Red blood cells (erythrocytes): normal values and interpretation | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Red blood cells transport oxygen through hemoglobin. Normal values, anemia, polycythemia, erythrocyte indices and interpretation in Quebec.\">\n<meta name=\"keywords\" content=\"globules rouges valeurs normales, \u00e9rythrocytes h\u00e9moglobine, an\u00e9mie globules rouges, polyglobulie \u00e9rythrocytose, VGM CCMH r\u00e9ticulocytes, NFS interpr\u00e9tation \u00e9rythrocytes, globules rouges Qu\u00e9bec bilan sanguin\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Hematology & Laboratory Medicine & Family Medicine<\/span>\n <h1>Red blood cells (erythrocytes)<\/h1>\n\n <div class=\"co-intro\">\n Red blood cells, or erythrocytes, are the most numerous blood cells in the body - there are around 25,000 billion of them in an adult, or 70 % of all cells in the human body. Devoid of nuclei and mitochondria at maturity, these biconcave discs measuring around 6-8 \u00b5m in diameter are specialized for a single function: transporting oxygen from the lungs to the tissues, and carbon dioxide in the opposite direction, thanks to hemoglobin, which occupies 33 % of their volume and accounts for 97 % of their proteins. Produced in the red bone marrow by erythropoiesis (the process by which hematopoietic stem cells differentiate into mature erythrocytes in 7 days), they circulate for a lifespan of 100-120 days before being phagocytosed by splenic and hepatic macrophages (reticuloendothelial system). Their production is finely regulated by erythropoietin (EPO), a glycoprotein synthesized at 90 % by the peritubular cells of the kidney in response to tissue hypoxia. The red cell count is an integral part of the complete blood count (CBC), which also includes the calculated erythrocyte indices: mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), mean corpuscular hemoglobin content (MCHC) and red cell distribution index (RCI). The combined interpretation of these parameters and the blood smear enables the etiological diagnosis of anemia, polycythemia and erythrocyte morphological abnormalities to be directed towards deficiency, hemolytic, bone marrow or constitutional causes.\n <\/div>\n\n <h2>Physiology, normal values and erythrocyte indices<\/h2>\n <ul class=\"co-list\">\n <li><strong>Erythropoiesis and regulation of erythrocyte production :<\/strong> medullary erythropoiesis: differentiation of pluripotent stem cells (HSC) \u2192 erythroid progenitors (BFU-E \u2192 CFU-E) \u2192 proerythroblast \u2192 basophilic erythroblast \u2192 polychromatophilic erythroblast \u2192 orthochromatic erythroblast \u2192 reticulocyte (extruded nucleus) \u2192 mature erythrocyte (loss of organelles) \u2192 total duration: 7 days in marrow \u2192 reticulocytes complete maturation in 1-2 days in peripheral blood (loss of residual ribosomes); EPO regulation: tissue hypoxia (altitude + anemia + hypoxemia) \u2192 renal peritubular cells \u2192 EPO secretion \u2192 binding to EPOR receptor on erythroid precursors \u2192 proliferation + differentiation + survival (inhibition of apoptosis) \u2192 increased erythrocyte production - human recombinant EPO (epoetin alfa - Eprex + darbepoetin alfa - Aranesp): used in anemia of chronic renal failure + chemotherapy + surgery + myelodysplastic syndromes; iron regulation: hemoglobin synthesis requires iron - its intestinal absorption is regulated by hepcidin (hepatic protein): elevated hepcidin (inflammation + martial overload) \u2192 degradation of ferroportin \u2192 blockage of iron absorption and release \u2192 inflammatory anemia; regulation by vitamins: vitamin B12 (cobalamin) and folate (vitamin B9): cofactors of DNA synthesis \u2192 essential for cell division of erythroid precursors \u2192 deficiency \u2192 inefficient erythropoiesis \u2192 megaloblastosis \u2192 macrocytosis + anemia; erythrocyte lifespan and destruction: 100-120 days \u2192 aging \u2192 reduced membrane deformability \u2192 splenic sequestration \u2192 phagocytosis by macrophages \u2192 hemoglobin degradation \u2192 globin \u2192 recycled amino acids + heme \u2192 biliverdin \u2192 unconjugated bilirubin \u2192 conjugated by liver \u2192 stercobilin (stool) + urobilinogen (urine) + iron \u2192 transferrin \u2192 marrow \u2192 recycling<\/li>\n <li><strong>Normal erythrocyte CBC values in adults :<\/strong> red blood cells (RBC - erythrocytes): adult man: 4.5-5.9 \u00d7 10\u00b9\u00b2\/L + adult woman: 4.0-5.2 \u00d7 10\u00b9\u00b2\/L + pregnant woman: physiologically lowered values (hemodilution - normal or slightly increased GMV); hemoglobin (Hb): man: 130-175 g\/L (13.0-17.5 g\/dL) + female: 120-155 g\/L (12.0-15.5 g\/dL) + pregnant: >110 g\/L (WHO - T1 and T3) + >105 g\/L (WHO - T2) + newborn: 140-220 g\/L (fetal Hb - dominant HbF) \u2192 physiological decline in first weeks of life; hematocrit (Ht): male: 40-52 % + female: 36-48 %; calculated erythrocyte indices - VGM (mean corpuscular volume): normal adult value: 80-100 fL - microcytosis: 100 fL (B12 or folate deficiency + alcohol + hypothyroidism + medications) - normocytosis: 80-100 fL (hemolytic anemia + renal failure + aplasia); MCHC (mean corpuscular hemoglobin concentration): normal: 320-360 g\/L - hypochromia: 360 g\/L (hereditary spherocytosis - MCHC sometimes >360 + severe dehydration); MCHC (mean corpuscular hemoglobin content): normal: 27-33 pg; RDI (red cell distribution index - anisocytosis): normal: 11.5-14.5 % - high RDI (>14.5 %): anisocytosis (size heterogeneity) \u2192 martial deficiency + B12 deficiency + folate deficiency + hemolytic anemia + recent transfusion; reticulocytes: immature erythroid cells - normal values: 20-100 \u00d7 10\u2079\/L (0.5-2.0 % of RBCs) - reticulocytosis (>100-120 \u00d7 10\u2079\/L): regenerative anemia (hemolysis + hemorrhage) \u2192 functional marrow that compensates - areticulocytosis (<20 \u00d7 10\u2079\/L): areticulocytic anemia (aplasia + erythroblastopenia + deficiency) \u2192 insufficient or substrate-deficient marrow.<\/li>\n <li><strong>Erythrocyte morphology on blood smear - main abnormalities :<\/strong> the stained blood smear (May-Gr\u00fcnwald-Giemsa - MGG) is irreplaceable for morphological analysis of red blood cells - in addition to automated indices; size anomalies: microcytes (diameter 9 \u00b5m - high GMV): B12 deficiency + folate deficiency + alcohol + hypothyroidism + drugs (hydroxyurea + methotrexate + azathioprine + antiretrovirals) + round macrocytes (non-ovalocytic): alcohol + hypothyroidism + liver disease + megaloblasts (ovalocytic macrocytes): B12 + folate deficiency; shape abnormalities (poikilocytosis): sickle cells (sickle-shaped): sickle cell disease (HbS) - pathognomonic + spherocytes (small round RBCs without central pallor): hereditary spherocytosis + autoimmune hemolytic anemia (AHAI) + schizocytes (erythrocyte fragments): thrombotic microangiopathy (TAM - PTT + HUS + DIC + malignant AH) + acanthocytes (irregular spicules): abetalipoproteinemia + severe hepatopathies + target cells: thalassemia + hemoglobinopathies + hepatopathy + martial deficiency + stomatocytes (central cleft): hereditary stomatocytosis + alcohol + elliptocytes: hereditary elliptocytosis + martial deficiency (mild) + dacryocytes (tears): myelofibrosis + extramedullary hematopoiesis + echinocytes (regularly crenulated): uremia + artifact + ATP depletion; intraerythrocyte inclusions: Heinz bodies (denatured hemoglobin - G6PD deficiency + unstable hemoglobinopathies - visible with cresyl blue only) + Howell-Jolly bodies (nucleus fragments - functional or surgical asplenia + megaloblastosis) + Cabot rings (mitotic spindle remnants - severe megaloblastosis + lead poisoning) + basophilic punctations (ribosome granules - lead poisoning + thalassemia + dyserythropoiesis) + intracellular parasites (Plasmodium - malaria + Babesia)<\/li>\n <\/ul>\n\n <h2>Clinical interpretation and management of erythrocyte abnormalities<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Erythrocyte abnormality<\/th><th>Etiologies and diagnostic