Jairo H Cajamarca B

Rheumatologist

[Internal Medicine @pgMedicine]

Microcytic anemia is not always iron deficiency.
Think TAILS: Thalassemia, Anemia of chronic disease/inflammation, Iron deficiency, Lead poisoning, and Sideroblastic anemia. A simple high-yield framework for quick differentiation in clinical practice and exam revision.

[Karla Chacon-Abril 🇪🇨 @karlita_chacon_]

What’s new in ILD 2025? 🫁
Nueva clasificación ERS/ATS:
🔹 Más allá de “idiopático”
🔹 Nuevos términos (BIP, DAD)
🔹 Patrón ≠ diagnóstico
🔹 Enfoque en comportamiento (PPF)

[ILLIASUL IBAD @IlliasulK]

Great slide from #WRF2026 — Myositis-related ILD: interpreting antibody testing

Not every positive antibody in an ILD patient means myositis-ILD. The clinical context matters.

Key patterns clinicians should remember:

🔴 ILD-dominant antibodies (high ILD risk)
• PL-12
• OJ
• KS
• MDA5

🔴 Myositis + ILD phenotype (antisynthetase spectrum)
• Jo-1
• PL-7
• EJ
• Ha
• Zo
• PM-Scl

🟡 Intermediate risk
• SAE
• Ku

🟢 Low / minimal ILD association
• SRP
• HMGCR
• NXP2
• TIF1
• Mi-2

⚠️ Ro52 can amplify ILD risk when co-existing with other myositis antibodies.

Take-home:
Antibody positivity ≠ diagnosis.
Interpret the panel with phenotype, HRCT pattern, and clinical context.

#Myositis #ILD #Rheumatology #AntisynthetaseSyndrome #Autoantibodies @DrAkhilX @IhabFathiSulima @CelestinoGutirr

[Jairo H Cajamarca B @jairo8702]

Not only systemic steroids matter. Higher cumulative topical corticosteroid exposure was associated with osteoporosis and major osteoporotic fractures. #BoneHealth #Dermatology

[Ritasman Baisya @RitasmanB]

💡SLE -PAH is an unexplored yet severe entity in lupus
💡RNP association - higher PAH, more anti-PAH therapy
💡 No antibody-associated PAH behaves refractorily
👉Multiple antibody positivity - inflammatory, more resolution of PAH
👉https://t.co/nrf9EoeOLH
PMID: 41607606

[Rheuma Doc @LastManStand85]

Azathioprine [thiopurines] ⬆️ risk of Intra-hepatic Cholestasis of pregnancy
🚩Safe but not risk free
➡️Use lowest effective dose
➡️Monitor metabolites if access [6-TGN & 6MMP ratio]
➡️Monitor for pruritus, rising bile acid, & LFTs
💊 Switch to tacrolimus if shunting or ICP

[Satyendra Dhar, MD SFHM @DharSaty]

RHEUMATOID LUNG DISEASE:
👉
▪️RA-associated interstitial lung disease (RA-ILD).
▪️Pleural disease (pleural thickening/effusions).
▪️Airway disease (Both upper & lower airway).
▪️Rheumatoid nodules
▪️Drug-induced lung toxicity (i.e., Methotrexate-induced lung injury)
▪️Fibro-bullous disease
▪️Thoracic cage immobility
▪️Venous thromboembolic disease
▪️Vasculitis
▪️Pneumonia.

👉RHEUMATOID EFFUSION:

▪️WCC <5000/mm3
▪️Fluid glucose <60 mg/Dl
▪️Pleural fluid to serum glucose ratio < 0.5
▪️pH < 7.3
▪️High pleural LDH level (ie, > 700 IU/L)
▪️Cytology: Slender or elongated multi-nucleated macrophages, round giant multi-nucleated macrophages, and necrotic background debris.

