Consuelo Arroyo Sch

Sureña. MD #UdeC. Medicina Interna #UChile.
📍Santiago. Pero extrañando el #SurdeChile.
Las decisiones, no las condiciones, determinan quiénes somos. (V Frankl)

[Abdelhamed Hamdy @Abdelhamed6261]

Lupus nephritis more clearly

[ReumaJoven @ReumaJoven]

🫁 #EULAR2026 Highlights
¿Cómo identificar a los pacientes con artritis reumatoide (AR) que deberían ser estudiados para enfermedad pulmonar intersticial (AR-EPI)?
Jeffrey A. Sparks (Harvard Medical School) revisó la evidencia actual sobre tamizaje y estratificación de riesgo🧵👇

[Dr.Mukesh , MD , DM @dr_immuno29]

SLE & Pregnancy: High-yield clinical guide 🧵

1️⃣ Core principle
• Disease activity at conception = strongest predictor
• Remission ≥6 months → ↓ flare, ↓ adverse outcomes

⸻

2️⃣ Fertility
• Slight ↓ fertility
• Drivers: activity, CKD, ↑ age, CYC exposure
• Ovarian reserve ↓ with CYC

⸻

3️⃣ High-risk markers 🚩
• Active disease
• Lupus nephritis
• APS / aPL +
• Anti-Ro/La +
• Prior adverse pregnancy

⸻

4️⃣ Maternal risks
• Flare (esp if active pre-pregnancy)
• Preeclampsia / HTN
• Thrombosis (APS)
• Infection

⸻

5️⃣ Fetal risks
• Miscarriage
• IUGR / LBW
• Preterm
• Stillbirth
• Neonatal lupus
• Congenital heart block (anti-Ro/La)

⸻

6️⃣ Pre-conception (gold step 💯)
✔ Remission ≥6 months
✔ Stop teratogens (MMF/MTX/CYC)
✔ Continue HCQ
✔ aPL, anti-Ro/La testing
✔ Renal + BP optimisation

⸻

7️⃣ Drugs
• Continue: HCQ (↓ flares, ↓ neonatal lupus risk)
• Safe: AZA, low-dose steroids, tacrolimus/CNI
• APS: add aspirin ± heparin
• Avoid: MMF, MTX, CYC

⸻

8️⃣ Monitoring
• Rheum + ObGyn care
• BP, urine protein, complements, dsDNA
• Serial growth scans
• Fetal echo (16–26 wks if anti-Ro/La +)

⸻

9️⃣ Flare vs preeclampsia ⚠️
• Complements ↓, dsDNA ↑ → flare
• Uric acid ↑, normal complements → preeclampsia

⸻

🔟 Post-partum
• Flare risk ↑
• Thrombosis risk ↑
• Restart/adjust meds

⸻

1️⃣1️⃣ Lactation
• HCQ, AZA, steroids → compatible
• Breastfeeding encouraged

⸻

🔑 Take-home
👉 Plan → Control → Monitor
👉 HCQ is cornerstone
👉 Controlled disease = successful pregnancy

⸻

DOI: https://t.co/bPQWO70QJe

#Rheumatology #SLE #Pregnancy #Lupus #MedTwitter #ObGyn #Autoimmune

[Dr.Mukesh , MD , DM @dr_immuno29]

Metabolic Masqueraders in Rheumatology ⚠️

🔑 Core
•IEM → mimic JIA / SLE / myositis / scleroderma
•Often misdiagnosed, DMARD-refractory

⸻

🧠 Mechanism
•Substrate ↑ → TLR4 / inflammasome → IL-1β, TNF
•Lysosome = inflammation hub

⸻

🚨 Think METABOLIC when:
•Early onset / atypical phenotype
•Multisystem (bone + neuro + organ)
•Dysmorphism / organomegaly
•Poor response to therapy
👉 Do genetic testing

⸻

🦴 Arthritis mimics (CLUES)
•Farber → nodules + arthritis + hoarseness
•MPS → contractures + coarse facies
👉 Child CTS = MPS
•Fabry → burning pain + angiokeratoma
👉 Pain + normal CRP
•Gaucher → bone pain + HSM
👉 Erlenmeyer deformity
•Alkaptonuria → AS-like spine
👉 Urine black on standing
•Purine defects → gout
👉 Childhood gout = metabolic

⸻

💪 Myositis mimics
•McArdle (GSD V)
👉 Second wind (+)
•Pompe (GSD II)
👉 Axial weakness + CK↑ + resp/cardio
•Danon
👉 Young + cardiomyopathy

