Mona vijayaran

DM (Clinical Hematology) AIIMS Delhi
Assistant Professor, SGPGI, Lucknow

[Dr. Iftikhar khan @DrIftikharkhann]

A narrative review can be your PubMed indexed publication. It is your own perception plus the literature, built around one gap.

Most people never attempt one because nobody teaches the process.

Here it is, start to finish

[Joshua Brody, MD @JoshuaBrodyMD]

Complete remission in 85% of patients with high-risk #DLBCL #lymphoma by adding #epcoritamab #immunotherapy to standard rx! Congrats to Drs. Falchi and Belada and the whole team and the patients and their families!
https://t.co/PUeylMAIqK

[Talha Badar @TalhaBadarMD]

Frontline AML therapy is rapidly evolving with targeted and lower-intensity options.

We created a quick upfront AML treatment algorithm to help guide initial therapy selection by patient fitness and disease biology.

Open Medicine link: https://t.co/3iGC8kBqxy

@OpenMedicineHQ #AML #Leukemia #leusm #PrecisionMedicine

[Rahul Banerjee, MD, FACP @RahulBanerjeeMD]

Another chapter of #downwithdex, this time for AL amyloidosis!

By the book, dex 20-40 mg QW for 6 months in ANDROMEDA. No need for this in real life.

No ∆ in efficacy; rise in CHF exacerbations and ⬆️ diuretics with prolonged dex.

I do 4-8 weeks of 12-20 mg then stop.

[Dr. Chokri Ben Lamine @abouabdrahman0]

🧬 Post-transplant AML relapse is not one disease.

Five overlapping mechanisms drive relapse after allo-HCT:

1️⃣ Immune escape: HLA loss/↓antigen presentation → consider NK-cell approaches
2️⃣ T-cell exhaustion: PD-1, TIM-3, LAG-3 ↑ → checkpoint blockade ⚠️ GVHD
3️⃣ Clonal evolution: FLT3/IDH/NPM1/KMT2A → genotype-directed therapy 🎯
4️⃣ Leukemic stem-cell persistence → hypomethylating agent-based strategies
5️⃣ Marrow-niche remodeling → rational combination therapy

💡 DLI requires intact antigen presentation; HLA-loss relapse may be intrinsically resistant. Reassess MRD, chimerism, HLA status and molecular evolution—then treat the dominant biology.

❓MCQ: Which relapse mechanism predicts poor DLI efficacy?
✅ Acquired HLA loss.

🩺 OSCE pearl: Before selecting salvage therapy, obtain marrow morphology/MRD, lineage chimerism, cytogenetics/NGS and evaluate immune-escape mechanisms.

👏 Credit: Antonella Bruzzese, Enrica Antonia Martino, Nicola Amodio, Fortunato Morabito, Massimo Gentile & Ernesto Vigna.

🔗 Bone Marrow Transplantation, 2026⁠

#AML #AlloHCT #BMT #MRD #Leukemia

[Henry C Fung| MM, lymphoma, leukemia & CART @HenrychihangFu1]

Modern first relapse after quadruplet therapy is increasingly characterized by what the myeloma has already escaped, not simply by the number of prior lines of therapy.

🧬 Match the patient
• Lenalidomide-refractory
• Dara + Len double-refractory
• True triple-class refractory

🧬 Match the biology
• Standard risk
• Functional/cytogenetic high risk
• Ultra-high-risk biology

🧬 Match the evidence
• CARTITUDE-4 and MajesTEC-9 provide the most relevant randomized evidence for early relapse, but neither trial fully reflects today's post-quadruplet, Dara-refractory population.
• CARTITUDE-1 and MajesTEC-1 complement these studies by providing important evidence in predominantly triple-class–refractory disease.

No single trial perfectly represents modern first-relapse, quadruplet-exposed myeloma. This framework integrates the most applicable evidence while recognizing the strengths and limitations of each study.

💡 Clinical pearl:
Match the patient. Match the biology. Match the evidence.

