Hemoglobin (Hb): normal values, anemia and interpretation | Omicron Clinic<\/title>\n<meta name=\"description\" content=\"Hemoglobin transports oxygen in the blood. Low hemoglobin (anemia), high hemoglobin (polycythemia), electrophoresis, sickle cell disease and management in Quebec.\">\n<meta name=\"keywords\" content=\"h\u00e9moglobine valeurs normales, h\u00e9moglobine basse an\u00e9mie, h\u00e9moglobine \u00e9lev\u00e9e, \u00e9lectrophor\u00e8se h\u00e9moglobine, h\u00e9moglobine A1c, dr\u00e9panocytose thalass\u00e9mie, h\u00e9moglobine grossesse Qu\u00e9bec, an\u00e9mie traitement\">\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 & Family Medicine & Internal Medicine<\/span>\n <h1>Hemoglobin (Hb)<\/h1>\n\n <div class=\"co-intro\">\n Hemoglobin (Hb) is the tetrameric protein found in red blood cells (erythrocytes), whose main function is to transport oxygen from the lungs to the tissues, and return carbon dioxide to the lungs. It represents around 33 % of the red blood cell's weight, and is made up of four polypeptide subunits (globins), each bearing a heme prosthetic group containing a ferrous iron atom (Fe\u00b2\u207a) capable of reversibly binding to an oxygen molecule. Hemoglobin concentration in blood is expressed in grams per liter (g\/L) or per deciliter (g\/dL) - 1 g\/dL = 10 g\/L. Normal adult values are 130 to 175 g\/L for men and 120 to 160 g\/L for women, according to Canadian laboratories. Hemoglobin is the reference parameter for diagnosing and classifying the severity of anemia (Hb below normal values, depending on age and sex) and polycythemia (Hb above normal values). It differs from hematocrit in that it measures the hemoglobin concentration itself - and not the volume occupied by red blood cells - making it a more stable parameter, less influenced by variations in mean corpuscular volume (MCV). Hemoglobin electrophoresis can be used to identify pathological structural variants (HbS in sickle cell disease, HbC, HbE) and abnormalities in globin chain synthesis (thalassemias), with major implications for preventive medicine and medical genetics.\n <\/div>\n\n <h2>Hemoglobin structure, function and variants<\/h2>\n <ul class=\"co-list\">\n <li><strong>Molecular structure and types of hemoglobin :<\/strong> structure of normal adult Hb (HbA): tetramer of two alpha (\u03b1) and two beta (\u03b2) chains \u2192 formula \u03b1\u2082\u03b2\u2082 \u2192 molecular weight: 64,500 Da \u2192 each chain carries a heme group (protoporphyrin IX + Fe\u00b2\u207a) \u2192 binding capacity: 1 molecule of O\u2082 per iron atom \u2192 4 molecules of O\u2082 per Hb molecule \u2192 allosteric cooperativity: binding of one O\u2082 molecule increases the affinity of the other three sites (sigmoid dissociation curve for oxyhemoglobin) \u2192 regulators of affinity for O\u2082: 2,3-diphosphoglycerate (2,3-DPG): binds to deoxyhemoglobin \u2192 decreases affinity for O\u2082 \u2192 promotes release of O\u2082 to tissues + pH (Bohr effect): low pH + high CO\u2082 (active tissues) \u2192 decreases affinity \u2192 release of O\u2082 + high temperature \u2192 decreases affinity \u2192 release of O\u2082; normal age-dependent hemoglobin types: fetal hemoglobin (HbF = \u03b1\u2082\u03b3\u2082): predominant in utero and in the first weeks of life \u2192 high affinity for O\u2082 (captures O\u2082 at placenta from maternal circulation) \u2192 gradually replaced by HbA after birth: HbF 70-90 % at birth \u2192 1 % in adulthood) under certain conditions: hemoglobinopathies + leukemias + aplasia + normal adult hemoglobin: HbA (\u03b1\u2082\u03b2\u2082): 96-98 % + HbA\u2082 (\u03b1\u2082\u03b4\u2082): 2-3.5 % \u2192 increased level in beta-thalassemia minor (trait): HbA\u2082 >3.5 % = diagnostic criterion + HbF: <1 %; pathological forms of