👉Pulmonary function testing in ILD (PFT):
▪️Reduced VC, lung volumes, & DLCO.
▪️Oxygen desaturation during exercise.
▪️Restrictive abnormalities common (poor muscle strength or kyphosis due to osteoporosis rather than ILD).

[ACR_Journals @ACR_Journals]

A subset of patients with Still’s disease had high type I IFN gene signature assoc with lung disease and drug-assoc immune reactions to IL-1/IL-6 inhibitors. These also linked to rare genetic variation in IFN-related immune pathways

A&amp;R
https://t.co/lu5yOt0Inc

[Mithu Maheswaranathan, MD @MithuRheum]

🆕 2023 ACR Guidelines for Management of Interstitial Lung Disease (#ILD) in Systemic Autoimmune Rheumatic Diseases 🫁

🔸 Screening &amp; Monitoring Recs
🔸 Treatment Guidelines ILD/RP-ILD

#RheumTwitter #PulmTwitter #MedTwitter #MedX

[Jairo H Cajamarca B @jairo8702]

iSLE/“incomplete lupus”: phenotype exists, entity debated (early SLE vs UCTD). SMILE reminds us: no precision biomarkers = diluted prevention trials. #Lupus

[Dr. John Cush @RheumNow]

Prevention in Lupus and Therapeutic Evolution in Sjögren’s explores the proactive approach in autoimmune diseases, moving from theory to empirical evaluation. Recent discussions on incomplete lupus and the SMILE trial, along with advancements in Sjögren’s treatments, underscore the promise and complexity of prevention and precision in systemic autoimmunity.

https://t.co/rSrefjkBV9

[The Journal of Rheumatology @jrheum]

Images in Rheumatology

An Uncommon Mimic of Spondyloarthritis

📖 https://t.co/QGAH5tuqVk

#ProgressivePseudorheumatoidDysplasia

[ILLIASUL IBAD @IlliasulK]

You know APS is antibody-mediated.

We test anti-β2GPI.

We test anticardiolipin.

We test lupus anticoagulant.

In pregnancy, we give heparin.

But lupus anticoagulant isn’t a single antibody.

And heparin isn’t just a blood thinner.

Yet both revolve around one molecule: β2GPI.

Let me explain.🧵👇

1-APS is NOT truly about phospholipids

Despite the name “antiphospholipid,”
the main pathogenic target is β2-glycoprotein I (β2GPI) -a phospholipid-binding protein.

Cardiolipin is the surface.
β2GPI is the antigen.

2-What is lupus anticoagulant (LA)?

LA is not a specific antibody.

It is a functional laboratory phenomenon:

An antibody that prolongs phospholipid-dependent clotting assays (like dRVVT or aPTT) and corrects with excess phospholipid.

3-Why does LA prolong clotting in vitro?

Clotting assays require phospholipid surfaces.

In many APS patients:

• β2GPI binds phospholipid
• Anti-β2GPI antibodies bind β2GPI
• This interferes with coagulation complex assembly

→ Clotting time prolongs.

That’s why it’s called “anticoagulant.”

4-But not all LA is anti-β2GPI

Important nuance:

Some LA activity is prothrombin-dependent (e.g., aPS/PT antibodies).

So LA is heterogeneous.

But in high-risk APS (especially triple positive patients),
LA is often β2GPI-dependent — and strongly associated with thrombosis.

5-Now shift to obstetric APS

Pregnancy loss in APS is not just thrombosis.

Placental studies and animal models show:

• Complement activation
• Trophoblast injury
• Impaired placental remodeling

Sometimes with minimal thrombosis.

This is immune-mediated placental dysfunction.

6-β2GPI at the maternal–fetal interface

β2GPI binds trophoblast membranes.

Anti-β2GPI antibodies:

• Inhibit trophoblast invasion
• Increase apoptosis
• Trigger complement cascade

The placenta becomes the target.

7-So why does heparin help?

If pregnancy loss were purely thrombotic,
aspirin alone should be enough.

But aspirin + heparin improves live birth rates.

Because heparin does more than anticoagulation..