#MultipleMyeloma #Medtwitter

[Benlazar S M A @smbenlazar]

Glofitamab plus gemcitabine and oxaliplatin for relapsed/refractory DLBCL: 3-year follow-up of STARGLO https://t.co/92fandxUph #lymsm

[Dr. Chokri Ben Lamine @abouabdrahman0]

🧵 How does CIBMTR classify conditioning intensity before HCT? 🧬🔥

Excellent explanation by Dr Shaikha Alotaibi, KFSHRC 🇸🇦👏

Understanding the difference between myeloablative conditioning (MAC), reduced-intensity conditioning (RIC), and non-myeloablative conditioning (NMA) is essential for transplant selection, toxicity assessment and CIBMTR reporting.

1/8 🧬 Why give conditioning before allo-HCT?

Conditioning aims to:

🔥 Reduce or eradicate malignant cells
🛡️ Suppress the recipient’s immune system
🚫 Prevent graft rejection
🏠 Create marrow space for donor hematopoiesis
🎯 Facilitate donor engraftment and chimerism
⚔️ Allow the donor graft-versus-tumour effect

The balance is always:

📈 Disease control + engraftment
versus
📉 Organ toxicity + non-relapse mortality

2/8 🔥 Myeloablative conditioning—MAC

MAC uses high-dose chemotherapy and/or radiation producing:

💥 Profound marrow ablation
🩸 Severe, prolonged pancytopenia
🧬 Near-complete recipient hematopoietic eradication
🦠 Marked immunosuppression
🩹 Mandatory stem-cell rescue

Without stem-cell infusion, hematopoietic recovery is generally not expected.

✅ Advantages: stronger cytoreduction and usually lower relapse risk
⚠️ Limitations: more mucositis, infections, organ toxicity, VOD/SOS and NRM

3/8 📉 Non-myeloablative conditioning—NMA

NMA uses substantially lower chemotherapy/radiation doses.

It primarily provides:

🛡️ Immunosuppression sufficient for engraftment
🩸 Minimal or relatively short cytopenia
🧬 Initial mixed donor–recipient chimerism
⚔️ Greater reliance on donor immune-mediated graft-versus-tumour activity

✅ Lower early organ toxicity and NRM
⚠️ Potentially more graft rejection, mixed chimerism and disease relapse

Common conceptual example: low-dose TBI-based conditioning, often with fludarabine.

4/8 ⚖️ Reduced-intensity conditioning—RIC

RIC lies between MAC and NMA:

🩸 Produces clinically significant cytopenia
🌱 Stem-cell support is required
↩️ Marrow suppression may not be irreversibly ablative
⚔️ Disease control depends on both chemotherapy and graft-versus-tumour activity

📌 Operationally, RIC includes regimens that meet neither full MAC nor classic NMA criteria.

RIC is commonly considered for:

👴 Older recipients
🫀 Significant comorbidities
🧾 High HCT-CI
🧪 Previous intensive therapy/HCT
⚠️ Patients unable to tolerate MAC

Chronological age alone should not determine intensity.

5/8 ☢️ CIBMTR operational MAC thresholds

Classify as myeloablative when the prescribed regimen exceeds these thresholds:

🔥 TBI:
• >500 cGy as a single fraction
• >800 cGy when fractionated

💊 Busulfan:
• >7.2 mg/kg IV
• >9 mg/kg orally
• >300 mg/m² IV
• >375 mg/m² orally

💊 Melphalan: >150 mg/m²
💊 Thiotepa: ≥10 mg/kg
💊 Treosulfan: >30 g/m²

Combination examples include:

🧪 Cyclophosphamide + high-dose TBI
🧪 Cyclophosphamide + etoposide + high-dose TBI
🧪 High-dose busulfan + cyclophosphamide
🧪 High-dose busulfan + melphalan >150 mg/m²

6/8 🌿 CIBMTR RIC/NMA operational examples

These fall within the combined RIC/NMA reporting category:

☢️ TBI:
• ≤500 cGy single fraction
• ≤800 cGy fractionated

💊 Busulfan:
• ≤7.2 mg/kg IV
• ≤9 mg/kg orally
• ≤300 mg/m² IV
• ≤375 mg/m² orally

💊 Melphalan: ≤150 mg/m²
💊 Thiotepa: <10 mg/kg
💊 Treosulfan: ≤30 g/m²

Regimen examples:

🧪 Fludarabine + low-dose TBI
🧪 Fludarabine + cyclophosphamide
🧪 Fludarabine + cytarabine
🧪 ATG + cyclophosphamide
🧪 Etoposide + cyclophosphamide
🧪 BEAM

[Dr. Chokri Ben Lamine @abouabdrahman0]

🔥 Subcutaneous Blinatumomab (SC Blina) – The Future of B-ALL Immunotherapy 🔥

💉 Why SC Blina?
✔️ Avoids 28-day continuous IV infusion
✔️ Outpatient-friendly
✔️ Better patient quality of life
✔️ Comparable efficacy & PK vs IV form

📊 Key Data (R/R B-ALL)
•Jabbour et al, AJH 2024 (Phase 1b)
✅ CR/CRh: 86–92%
✅ High MRD-negativity
✅ No grade ≥4 CRS/ICANS
•Jabbour et al, Lancet Haematology 2025
✅ CR/CRh: 75–79%
✅ Manageable safety (22% neutropenia, 17% ICANS)
•Blood 2022 (early cohort)
✅ Promising activity
✅ Low CRS
✅ 0% treatment-related mortality

🔬 Dose Examples Under Study
•250→500 μg QD TIW
•500→1000 μg QD TIW (step-up strategy)

✅ Conclusion
SC Blinatumomab = high efficacy + manageable safety + PK equivalence → practical alternative to IV and ideal for global access.

#ALL #Blinatumomab #SubcutaneousTherapy #Immunotherapy #Leukemia #Hematology #SOHOKSA #SOHO

[Vincent Rajkumar @VincentRK]

Updated FAQs on newly diagnosed multiple myeloma for 2026!

1. Which frontline regimen to use?
Quad regimen, either Dara-VRd or Isa-VRd

2. How long to give the Quad regimen?

4 months and then transplant, or
6 months if transplant ineligible or deferred

3. What maintenance after initial therapy?

Standard risk: Dara or Isa plus Lenalidomide

High Risk: Dara or Isa plus Lenalidomide; or bortezomib plus Lenalidomide

4. How long to give maintenance?

Standard risk: Lenalidomide for 2 years and stop; Dara or Isa till progression.

High risk: Till progression.

5. Is transplant still recommended in eligible patients?

High risk myeloma: Yes.
Standard risk: Early vs delayed- Shared decision making based on age and patient preference.

6. Definition of High risk myeloma?

Del 17p is high risk by itself
All the others (4;14, 1q, 1p, etc) all need two abnormalities together to call as high risk.
(P53 mutation and bi-allelic del 1p also high risk; but small numbers)

Check out https://t.co/qeXZaqzOpV to make this assessment easily.

7. What about CART or bispecifics in newly diagnosed myeloma.

Totally Investigational. Done only on approved clinical trials

8. What about frail patients who cannot tolerate quadruplet?

Triplet: DaraRd or IsaRd; if that’s not possible or safe: Rd or even single agent Dara may sometimes be needed at least initially till performance status improves.

9. What about patients with acute renal failure?

Prefer Dara-VCd rather than Dara-VRd

10. How long to give the Dex?

Keep Dex only for initial 4-6 months. No dex in maintenance.