hemoglobin: HbS (sickle cell disease): glutamate \u2192 valine substitution in position 6 of \u03b2 chain (\u03b26Glu\u2192Val) + GAG\u2192GTG mutation \u2192 deoxygenated HbS polymerizes \u2192 RBC sickling + HbC: \u03b26Glu\u2192Lys substitution \u2192 crystallizes \u2192 moderate hemolysis + HbE: \u03b226Glu\u2192Lys substitution + splicing mutations \u2192 microcytosis + frequent in Southeast Asia + other variants: HbD-Punjab + HbO-Arab + Hb Constant Spring (\u03b1-chain extension); hemoglobin measurement on modern automatons: cyanmhemoglobin method (ICSH - reference method): RBC lysis + oxidation of Fe\u00b2\u207a to Fe\u00b3\u207a (methemoglobin) + transformation to cyanmethemoglobin + spectrophotometric reading at 540 nm \u2192 but most modern automata (Sysmex XN + Beckman-Coulter DxH) use the cyanide-free method (SLS - sodium lauryl sulfate) \u2192 coefficient of variation <1 % \u2192 interference: severe lipemia + massive hyperleukocytosis + carboxyhemoglobin \u2192 false high Hb if uncorrected<\/li>\n <li><strong>Normal values, physiological variations and definition of anemia :<\/strong> hemoglobin reference values (Canadian laboratories - venous plasma - calibrated automatons): adult male (18-70 years): 130-175 g\/L + adult female (18-70 years): 120-160 g\/L + pregnancy: Hb <110 g\/L = anemia (WHO) in 1st and 3rd trimester + Hb 70 years): slight physiological decline expected but any Hb <120 g\/L (H) or <110 g\/L (F) merits investigation + altitude: +10 g\/L for 1,000 m altitude above 1,500 m (hypoxia-stimulated EPO) + smoking: slightly higher Hb (carboxyhemoglobin \u2192 shift in dissociation curve \u2192 relative hypoxia \u2192 EPO stimulation) \u2192 correct Hb for smoking in population; WHO definition of anemia (2001): adult male: Hb <130 g\/L + adult non-pregnant female: Hb <120 g\/L + pregnant female 1st + 3rd trimester: Hb <110 g\/L + pregnant female 2nd trimester: Hb <105 g\/L + child 6 months-5 years: Hb <110 g\/L + child 5-11 years: Hb <115 g\/L + child 12-14 years: Hb <120 g\/L; classification of anemia severity: mild: Hb 100-130 g\/L (H) or 100-120 g\/L (F) \u2192 mild symptoms on exertion + moderate: Hb 70-100 g\/L \u2192 fatigue + dyspnea on exertion + palpitations + severe: Hb <70 g\/L \u2192 rest dyspnea + rest tachycardia + high output heart failure + angina + very severe (critical): Hb <50 g\/L \u2192 life-threatening \u2192 indication for near-absolute transfusion<\/li>\n <li><strong>Hemoglobin electrophoresis and neonatal screening :<\/strong> hemoglobin electrophoresis: method: separation of Hb variants according to their electrical charge in agarose or cellulose acetate gel (alkaline pH 8.6 and\/or acid pH 6.2) \u2192 HPLC (High Performance Liquid Chromatography): current reference method \u2192 separation + quantification of Hb fractions (HbA + HbA\u2082 + HbF + variants) on cation exchange column \u2192 automatic detection \u2192 highly sensitive and reproducible \u2192 interpretation of fractions: HbA\u2082 >3.5 %: beta-thalassemic trait (\u03b2TA or \u03b2TB) \u2192 HbA\u2082 4-7 % in beta-thalassemia minor \u2192 if >7 %: associated hemoglobin D + HbF >5 % in adults: thalassemic syndrome + hereditary persistence of HbF (PHHF) + sickle cell anemia treated with hydroxyurea + hemopathies \u2192 presence of an HbS fraction: sickle cell anemia (SS if HbA absent + SA if HbA present = sickle cell trait) + presence of HbC: HbCC (moderate chronic hemolytic anemia) or HbSC (major sickle cell syndrome with moderate phenotype); neonatal screening in Quebec: provincial neonatal screening program (Quebec) \u2192 screening for sickle cell disease + major sickle cell syndromes by HPLC on dried blood (blotting paper - \u00abGuthrie test\u00bb) at D2-J5 of life \u2192 indication: high-risk population (sub-Saharan Africa + Caribbean + Mediterranean + India + Southeast Asia) \u2192 Programme Qu\u00e9b\u00e9cois de D\u00e9pistage N\u00e9onatal (PQDN - MSSS) \u2192 if screening positive \u2192 confirmation by HPLC on venous sample + genotyping \u2192 genetic consultation + pediatric hematological follow-up \u2192 genetic counseling: if both parents are carriers (trait) \u2192 risk 1\/4 homozygous form (disease) + 1\/2 trait + 1\/4 non-carrier child<\/li>\n <\/ul>\n\n <h2>Anemia, hemoglobinopathies and special clinical situations<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Clinical situation<\/th><th>Assessment and diagnosis<\/th><th>Treatment and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Diagnostic approach to low Hb - etiological algorithm<br><small style=\"font-weight:400;color:#7a8fa0;\">VGM - reticulocytes - ferritin - B12 - hemolysis<\/small><\/td>\n <td>Low hemoglobin requires a structured diagnostic approach based on erythrocyte indices, reticulocytosis and biochemical tests; first step - VGM as a morphological orientation tool: microcytic anemia (VGM <80 fL) : martial deficiency (most frequent cause - low ferritin + CST 100 fL) : vitamin B12 deficiency (autoimmune gastric atrophy - Biermer's disease - anti-FI positive + gastrostomy + strict veganism) + folate deficiency (pregnancy + alcoholism + drugs: MTX + carbamazepine + trimethoprim) + alcoholism (direct macrocytosis independent of deficiencies) + hypothyroidism + MDS (myelodysplastic syndrome - macrocytosis + dysplasia on CBC + pancytopenia) + drugs (hydroxyurea + zidovudine + capecitabine); second stage - reticulocytes : regenerative anemia (high reticulocytes - RPN >2) \u2192 marrow actively producing \u2192 look for hemolysis or bleeding + aregenerative anemia (low reticulocytes - RPN <2) \u2192 insufficient production \u2192 nutritional deficiency + marrow insufficiency + chronic disease<\/td>\n <td>Biological work-up oriented according to the type of anemia: systematic 1st-line work-up: complete CBC with blood smear (RBC morphology: microcytes + hypochromia + elliptocytes + spherocytes + schizocytes + sickle cells + targets + Howell-Jolly bodies + nucleated RBCs) + reticulocytes + ferritin + CRP (ferritin = acute-phase reactant \u2192 interpret with CRP) + vitamin B12 + serum folate + TSH + creatinine + GFR; if regenerative anemia (elevated reticulocytes) \u2192 hemolysis workup: LDH (elevated if intravascular or intracorpuscular hemolysis) + haptoglobin (collapsed if intravascular hemolysis - haptoglobin binds to free Hb \u2192 complex catabolized by liver) + total bilirubin + indirect (elevated if hemolysis \u2192 hemolytic jaundice) + direct antiglobulin test (DAT or direct Coombs): positive if autoantibodies (IgG) or complement (C3d) on RBCs \u2192 autoimmune hemolytic anemia (AHAI) \u2192 GS Rh + phenotyping + hematology opinion + smear : spherocytes (AHAI + hereditary spherocytosis) + schizocytes (MAT - thrombotic microangiopathy - PTT + SHU + CIVD) + sickle cells + Heinz bodies (after special staining - G6PD deficiency + methemoglobinemia); if aregenerative anemia + macrocytosis: B12 (<148 pmol\/L \u2192 deficiency) + methylmalonic acid (AMM) + homocysteine : functional markers of B12 deficiency (more sensitive than serum B12 levels) + antiintrinsic factor (Biermer's disease - specificity 95-99 % but sensitivity 50-70 %) + anti-gastric parietal cells (APC - sensitivity 85 % but not very specific) + gastroscopy + gastric biopsy if Biermer's suspected \u2192 atrophic fundic gastritis<\/td>\n <\/tr>\n <tr>\n <td>Sickle cell disease - HbSS and major sickle cell syndromes<br><small style=\"font-weight:400;color:#7a8fa0;\">Vaso-occlusive crisis - hydroxyurea - transfusion - transplantation<\/small><\/td>\n <td>Sickle cell disease is the most