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Leucocytoses & leucopenia Jo Caers Dept of Clinical Hematology [email protected] Bone marrow Blood Granulopoiesis Proliferation & 5 days maturation Storage 1 day Marginisation& Circulation 1 day Tissues 1-2 days Granulopoiesis Proliferation & 5 days maturation Storage 1 day Marginisation& Circulation 1 day Tissues 1-2 days Granulopoiesis Proliferation & 5 days maturation Storage 1 day Marginisation& Circulation 1 day Tissues 1-2 days Lymphocytes Monocytes NORMAL BLOOD CELL COUNT Hemoglobin 12.0 – 15.0 g/dl (F) 13.0 – 17.0 g/dl (M) Red Blood Cells 3.9 – 5.6 x 10 6/µl (F) 4.5 – 6.5 x 10 6/µl (M) Hematocrit 36 – 48% (F) 40 – 52% (M) Mean Corpuscular Volume 80 – 95µ³ Mean Hb Concentration 27 – 34 pg Conc corp mean Hb 30 – 35 g/dl Reticulocytes 0.5 – 20 % Leucocytes 4.0 – 10.0 x 10 3/µl ¨ Neutophils 1.8 – 7.5 Lymphocytes 1.5 – 3.5 Monocytes 0.2 – 0.8 Eosinophils 0.04 – 0.45 Basophils 0.01 – 0.1 Platelets 100 – 400 x 10 3/dl Hyperleucocytosis > 10.000 WBC/mm³ Normal Cells Abnormal cells or blastic cells Infections ? Neutrophilia (> 7.500/mm³) Acute Leukemias Lymphocytosis (> 4.500/mm³) Chronic Myelomonocytic Leukemias Chronic Lymhocytic leukemia Chronic Myeloid Leukemia Non Hodgkin Lymphoma Chronic Monocytosis (> 800/mm³) … Inflammations? Eosinophilia (> 400/mm³) Basophilia (> 100/mm³) Leukoerythroblastic reaction Cytopenia with immature RBCs (normoblasts) immature WBCs (agranular neutrophils, myelocytes, metamyelocytes ) Causes BM infiltration • Solid tumor or hematological malignancy • Myelofibrosis Strong BM stimulation • Infection, inflammation, hypoxia, trauma • Severe Hemolytic or megaloblastic anemia • Massive bleeding Leukemoid reaction Leucocytosis ( > 50.000) similar to CML Causes - Infection (TB…) - Stress or infection in newborns - Intensive care Laboratory abnormalities - WBC > 50,000/µL - Formula deviated: immature WBC → hyposegmented neutrophils → métamyelocytes, myelocytes, promyelocytes, Neutropenia Neutrophilcount Riskof infection 1.000-1.500 No significant increase in infection risk 0.500-1,000 Some increased risk in infection (can generally be treated as an outpatient) <0.500 Major increased infection risk (treat all fevers with broad spectrum IV antibiotics as an inpatient CASE 1: ♂ 26 years old BLOOD CELL COUNT Differential Counts (%) - Blasts 1.77 WBC (10 9/L) - Myélocytes 5.88 RBC(10 12 /L) - Métamyelocytes 16.8 Hb(g/dl) 44 Hct (%) - Non segmented 80.7 MCV (fl) 15 Neutrophils 28.4 CMH (pg) 74 Lymphocytes 34 CCMH (g/L) 11 Monocytes 9 MPV (fl) 0.0 Eosinophils 183 Platelets 0.0 Basophils Inherited - Benign familial or racial neutropenia (Africa) - Kostmann Syndrome - Chediak-Higashi - Shwachman-Diamond syndrome - Cyclic Neutropenia: cycles of 3-4 weeks Acquired - Infection * Sepsis * Viral (HIV, HC, CMV, influenza…) - Drug induced - Immune * Auto-immune (Ac anti-neutrophils) * Lupus * Felty = RA + neutropenia and splenomegaly * Chronic benign neutropenia - Hypersplénism - Idiopathic - Pancytopenia (AA, MF, MDS, hematological malignancies) Drug-induced • Definitions - Neutropenia < 2,000 / µL - Agranulocytosis < 500 / µL • Plusieurs mécanismes (1) Central : ↓ granulopoiesis : dose-response effect (2) Central : ineffective granulopoïesis : dose-response