approach<\/th><th>Care and referral<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Hypochromic microcytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">VGM <80 fL - CCMH <320 g\/L<\/small><\/td>\n <td>Microcytic hypochromic anemia is the most frequent form of anemia worldwide - martial deficiency is the cause in the vast majority of cases; martial deficiency (iron deficiency anemia): most frequent cause of anemia worldwide - mechanism: depletion of iron stores \u2192 insufficient hemoglobin synthesis \u2192 microcytosis + progressive hypochromia - martial workup: serum ferritin (best reflection of reserves - low if <15-20 \u00b5g\/L) + low serum iron + high transferrin (TIBC) + low transferrin saturation coefficient (TSC) (<16 %) - caution: ferritin is an acute-phase protein - may be falsely normal or elevated in inflammatory context despite true deficiency - in this case : CRP + soluble transferrin receptor (sTfR) + sTfR\/log ferritin index (Thomas index) - look for causes of martial deficiency: occult digestive bleeding (colorectal cancer + ulcer + inflammatory bowel disease) in any adult \u2192 FOGD + colonoscopy + gynecological bleeding (menorrhagia - main cause in women of childbearing age) + malabsorption (celiac disease + gastrectomy + gastric bypass) + inadequate intakes (strict veganism + infants) + intrapulmonary hemorrhage (hemosiderosis - rare); thalassemias (alpha and beta): genetic abnormality of globin chain synthesis \u2192 microcytosis disproportionate to degree of anemia (VGM often 3.5 % in beta-thalassemia minor + normal HbA2 in alpha-thalassemia - molecular diagnosis PCR) + normal or elevated ferritin (no deficiency) - target population: Mediterranean Basin + Africa + Middle East + Southeast Asia natives; anemia of chronic diseases (ACD): moderate microcytosis (often normocytic - GMV 75-85 fL) + hypochromia + normal or high ferritin + low TIBC + normal or low CST - mechanism: hepcidin elevated by inflammation \u2192 blockade of ferroportin \u2192 sequestration of iron in macrophages \u2192 reduced availability for erythropoiesis - context: chronic inflammatory diseases (RA + Crohn's + lupus) + cancers + chronic infections (HIV + tuberculosis + hepatitis) + chronic renal failure; sideroblastic anemia: crown sideroblasts (mitochondrial sideroblasts in perinuclear ring - visible with Perls stain on myelogram) + microcytosis + hypochromia + elevated ferritin (martial overload) \u2192 causes: acquired (alcohol ++ + lead + isoniazid + chloramphenicol + pyridoxine deficiency) + congenital (XLSA - X-linked sideroblastic anemia - ALAS2 mutation)<\/td>\n <td>Treatment of martial deficiency: oral iron: ferrous sulfate (Fer-In-Sol + Palafer + generics): 150-200 mg\/d of elemental iron in 2-3 doses - optimal absorption on an empty stomach or with vitamin C - frequent digestive side effects (nausea + constipation + black stools) \u2192 if intolerant: reduce dose + take with meals (absorption reduced by 40 % but better tolerated) + ferrous gluconate + ferrous fumarate - duration: minimum 3-6 months after Hb normalization (to replenish reserves - target ferritin \u226550 \u00b5g\/L) - CBC check + ferritin at 1-2 months (expected Hb increase +1 g\/dL\/week from D10-14 if effective treatment and cause treated); IV iron: ferric carboxymaltose (Ferinject): IV administration as a single infusion (up to 1,000 mg in 15 min) or iron sucrose (Venofer): 200 mg in 3 spaced infusions - indications: intolerance to oral iron + malabsorption (celiac disease + active Crohn's + bariatric) + severe deficiency requiring rapid correction (preoperative + advanced pregnancy) + chronic renal failure on erythropoietin; treatment of cause: indispensable - treatment of menorrhagia (hormonal contraception + Mirena hormonal IUD) + treatment of celiac disease (gluten-free diet) + resection of a bleeding digestive cancer + anti-ulcer treatment (PPI + H. pylori eradication); thalassemias - treatment: thalassemia minor (thalassemic trait): no martial therapy (risk of overload) + genetic counseling if pregnancy planned + prenatal diagnosis if both parents are carriers - thalassemia major (homozygous beta-thalassemia): iterative transfusions + iron chelation (deferasirox - Exjade PO) + hematopoietic stem cell allograft (HSCT) + gene therapy (Zynteglo - available in Europe + under evaluation in Canada)<\/td>\n <\/tr>\n <tr>\n <td>Macrocytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">VGM >100 fL - megaloblastosis - alcohol<\/small><\/td>\n <td>Macrocytosis (VGM >100 fL) is a frequent call sign discovered on routine CBC - its causes are varied and require a systematic diagnostic approach; vitamin B12 (cobalamin) deficiency: prevalence: 5-15 % of elderly + vegans + strict vegetarians - mechanism: B12 required for thymidine synthase + methionine synthase \u2192 deficiency \u2192 blockage of DNA synthesis \u2192 megaloblastosis + neurological disorders (subacute combined degeneration - involvement of the posterior and lateral cords of the medulla: paresthesias + ataxia + Lhermitte's sign) - causes: autoimmune atrophic gastritis (Biermer's anemia - antiintrinsic factor + anti-parietal cell antibodies - 60-70 % of B12 deficiencies in developed countries) + gastrectomy + ileal resection + celiac disease + Crohn's + bacterial overgrowth + strict veganism + drugs (metformin - blocks ileal B12 absorption - after \u22655 years of treatment + long-term PPIs + colchicine); folate (vitamin B9) deficiency: mechanism similar to B12 (cofactor in DNA synthesis) - no neurological impairment - causes : inadequate intake (alcoholism + anorexia + malnutrition) + malabsorption (celiac disease) + increased requirements (pregnancy + chronic hemolytic anemia + hemodialysis) + antifolate drugs (methotrexate + trimethoprim + phenytoin); macrocytosis without megaloblastic anemia: alcoholism (VGM often 100-110 fL without frank megaloblastosis - mechanism: direct toxicity of alcohol on erythropoiesis + associated folate deficiency) + hypothyroidism (slightly increased GMV + elevated TSH) + hepatopathies (membrane lipid loading \u2192 round - not ovalocytic - macrocytes) + drugs (hydroxyurea + methotrexate + azathioprine + zidovudine + d4T - antiretrovirals) + myelodysplastic syndromes (MDS): macrocytosis + cytopenias \u00b1 blastosis \u2192 smear + myelogram + osteo-medullary biopsy; diagnostic workup for macrocytosis: serum B12 + erythrocyte folates (more reliable than serum folates) + TSH + liver workup + protein electrophoresis + blood smear (ovalocytic megalocytes + hypersegmented polynuclei = megaloblastosis \u2192 B12 or folate) + LDH + bilirubin (ineffective erythropoiesis \u2192 intramedullary cytolysis) + antiintrinsic factor + anti-parietal cell antibodies (if Biermer suspected)<\/td>\n <td>Treatment of vitamin B12 deficiency: mild forms without neurological impairment (Biermer + partial gastrectomy + veganism without documented malabsorption): cyanocobalamin or hydroxocobalamin IM: standard protocol: 1,000 \u00b5g IM\/d \u00d7 7 days \u2192 then 1,000 \u00b5g IM\/week \u00d7 4 weeks \u2192 then 1,000 \u00b5g IM\/month for life (if uncorrectable cause - Biermer + total gastrectomy); forms with severe neurological impairment: 1,000 \u00b5g IM\/d \u00d7 2-3 weeks \u2192 monthly maintenance for life + physiotherapy if ataxia + neurological follow-up; oral B12 (cyanocobalamin PO 1,000-2,000 \u00b5g\/d): as effective as IM in most situations (passive absorption not dependent on intrinsic factor at high doses) - convenient alternative for patients without severe neurological impairment or complete intestinal malabsorption - increasing Quebec preference for oral route (avoids injections) + less effective in cases of severe Biermer or total ileal resection; sublingual or nasal B12 (Nascobal): possible alternatives; follow-up: reticulocytosis as early as D5-7 (peak at D7-10) + normalization of Hb in 6-8 weeks + normalization of VGM in 2-3 months + monitoring of kalemia (hypokalemia possible in correction phase - rapid erythroid regeneration) + neurological follow-up (improvement possible but