[Talha Badar @TalhaBadarMD]

Blinatumomab moves the needle in frontline high-risk Ph-negative B-#ALL @BloodPortfolio

In the GRAALL-2014/B QUEST study, blinatumomab consolidation:
✅ Higher MRD negativity: 72% vs 54% (P=0.04)
✅ Improved disease-free survival: ~70% vs ~45% at 5 years (P=0.001)
✅ Improved overall survival: ~75% vs ~60% at 5 years (P=0.03)

The remaining question is whether allogeneic HCT is still required for patients with MRD neg after blinatumomab, an area that warrants prospective evaluation.

Congratulations to Boissel and colleagues on this important contribution.

[Jayant Gadrey @JayantYGadrey6]

Beyond thrilled to share our (w/ @HannahUckelmann & @BrunettiLab) Spotlight article in @BloodPortfolio !!🤩NPM1-mutant AML is the most common subset of AML worldwide. For ~20 years since defining this subset, researchers wondered: how does a mainly cytoplasmic protein drive leukemia causing gene expression programs? What does this mean for treating these patients? We NOW have answers!

@Armstrong_dfci @Goodell_Lab

@rosslevinemd @Daver_Leukemia @jayastuMD @LeukDocJZ @beatalleukemia @DrGauravNarula @nvpatkar @AML_Hub @oncodaily @OncoAlert

https://t.co/cNjnxk02AS

[Dr. Chokri Ben Lamine @abouabdrahman0]

🌱 Engraftment Syndrome (ES) vs Sepsis vs Other Differential Diagnoses After HSCT 🧵

🔥 Engraftment Syndrome (ES)
📅 Typically occurs around neutrophil recovery (ANC > 500/µL), usually D+7 to D+14 after auto-SCT and allo-SCT.
🌡️ Non-infectious inflammatory syndrome due to cytokine surge.
🧬 Mediated by IL-1, IL-6, TNF-α, and capillary leak.

🔑 Classic Clinical Features
🌡️ Fever ≥38.3°C without documented infection.
🌬️ Non-cardiogenic pulmonary infiltrates/hypoxemia.
⚖️ Weight gain >2.5%.
💧 Edema/capillary leak.
🩹 Erythematous maculopapular rash.
🫀 Hypotension.
🧠 Occasionally encephalopathy.
🫁 Pleural effusions.
💧 Renal dysfunction.

📌 Spitzer Criteria
Major:
🌡️ Fever
🩹 Rash >25% BSA
🫁 Non-cardiogenic pulmonary edema

Minor:
💧 Weight gain
🫀 Hepatic dysfunction
🩸 Renal dysfunction
🧠 Encephalopathy

Diagnosis:
✅ 3 major OR
✅ 2 major + 1 minor within 96 hours of engraftment.

⚡ Maiolino Criteria
🌡️ Non-infectious fever +
🩹 Rash OR
🫁 Pulmonary infiltrates OR
💩 Diarrhea.

🧪 Typical Laboratory Findings
📈 Rising CRP and ferritin.
📉 Hypoalbuminemia.
📈 Creatinine.
📈 LFTs.
🦠 Blood cultures negative.

💉 Treatment
💊 Methylprednisolone 1–2 mg/kg/day.
⏱️ Dramatic response within 24–48 hours strongly supports ES.
📉 Taper over 3–5 days if improving.

🚨 Sepsis
🦠 Proven or presumed infection with systemic inflammatory response.
🌡️ Fever or hypothermia.
🫀 Persistent hypotension.
🧪 Positive cultures may be present.
📈 Procalcitonin often elevated.
⚠️ Usually no rapid steroid response.

💊 Management
🧫 Cultures.
🧪 Lactate.
💉 Broad-spectrum antimicrobials immediately.
💧 Fluid resuscitation.
🫀 Vasopressors if needed.

🔍 How to Differentiate ES vs Sepsis
📅 ES coincides with neutrophil recovery.
🩹 Rash and weight gain favor ES.
🫁 Diffuse pulmonary infiltrates with rapid steroid response favor ES.
🦠 Positive cultures or focal infection favor sepsis.
📈 Very high procalcitonin supports infection (not perfect).

