Ольга Костенчак-Свистак Olha Kostenchak-Svystak

PhD, hematologist in Ukraine. 🇺🇦 Admire hematology, science, travelling and literature. Believe in God, good, miracles and medicine

[Aravind Palraj @Rheumat_Aravind]

Ever seen ESR 100 with a normal CRP? Or CRP 150 with ESR 15?

ESR and CRP measure different aspects of inflammation and often tell different stories.

Understanding when they disagree can prevent diagnostic errors and improve clinical decision-making.

What is the biggest ESR–CRP mismatch you’ve encountered in practice?

#Rheumatology #MedTwitter #InternalMedicine @docakx @IhabFathiSulima #MedicalEducation #ClinicalPearls #FOAMed #ESR #CRP #Inflammation #RheumatologyPearls

[Aravind Palraj @Rheumat_Aravind]

Normal CRP ≠ No Inflammation.

Active disease may occur with a normal CRP in:
🔹 SLE (especially lupus nephritis)
🔹 Sjögren disease
🔹 Inflammatory myopathies
🔹 Systemic sclerosis
🔹 Some ANCA-associated vasculitis

Also remember:
💊 IL-6 inhibitors, steroids & JAK inhibitors can suppress CRP
🦠 Early/localized infections may have a normal CRP

Treat the patient, not the number.

#Rheumatology #CRP #Lupus #Vasculitis #Myositis @docakx @IhabFathiSulima #MedTwitter #FOAMed

[British Journal of Haematology @BrJHaem]

📢 Explore the May 2026 issue of @BrJHaem: https://t.co/pHUW9IU345

✨ Congratulations to authors Ashleigh P. Scott and colleagues for their cover figure featured from their article: https://t.co/lnBw4YMoai

@DrAEvens | @WileyHealth

[British Journal of Haematology @BrJHaem]

In a nutshell: The association of thrombocytopenia with haematological malignancy
https://t.co/fyXco8i4uj

[European Hematology Association @EHA_Hematology]

How experts treat Peripheral T- and NK-cell lymphomas 

Prof Francesco D’Amore and Prof Massimo Federico break down the latest ESMO–EHA guideline for peripheral T‑ and natural killer‑cell lymphomas, highlighting the importance of accurate diagnosis in these rare, biologically diverse and often aggressive diseases. Essential listening for clinicians treating PTCLs.

🎧 Listen to the podcast: https://t.co/NDZBnBgpKN
🗃️ Access the guideline: https://t.co/BwKbBWfkr5

[Dr. Chokri Ben Lamine @abouabdrahman0]

🩸 ET with PLT 1600 ×10⁹/L + IDH1+ — high-yield management

⸻

🚨 Red flag
➡️ PLT >1500 → extreme thrombocytosis
➡️ ↑ bleeding risk → acquired VWD until proven otherwise

⸻

🧠 Interpretation

➡️ ET diagnosis + IDH1 mutation
👉 atypical for classical ET
👉 think MPN/MDS overlap or clonal evolution

➡️ Requires:
👉 marrow review + NGS context (ASXL1, SRSF2, etc.)

⸻

🧪 Immediate workup

➡️ vWF activity + Ag
➡️ FVIII level
➡️ Peripheral smear
➡️ Bone marrow morphology review

⸻

💊 Immediate management (do NOT delay)

➡️ Start cytoreduction:
👉 Hydroxyurea (first-line)

➡️ Target:
👉 PLT <400–600

⸻

⚠️ Aspirin decision (CRITICAL)

🚫 If vWF activity <30–40%
👉 NO aspirin

✅ If vWF adequate
👉 low-dose aspirin can be used (especially if JAK2+)

⸻

⚡ If bleeding or urgent surgery
➡️ Consider:
👉 Plateletpheresis (rapid drop)
👉 vWF concentrate if significant bleeding

⸻

🧬 IDH1 significance

➡️ Rare in ET
➡️ Seen in:
👉 clonal hematopoiesis
👉 MDS/MPN overlap
👉 AML evolution

➡️ Action:
👉 closer monitoring for progression

⸻

📊 Risk category

➡️ Regardless of age:
👉 PLT >1500 = cytoreduction indicated

⸻

🧠 Key pearl

➡️ Extreme thrombocytosis ≠ only thrombosis
👉 bleeding risk dominates due to acquired VWD

⸻

🎯 MCQ
ET patient PLT 1.6M → first step before aspirin?
✅ Check vWF activity

⸻

🩺 OSCE
ET + IDH1 + PLT 1600:
➡️ Start hydroxyurea immediately
➡️ Screen for acquired VWD
➡️ Avoid aspirin if vWF low
➡️ Reassess diagnosis (overlap syndrome?)