incomplete if old damage - spinal cord lesions established >6 months partially recover); treatment of folate deficiency: folic acid 1-5 mg\/d PO \u00d7 4 months (or for life if uncorrectable cause) + NEVER correct folates without having excluded or treated B12 deficiency: risk of worsening neurological disorders by correcting anemia without correcting B12 deficiency \u2192 always treat B12 first or simultaneously if both deficiencies coexist; preventive folate supplementation: 0.4 mg\/d periconceptionally (prevention of neural tube closure defects - spina bifida) + 5 mg\/d if pregnancy with chronic hemolytic anemia or antifolate treatment<\/td>\n <\/tr>\n <tr>\n <td>Hemolytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">Hemolysis - reticulocytosis - Coombs<\/small><\/td>\n <td>Hemolytic anemia results from premature destruction of erythrocytes (lifespan 120 \u00d7 10\u2079\/L or >2 % of RBCs) + elevated LDH (released by erythrocyte lysis) + elevated unconjugated (indirect) bilirubin + collapsed haptoglobin (captures free \u2192 saturated and degraded Hb during intravascular hemolysis) + in intravascular hemolysis: hemoglobinemia + hemoglobinuria + methemalbumin; direct Coombs test (DCT): detects antibodies or complement attached to RBCs - positive DCT \u2192 immune hemolysis: AHAI (autoimmune hemolytic anemia) + transfusional hemolysis + drugs + hemolytic disease of the newborn (fetal-maternal incompatibility) - TCD negative \u2192 non-immune hemolysis: intrinsic RBC abnormalities (hemoglobinopathies + membranopathies + enzymopathies) + thrombotic microangiopathy (TMA - schizocytes +++) + malaria + physical agents (burns); etiological classification of hemolytic anemias: corpuscular causes (intrinsic - most often constitutional): hereditary membranopathies (hereditary spherocytosis + elliptocytosis - mutation of erythrocyte membrane proteins: spectrin + ankyrin + protein 4.2 + band 3) + enzymopathies (G6PD deficiency + pyruvate kinase deficiency) + hemoglobinopathies (sickle cell disease + thalassemias + HbC + HbE) + HPN (paroxysmal nocturnal hemoglobinuria - acquired clonal abnormality of GPI-anchor \u2192 complement sensitivity); extra-corpuscular causes: AHAI (autoimmune - TCD+) + allo-immune hemolysis (transfusion + fetal-maternal alloimmunization) + MAT (PTT + SHU - schizocytes + ADAMTS13 low in PTT) + infection (malaria + Clostridium + Bartonella) + drugs (methyldopa + penicillin + ceftriaxone + NSAIDs - variable immunological mechanisms)<\/td>\n <td>Management of autoimmune hemolytic anemias (AHAI): AHAI with warm antibodies (IgG - TCD IgG positive - most frequent - 80 % of AHAI): 1st-line corticosteroid therapy: prednisone 1 mg\/kg\/d PO \u2192 response expected in 1-3 weeks (Hb rises + reticulocytes increase then decrease) \u2192 gradual decrease over 3-6 months \u2192 60-80 % initial response - but frequent relapse on decrease (50 % of patients) \u2192 2nd-line treatment: rituximab (anti-CD20 - Rituxan + biosimilar generics): 375 mg\/m\u00b2 IV \u00d7 4 weekly infusions \u2192 durable remission in 60-80 % - splenectomy: curative option in corticoresistant or corticodependent AHAI (response in 50-70 %) + immunosuppressants (azathioprine + mycophenolate mofetil) + fostamatinib (Syk kinase inhibitor - FDA 2023 approved for refractory AHAI) \u2192 awaiting Health Canada approval; Cold antibody AHAI (IgM - cold agglutinins - TCD positive C3 complement): cold avoidance (warm clothing + temperate environment) + rituximab \u00b1 bendamustine + no splenectomy (mainly hepatic hemolysis); HPN (paroxysmal nocturnal hemoglobinuria): eculizumab (Soliris - anti-C5 - terminal complement inhibitor): first treatment approved - 900 mg IV\/2 weeks then 1,200 mg\/4 weeks - normalizes hemolysis + prevents thrombosis (main cause of death in HPN) + meningococcal vaccination mandatory before initiation + ravulizumab (Ultomiris - long-acting anti-C5 - 4 infusions\/year) : Health Canada approved + iptacopan (alternate pathway factor B inhibitor - PO - APPLY + APPOINT 2023 trials - response under evaluation Health Canada); transfusion in hemolytic anemias: packed red blood cells compatibilized + phenotyped (prevention of alloimmunization) + washed if severe AHAI or HPN<\/td>\n <\/tr>\n <tr>\n <td>Polycythemia and erythrocytosis<br><small style=\"font-weight:400;color:#7a8fa0;\">High GR - JAK2 mutation - Vaquez<\/small><\/td>\n <td>Polycythemia (erythrocytosis) is defined by an increase in erythrocyte mass - diagnosed in practice by an Hb >185 g\/L in men + >165 g\/L in women (WHO 2016) or a hematocrit >52 % (men) + >48 % (women); erythrocytosis classification: true absolute erythrocytosis (actual increase in erythrocyte mass): primary - Vaquez disease (polycythemia vera - PV): clonal myeloproliferative neoplasm - JAK2 V617F mutation (exon 14) in >95 % of cases + JAK2 exon 12 mutation in <5 % - workup: CBC (polycythemia + often associated thrombocytosis + leukocytosis) + low EPO (autonomous GR production - physiological EPO braking) + JAK2 V617F mutation (key diagnostic test) + bone-medullary biopsy (tri-lineage hypercellularity with panmyelosis) - WHO 2016 diagnostic criteria (3 major criteria or 2 major + 1 minor required); secondary erythrocytosis (high EPO): hypoxic causes: severe COPD + obstructive sleep apnea syndrome (OSAS) + cyanogenic congenital heart disease + high altitude + smoking (CO \u2192 HbCO \u2192 functional tissue hypoxia \u2192 smoker's polyglobulia) + high-affinity hemoglobin for O2 (high-affinity hemoglobins: left-shifted dissociation curve \u2192 tissue hypoxia \u2192 high EPO \u2192 polyglobulia); non-hypoxic causes (non-physiological high EPO): clear cell renal cell carcinoma (ectopic EPO secretion - paraneoplastic polycythemia) + hepatocarcinoma + cerebellar hemangioblastoma (Von Hippel-Lindau) + renal cyst + renal artery stenosis (focal renal ischemia \u2192 elevated local EPO); relative erythrocytosis (Gaisbock pseudopolycythemia): normal erythrocyte mass - hemoconcentration by reduction of plasma volume (dehydration + diuretics + visceral obesity + hypertension + smoking + stress) \u2192 elevated hematocrit and Hb but normal RBCs on isotopic measurement of erythrocyte mass<\/td>\n <td>Treatment of Vaquez disease (polycythemia vera): main therapeutic objective: reduce the risk of thrombosis (main cause of mortality in PV) by maintaining hematocrit <45 % (male) + 60 + history of thrombosis + platelets >1,500 G\/L + polycythemia difficult to control with bloodletting alone): hydroxyurea (Hydrea): 1st line of cytoreduction - 500-1,500 mg\/d PO + theoretical leukemogenic risk (low but real in the long term) + pegylated interferon alfa (Besremi - ropeginterferon alfa-2b): approved by Health Canada 2022 for PV - SC every 2 weeks \u2192 reduction of JAK2 allelic load (possible molecular remission) \u2192 preferred alternative in young patients + pregnancy considered (with precautions) + intolerance or resistance to hydroxyurea + ruxolitinib (Jakafi - JAK1\/JAK2 inhibitor): 2nd line if resistant or intolerant to hydroxyurea - approved by Health Canada for refractory PV; secondary erythrocytosis : treatment of cause (smoking cessation + CPAP if OSA + COPD treatment + renal cell carcinoma resection) + bloodletting if polycythaemia-related symptoms (hyperviscosity - headache + facial erythrosis + tinnitus + aquagenic pruritus) + target hematocrit <50 % in hypoxic secondary polycythaemias<\/td>\n <\/tr>\n <tr>\n <td>Aregenerative normocytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">Aplasia - renal failure - MDS<\/small><\/td>\n <td>Aregenerative normocytic anemia (low reticulocytes + normal GMV) points to insufficient bone marrow production (aplasia) or inefficient erythropoiesis (MDS + incipient deficiencies); chronic renal failure (CKD): anemia in CKD is the most frequent of the aregenerative anemias - mechanism: insufficient EPO production by fibrosed renal peritubular cells + reduced erythrocyte lifespan + frequent relative martial deficiency + uremic toxicity on erythropoiesis + chronic inflammation (hepcidin) - prevalence: 