common monogenic disease in the world - its management has been transformed by hydroxyurea, erythrocyte exchange and new targeted therapies; pathophysiology: deoxygenated HbS polymerizes into rigid fibers \u2192 sickling of RBCs \u2192 3 major consequences: chronic hemolysis (lifespan of sickled RBCs : 10-20 days vs 120 days for normal RBCs \u2192 severe chronic hemolytic anemia - baseline Hb 60-90 g\/L) + vaso-occlusion (sickle + rigid RBCs block capillaries \u2192 tissue ischemia \u2192 intense pain + organ necrosis) + endothelial dysfunction (intravascular hemolysis \u2192 free Hb \u2192 NO scavenging \u2192 vasoconstriction + hypercoagulability); major sickle cell syndromes: HbSS (homozygous sickle cell disease): most severe \u2192 70-80 % sickle cell RBCs + HbSC (HbS + HbC in trans): moderate phenotype \u2192 proliferative retinopathy + thromboembolic complications + Hb often 90-110 g\/L + HbS\u03b2\u2070-thalassemia: HbS + no \u03b2 chain \u2192 picture close to SS + HbS\u03b2\u207a-thalassemia: HbS + little \u03b2 chain \u2192 moderate phenotype; major clinical manifestations: painful vaso-occlusive crisis (CVO): intense osteoarticular pain (back + hips + limbs) \u2192 management: level 3 immediately if VAS >7 (morphine IV or SC) + NSAIDs + ketorolac + NaCl 0.9 % (hyperhydration) + local heat \u2192 hospitalization if VAS >7 or duration >4h + acute chest syndrome (ACS): pulmonary infiltrate + chest pain + fever + hypoxemia \u2192 main cause of sickle cell mortality \u2192 treatment: urgent transfusion (single or exchange) + antibiotic (ceftriaxone + azithromycin) + bronchodilators + O\u2082 + ischemic stroke (20 % of HbSS before age 20 without prevention) + splenic sequestration (especially child <5 years) + priapism + sickle cell nephropathy<\/td>\n <td>Treatment of sickle cell disease - therapeutic options: hydroxyurea (HU): mechanism: increase in HbF (inhibits polymerization of HbS) + reduction in reticulocytes and leukocytes + improvement in RBC hydration \u2192 dose: 15-35 mg\/kg\/d PO + titration to maximum tolerated dose (nadir Platelets >80,000 + PNN >2,000) \u2192 proven efficacy: 1995 MSH trial (Charache - NEJM): reduction of CVO by 44 % + of STA by 50 % + of transfusions by 50 % + recommended from 9 months (child) by NHLBI 2014 guidelines + adverse effects: myelosuppression (CBC monitoring every 4-8 weeks) + macrocytosis (benign - compliance marker) + theoretical mutagen but no clinically documented leukemic surrisk + reimbursed RAMQ on drug list + voxelotor (Oxbryta): HbS polymerization inhibitor (increases HbS affinity for O\u2082) \u2192 HOPE 2019 trial (Vichinsky - NEJM): Hb improvement +1.5 g\/dL + hemolysis reduction + FDA approval 2019 \u2192 under INESSS evaluation in Quebec + crizanlizumab (Adakveo): anti-P-selectin (inhibits sickle cell RBC adhesion to endothelium) \u2192 SUSTAIN 2017 trial (Ataga - NEJM): CVO reduction of 45 % vs placebo \u2192 FDA approval 2019 + Health Canada 2021 + L-glutamine (Endari): reduces oxidative stress in sickle cell RBCs \u2192 FDA approval 2017 + hematopoietic stem cell transplantation (allograft): only curative treatment available \u2192 indication: HbSS + recurrent APS + stroke + frequent CVO \u00b1 comorbidities + HLA-compatible donor (ideally sibling) \u2192 cure rate: 85-95 % if genotypic donor \u2192 gene therapy (LentiGlobin bb1111 - Bluebird Bio + CRISPR-Cas9 - Vertex\/CRISPR Therapeutics): BCL11A gene editing or direct correction of HbS mutation \u2192 FDA approval December 2023 (exagamglogene autotemcel - Casgevy - world's first approved CRISPR therapy) \u2192 availability in Canada: under evaluation Health Canada \/ INESSS 2024-2025<\/td>\n <\/tr>\n <tr>\n <td>Thalassemias - alpha and beta<br><small style=\"font-weight:400;color:#7a8fa0;\">Thalassemia trait - thalassemia major - iron - Desferal<\/small><\/td>\n <td>Thalassemias are quantitative abnormalities of globin chain synthesis - reduction or absence of production of one or more chains \u2192 imbalance \u2192 precipitation of excess chains \u2192 intramedullary destruction + peripheral hemolysis; beta-thalassemia: mutations in the HBB gene (chromosome 11) \u2192 reduction (\u03b2\u207a) or absence (\u03b2\u2070) of \u03b2-chain synthesis + clinical classification: beta-thalassemia trait (\u03b2Thal minor or \u00abthalassemia minor\u00bb): heterozygous \u03b2\u2070 or \u03b2\u207a \u2192 slightly low Hb (100-120 g\/L in F) + very low VGM (3.5 % on HPLC \u2192 no treatment \u2192 important for genetic counseling + thalassemia intermediate (\u03b2Thal intermediate): genotype \u03b2\u207a\/\u03b2\u207a or \u03b2\u2070\/\u03b2\u207a + moderate mutations \u2192 Hb 70-100 g\/L \u2192 intermittent transfusion + iron overload possible + thalassemia major (Cooley - \u03b2Thal major - \u03b2\u2070\/\u03b2\u2070): Hb <70 g\/L requiring regular transfusions + extramedullary erythropoiesis + hepatosplenomegaly + bone deformities (thalassemic facies) \u2192 management in specialized center; alpha-thalassemia: deletions of the HBA1\/HBA2 gene (chromosome 16) - 4 alleles: 1 deletion (\u03b1\u03b1\/\u03b1-): silent carrier \u2192 asymptomatic \u2192 normal Hb + VGM \u2192 2 deletions (\u03b1-\/\u03b1- or \u03b1\u03b1\/--): alpha-thalassemic trait \u2192 low VGM + normal or slightly low Hb + normal HbA\u2082 (different from beta!) \u2192 diagnosis by PCR\/genotyping \u2192 3 deletions (--\/\u03b1-): HbH (\u03b2\u2084) - HbH disease \u2192 moderate chronic haemolytic anaemia + haemoglobin H precipitates + Heinz bodies \u2192 Hb 80-110 g\/L \u2192 4 deletions (--\/--): Hb Bart (\u03b3\u2084) - hydrops fetalis \u2192 incompatible with ectopic life \u2192 immediate fetal death in utero or neonatal.<\/td>\n <td>Treatment of severe thalassemias: regular transfusions (thalassemia major): goal: maintain pre-transfusion Hb >95-100 g\/L \u2192 suppression of inefficient erythropoiesis (main source of iron overload) \u2192 pheno-compatible RBCs (Rh + Kell at least) \u2192 leukodepleted \u2192 interval: every 2-4 weeks according to regimen + iron chelation: necessary in all polytransfused patients (iron overload \u2192 cardiac + hepatic + endocrine hemosiderosis): deferasirox (Exjade - Jadenu): 10-20 mg\/kg\/d PO \u2192 1st line \u2192 well tolerated \u2192 monitor creatinine + hepatic workup + deferoxamine (Desferal): 20-40 mg\/kg\/d SC nightly infusion \u00d7 8-10h \u2192 effective but restrictive (nightly SC injection) \u2192 reserved if deferasirox CI + deferiprone (Ferriprox): 75-100 mg\/kg\/d PO \u00d7 3\/d \u2192 useful for cardiac chelation + in combination with deferoxamine if advanced cardiac fibrosis \u2192 chelation goal: serum ferritin 20 ms (cardiac siderosis monitoring - CMR method); hematopoietic stem cell transplantation: curative treatment of thalassemia major \u2192 cure rate: 85-90 % if genoidentical HLA donor + patient in Pesaro class I (absence of hepatomegaly + no portal fibrosis + regular chelation before transplantation) \u2192 betibeglogene autotemcel gene therapy (Zynteglo - Bluebird Bio): lentiviral vector \u2192 insertion of a functional copy of the \u03b2-globin gene \u2192 FDA 2022 approval + Health Canada under evaluation; luspatercept (Reblozyl): traps TGF-\u03b2 ligands \u2192 reduces inefficient erythropoiesis \u2192 FDA + EMA approval for transfusion-dependent beta-thalassemia \u2192 BELIEVE 2020 trial (Cappellini - NEJM): reduction in transfusion requirement of \u226533 % in 21.4 % vs. 4.5 % on placebo \u2192 Health Canada approval 2021<\/td>\n <\/tr>\n <tr>\n <td>Methemoglobinemia and carboxyhemoglobin - Dysfunctional