplained pleural effusion/thickening •Unexplained pericardial effusion/thickening •Unexplained intrinsic airway disease •Unexplained pulmonary vasculopathy 🔮 Prognosis IPAF has a heterogeneous course. 📊 Overall •Prognosis is intermediate between IPF and CTD-ILD •Better than IPF (overall) •Worse than classical CTD-ILD (in many cohorts) 🔎 Factors Affecting Prognosis 1️⃣ HRCT Pattern •NSIP pattern → Better prognosis •UIP pattern → Prognosis similar to IPF •OP pattern → Often steroid responsive UIP in IPAF behaves more like fibrotic ILD. 2️⃣ Disease Behavior •Progressive fibrosing phenotype → Poorer outcome •Inflammatory phenotype → Better response to immunosuppression 3️⃣ Evolution to CTD •~10–20% progress to defined CTD over time (RA, SSc, IIM most common) Higher risk of progression if: •Specific autoantibodies present •Strong clinical autoimmune features 📉 Mortality Predictors •Older age •Male sex •UIP pattern •Reduced DLCO •Progressive fibrosis 💊 Treatment ⚠ No RCT-based specific IPAF guidelines. Management extrapolated from CTD-ILD and progressive fibrosing ILD data. 🔹 Step 1: Determine Phenotype Inflammatory predominant (NSIP, OP, cellular features) → Immunosuppression preferred Fibrotic predominant (UIP, progressive fibrosis) → Consider antifibrotics ± immunosuppression 🔹 Immunosuppressive Options First-line •Mycophenolate mofetil (MMF) – most commonly used •Azathioprine Moderate–severe disease •Cyclophosphamide (selected cases) Refractory cases •Rituximab •Tacrolimus (in antisynthetase phenotype) 🔹 Antifibrotic Therapy For progressive fibrosing IPAF: •Nintedanib (supported by INBUILD trial subgroup data) •Pirfenidone (less data) Especially useful in: •UIP pattern •Progressive FVC decline 🔹 Steroids •Useful in OP or inflammatory NSIP •Not ideal long-term for fibrotic UIP 🔹 Monitoring •PFT every 3–6 months •HRCT if clinical worsening •Watch for evolution into defined CTD #RheumattDoc #MedTwitter #RheumTwitter #Medicine #rheumatology @DrAkhilX @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1

VEXAS syndrome is a newly discovered multisystemic disease affecting most organs. A new Review provides a comprehensive overview of VEXAS syndrome, including the disease's discovery, diagnosis, and treatment: spkl.io/6014AsjYw

NEW RESEARCH—Patient profiles and early response in patients with systemic #lupus erythematosus initiating #anifrolumab: interim analysis from the ongoing multicentre observational REVEAL study bit.ly/4aj9YWz @MartaMartamosca Plus, linked Comment bit.ly/3ZliHT6

🩸 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