40-50 % of stage 3b-5 CKD patients (GFR <45 mL\/min\/1.73 m\u00b2) - workup: serum EPO (inadequately low for degree of anemia) + ferritin + CST + inflammatory workup; bone marrow aplasia (pure aplasia or aplastic pancytopenia): disappearance of hematopoietic cells from marrow \u2192 anemia + thrombocytopenia + neutropenia - acquired aplasia (idiopathic - autoimmune mechanism T \u2192 70 % of acquired aplasias + drugs: chloramphenicol + carbamazepine + ticlopidine + sulfonamides + gold) + constitutional aplasias (Fanconi anemia - chromosomal breaks + congenital anomalies + dyskeratosis congenita - TERC + TERT mutation); pure red cell aplasia (PRCA) : selective aplasia of the erythroid lineage \u2192 severe aregenerative anemia without thrombocytopenia or neutropenia - causes: parvovirus B19 (in immunocompromised or chronic hemolytics) + thymoma + autoimmune + drugs (epoetin - anti-EPO antibodies); myelodysplastic syndromes (MDS): dysplastic bone marrow clones \u2192 ineffective erythropoiesis \u2192 anemia + sometimes macrocytosis + smear: dysgranulopoiesis + abnormal megakaryocytes + myelogram + BOM + karyotype + NGS \u2192 WHO 2022 classification \u2192 IPSS-R score \u2192 therapeutic decision (monitoring + azacitidine + allograft); acquired aplastic anemia - severity criteria: severe aplasia (SAA): neutrophils <0.5 G\/L + platelets <20 G\/L + reticulocytes <20 G\/L + marrow <25 % cellularity + very severe aplasia (VSAA): neutrophils <0.2 G\/L<\/td>\n <td>Treatment of anemia in CKD: erythropoiesis-stimulating agents (ESAs): epoetin alfa (Eprex) + epoetin beta (NeoRecormon) + darbepoetin alfa (Aranesp): EPO \u2192 receptor agonists stimulate erythropoiesis \u2192 indications: Hb <100 g\/L + GFR 130 g\/L - increased cardiovascular and thromboembolic risk) - administration: SC (better than IV for efficacy) or IV if hemodialysis + concomitant martial supplementation mandatory (IV iron preferably in hemodialysis) \u2192 target ferritin >200 \u00b5g\/L + CST >20 %; HIF-PH (hypoxia-inducible factor prolyl hydroxylase) inhibitors: new oral therapeutic class: roxadustat (Evrenzo - AstraZeneca): approved by Health Canada 2021 for CKD anemia in dialysis and pre-dialysis - mechanism: inhibition of HIF prolyl hydroxylases \u2192 stabilization of HIF-1\u03b1 and HIF-2\u03b1 factors \u2192 endogenous increase in EPO secretion + increase in intestinal iron absorption \u2192 dual effect - advantages vs ESA: oral route + effective in inflammatory setting (reduced hepcidin) + lower risk of hypertension - monitoring: HbA1c + lipids (decreased under roxadustat) + thromboses; treatment of acquired bone marrow aplasia: hematopoietic stem cell allograft transplantation (HSCT): reference curative treatment for patients 40 years old): anti-thymocyte serum (SAT - horse or rabbit) + cyclosporine + eltrombopag (Revolade - thrombopoietin receptor agonist - TPO-RA): data RACE + STRONG-SAA \u2192 improved response rate + complete remission rate 40-50 % under triple therapy SAT + cyclosporine + eltrombopag<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>Interpretation of erythrocyte CBC - 4-step systematic approach:<\/strong> (1) Presence or absence of anemia (low Hb) or polycythemia (high Hb) - (2) VGM: microcytosis (100 fL) \u2192 B12\/folate deficiency or drugs - (3) Regenerative (reticulocytes >120 \u00d7 10\u2079\/L \u2192 hemolysis or hemorrhage) or aregenerative (low reticulocytes \u2192 insufficient production) character - (4) Blood smear for morphology (schizocytes \u2192 MAT; sickle cells \u2192 sickle cell anemia; PNN hypersegmentation \u2192 megaloblastosis). This cascade approach leads to a precise etiological diagnosis before prescribing targeted complementary examinations.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Severe anemia (Hb <70 g\/L) + signs of poor tolerance (dyspnea at rest + tachycardia + hypotension + chest pain + confusion)<\/strong> \u2192 urgent erythrocyte transfusion + etiological workup + hospitalization.<\/p>\n <p><strong>Schizocytes on smear + anemia + severe thrombocytopenia \u00b1 fever + neurological or renal impairment<\/strong> \u2192 thrombotic microangiopathy (PTT or SHU) \u2192 ADAMTS13 urgently + plasma exchanges if PTT \u2192 urgent hematology opinion.<\/p>\n <p><strong>Polyglobulia (Hb >185 g\/L male + >165 g\/L female) + thrombosis (stroke + MI + Budd-Chiari) or signs of hyperviscosity<\/strong> \u2192 probable Vaquez disease \u2192 JAK2 V617F mutation + urgent bleeding if hematocrit >55 % + aspirin + hematology.<\/p>\n <p><strong>Pancytopenia (anemia + neutropenia + thrombocytopenia) + fever in a patient taking a potentially myelotoxic drug<\/strong> \u2192 drug-induced bone marrow aplasia \u2192 immediate discontinuation of incriminating drug + urgent CBC + hematology opinion + hospitalization if severe neutropenia.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron's physicians prescribe and interpret erythrocyte CBCs as part of the work-up for unexplained fatigue, incidentally discovered anemia, pregnancy monitoring, chronic illness or pre-operative work-up. Referral to specialized hematology (hemolytic anemias, polycythemia, aplasia), prescription of appropriate martial or vitamin supplementation and screening for underlying causes (digestive bleeding, celiac disease, nutritional deficiencies) are all part of the clinical approach available at several points of service in Quebec and via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The contents of this page are provided for information purposes only and do not replace the advice of a physician or hematologist. The interpretation of a CBC must always be carried out in the patient's clinical context.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Globules rouges (\u00e9rythrocytes) : valeurs normales et interpr\u00e9tation | Clinique Omicron H\u00e9matologie & M\u00e9decine de laboratoire & M\u00e9decine de famille Globules rouges (\u00e9rythrocytes) Les globules rouges, ou \u00e9rythrocytes, sont les cellules sanguines les plus nombreuses de l’organisme \u2014 on en d\u00e9nombre environ 25 000 milliards chez un adulte, soit 70 % de toutes les cellules… <a href=\"https:\/\/cliniqueomicron.ca\/en\/globules-rouges-erythrocytes\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Red blood cells (erythrocytes): normal values and interpretation | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Globules rouges (\u00e9rythrocytes) : | Brossard | Clinique Omicron","_metasync_otto_description":"Les globules rouges transportent l'oxyg\u00e8ne gr\u00e2ce \u00e0 l'h\u00e9moglobine. Valeurs normales, an\u00e9mie, polyglobulie, indices \u00e9rythrocytaires et interpr\u00e9tation au Qu\u00e9bec.","_metasync_otto_keywords":"","_metasync_otto_og_title":"Globules rouges (\u00e9rythrocytes) : | Brossard | Clinique Omicron","_metasync_otto_og_description":"","_metasync_otto_twitter_title":"Globules rouges (\u00e9rythrocytes) : | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"Les globules rouges transportent l'oxyg\u00e8ne gr\u00e2ce \u00e0 l'h\u00e9moglobine. Valeurs normales, an\u00e9mie, polyglobulie, indices \u00e9rythrocytaires et interpr\u00e9tation au Qu\u00e9bec.","rank_math_title":"","rank_math_description":"","_yoast_wpseo_title":"","_yoast_wpseo_metadesc":"","_aioseo_title":"Globules rouges (\u00e9rythrocytes) : valeurs normales et interpr\u00e9tation | Clinique Omicron","_aioseo_description":"Les globules rouges transportent l'oxyg\u00e8ne gr\u00e2ce \u00e0 l'h\u00e9moglobine. 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\n\t\t\t\t\t\n\n\n\n\nRed blood cells (erythrocytes): normal values and interpretation | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Red blood cells transport oxygen through hemoglobin. Normal values, anemia, polycythemia, erythrocyte indices and interpretation in Quebec.