⸻

🔥 Autoimmune mimics
•Lysinuric PI
👉 SLE-like + post-meal NH₃↑
•MKD
👉 Recurrent fever (3–7 d), vaccine trigger
•α-Mannosidosis
👉 Hearing loss + coarse facies
•Prolidase def.
👉 Chronic leg ulcers

⸻

🧪 Tests
•Enzyme assays
•Urine: GAGs / organic acids / purines
•Genetics = confirm
•X-ray: dysostosis multiplex

⸻

🎯 Punchlines
•Atypical = metabolic until proven otherwise
•Refractory JIA → rethink diagnosis
•Early dx = treatable (ERT / targeted Rx)

⸻

DOI: 10.1038/s41584-026-01352-y

#Rheumatology #MedEd #Genetics #RareDisease

[Dr.Mukesh , MD , DM @dr_immuno29]

Hydroxychloroquine Retinopathy Screening 2026-🧵

• HCQ retinopathy = silent early, irreversible late
→ Retina normal for yrs → sudden thinning → rapid damage

• Dose matters MOST ⚠️
→ Safe: ≤5 mg/kg/day (real wt)
→ >6 mg/kg → sharp ↑ toxicity risk

• Risk timeline ⏳
→ <1% (5 yrs) | <2% (10 yrs)
→ ↑ steep after long duration
→ Even @20 yrs: annual risk <5% (if safe dose)

• Key risk factors 🚩
→ High dose + long duration
→ Renal disease
→ Tamoxifen
→ Older age at start

• Patterns differ 👁️
→ Parafoveal (Indians/Europeans)
→ Pericentral (East Asians)
→ Screen BOTH

• Screening = game changer 🔍
→ Baseline: Fundus + OCT + FAF
→ Annual (delay till 5 yrs if low risk)

• Gold standard tests 🥇
→ OCT (primary)
→ Wide-field FAF
→ VF/mfERG = confirmatory

• Earliest sign ⚡
→ Outer retinal thinning (OCT)
→ BEFORE symptoms / VF changes

• Progression 🚨
→ Early → stabilises after stopping
→ Late (EZ/RPE loss) → keeps worsening

• Management 🎯
→ Stop/reduce HCQ = ONLY proven step
→ Decision = shared (rheum + patient)

• Clinical pearl 💡
→ Detect thinning early → save vision
→ Bull’s eye maculopathy = failure of screening

📄 DOI: 10.1016/j.ophtha.2025.11.001

#Hydroxychloroquine #Retinopathy #OCT #Rheumatology #Ophthalmology #SLE #MedTwitter #Screening #PatientSafety

[Dr.Mukesh , MD , DM @dr_immuno29]

Behçet’s 2025 — decode in 60 seconds

—

🧠 WHAT CHANGED
Organ > disease label
Phenotype-driven Rx
Early biologics (not last line)

—

🩺 MUCOSA (oral/genital/skin)
Colchicine → base
Apremilast/AZA if needed
🚫 Don’t overkill

—

👁 EYE = CLOCK IS TICKING
Posterior uveitis = emergency
AZA / Anti-TNF early
Delay → blindness

—

🧠 BRAIN ≠ BODY RULES
Parenchymal → steroids + AZA/CYC
🚫 No cyclosporine
Think aggressive

—

🩸 VESSELS THINK DIFFERENT
Clot = inflammation
IS > anticoag
Venous > arterial
Aneurysm = danger

—

🍽 GUT (IBD mimic)
Steroids → AZA / Anti-TNF
Treat like inflammatory ulcer disease

—

💉 BIOLOGICS RESET TIMELINE
Anti-TNF = frontline in severe
Not “after everything fails”

—

💊 STEROID PHILOSOPHY
Use fast
Exit faster
Avoid chronic

—

🔁 DISEASE IS NOT STATIC
Phenotype shifts
Rx must evolve

—

🚨 RED FLAGS = ACT FAST
Eye pain
Neuro signs
Hemoptysis

—

⚡ CLINICAL CODE
Right organ
Right timing
Right intensity

—

📄 DOI: https://t.co/AdqzEUivRF

—

#Behcets #Rheumatology #Vasculitis #MedTwitter #RheumTwitter #Immunology #EULAR #ClinicalPearls

[Alberto Giraldo @alb_giraldo]

#Hypoxia-inducible factor 1 α (HIF-1α) acts as a central metabolic switch in #gout, linking nutrient excess, oxidative stress, and #hypoxia to altered #purine metabolism, #hyperuricemia, and IL-1β-driven inflammation.