🧠 Other Important Differential Diagnoses

🦠 Bacterial, fungal, or viral infection (CMV, HHV-6, adenovirus).
🫁 Diffuse alveolar hemorrhage.
💊 Drug fever (e.g., β-lactams, amphotericin, G-CSF).
🫀 Fluid overload or heart failure.
🩸 SOS/VOD.
🫁 Idiopathic pneumonia syndrome.
🧬 Acute GVHD.
🧫 HLH/MAS.
🧠 PRES.
🩸 TA-TMA.
💉 Cytokine release syndrome (post CAR-T).
🦠 Pneumocystis jirovecii pneumonia.

🧪 Suggested Workup
🩸 CBC, CMP, CRP, ferritin, procalcitonin.
🧫 Blood/urine cultures.
🦠 Viral PCRs.
🫁 CT chest.
🫀 BNP, echocardiography if fluid overload suspected.
🩸 Coagulation profile if DAH suspected.

💎 Practical Pearl
🌱 Fever + rash + weight gain + hypoxemia at neutrophil recovery with negative cultures and rapid steroid response = think Engraftment Syndrome until proven otherwise.

📚 References:
🔹 European Society for Blood and Marrow Transplantation Handbook.
🔹 American Society for Transplantation and Cellular Therapy supportive care guidance.
🔹 Spitzer TR. Bone Marrow Transplant. 2001.
🔹 Maiolino A. Bone Marrow Transplant. 2003.

#Hematology #HSCT #BMT #EngraftmentSyndrome #Sepsis #TransplantMedicine

[Dr. Chokri Ben Lamine @abouabdrahman0]

🧬 Immunology / IEI Classification — Consultant-Level Pearls (IUIS Framework)

⸻

🧠 BIG PICTURE

🧬 Inborn Errors of Immunity (IEI) → >450 disorders
👉 2 major axes:
🔹 Immunodeficiency (infection)
🔹 Immune dysregulation (autoimmunity/inflammation)

⸻

🔴 1. COMBINED IMMUNODEFICIENCIES (CID)

🧬 T-cell ± B-cell defects
👉 Severe infections (viral, fungal, opportunistic)

📌 Examples:
👉 SCID (IL2RG, ADA)
👉 ZAP70 deficiency

🧠 Key pearl → early, severe, multi-organ infections

⸻

🔴 2. COMBINED IMMUNODEFICIENCY WITH SYNDROMIC FEATURES

🧬 Immune + extra features (neuro, skeletal, dysmorphism)

📌 Examples:
👉 Wiskott-Aldrich → thrombocytopenia + eczema
👉 Ataxia-telangiectasia → neuro + cancer risk
👉 DiGeorge (22q11)

🧠 Pearl → if syndromic → think this group

⸻

🔴 3. PREDOMINANT ANTIBODY DEFICIENCIES

🧬 B-cell / Ig defects

📌 Examples:
👉 CVID
👉 X-linked agammaglobulinemia

🧠 Pearl → recurrent sinopulmonary bacterial infections

⸻

🔴 4. DISEASES OF IMMUNE DYSREGULATION (PIRD)

🧬 Failure of immune tolerance

📌 Examples:
👉 CTLA-4 deficiency
👉 LRBA deficiency
👉 STAT3 GOF
👉 FOXP3 (IPEX)

🧠 Pearl → autoimmunity + cytopenias + lymphoproliferation

⸻

🔴 5. CONGENITAL DEFECTS OF PHAGOCYTES

🧬 Neutrophil number/function defects

📌 Examples:
👉 CGD
👉 Severe congenital neutropenia

🧠 Pearl → recurrent abscesses, catalase+ organisms

⸻

🔴 6. DEFECTS IN INTRINSIC & INNATE IMMUNITY

🧬 Pathogen-specific susceptibility

📌 Examples:
👉 IL-12/IFN-γ axis → mycobacteria
👉 TLR defects

🧠 Pearl → unusual infections in otherwise healthy pts

⸻

🔴 7. AUTOINFLAMMATORY DISORDERS

🧬 Innate immune overactivation (NO autoantibodies)