\">\n<meta name=\"keywords\" content=\"globules rouges valeurs normales, \u00e9rythrocytes h\u00e9moglobine, an\u00e9mie globules rouges, polyglobulie \u00e9rythrocytose, VGM CCMH r\u00e9ticulocytes, NFS interpr\u00e9tation \u00e9rythrocytes, globules rouges Qu\u00e9bec bilan sanguin\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Hematology & Laboratory Medicine & Family Medicine<\/span>\n <h1>Red blood cells (erythrocytes)<\/h1>\n\n <div class=\"co-intro\">\n Red blood cells, or erythrocytes, are the most numerous blood cells in the body - there are around 25,000 billion of them in an adult, or 70 % of all cells in the human body. Devoid of nuclei and mitochondria at maturity, these biconcave discs measuring around 6-8 \u00b5m in diameter are specialized for a single function: transporting oxygen from the lungs to the tissues, and carbon dioxide in the opposite direction, thanks to hemoglobin, which occupies 33 % of their volume and accounts for 97 % of their proteins. Produced in the red bone marrow by erythropoiesis (the process by which hematopoietic stem cells differentiate into mature erythrocytes in 7 days), they circulate for a lifespan of 100-120 days before being phagocytosed by splenic and hepatic macrophages (reticuloendothelial system). Their production is finely regulated by erythropoietin (EPO), a glycoprotein synthesized at 90 % by the peritubular cells of the kidney in response to tissue hypoxia. The red cell count is an integral part of the complete blood count (CBC), which also includes the calculated erythrocyte indices: mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), mean corpuscular hemoglobin content (MCHC) and red cell distribution index (RCI). The combined interpretation of these parameters and the blood smear enables the etiological diagnosis of anemia, polycythemia and erythrocyte morphological abnormalities to be directed towards deficiency, hemolytic, bone marrow or constitutional causes.\n <\/div>\n\n <h2>Physiology, normal values and erythrocyte indices<\/h2>\n <ul class=\"co-list\">\n <li><strong>Erythropoiesis and regulation of erythrocyte production :<\/strong> medullary erythropoiesis: differentiation of pluripotent stem cells (HSC) \u2192 erythroid progenitors (BFU-E \u2192 CFU-E) \u2192 proerythroblast \u2192 basophilic erythroblast \u2192 polychromatophilic erythroblast \u2192 orthochromatic erythroblast \u2192 reticulocyte (extruded nucleus) \u2192 mature erythrocyte (loss of organelles) \u2192 total duration: 7 days in marrow \u2192 reticulocytes complete maturation in 1-2 days in peripheral blood (loss of residual ribosomes); EPO regulation: tissue hypoxia (altitude + anemia + hypoxemia) \u2192 renal peritubular cells \u2192 EPO secretion \u2192 binding to EPOR receptor on erythroid precursors \u2192 proliferation + differentiation + survival (inhibition of apoptosis) \u2192 increased erythrocyte production - human recombinant EPO (epoetin alfa - Eprex + darbepoetin alfa - Aranesp): used in anemia of chronic renal failure + chemotherapy + surgery + myelodysplastic syndromes; iron regulation: hemoglobin synthesis requires iron - its intestinal absorption is regulated by hepcidin (hepatic protein): elevated hepcidin (inflammation + martial overload) \u2192 degradation of ferroportin \u2192 blockage of iron absorption and release \u2192 inflammatory anemia; regulation by vitamins: vitamin B12 (cobalamin) and folate (vitamin B9): cofactors of DNA synthesis \u2192 essential for cell division of erythroid precursors \u2192 deficiency \u2192 inefficient erythropoiesis \u2192 megaloblastosis \u2192 macrocytosis + anemia; erythrocyte lifespan and destruction: 100-120 days \u2192 aging \u2192 reduced membrane deformability \u2192 splenic sequestration \u2192 phagocytosis by macrophages \u2192 hemoglobin degradation \u2192 globin \u2192 recycled amino acids + heme \u2192 biliverdin \u2192 unconjugated bilirubin \u2192 conjugated by liver \u2192 stercobilin (stool) + urobilinogen (urine) + iron \u2192 transferrin \u2192 marrow \u2192 recycling<\/li>\n <li><strong>Normal erythrocyte CBC values in adults :<\/strong> red blood cells (RBC - erythrocytes): adult man: 4.5-5.9 \u00d7 10\u00b9\u00b2\/L + adult woman: 4.0-5.2 \u00d7 10\u00b9\u00b2\/L + pregnant woman: physiologically lowered values (hemodilution - normal or slightly increased GMV); hemoglobin (Hb): man: 130-175 g\/L (13.0-17.5 g\/dL) + female: 120-155 g\/L (12.0-15.5 g\/dL) + pregnant: >110 g\/L (WHO - T1 and T3) + >105 g\/L (WHO - T2) + newborn: 140-220 g\/L (fetal Hb - dominant HbF) \u2192 physiological decline in first weeks of life; hematocrit (Ht): male: 40-52 % + female: 36-48 %; calculated erythrocyte indices - VGM (mean corpuscular volume): normal adult value: 80-100 fL - microcytosis: 100 fL (B12 or folate deficiency + alcohol + hypothyroidism + medications) - normocytosis: 80-100 fL (hemolytic anemia + renal failure + aplasia); MCHC (mean corpuscular hemoglobin concentration): normal: 320-360 g\/L - hypochromia: 360 g\/L (hereditary spherocytosis - MCHC sometimes >360 + severe dehydration); MCHC (mean corpuscular hemoglobin content): normal: 27-33 pg; RDI (red cell distribution index - anisocytosis): normal: 11.5-14.5 % - high RDI (>14.5 %): anisocytosis (size heterogeneity) \u2192 martial deficiency + B12 deficiency + folate deficiency + hemolytic anemia + recent transfusion; reticulocytes: immature erythroid cells - normal values: 20-100 \u00d7 10\u2079\/L (0.5-2.0 % of RBCs) - reticulocytosis (>100-120 \u00d7 10\u2079\/L): regenerative anemia (hemolysis + hemorrhage) \u2192 functional marrow that compensates - areticulocytosis (<20 \u00d7 10\u2079\/L): areticulocytic anemia (aplasia + erythroblastopenia + deficiency) \u2192 insufficient or substrate-deficient marrow.<\/li>\n <li><strong>Erythrocyte morphology on blood smear - main abnormalities :<\/strong> the stained blood smear (May-Gr\u00fcnwald-Giemsa - MGG) is irreplaceable for morphological analysis of red blood cells - in addition to automated indices; size anomalies: microcytes (diameter 9 \u00b5m - high GMV): B12 deficiency + folate deficiency + alcohol + hypothyroidism + drugs (hydroxyurea + methotrexate + azathioprine + antiretrovirals) + round macrocytes (non-ovalocytic): alcohol + hypothyroidism + liver disease + megaloblasts (ovalocytic macrocytes): B12 + folate deficiency; shape abnormalities (poikilocytosis): sickle cells (sickle-shaped): sickle cell disease (HbS) - pathognomonic + spherocytes (small round RBCs without central pallor): hereditary spherocytosis + autoimmune hemolytic anemia (AHAI) + schizocytes (erythrocyte fragments): thrombotic microangiopathy (TAM - PTT + HUS + DIC + malignant AH) + acanthocytes (irregular spicules): abetalipoproteinemia + severe hepatopathies + target cells: thalassemia + hemoglobinopathies + hepatopathy + martial deficiency + stomatocytes (central cleft): hereditary stomatocytosis + alcohol + elliptocytes: hereditary elliptocytosis + martial deficiency (mild) + dacryocytes (tears): myelofibrosis + extramedullary hematopoiesis + echinocytes (regularly crenulated): uremia + artifact + ATP depletion; intraerythrocyte inclusions: Heinz bodies (denatured hemoglobin - G6PD deficiency + unstable hemoglobinopathies - visible with cresyl blue only) + Howell-Jolly bodies (nucleus fragments - functional or surgical asplenia + megaloblastosis) + Cabot rings (mitotic spindle remnants - severe megaloblastosis + lead poisoning) + basophilic punctations (ribosome granules - lead poisoning + thalassemia + dyserythropoiesis) + intracellular parasites (Plasmodium - malaria + Babesia)<\/li>\n <\/ul>\n\n <h2>Clinical interpretation and management of erythrocyte abnormalities<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Erythrocyte abnormality<\/th><th>Etiologies and diagnostic approach<\/th><th>Care and referral<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Hypochromic microcytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">VGM <80 fL - CCMH <320 g\/L<\/small><\/td>\n <td>Microcytic hypochromic anemia is the most frequent form of anemia worldwide - martial deficiency is the cause in the vast majority of cases; martial deficiency (iron deficiency anemia): most frequent cause of anemia worldwide - mechanism: depletion of iron stores \u2192 insufficient hemoglobin