𝗞𝗲𝘆 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺𝘀:
◦ Systemic level: Enhanced HIF-1α activity (via genetic variants or metabolic stress) reprograms hepatocyte metabolism, increasing purine flux, urate production (through NT5C2, XDH, glycolysis, and AMP accumulation), and gout risk.
◦ Bidirectional loop: Hyperuricemia further stabilizes HIF-1α, promoting glycolysis, oxidative stress, inflammasome activation, and multisystem damage (liver, kidney).
◦ Local/tissue level: In immune cells, MSU crystals activate the mTOR/HIF-1α/glycolysis axis, driving proinflammatory macrophage and neutrophil responses, NETosis, Th17 differentiation, and IL-1β production. Pharmacologic HIF-1α inhibition suppresses these effects.
◦ Environmental triggers: Hypoxia (high altitude, obstructive sleep apnea) and pseudohypoxia stabilize HIF-1α via oxidative stress, elevating urate and creating feed-forward loops that explain environmentally triggered flares.

𝗧𝗵𝗲𝗿𝗮𝗽𝗲𝘂𝘁𝗶𝗰 𝗜𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀:
Metabolic interventions (e.g., SGLT2 inhibitors, metformin) that indirectly dampen mTOR/HIF-1α signaling reduce urate levels and inflammation, supporting treatment of gout as a metabolic-inflammatory disease rather than solely urate-lowering.

*Rasheed N, Reyes C, Weisman MH. HIF-1α in gout: a central regulator of metabolism, inflammation, and environmental stress. Semin Arthritis Rheum. 2026;78:152971.
🔗https://t.co/C6xkfQE7dO

[Rheuma Doc @LastManStand85]

Leflunomide washout plan 👇👇

[Dr. Chokri Ben Lamine @abouabdrahman0]

✅ Autoimmune diseases associated with Myelodysplastic Syndrome (MDS)

🧬 MDS & Autoimmunity — Key Facts
• Autoimmune diseases (ADs) occur in 10–30% of MDS patients
• May precede, coincide or follow MDS by months–years
• Driven by immune dysregulation + clonal hematopoiesis

⸻

🔥 Common autoimmune associations in MDS
• Vasculitis (32%) → PAN-like, GCA, ANCA− vasculitis, Behçet-like 🩸
• Connective tissue disease (25–30%) → relapsing polychondritis, SLE, Sjögren’s 💧
• Inflammatory arthritis (23%) → seronegative polyarthritis, PMR 🤲
• Neutrophilic dermatoses (10%) → Sweet syndrome ⚡
• Autoimmune cytopenias → AIHA, ITP (rare ~3–5%) 🔴
• Other organ ADs → inflammatory bowel disease, pulmonary alveolar proteinosis 🌬️

⸻

⚕️ Clinical Clues
• Older patient with cytopenias + autoimmune symptoms
• Sweet syndrome may signal underlying MDS
• Relapsing polychondritis strongly associated with MDS
• Autoimmunity does not significantly worsen MDS survival

⸻

💊 Treatment Pearls
• First-line for AD symptoms → steroids (GCs)
• Steroid-sparing agents: methotrexate, azathioprine (limited benefit)
• Azacitidine ✅ improves both MDS + autoimmune symptoms
• HMA benefit on immune disease needs more data
• HSCT 💥 cures MDS + refractory autoimmune disease
• Avoid long-term steroids alone → infection risk + clonal evolution

⸻

🚨 When to suspect underlying MDS in autoimmune disease?
✅ Cytopenia unexplained by AD
✅ Elderly with new autoimmune vasculitis
✅ Refractory Sweet syndrome
✅ Macrocytosis + anemia + normal B12/folate
✅ Splenomegaly + abnormal smear

⸻

📚 Reference
• Mekinian et al. Autoimmunity in MDS. Crit Rev Oncol Hematol
• NCCN MDS v3.2025
• PMID: 35090834

[Lupus Hub @lupus_hub]