📌 Examples:
👉 FMF
👉 CAPS

🧠 Pearl → recurrent fevers + inflammation

⸻

🔴 8. COMPLEMENT DEFICIENCIES

🧬 Complement pathway defects

📌 Examples:
👉 C5–C9 → Neisseria infections
👉 C1q/C2 → lupus-like disease

🧠 Pearl → encapsulated bacteria + autoimmunity

⸻

🔴 9. BONE MARROW FAILURE / HEMATOPOIETIC DEFECTS

🧬 Stem cell / marrow disorders

📌 Examples:
👉 Fanconi anemia
👉 Dyskeratosis congenita

🧠 Pearl → cytopenias + cancer predisposition

⸻

🔴 10. PHENOCOPIES OF IEI

🧬 Acquired but mimic IEI

📌 Examples:
👉 Anti–IFN-γ antibodies
👉 Somatic mutations

🧠 Pearl → adult onset “genetic-like” disease

⸻

🧠 HEMATOLOGY LINK (VERY HIGH-YIELD)

🩸 Autoimmune cytopenias → think PIRD
🩸 HLH → immune dysregulation / cytotoxic defect
🩸 Recurrent infections → antibody / CID
🩸 Neutropenia → phagocyte disorders

⸻

🎯 OSCE CLASSIFICATION TEMPLATE

🗣️ “This falls under IEI, specifically [category], based on dominant phenotype: infection vs immune dysregulation vs syndromic features.”

⸻

🔥 CONSULTANT TAKE-HOME

🧠 Infection → think deficiency
🧠 Autoimmunity → think dysregulation
🧠 Syndromic → think combined + extra features
🧠 Always classify BEFORE diagnosing

⸻

[Benlazar S M A @smbenlazar]

Glofitamab crosses the blood-brain barrier and exhibits activity against primary and secondary CNS lymphoma https://t.co/94OgAHK1fY #lymsm

[Henry C Fung| MM, lymphoma, leukemia & CART @HenrychihangFu1]

💣 AZA + VEN doesn’t fail—execution does.

Day 21 marrow decides everything.
Shorten VEN, not AZA.
Don’t wait for perfect counts.

Here’s how we induce AML in 2026 👇

Please let us know your approach.

#AML #HemeTwitter

Dr Fun + G

[Benlazar S M A @smbenlazar]

NPM1-mutated AML: 2 faces of the same coin https://t.co/w1jWmj2rUD #leusm

[Dr Rudra Narayan Swain M.D , D.M @rudra09s025]

What should be the optimal strategy after AZA–VEN–induced remission in younger AML patients not proceeding to allo-HSCT?

Our recent work explores this clinically relevant question.
Read more in @BloodCancerJnl : 👉https://t.co/D2qYE1Vjbm

Grateful to @ArihantDr, @DrGPrakash, and @DrPMPGI Sir, for their invaluable support and conceptual guidance.
@AML_Hub #leusm #Hematology @blood_academy @SOAsocialmedia @ims_sum

[Henry C Fung| MM, lymphoma, leukemia & CART @HenrychihangFu1]

Myeloma Signal: TP53

TP53 is the guardian of genomic integrity.

Cyclin D powers the cell.
TP53 keeps it under control.

Monoallelic loss:
→ genomic instability begins
→ subclones emerge

Biallelic inactivation:
→ checkpoint failure
→ clonal evolution accelerates
→ therapy resistance dominates

This is not just high-risk disease.

This is evolution without control.

[ALL Hub @ALL_Hub_]

Explore the @ASH_hematology 2026 #AcuteLymphoblasticLeukemia guidelines for asparaginase management, including recommendations on dosing, premedication, TDM, and switching formulations in AYA patients with #ALL.

https://t.co/2pnJBVG0a7

#ALLsm #leusm #MedEd