synthesis \u2192 microcytosis + progressive hypochromia - martial workup: serum ferritin (best reflection of reserves - low if <15-20 \u00b5g\/L) + low serum iron + high transferrin (TIBC) + low transferrin saturation coefficient (TSC) (<16 %) - caution: ferritin is an acute-phase protein - may be falsely normal or elevated in inflammatory context despite true deficiency - in this case : CRP + soluble transferrin receptor (sTfR) + sTfR\/log ferritin index (Thomas index) - look for causes of martial deficiency: occult digestive bleeding (colorectal cancer + ulcer + inflammatory bowel disease) in any adult \u2192 FOGD + colonoscopy + gynecological bleeding (menorrhagia - main cause in women of childbearing age) + malabsorption (celiac disease + gastrectomy + gastric bypass) + inadequate intakes (strict veganism + infants) + intrapulmonary hemorrhage (hemosiderosis - rare); thalassemias (alpha and beta): genetic abnormality of globin chain synthesis \u2192 microcytosis disproportionate to degree of anemia (VGM often 3.5 % in beta-thalassemia minor + normal HbA2 in alpha-thalassemia - molecular diagnosis PCR) + normal or elevated ferritin (no deficiency) - target population: Mediterranean Basin + Africa + Middle East + Southeast Asia natives; anemia of chronic diseases (ACD): moderate microcytosis (often normocytic - GMV 75-85 fL) + hypochromia + normal or high ferritin + low TIBC + normal or low CST - mechanism: hepcidin elevated by inflammation \u2192 blockade of ferroportin \u2192 sequestration of iron in macrophages \u2192 reduced availability for erythropoiesis - context: chronic inflammatory diseases (RA + Crohn's + lupus) + cancers + chronic infections (HIV + tuberculosis + hepatitis) + chronic renal failure; sideroblastic anemia: crown sideroblasts (mitochondrial sideroblasts in perinuclear ring - visible with Perls stain on myelogram) + microcytosis + hypochromia + elevated ferritin (martial overload) \u2192 causes: acquired (alcohol ++ + lead + isoniazid + chloramphenicol + pyridoxine deficiency) + congenital (XLSA - X-linked sideroblastic anemia - ALAS2 mutation)<\/td>\n <td>Treatment of martial deficiency: oral iron: ferrous sulfate (Fer-In-Sol + Palafer + generics): 150-200 mg\/d of elemental iron in 2-3 doses - optimal absorption on an empty stomach or with vitamin C - frequent digestive side effects (nausea + constipation + black stools) \u2192 if intolerant: reduce dose + take with meals (absorption reduced by 40 % but better tolerated) + ferrous gluconate + ferrous fumarate - duration: minimum 3-6 months after Hb normalization (to replenish reserves - target ferritin \u226550 \u00b5g\/L) - CBC check + ferritin at 1-2 months (expected Hb increase +1 g\/dL\/week from D10-14 if effective treatment and cause treated); IV iron: ferric carboxymaltose (Ferinject): IV administration as a single infusion (up to 1,000 mg in 15 min) or iron sucrose (Venofer): 200 mg in 3 spaced infusions - indications: intolerance to oral iron + malabsorption (celiac disease + active Crohn's + bariatric) + severe deficiency requiring rapid correction (preoperative + advanced pregnancy) + chronic renal failure on erythropoietin; treatment of cause: indispensable - treatment of menorrhagia (hormonal contraception + Mirena hormonal IUD) + treatment of celiac disease (gluten-free diet) + resection of a bleeding digestive cancer + anti-ulcer treatment (PPI + H. pylori eradication); thalassemias - treatment: thalassemia minor (thalassemic trait): no martial therapy (risk of overload) + genetic counseling if pregnancy planned + prenatal diagnosis if both parents are carriers - thalassemia major (homozygous beta-thalassemia): iterative transfusions + iron chelation (deferasirox - Exjade PO) + hematopoietic stem cell allograft (HSCT) + gene therapy (Zynteglo - available in Europe + under evaluation in Canada)<\/td>\n <\/tr>\n <tr>\n <td>Macrocytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">VGM >100 fL - megaloblastosis - alcohol<\/small><\/td>\n <td>Macrocytosis (VGM >100 fL) is a frequent call sign discovered on routine CBC - its causes are varied and require a systematic diagnostic approach; vitamin B12 (cobalamin) deficiency: prevalence: 5-15 % of elderly + vegans + strict vegetarians - mechanism: B12 required for thymidine synthase + methionine synthase \u2192 deficiency \u2192 blockage of DNA synthesis \u2192 megaloblastosis + neurological disorders (subacute combined degeneration - involvement of the posterior and lateral cords of the medulla: paresthesias + ataxia + Lhermitte's sign) - causes: autoimmune atrophic gastritis (Biermer's anemia - antiintrinsic factor + anti-parietal cell antibodies - 60-70 % of B12 deficiencies in developed countries) + gastrectomy + ileal resection + celiac disease + Crohn's + bacterial overgrowth + strict veganism + drugs (metformin - blocks ileal B12 absorption - after \u22655 years of treatment + long-term PPIs + colchicine); folate (vitamin B9) deficiency: mechanism similar to B12 (cofactor in DNA synthesis) - no neurological impairment - causes : inadequate intake (alcoholism + anorexia + malnutrition) + malabsorption (celiac disease) + increased requirements (pregnancy + chronic hemolytic anemia + hemodialysis) + antifolate drugs (methotrexate + trimethoprim + phenytoin); macrocytosis without megaloblastic anemia: alcoholism (VGM often 100-110 fL without frank megaloblastosis - mechanism: direct toxicity of alcohol on erythropoiesis + associated folate deficiency) + hypothyroidism (slightly increased GMV + elevated TSH) + hepatopathies (membrane lipid loading \u2192 round - not ovalocytic - macrocytes) + drugs (hydroxyurea + methotrexate + azathioprine + zidovudine + d4T - antiretrovirals) + myelodysplastic syndromes (MDS): macrocytosis + cytopenias \u00b1 blastosis \u2192 smear + myelogram + osteo-medullary biopsy; diagnostic workup for macrocytosis: serum B12 + erythrocyte folates (more reliable than serum folates) + TSH + liver workup + protein electrophoresis + blood smear (ovalocytic megalocytes + hypersegmented polynuclei = megaloblastosis \u2192 B12 or folate) + LDH + bilirubin (ineffective erythropoiesis \u2192 intramedullary cytolysis) + antiintrinsic factor + anti-parietal cell antibodies (if Biermer suspected)<\/td>\n <td>Treatment of vitamin B12 deficiency: mild forms without neurological impairment (Biermer + partial gastrectomy + veganism without documented malabsorption): cyanocobalamin or hydroxocobalamin IM: standard protocol: 1,000 \u00b5g IM\/d \u00d7 7 days \u2192 then 1,000 \u00b5g IM\/week \u00d7 4 weeks \u2192 then 1,000 \u00b5g IM\/month for life (if uncorrectable cause - Biermer + total gastrectomy); forms with severe neurological impairment: 1,000 \u00b5g IM\/d \u00d7 2-3 weeks \u2192 monthly maintenance for life + physiotherapy if ataxia + neurological follow-up; oral B12 (cyanocobalamin PO 1,000-2,000 \u00b5g\/d): as effective as IM in most situations (passive absorption not dependent on intrinsic factor at high doses) - convenient alternative for patients without severe neurological impairment or complete intestinal malabsorption - increasing Quebec preference for oral route (avoids injections) + less effective in cases of severe Biermer or total ileal resection; sublingual or nasal B12 (Nascobal): possible alternatives; follow-up: reticulocytosis as early as D5-7 (peak at D7-10) + normalization of Hb in 6-8 weeks + normalization of VGM in 2-3 months + monitoring of kalemia (hypokalemia possible in correction phase - rapid erythroid regeneration) + neurological follow-up (improvement possible but incomplete if old damage - spinal cord lesions established >6 months partially recover); treatment of folate deficiency: folic acid 1-5 mg\/d PO \u00d7 4 months (or for life if uncorrectable cause) + NEVER correct folates without having excluded or treated B12 deficiency: risk of worsening neurological disorders by correcting anemia without correcting B12 deficiency \u2192 always treat B12 first or simultaneously if both deficiencies coexist; preventive folate supplementation: 0.4 mg\/d