effect (3) Periphery: Ab-mediated destruction : no dose-response Central Peripheral • production • destruction • Toxic • Immunologic • Dose-response effect • No dose-response effect • Progressive • Abruptly • Recovery: 2-4 weeks • Recovery: 1-2 weeks eg : chemotherapy eg : phenylbutazone • Médicaments - Rituximab delayed - Azathioprime, MMF C - Metamizol / amidopyrine / noramidopyrine 1/100 P - Phenylbutazone 1/100 P - Phenothiazine C - Thyroid (propylthiouracil , carbimazol) 1/100 C - Anti-epileptics (phenobarbital, DPH, mysoline, carbamazepine) C - Sulfonamides (cotrimoxazole , salazopyrine, chlorpropamide, dapsone) C/P - Indomethacine, diclofenac - Levamizole 2/100 P - Ticlopidine 2/100 P - Deferiprone 5/100 P - Clozapine 1/100 P - Antibiotics β-lactams P - Spironolactone - Procainamide CASE 1: ♂ 26 years old • BM cytology: normal granulopoiesis (normal differentiation) and erythropoiesis • Ultrasound abdomen: nl • Nl iron and vitamin status • Anti-nuclear antibodies: 1/1280 anti-SSA • Anca – • Rheumatoid factor - CASE 2 : ♂ 42 years old Leukocytosis discovered during routine « check-up » Complaints of fatigue and flu-like syndrome Examination: mild splenomegaly CASE 2 : ♂ 42 years old BLOOD CELL COUNTS DIFFERENTIAL (%) - Blasts 39.86 + WBC (10 9/L) 1+ Myelocytes 5.13 RBC (10 12 /L) 2+ Métamyelocytes 15.0 Hb (g/dl) Non segmented 44.6 Hct (%) + 86.9 MCV (fl) 84 Neutrophils 29.3 CMH (pg) 2- Lymphocytes 33.8 CCMH(g/L) 2 Monocytes 13.3 MPV (fl) - Eosinophils 695 + Platelets 9+ Basophils Neutrophilia • Etiologie - Infection - Inflammation (trauma, infarctus, vasculitis, rheumatology) - Drugs G-CSF, GM-CSF ( production & liberation) Corticosteroides (demargination ) Adrenalin (demargination ) - Tabac - Anesthesia, surgery - Exercice - Cold, heat stroke, burns, seizures - Cancer - Chronic stimulation of the BM (bleeding, hemolysis, iTP) - Post-splenectomy - Myéloproliferative disorders - Idiopathic MYELOPROLIFERATIVE NEOPLASMS CML MF PV ET Hématocrit N ou ↑ ↓↓ ↑↑ N Leucocytes ↑↑ ↑ ou ↑↑ ↑↑ ou N N Platelets ↑↑ ou N N ou ↓ ↑ ou N ↑↑ Splénomégaly +++ +++ + + LAP ↓ N ↑↑ N Fibrosis N ou ↑↑ +++ N ou ↑↑ N ou ↑↑ Cytogénétics Phi + Jak2 Jak2 (95%) Jak2/CalR Median Survival 12 1 –5 ans 10 + ans 10 + ans Acute leukemia <20% ? 10% < 10% < 10% Basophilia • Causes - Myeloproliferative neoplasms – CML – PV – TE – MF – Basophilic leucemia • Hypersensitivity reactions IgE–mediated • Inflammatory diseases (RA, RCUH, Crohn) Viral infections • Hypothyroidism • Hyperlipidemai • Oestrogens • Hyperlipidemia CASE 3: ♀ 45 years old • Leucocytosis discovered during « check-up » for asthenia • past History : unremarkable • Physical exam : Slenomegaly 2 cm below costal margin, No hepatomegaly, no lymphnodes. CASE 3: ♀ 45 years old BLOOD CELL COUNT Differential Counts (%) 22 +++ WBC (10 9/L) - Blasts - Myélocytes 4.88 RBC(10 12 /L) - Métamyelocytes 14.8 Hb (g/dl) 44 Hct (%) - Non segmented 90 MCV (fl) 12.3 Neutrophils 30.3 CMH (pg) 85.9 + Lymphocytes 34 CCMH (g/L) 0.0 - Monocytes 9 MPV (fl) 0.9 Eosinophils 183 Platelets 0.9 Basophils Lymphocytosis > 4.500 Ly/mm³ Atypical lympocytes ? EBV serology monoclonality pos neg B monoclonality T monoclonality Infectious CMV (T8↑) CLL / HCL / NHL mononucleosis Hepas (T8↑) ATCL/LGL MM (Ig