⸻

#Hematology #ET #MPN #IDH1 #Thrombocytosis #KFSHRC

[Adriana Zucchiatti @zucchiatti_]

Advances in the pathophysiology, diagnosis, and management of celiac disease
https://t.co/oQqMrKMHfy
#GIpath #celiacdisease

[British Journal of Haematology @BrJHaem]

Renal dysfunction in symptomatic Waldenström macroglobulinaemia: A nationwide Italian multicentre study
https://t.co/p0iM4DXv50

[British Journal of Haematology @BrJHaem]

✨️ BJHaem Editor's pick - March ✨️
Assessment of measurable residual disease in ovarian tissue collected for fertility preservation in patients in remission from acute myeloid leukaemia: A pilot study
https://t.co/vYNR7y7rKa
@DrAEvens | @WileyHealth

[Only Cells @OnlyCellsLTD]

🩸#MorphologyMonday | Case MM251110: May Hegglin anomaly

https://t.co/uiW9ndzY8b

✅ 28-year-old patient
✅ Mild symptoms only: occasional easy bruising, no major bleeding history.
✅ Platelets 62 × 10⁹/L
✅ Blood film: Large platelets + pale blue Dӧhle body like inclusions in neutrophils.

Diagnosis: May Hegglin anomaly

#OnlyCells #BloodFilm #Platelets #Genetics #LabDiagnostics

[Dr. Chokri Ben Lamine @abouabdrahman0]

📘 Low-Dose Dasatinib (50 mg/day) vs Standard-Dose (100 mg/day) as Frontline Therapy in CML-CP
(Jabbour E. et al., Am J Hematol 2022;97(11):1413–1418)

⸻

👨‍⚕️ Study Design:
•233 patients with CML-CP treated with dasatinib 50 mg/day (n=83) or 100 mg/day (n=150).
•Propensity score–matched cohort: 77 patients per group.
•Median follow-up: 48 months.

⸻

📊 Key Results:
•🧬 1-year MR4: 63% vs 43% (p=0.009)
•🧬 1-year MR4.5: 53% vs 36% (p=0.03)
•🧬 1-year CMR: 46% vs 33% (p=0.06)
•💨 Pleural effusions: 3% (DAS50) vs 21% (DAS100) (p=0.016)
•🕒 4-year Failure-Free Survival (FFS): 89% vs 77% (p=0.04)
•TFS: 100% both arms
•EFS: 95% vs 92% (NS)

⸻

💡 Interpretation:
•Dasatinib 50 mg daily maintained comparable molecular responses with lower toxicity and superior 4-year FFS.
•Supports FDA/academic trend toward dose optimization rather than maximal tolerated dosing.

⸻

📚 Reference:
Jabbour E, et al. Am J Hematol. 2022;97(11):1413–1418. DOI: 10.1002/ajh.26689

#CML #Dasatinib #LowDoseTKI #DoseOptimization #Hematology #MDAnderson #ASH #KFSHRC

[Dr. Chokri Ben Lamine @abouabdrahman0]

🧪 Reticulocyte Index (RI) – Quick Hematology Pearl

🩸 Why we use it?
RI helps judge bone marrow response to anemia ✅ (Is marrow compensating or not?)

📊 Formula
RI = Retic % × (Patient Hct / Normal Hct) ÷ Maturation Factor
🔧 Normal Hct ~ 45%

⏳ Maturation Factor (reflects marrow stress):
•Hct 40–45% → ×1
•Hct 30–39% → ×1.5
•Hct 20–29% → ×2
•Hct <20% → ×2.5

📈 Interpretation
•RI <2 → Hypoproliferative anemia ❌ (marrow NOT responding)
🔎 Causes: Iron deficiency 🧲, ACD/inflammation 🔥, CKD ↓EPO, marrow failure (AA/MDS), chemo
•RI >2 → Hyperproliferative anemia ✅ (marrow responding)
🔎 Causes: Hemolysis 🧨, acute blood loss 💉, hemoglobinopathies

🧭 Example
Retic 4%, Hct 20%
RI = 4 × (20/45) ÷ 2.5 = 0.7 ➝ Inadequate response → hypoproliferative

💡 Tips
•Always correct retics with RI before interpreting anemia 🔍
•Combine with LDH, bilirubin, haptoglobin for hemolysis workup 🧬
•Retic % alone is misleading in anemia ➝ use RI

#Hematology #BoneMarrow #Anemia #ClinicalPearls #MedEd #HemeFellows #BoardReview

[Reumatoscience @reumatoscience]

#ACR2025

[Vincent Rajkumar @VincentRK]

One of the main goals of our review article in @NEJM on MGUS was to provide clear clarifications on the concept of “monoclonal gammopathy of clinical significance” (MGCS). It’s all very confusing in the literature and can cause problems for patients if we are not totally clear of the concepts.