8-Heparin disrupts β2GPI biology

Heparin binds a heparin-binding region in domain V of β2GPI.

This can:

• Reduce β2GPI binding to phospholipids
• Interfere with antibody clustering
• Promote β2GPI inactivation in some settings

9-Complement may be the key

Animal models show:

Block complement → prevent aPL-mediated fetal loss.

Heparin reduces complement activation at the placenta.

This may be central to its benefit in obstetric APS.

10- The concept

APS revolves around β2GPI.

Lupus anticoagulant is a functional manifestation, often reflecting antibodies that disrupt phospholipid surfaces (frequently β2GPI-dependent, but not always).

And in pregnancy:

Heparin works not only by preventing clots..
but by modulating β2GPI interactions and complement activation.

Same axis.
Different angles.
One central protein.

β2GPI.

#Rheumatology #APS #ObstetricAPS #Lupus #Immunology @DrAkhilX @IhabFathiSulima

[Alberto Giraldo @alb_giraldo]

𝗠𝗲𝗹𝘁𝘇𝗲𝗿'𝘀 𝘁𝗿𝗶𝗮𝗱 (𝗰𝗿𝘆𝗼𝗴𝗹𝗼𝗯𝘂𝗹𝗶𝗻𝗲𝗺𝗶𝗮)
◦ The triad of palpable purpura, weakness (often manifesting as fatigue), and arthralgia is known as Meltzer's triad.
◦ It was identified in 1966 by M. Meltzer and E.C. Franklin (along with colleagues) in a landmark study of 29 patients suffering from cryoglobulinemia.
◦ This triad is characteristically associated with mixed cryoglobulinemia (types II and III), often triggered by chronic conditions such as hepatitis C virus infection, autoimmune diseases, or certain hematologic malignancies.
◦ Cryoglobulinemia is a rare medical condition characterized by the presence of abnormal proteins called cryoglobulins in the blood, which precipitate or clump together at low temperatures.
◦ These cryoglobulins, composed of immunoglobulins and sometimes complement components, deposit in small- to medium-sized blood vessels throughout the body, causing endothelial injury and end-organ damage.
◦ Cryoglobulins can cause a range of symptoms, including joint pain, skin rashes, and kidney problems, due to their tendency to obstruct blood vessels and trigger inflammatory reactions.

📸 Clinical, serological and pathological hallmarks of cryoglobulinemia.

*From: Roccatello, D., Saadoun, D., Ramos-Casals, M. et al. Cryoglobulinaemia. Nat Rev Dis Primers 4, 11 (2018).
🔗https://t.co/a0ergqppAg

[Dr.Mukesh , MD , DM @dr_immuno29]

🫀 Systemic Sclerosis (SSc) & the Heart — Serial CMR changes predict outcomes

📄 RMD Open 2026 | DOI: 10.1136/rmdopen-2025-006562

🔬 44 SSc pts | 2 cardiac MRIs | median FU 6.3 yrs

🔑 Core signals

📌 36% developed MACE (death / HF admission / VT)
📌 Baseline CMR ≠ predictive
📌 Progression of diffuse myocardial fibrosis (↑ max T1) = mortality risk

👉 It’s the CHANGE over time that matters.

🧬 Imaging biomarkers

⬆️ Max T1 (diffuse fibrosis) → ↑ all-cause mortality
LGE alone → not enough
Serial T1 mapping = strongest prognostic tool

💊 Treatment effects (real-world data)

✅ Methotrexate
•↑ LVEF
•↓ MACE (significant)
➡️ Possible cardioprotective role

✅ Rituximab
•↓ maximal T1
➡️ First clinical signal of myocardial antifibrotic effect

🚫 MMF / cyclophosphamide / steroids
→ No significant impact on fibrosis, LVEF, or MACE

⸻

⚠️ High-risk features

🔴 Diffuse myocardial fibrosis
🔴 Pulmonary hypertension
🔴 Anti–Scl-70 positivity
🔴 Primary cardiac SSc → ~50% MACE

Vasodilators: no clear benefit (underpowered)

⸻

🧠 Clinical takeaways

🫀 Repeat CMR beats single scan
🧬 Track T1 = track prognosis
💊 MTX may reduce CV events
🧪 RTX may reverse fibrosis
📊 Diffuse fibrosis = RED FLAG

⸻

✨ Bottom line:
Serial cardiac MRI + smart immunosuppression could redefine cardiac risk stratification in SSc. Prospective trials urgently needed.