CONGRESS | #EULAR2025 | PLENARY SESSION
Antonis Fanouriakis, National and Kapodistrian University of Athens, gave a talk about recent advances in #SLE including pathogenesis, treatment strategy and major clinical trials in 2024-2025.
· Genetic burden of SLE may lead to transition from normal to preclinical autoimmunity and an IFN signature predicts progression from ANA positivity to SLE.
· Summary of 2025 ACR guidelines for SLE has been published.
· HCQ was associated with a reduced risk for any CV outcome but there was no protective role in the preeclampsia.
· HCQ continuation during GC withdrawal may help prevent flares.
· Early use of MMF prevents flares.
Achievement of remission and low disease activity is still low with belimumab and anifrolumab in clinical trials.
· Many trials are ongoing to investigate new agents for treating SLE, including CAR T-cell therapy.
Follow our live feed for more updates: https://t.co/fJPOBGgcwh
#RheumTwitter #rheumatology #MedNews #MedEd #MedicalCongress

[Dr. Dinesh Khanna @sclerodermaUM]

⏩Lecture by Prof Takeuchi on Sjogren Syndrome. Anti-centromere ab is seen in 10% of primary Sjogren syndrome. more likely to have sclerodactyly. https://t.co/mVry2OaNmq @IRACON24Blr

[Steven Zhao @SteZhao]

🚨#Tofacitinib ⬆️ #cardiovascular &amp; #cancer risk in RA. But how relevant is this risk to people with #AxialSpondyloarthritis or #PsoriaticArthritis?

This study did not find⬆️risk of JAK compared to TNF/IL17 inhibitors in SpA. Funded by @PsoriasisInfo https://t.co/jCutAt1rRJ

[ILLIASUL IBAD @IlliasulK]

🧵 Thread: Understanding Panniculitis 🔬

1/ Panniculitis = Inflammation of subcutaneous fat
🧠 The subcutaneous fat has 2 components:
•Septa
•Lobules

It has many causes, best remembered by the TIMED mnemonic👇
#Rheumatology #Panniculitis #trump #Sullysrounds

[Janet Pope @Janetbirdope]

#JAKi May be more similar in #rheumatoid #arthritis than different

With respect to safety events

#EULAR2024 #EULARBEST
@RheumNow @drdavidliew @eular_org

I gracefully was defeated by David who had a voice of reason on the safety alerts of #EMEA #FDA and others

[Janet Pope @Janetbirdope]

Top 3 messages
Re
#JAKi #safety

Shared decision w benefit/risk info

Some #CV risks are more Impt than others- stratify your pt into risk categories

#Smoking is a big risk for #MACE &amp;
#malignancy-So work on facilitating
Smoking #cessation

#EULAR2024 @eular_org @RheumNow

[Janet Pope @Janetbirdope]

ACR24 take homes

➡️#Inflammatory #myositis
#Upadacitinib improved MDA5 ILD
#Baricitinib 4mg/d good in myositis delayed start #RCT
#Tofacitinb ➡️help for skin, calcinosis, rash in case series
➡️RCT ongoing

JAKi is ‘jacked’ in muscles 💪🏿

#ACR24 @RheumNow @ACRheum
1731 0348

[Laurent ARNAUD @Lupusreference]

🆕 HOW TO MAKE A #DIAGNOSIS OF #LUPUS ?!? is the most common question 🧐 I get ➡️ Well, certainly NOT ⛔ by checking ✔️ if you have at least 4 criteria 📑 on a list ! #SLE diagnosis is a complex process 👨‍🎓 and requires expertise. Ask your #rheumatologist 👍 if you are unsure 🏥.

[Ross Prager @ross_prager]

'Problem representation' is one of the most fundamental skills of clinical diagnosis, yet is often taken for granted.

Here's how to get it right.

A 🧵

(1/x)

[Deepti Agarwal @deepti_pramod]

#WrapItUpWednesday 🎁

🔬 ANA IF – One of the screening test to detect MSA &amp; MAA!

✨ Pattern helps to decide which line blot to order next

⚠️ MSA/MAA can still be +ve in ~2/3 of ANA (IF) -ve pts : if suspicion high, don’t stop at ANA! 🚀

📸 Image: ICAP ANA
#rheumtwitter

[Alberto Giraldo @alb_giraldo]

#Chilblain #lupus erythematosus usually develops in subjects with circulating anti-Ro/SSA autoantibodies (up to 89% of the cases). Because of this association, it is considered that the chilblain lupus erythematosus should be included in the spectrum of anti-Ro/SSA-associated cutaneous disease in addition to subacute cutaneous lupus erythematosus, hypergammaglobulinemic purpura, and neonatal lupus.

*Franceschini F, Calzavara-Pinton P, Quinzanini M, et al. Chilblain lupus erythematosus is associated with antibodies to SSA/Ro. Lupus. 1999;8(3):215-219.
🔗https://t.co/pde1Lbn4e7