Read on to be 100% sure of the concepts so you can take care of your patients correctly!

1) First key concept: MGUS is a clinically indolent condition that usually remains quiet for an entire lifetime. The problem with MGUS is that it can progress to symptomatic malignancy (like multiple myeloma), or cause a variety of non-malignant, serious, and clinically important diseases that are collectively referred to as “monoclonal gammopathy of clinical significance” (MGCS).

2) Second key concept: MGCS is like the title of chapter in a textbook. It is NOT the name of a disease. Within the term “MGCS” are several distinct diseases, each of which has its own diagnostic criteria, clinical manifestations, and treatment strategies. So you simply cannot diagnose “MGCS” and treat but need to identify the specific disease. All that the term MGCS does is to alert you that MGUS can cause serious non-malignant diseases besides progression to malignancy.

3) Third key concept is: Some of the MGCS conditions are multi-system disorders like light chain amyloidosis and light chain deposition disease. Some MGCS disorders on the other hand are restricted to one organ leading to more confusing terms like “monoclonal gammopathy of renal significance” (MGRS), “monoclonal gammopathy of dermatologic significance” (MGDS), monoclonal gammopathy of neurological significance” (MGNS), and so on. These are also like titles of book chapters NOT the names of a disease. Within each term are specific unique diseases.

4) Fourth key concept is: For taking care of the patient you need to know the name of the exact disease. Not just add an umbrella term like “MGCS” or “MGRS”. So for example instead of diagnosing “MGRS” you need to be clear exactly which kidney disease the monoclonal protein is accused of causing! MGUS is so common and so many people can have a MGUS and a completely unrelated kidney disease. MGUS plus kidney disease doesn’t mean “MGRS”. Most of the time the two have nothing to do with each other.

There are specific kidney diseases that are casually related to the monoclonal protein and if we suspect MGRS for some reason we need to work up and make the specific diagnosis which needs a kidney biopsy: proliferative glomerulonephritis with immunoglobulin deposits (PGNMID), C3 glomerulonephritis, and so on. Each of these disease have their unique clinical and lab manifestations, and treatment strategies.

5) Fifth key concept is: with more and more sensitive tests for MGUS and more and more testing done for MGUS we are all going to find M proteins associated with a variety of clinical problems, 99% of which are NOT caused by the M protein. I am hugely concerned with labels like MGCS and MGRS wrongly applied. And the last thing we want is Dara-VRd for a DVT just because there is a paper that says M proteins can cause blood clots!

This Review will be a good place to start for getting all the key concepts straight. https://t.co/XErNkLVA48

[Bread & Butter Haematology @MorphologyAmigo]

Leucocytosis ...
The Handy Chart to Keep for Everyday Clinical Work

#medicine #meded #medtwitter #hematology
From My Undergraduate Teaching Slide Set
Learning Lesson : Not every WCC is Malignant :)

[British Journal of Haematology @BrJHaem]

2025 British Society for Haematology Guideline for the treatment of chronic lymphocytic leukaemia
https://t.co/QoWhUXDEto

[Jasmine Sethi @JasmineNephro]

🧵Great info on ANA interpretetion

⏬

[Aravind Palraj @Rheumat_Aravind]

ANCA Patterns — Simplified 🔬
• c-ANCA → Cytoplasmic glow → PR3 → Granulomatosis with polyangiitis (GPA)
• p-ANCA → Perinuclear halo → MPO → MPA, EGPA, autoimmune liver disease
• Atypical ANCA → Patchy fluorescence → IBD, autoimmune hepatitis, infections, drugs

👉 Always confirm with PR3/MPO ELISA + clinical context.
@DrAkhilX @IhabFathiSulima
#Rheumatology #Vasculitis #LabMedicine #MedEd #MedTwitter

[Manual Of Medicine @ManualOMedicine]

Anticoagulation Dosing Cheat Sheet

#medtwitter #foamed #meded

[Ahmed Kotb @AhmedKo45911157]

🧪 Thrombophilia testing pitfalls
⚠️ False ↓ PC/PS/AT in: acute VTE, heparin, warfarin, pregnancy, liver disease, chemo
💊 DOACs affect functional assays → confirm assay type
👉 Always interpret results in clinical context
#ASH #VTE