⸻

#SystemicSclerosis #Scleroderma #CardioRheum #CMR #T1Mapping #MyocardialFibrosis #Methotrexate #Rituximab #Autoimmune #MedTwitter #Rheumatology

[Rheuma Doc @LastManStand85]

New autoantibodies in Sjögren's disease
#Rheumatology #MedTwitter These findings strongly suggest that a multi-marker panel approach is the most promising strategy for developing a new diagnostic test for seronegative SjD…

[Ravi Kumar @RheumattDoc]

👁️ Takayasu Retinopathy (Uyama & Asayama Classification)

Stage I – Dilatation of small vessels
•Dilated retinal veins
•Mild venous tortuosity

Stage II – Capillary microaneurysms
•Multiple microaneurysms
•Early Arteriovenous anastomoses

Stage III – Arteriovenous shunts
•Marked AV anastomoses
•Venous beading

Stage IV – Ocular complications
•Neovascularization
•Vitreous hemorrhage
•Retinal detachment
•Neovascular glaucoma

#RheumattDoc #MedTwitter #RheumTwitter #Medicine #rheumatology @DrAkhilX @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1 @Urchilla01

[CardiovascularCorner @TrackYourHeart]

What clinical sign is demonstrated in this nail lesion?

[KIReports @KIReports]

Kidney Outcomes in #ANCA-Glomerulonephritis According to Induction #Immunosuppression and #Histopathology

#VisualAbstract by @DrPallaviPrasad

https://t.co/K9TT0EGtUh

[Alberto Giraldo @alb_giraldo]

Primary heart involvement in systemic sclerosis (SSc-PHI) refers to cardiac abnormalities directly attributable to SSc, excluding those secondary to other SSc manifestations (e.g., pulmonary hypertension, interstitial lung disease, renal crisis) or unrelated conditions (e.g., ischemic heart disease). It is an important cause of mortality in SSc and accounts for ~12% of deaths in the EUSTAR cohort.

SSc-PHI may manifest as pericarditis, myocarditis, myocardial fibrosis with conduction defects, or biventricular diastolic/systolic dysfunction. Both microvascular ischaemia and myocardial inflammation contribute to perivascular and myocardial fibrosis in SSc, with an increasing recognition of the role of accelerated macrovascular disease.

Distinguishing primary from secondary cardiac involvement is often difficult due to overlapping symptoms, masked presentations, and shared abnormalities on biomarkers and imaging (e.g., pulmonary arterial hypertension and/or interstitial lung disease vs. right ventricular dysfunction or SSc-PHI).

Management requires a multidisciplinary team (rheumatologist + cardiologist experienced in SSc), however, evidence is limited (mostly small cohorts/case series). Treatment is tailored to the specific cardiac presentation, but key principles include:
◦ Controlling overall SSc disease activity
◦ Supportive care aligned with standard cardiovascular management
◦ First-line immunosuppression: mycophenolate mofetil
◦ Alternatives: tocilizumab or rituximab
◦ Frequent addition of calcium channel blockers or vasodilators

*Soo CY, Jex N, Bissell L-A, Del Galdo F, Plein S. Cardiac involvement in systemic sclerosis: mechanisms, manifestations and management. Rheumatology (Oxford). Published online February 4, 2026.
🔗https://t.co/xaxmgvYsMx

[ERM @Owner_X429]

Old and new autoantibodies in systemic lupus erythematosus