intraC) (T8↑, T4/T8↓) Toxoplasmosis T NHL HIV (T4↓) Sezary S. (T4↑) Lymphocytosis > 4.500 Ly/mm³ Atypical lympocytes Normal lympocytes No monoclonolity EBV serology monoclonality Viral Acute Brucellosis Mycoplasma B monoclonality T monoclonality Pertussis Chronic Tuberculosis Infectious CMV serology ATCL/LGL CLL / HCL / NHL mononucleosis (T8↑) T NHL Sarcoïdosis MM (Ig intraC) (T8↑, T4/T8↓) Hepas (T8↑) Sezary S. (T4↑) Wegener Toxoplasmosis Syphilis III HIV serology (T4↓) Thyreotoxicosis adrenal insufficiency Pereira I et al Atlas of Peripheral Blood, 2012. B-polyclonal Lymphocytosis related to heavy smoking • Young ladies • Binucleated Lymphocytes • Polyclonal lymphocytes population • Splenomégaly : +/- • ↑ polyclonal IgM • Association with HLA-DR7 • Benign Evolution Leukemia – Lymphoma 1996: 275-279 Phenotype of Peripheral Blood LYMPHOCYTES T = CD3: 60 - 85% CD4: 40 - 60% CD4/CD8: 1.5 - 3 CD8: 20 - 40% B = CD19: 5 - 15% κ/λ : 1.5 à 2 Values in our patient : • Phenotype : 45% of B- lymphocytes (IgM, λ) , CD5 - CD23 - FMC7 +, CD25 + • CRP : < 0.5 mg/dl , LDH : NL , Viral Serology : NL DIFFERENTIAL DIAGNOSIS OF B- LYMPHOCYTOSIS F Chronic Hairy cell LK Prolymphocytic Follicular Mantle Cell Splenic vilous lymphocytic LK LK Lymphoma Lymphomas lymphomas CLL HCL PLL F NHL MCL* SVL ↑↑ lympho ++ + +++ + + +++ Spleen +/- ++ ++ +/- +/- +++ CD19 + + ++ ++ ++ ++ ++ CD5 ++ - -/+ - ++ - CD23 + - - -/+ - - CD10 - - + - - CD11c +/- ++ - - - - FMC7 - - ++ + + + CD103/25 - + - - - -/+ Mature T-cell lymphoproliferative disorders Marker T-LGLL NK-LGLL T-PLL ATLL SS TdT* ----- CD2 + + + + + CD3 ++ - ++ ++ ++ CD4 - - +/- ++ ++ CD5 + + + + + CD7 -/+ - +++ - -/+ CD8 ++ - -/+ - - CD16 + + - - - CD25 - - -/+ ++ -- CD56 -/+ + - - - Other CD11b+ HTLV1+ CD16+ CD57+ T-LGLL, T-cell large granular lymphocyte leukemia; NK-LGLL, NK-cell large granular lymphocyte leukemia; T- PLL, T cell prolymphocytic leukemia; ATLL, adult T cell leukemia/lymphoma; SS, Serazy syndrome. *TdT : terminal deoxynucleotidyl transferase differentiates these cells from lymphoblasts of ALL CASE 4: ♂ 23 years old Back from a stay in China for professional reasons Complaints : Fatigue, NS, subT ° , Weight loss +/- 2kg, No pruritus , no diarrhea. Past history : unremarkable Treatment : none Alcohol / tabacco : moderate Phys Exam : 5 cm diameter left Sub-clavicular LN CASE 4: ♂ 23 years old Differential (%) BLOOD CELL COUNT - Blasts 19.6 + WBC (10 9/L) - Myelocytes 12 4.3 RBC (10 /L) - Métamyelocytes 12.8 Hb (g/dl) - Non segmented 37.7 Hct (%) + 88.5 MCV (fl) 66.2 Neutrophils 29.6 MCH(pg) 7.9 Lymphocytes 33.9 MCCH (g/L) 7.3 + Monocytes 6.6 MPV (fl) 18.3 + Eosinophils 473.000 + Platelets 0.6 Basophils Causes of Eosinophilia Mild > 500, Moderate >1500, high >5000/ul • Allergies (industrialised countries) – atopia – Drug (Il-2 treatment) • Parasitosis (especially in developing countries) • Neoplasia – Hematological – - clonal eosinophilia in myeloid pathologies – - Polyclonal paraneoplasic eosinophilia in lymphoid pathologies – Solid tumors (uterus, lung, colon) • Idiopathic (SHE, GI eosinophilia, Eos pneumonia, Eosinophilic
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  • ICON: Eosinophil Disorders

    ICON: Eosinophil Disorders