periconceptionally (prevention of neural tube closure defects - spina bifida) + 5 mg\/d if pregnancy with chronic hemolytic anemia or antifolate treatment<\/td>\n <\/tr>\n <tr>\n <td>Hemolytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">Hemolysis - reticulocytosis - Coombs<\/small><\/td>\n <td>Hemolytic anemia results from premature destruction of erythrocytes (lifespan 120 \u00d7 10\u2079\/L or >2 % of RBCs) + elevated LDH (released by erythrocyte lysis) + elevated unconjugated (indirect) bilirubin + collapsed haptoglobin (captures free \u2192 saturated and degraded Hb during intravascular hemolysis) + in intravascular hemolysis: hemoglobinemia + hemoglobinuria + methemalbumin; direct Coombs test (DCT): detects antibodies or complement attached to RBCs - positive DCT \u2192 immune hemolysis: AHAI (autoimmune hemolytic anemia) + transfusional hemolysis + drugs + hemolytic disease of the newborn (fetal-maternal incompatibility) - TCD negative \u2192 non-immune hemolysis: intrinsic RBC abnormalities (hemoglobinopathies + membranopathies + enzymopathies) + thrombotic microangiopathy (TMA - schizocytes +++) + malaria + physical agents (burns); etiological classification of hemolytic anemias: corpuscular causes (intrinsic - most often constitutional): hereditary membranopathies (hereditary spherocytosis + elliptocytosis - mutation of erythrocyte membrane proteins: spectrin + ankyrin + protein 4.2 + band 3) + enzymopathies (G6PD deficiency + pyruvate kinase deficiency) + hemoglobinopathies (sickle cell disease + thalassemias + HbC + HbE) + HPN (paroxysmal nocturnal hemoglobinuria - acquired clonal abnormality of GPI-anchor \u2192 complement sensitivity); extra-corpuscular causes: AHAI (autoimmune - TCD+) + allo-immune hemolysis (transfusion + fetal-maternal alloimmunization) + MAT (PTT + SHU - schizocytes + ADAMTS13 low in PTT) + infection (malaria + Clostridium + Bartonella) + drugs (methyldopa + penicillin + ceftriaxone + NSAIDs - variable immunological mechanisms)<\/td>\n <td>Management of autoimmune hemolytic anemias (AHAI): AHAI with warm antibodies (IgG - TCD IgG positive - most frequent - 80 % of AHAI): 1st-line corticosteroid therapy: prednisone 1 mg\/kg\/d PO \u2192 response expected in 1-3 weeks (Hb rises + reticulocytes increase then decrease) \u2192 gradual decrease over 3-6 months \u2192 60-80 % initial response - but frequent relapse on decrease (50 % of patients) \u2192 2nd-line treatment: rituximab (anti-CD20 - Rituxan + biosimilar generics): 375 mg\/m\u00b2 IV \u00d7 4 weekly infusions \u2192 durable remission in 60-80 % - splenectomy: curative option in corticoresistant or corticodependent AHAI (response in 50-70 %) + immunosuppressants (azathioprine + mycophenolate mofetil) + fostamatinib (Syk kinase inhibitor - FDA 2023 approved for refractory AHAI) \u2192 awaiting Health Canada approval; Cold antibody AHAI (IgM - cold agglutinins - TCD positive C3 complement): cold avoidance (warm clothing + temperate environment) + rituximab \u00b1 bendamustine + no splenectomy (mainly hepatic hemolysis); HPN (paroxysmal nocturnal hemoglobinuria): eculizumab (Soliris - anti-C5 - terminal complement inhibitor): first treatment approved - 900 mg IV\/2 weeks then 1,200 mg\/4 weeks - normalizes hemolysis + prevents thrombosis (main cause of death in HPN) + meningococcal vaccination mandatory before initiation + ravulizumab (Ultomiris - long-acting anti-C5 - 4 infusions\/year) : Health Canada approved + iptacopan (alternate pathway factor B inhibitor - PO - APPLY + APPOINT 2023 trials - response under evaluation Health Canada); transfusion in hemolytic anemias: packed red blood cells compatibilized + phenotyped (prevention of alloimmunization) + washed if severe AHAI or HPN<\/td>\n <\/tr>\n <tr>\n <td>Polycythemia and erythrocytosis<br><small style=\"font-weight:400;color:#7a8fa0;\">High GR - JAK2 mutation - Vaquez<\/small><\/td>\n <td>Polycythemia (erythrocytosis) is defined by an increase in erythrocyte mass - diagnosed in practice by an Hb >185 g\/L in men + >165 g\/L in women (WHO 2016) or a hematocrit >52 % (men) + >48 % (women); erythrocytosis classification: true absolute erythrocytosis (actual increase in erythrocyte mass): primary - Vaquez disease (polycythemia vera - PV): clonal myeloproliferative neoplasm - JAK2 V617F mutation (exon 14) in >95 % of cases + JAK2 exon 12 mutation in <5 % - workup: CBC (polycythemia + often associated thrombocytosis + leukocytosis) + low EPO (autonomous GR production - physiological EPO braking) + JAK2 V617F mutation (key diagnostic test) + bone-medullary biopsy (tri-lineage hypercellularity with panmyelosis) - WHO 2016 diagnostic criteria (3 major criteria or 2 major + 1 minor required); secondary erythrocytosis (high EPO): hypoxic causes: severe COPD + obstructive sleep apnea syndrome (OSAS) + cyanogenic congenital heart disease + high altitude + smoking (CO \u2192 HbCO \u2192 functional tissue hypoxia \u2192 smoker's polyglobulia) + high-affinity hemoglobin for O2 (high-affinity hemoglobins: left-shifted dissociation curve \u2192 tissue hypoxia \u2192 high EPO \u2192 polyglobulia); non-hypoxic causes (non-physiological high EPO): clear cell renal cell carcinoma (ectopic EPO secretion - paraneoplastic polycythemia) + hepatocarcinoma + cerebellar hemangioblastoma (Von Hippel-Lindau) + renal cyst + renal artery stenosis (focal renal ischemia \u2192 elevated local EPO); relative erythrocytosis (Gaisbock pseudopolycythemia): normal erythrocyte mass - hemoconcentration by reduction of plasma volume (dehydration + diuretics + visceral obesity + hypertension + smoking + stress) \u2192 elevated hematocrit and Hb but normal RBCs on isotopic measurement of erythrocyte mass<\/td>\n <td>Treatment of Vaquez disease (polycythemia vera): main therapeutic objective: reduce the risk of thrombosis (main cause of mortality in PV) by maintaining hematocrit <45 % (male) + 60 + history of thrombosis + platelets >1,500 G\/L + polycythemia difficult to control with bloodletting alone): hydroxyurea (Hydrea): 1st line of cytoreduction - 500-1,500 mg\/d PO + theoretical leukemogenic risk (low but real in the long term) + pegylated interferon alfa (Besremi - ropeginterferon alfa-2b): approved by Health Canada 2022 for PV - SC every 2 weeks \u2192 reduction of JAK2 allelic load (possible molecular remission) \u2192 preferred alternative in young patients + pregnancy considered (with precautions) + intolerance or resistance to hydroxyurea + ruxolitinib (Jakafi - JAK1\/JAK2 inhibitor): 2nd line if resistant or intolerant to hydroxyurea - approved by Health Canada for refractory PV; secondary erythrocytosis : treatment of cause (smoking cessation + CPAP if OSA + COPD treatment + renal cell carcinoma resection) + bloodletting if polycythaemia-related symptoms (hyperviscosity - headache + facial erythrosis + tinnitus + aquagenic pruritus) + target hematocrit <50 % in hypoxic secondary polycythaemias<\/td>\n <\/tr>\n <tr>\n <td>Aregenerative normocytic anemia<br><small style=\"font-weight:400;color:#7a8fa0;\">Aplasia - renal failure - MDS<\/small><\/td>\n <td>Aregenerative normocytic anemia (low reticulocytes + normal GMV) points to insufficient bone marrow production (aplasia) or inefficient erythropoiesis (MDS + incipient deficiencies); chronic renal failure (CKD): anemia in CKD is the most frequent of the aregenerative anemias - mechanism: insufficient EPO production by fibrosed renal peritubular cells + reduced erythrocyte lifespan + frequent relative martial deficiency + uremic toxicity on erythropoiesis + chronic inflammation (hepcidin) - prevalence: 40-50 % of stage 3b-5 CKD patients (GFR <45 mL\/min\/1.73 m\u00b2) - workup: serum EPO (inadequately low for degree of anemia) + ferritin + CST + inflammatory workup; bone marrow aplasia (pure aplasia or aplastic pancytopenia): disappearance of hematopoietic cells from marrow \u2192 anemia + thrombocytopenia + neutropenia - acquired aplasia (idiopathic - autoimmune mechanism T \u2192 70 % of acquired aplasias + drugs: chloramphenicol + carbamazepine + ticlopidine + sulfonamides + gold) + constitutional aplasias (Fanconi anemia - chromosomal breaks + congenital anomalies + dyskeratosis congenita - TERC + TERT mutation); pure red cell aplasia (PRCA) : selective aplasia of the erythroid lineage \u2192 severe aregenerative anemia without thrombocytopenia or neutropenia - causes: parvovirus B19 (in immunocompromised or chronic hemolytics) + thymoma + autoimmune + drugs (epoetin - anti-EPO antibodies); myelodysplastic syndromes (MDS): dysplastic bone marrow clones \u2192 ineffective erythropoiesis \u2192 anemia + sometimes macrocytosis + smear: dysgranulopoiesis + abnormal megakaryocytes + myelogram + BOM + karyotype + NGS \u2192 WHO 2022 classification \u2192 IPSS-R score \u2192 therapeutic decision (monitoring + azacitidine + allograft); acquired aplastic anemia - severity criteria: severe aplasia (SAA): neutrophils <0.5 G\/L + platelets <20 G\/L + reticulocytes <20 G\/L + marrow <25 % cellularity + very severe aplasia (VSAA): neutrophils <0.2 G\/L<\/td>\n <td>Treatment of anemia in CKD: erythropoiesis-stimulating agents (ESAs): epoetin alfa (Eprex) + epoetin beta (NeoRecormon) + darbepoetin alfa (Aranesp): EPO \u2192 receptor agonists stimulate erythropoiesis \u2192 indications: Hb <100 g\/L + GFR 130 g\/L - increased cardiovascular and thromboembolic risk) - administration: SC (better than IV for efficacy) or IV if hemodialysis + concomitant martial supplementation mandatory (IV iron preferably in hemodialysis) \u2192 target ferritin >200 \u00b5g\/L + CST >20 %; HIF-PH (hypoxia-inducible factor prolyl hydroxylase) inhibitors: new oral therapeutic class: roxadustat (Evrenzo - AstraZeneca): approved by Health Canada 2021 for CKD anemia in dialysis and pre-dialysis - mechanism: inhibition of HIF prolyl hydroxylases \u2192 stabilization of HIF-1\u03b1 and HIF-2\u03b1 factors \u2192 endogenous increase in EPO secretion + increase in intestinal iron absorption \u2192 dual effect - advantages vs ESA: oral route + effective in inflammatory setting (reduced hepcidin) + lower risk of hypertension - monitoring: HbA1c + lipids (decreased under roxadustat) + thromboses; treatment of acquired bone marrow aplasia: hematopoietic stem cell allograft transplantation (HSCT): reference curative treatment for patients 40 years old): anti-thymocyte serum (SAT - horse or rabbit) + cyclosporine + eltrombopag (Revolade - thrombopoietin receptor agonist - TPO-RA): data RACE + STRONG-SAA \u2192 improved response rate + complete remission rate 40-50 % under triple therapy SAT + cyclosporine + eltrombopag<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>Interpretation of erythrocyte CBC - 4-step systematic approach:<\/strong> (1) Presence or absence of anemia (low Hb) or polycythemia (high Hb) - (2) VGM: microcytosis (100 fL) \u2192 B12\/folate deficiency or drugs - (3) Regenerative (reticulocytes >120 \u00d7 10\u2079\/L \u2192 hemolysis or hemorrhage) or aregenerative (low reticulocytes \u2192 insufficient production) character - (4) Blood smear for morphology (schizocytes \u2192 MAT; sickle cells \u2192 sickle cell anemia; PNN hypersegmentation \u2192 megaloblastosis). This cascade approach leads to a precise etiological diagnosis before prescribing targeted complementary examinations.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Severe anemia (Hb <70 g\/L) + signs of poor tolerance (dyspnea at rest + tachycardia + hypotension + chest pain + confusion)<\/strong> \u2192 urgent erythrocyte transfusion + etiological workup + hospitalization.<\/p>\n <p><strong>Schizocytes on smear + anemia + severe thrombocytopenia \u00b1 fever + neurological or renal impairment<\/strong> \u2192 thrombotic microangiopathy (PTT or SHU) \u2192 ADAMTS13 urgently + plasma exchanges if PTT \u2192 urgent hematology opinion.<\/p>\n <p><strong>Polyglobulia (Hb >185 g\/L male + >165 g\/L female) + thrombosis (stroke + MI + Budd-Chiari) or signs of hyperviscosity<\/strong> \u2192 probable Vaquez disease \u2192 JAK2 V617F mutation + urgent bleeding if hematocrit >55 % + aspirin + hematology.<\/p>\n <p><strong>Pancytopenia (anemia + neutropenia + thrombocytopenia) + fever in a patient taking a potentially myelotoxic drug<\/strong> \u2192 drug-induced bone marrow aplasia \u2192 immediate discontinuation of incriminating drug + urgent CBC + hematology opinion + hospitalization if severe neutropenia.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron's physicians prescribe and interpret erythrocyte CBCs as part of the work-up for unexplained fatigue, incidentally discovered anemia, pregnancy monitoring, chronic illness or pre-operative work-up. Referral to specialized hematology (hemolytic anemias, polycythemia, aplasia), prescription of appropriate martial or vitamin supplementation and screening for underlying causes (digestive bleeding, celiac disease, nutritional deficiencies) are all part of the clinical approach available at several points of service in Quebec and via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The contents of this page are provided for information purposes only and do not replace the advice of a physician or hematologist. The interpretation of a CBC must always be carried out in the patient's clinical context.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Globules rouges (\u00e9rythrocytes) : valeurs normales et interpr\u00e9tation | Clinique Omicron H\u00e9matologie & M\u00e9decine de laboratoire & M\u00e9decine de famille Globules rouges (\u00e9rythrocytes) Les globules rouges, ou \u00e9rythrocytes, sont les cellules sanguines les plus nombreuses de l’organisme \u2014 on en d\u00e9nombre environ 25 000 milliards chez un adulte, soit 70 % de toutes les cellules… <a href=\"https:\/\/cliniqueomicron.ca\/en\/globules-rouges-erythrocytes\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Red blood cells (erythrocytes): normal values and interpretation | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Globules rouges (\u00e9rythrocytes) : | Brossard | Clinique Omicron","_metasync_otto_description":"Les globules rouges transportent l'oxyg\u00e8ne gr\u00e2ce \u00e0 l'h\u00e9moglobine. Valeurs normales, an\u00e9mie, polyglobulie, indices \u00e9rythrocytaires et interpr\u00e9tation au Qu\u00e9bec.","_metasync_otto_keywords":"","_metasync_otto_og_title":"Globules rouges (\u00e9rythrocytes) : | Brossard | Clinique Omicron","_metasync_otto_og_description":"","_metasync_otto_twitter_title":"Globules rouges (\u00e9rythrocytes) : | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"Les globules rouges transportent l'oxyg\u00e8ne gr\u00e2ce \u00e0 l'h\u00e9moglobine. Valeurs normales, an\u00e9mie, polyglobulie, indices \u00e9rythrocytaires et interpr\u00e9tation au Qu\u00e9bec.","rank_math_title":"","rank_math_description":"","_yoast_wpseo_title":"","_yoast_wpseo_metadesc":"","_aioseo_title":"Globules rouges (\u00e9rythrocytes) : valeurs normales et interpr\u00e9tation | Clinique Omicron","_aioseo_description":"Les globules rouges transportent l'oxyg\u00e8ne gr\u00e2ce \u00e0 l'h\u00e9moglobine. Valeurs normales, an\u00e9mie, polyglobulie, indices \u00e9rythrocytaires et interpr\u00e9tation au Qu\u00e9bec.","_metasync_seo_title":"","_metasync_seo_desc":"","_metasync_breadcrumb_title":"","_metasync_primary_category":0,"_metasync_primary_product_cat":0,"_metasync_otto_disabled":"","_metasync_hreflang":"","_metasync_plugin_sync_ts":"{\"aioseo\":\"2026-05-04T15:31:20+00:00\"}","_metasync_robots_advanced":"","footnotes":""},"class_list":["post-24609","page","type-page","status-publish","hentry"],"aioseo_notices":[],"_links":{"self":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages\/24609","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/comments?post=24609"}],"version-history":[{"count":4,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages\/24609\/revisions"}],"predecessor-version":[{"id":29004,"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/pages\/24609\/revisions\/29004"}],"wp:attachment":[{"href":"https:\/\/cliniqueomicron.ca\/en\/wp-json\/wp\/v2\/media?parent=24609"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}