    ICON: Eosinophil Disorders The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Valent, P., A. D. Klion, L. J. Rosenwasser, M. Arock, B. S. Bochner, J. H. Butterfield, J. Gotlib, et al. 2012. “ICON: Eosinophil Disorders.” The World Allergy Organization Journal 5 (12): 174-181. doi:10.1097/WOX.0b013e31827f4192. http://dx.doi.org/10.1097/ WOX.0b013e31827f4192. Published Version doi:10.1097/WOX.0b013e31827f4192 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:11717517 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA CONSENSUS DOCUMENT ICON: Eosinophil Disorders Peter Valent, MD,1 Amy D. Klion, MD,2 Lanny J. Rosenwasser, MD,3 Michel Arock, PharmD, PhD,4 Bruce S. Bochner, MD,5 Joseph H. Butterfield, MD,6 Jason Gotlib, MD,7 Torsten Haferlach, MD,8 Andrzej Hellmann, MD,9 Hans-Peter Horny, MD,10 Kristin M. Leiferman, MD,11 Georgia Metzgeroth, MD,12 Kenji Matsumoto, MD, PhD,13 Andreas Reiter, MD,12 Florence Roufosse, MD, PhD,14 Marc E. Rothenberg, MD, PhD,15 Hans-Uwe Simon, MD, PhD,16 Karl Sotlar, MD,9 Peter Vandenberghe, MD, PhD,17 Peter F. Weller, MD,18 and Gerald J. Gleich, MD11,19 Key Words: eosinophil disorders, hypereosinophilic syndrome Several different neoplastic, paraneoplastic, infectious, and aller- (HES), global consensus, classification gic disorders may underlie HE.
  • The Idiopathic Hypereosinophilic Syndrome and Eosinophilic Leukemias

    The Idiopathic Hypereosinophilic Syndrome and Eosinophilic Leukemias

    Editorials, Comments & Views Editorials, Comments & Views tion event permitted the diagnosis to be made. The idiopathic hypereosinophilic syndrome and For several decades the true nature of many exam- eosinophilic leukemias ples of idiopathic HES remained obscure although the striking male dominance suggested that one or more he idiopathic hypereosinophilic syndrome (idio- entities were there to be discovered. Recent research pathic HES) was first defined by Chusid et al. in has revealed at least two explanations of such cases T1975 as a condition in which there was unex- of chronic eosinophilia: (i) reactive eosinophilia as a plained eosinophilia (eosinophil count greater than response to cytokines secreted by aberrant T cells; (ii) 1.5×109/L) persisting for at least 6 months and lead- chronic eosinophilic leukemia with clonal molecular ing to tissue damage.1 The requirement for the genetic abnormalities but generally without cytoge- eosinophilia to persist and remain unexplained for six netic abnormalities. With the application of appropri- months served to exclude examples of reactive ate diagnostic techniques, the number of patients in eosinophilia in which an explanation emerged during whom the eosinophilia remains idiopathic has been this time. The requirement for tissue damage, such as reduced considerably. cardiac damage, would appear to be less important since there is likely to be a phase of this disease that Eosinophilia as a response to cytokines precedes tissue damage. Such patients can be regard- secreted by aberrant T cells ed as having chronic idiopathic eosinophilia (CIE), with Lymphoma, either Hodgkin’s disease or non- the recognition that they may well have the same Hodgkin’s lymphoma, is one of the well recognized spectrum of underlying disorders as those with idio- causes of reactive cytokine-driven eosinophilia.