Hb<br><small style=\"font-weight:400;color:#7a8fa0;\">Methylene blue - CO - co-oximetry - intoxication<\/small><\/td>\n <td>Some forms of hemoglobin are unable to transport oxygen - their accumulation leads to tissue hypoxia despite sometimes normal total Hb; methemoglobinemia: mechanism: oxidation of Fe\u00b2\u207a to Fe\u00b3\u207a in the heme moiety \u2192 methemoglobin (MetHb) unable to bind O\u2082 + left Bohr effect on the curve of remaining Hb \u2192 worsening hypoxia \u2192 clinical thresholds: MetHb >10 %: central cyanosis (grey-slate hue) + low SpO\u2082 pulse saturation (~85 % regardless of actual O\u2082 level) \u2192 \u00absaturation set at 85 % by pulse oximeter\u00bb \u2192 major diagnostic pitfall as pulse oximeter does not distinguish MetHb from OxyHb + MetHb >20-30 %: headache + dizziness + dyspnoea + confusion + MetHb >50 %: convulsions + coma + life-threatening + MetHb >70 %: potentially fatal; causes of acquired methemoglobinemia: drugs: dapsone ++ + primaquine + nitrates + nitrites (contaminated water + excess nitrite-treated deli meats) + benzocaine + topical lidocaine + chloroquine + metoclopramide + nitrofurantoin + rasburicase \u2192 at-risk populations: G6PD deficiency (reduced NADPH oxidase pathway \u2192 less reducing power) + infants (50 % + mechanical ventilation; co-oxymetry: reference method for measuring Hb fractions: OxyHb + DeoxyHb + MetHb + COHb + SulfHb \u2192 available on blood gas co-oximeters (ABL from Radiometer + EPOC) \u2192 do not rely on pulse-oximeter alone if CO intoxication or methemoglobinemia suspected<\/td>\n <td>Carbon monoxide (CO) intoxication and carboxyhemoglobin: CO binds to hemoglobin with 240\u00d7 higher affinity than O\u2082 \u2192 carboxyhemoglobin (COHb) \u2192 displaces O\u2082 \u2192 tissue hypoxia \u2192 also blocks mitochondrial cytochrome c oxidase (direct cellular toxicity) \u2192 left-shifted dissociation curve (less O\u2082 delivered to tissues); CO sources: incomplete combustion (gas + fuel oil + wood + coal + propane + gasoline) + fire + engine in enclosed space + motor-driven electric generator; clinical picture according to COHb: COHb 50 %: coma + convulsions + cardiorespiratory arrest + COHb >70 %: fatal; diagnostic pitfall: SpO\u2082 on pulse-oximeter normal or subnormal (COHb absorbs light like OxyHb at 660 nm \u2192 false high saturation) \u2192 always assay COHb by co-oximetry if CO intoxication suspected; treatment: O\u2082 normobaric at 100 % (reservoir mask or intubation) \u2192 COHb half-life: ambient air 5-6h \u2192 O\u2082 100 % 60-90 min \u2192 O\u2082 hyperbaric (HBOT) 2.5-3 ATA \u2192 20-30 min \u2192 HBOT indications (Weaver 2002 NEJM): COHb >25 % + pregnancy + loss of consciousness + neurological symptoms + cardiac ischemia \u2192 available in Quebec: CHU de Qu\u00e9bec + IUCPQ hyperbaric center + SMOH (Service M\u00e9dical d'Oxyg\u00e9noth\u00e9rapie Hyperbare) \u2192 neurological sequelae: lucid post-interval syndrome (dementia + personality disorders + parkinsonism) \u2192 10-30 % of severe forms \u2192 brain MRI: lesions of the pallidums + periventricular white matter. <\/tr>\n <tr>\n <td>Hemoglobin and pregnancy - Gestational anemia and screening<br><small style=\"font-weight:400;color:#7a8fa0;\">Iron - folates - B12 - screening for hemoglobinopathies - thalassemia<\/small><\/td>\n <td>Pregnancy profoundly modifies hemoglobin and exposes to specific risks that justify systematic screening; physiological modifications of pregnancy on Hb: hemodilution: expansion of plasma volume by 40-50 % in 2nd trimester + increase in erythrocyte mass by 20-30 % \u2192 Hb dilutes \u2192 \u00abphysiological anemia\u00bb \u2192 minimum acceptable Hb in pregnancy according to WHO: 110 g\/L (1st + 3rd trimester) + 105 g\/L (2nd trimester) \u2192 caution: the 'physiological anemia\u00ab of pregnancy should not lead to overlooking a true iron deficiency anemia \u2192 ferritin <30 \u00b5g\/L \u2192 martial deficiency \u2192 treat + increase needs: iron: iron needs increase from 1 mg\/d (outside pregnancy) to 6-7 mg\/d at the end of pregnancy \u2192 needs covered by a varied diet + systematic supplementation if ferritin <30 \u00b5g\/L + folates: needs double in pregnancy \u2192 systematic pre-conceptional supplementation: folic acid 0.4-5 mg\/d (0.4 mg if no particular risk + 4 mg if history of AFTN + valproate + morbid obesity + diabetes) \u2192 recommendation Society of Obstetricians and Gynaecologists of Canada (SOGC) 2015 + MSSS Quebec \u2192 reduces the risk of neural tube defects by 70 % + vitamin B12: supplementation recommended if strict vegan diet (risk of maternal + neonatal deficiency) \u2192 B12 1,000 \u00b5g\/d PO; screening for hemoglobinopathies in pregnancy in Quebec: SOGC 2008 recommendation (J Obstet Gynaecol Can): Hb electrophoresis recommended for all high-risk pregnant women (African + Caribbean + Mediterranean + Middle Eastern + Asian origin) \u2192 in Quebec: universal screening recommended by several pediatric associations \u2192 if maternal sickle cell trait (HbAS) \u2192 paternal screening \u2192 if both parents carriers \u2192 genetic counseling + prenatal diagnosis (amniocentesis + villocentesis \u2192 HBB + HBA genotyping) \u2192 universal neonatal screening available in Quebec if at-risk origin.<\/td>\n <td>Management of anemia in pregnancy: iron-deficiency anemia in pregnancy: 1st-line oral iron: ferrous sulfate 300 mg\/d or ferrous fumarate (Palafer) + ascorbic acid \u2192 Hb monitoring + ferritin at 4 weeks \u2192 if severe anemia (Hb <90 g\/L in 2nd-3rd trimester) or intolerance to oral iron + urgent need for correction: IV iron : carboxymaltose iron (Ferinject) \u2192 reassuring safety data after 1st trimester (no sufficient data in 1st trimester) \u2192 superior efficacy to oral iron for rapid correction of Hb + avoid transfusion in pregnancy unless life-threatening emergency (risk of maternal-fetal erythrocyte alloimmunization); megaloblastic anemia in pregnancy: folate deficiency: folic acid 5 mg\/d \u00d7 4-6 weeks + B12 deficiency: B12 1,000 \u00b5g\/d PO or 1,000 \u00b5g IM \u00d7 7 days (cyanocobalamin or hydroxocobalamin) if malabsorption; prenatal screening for sickle cell risk: if two parents carry a sickle cell trait (HbAS + HbAS) or another risk combination (HbAS + HbAC + HbAS + \u03b2Thal) \u2192 risk: 1\/4 affected child \u2192 prenatal diagnosis possible: villocentesis (SA 10-13) or amniocentesis (SA 15-18) \u2192 HBB genotyping \u2192 couple's informed decision \u2192 medical genetics consultation (Cliniques de g\u00e9n\u00e9tique m\u00e9dicale at CHU de Qu\u00e9bec + CHUM + CHU Ste-Justine + McGill University Health Centre); postpartum transfusion: postpartum hemorrhage (PPH): major cause of maternal mortality \u2192 Hb <70 g\/L + hemodynamic instability \u2192 packed red blood cells + PFC + cryoprecipitate + tranexamic acid (1 g IV \u00d7 2\/d - WOMAN Trial 2017 Lancet) \u2192 oxytocin + uterotonics \u2192 interventional radiology (uterine artery embolization) if possible before surgery <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>The pulse oximeter does not measure hemoglobin:<\/strong> SpO\u2082 measured by the digital sensor reflects the oxygen saturation of available hemoglobin - but detects neither anemia (low Hb), nor methemoglobinemia, nor CO intoxication. A SpO\u2082 at 98 % with Hb at 60 g\/L represents severe tissue hypoxemia despite normal saturation. Blood gas co-oximetry is the only method for determining OxyHb, DeoxyHb, COHb and MetHb fractions.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Hb <65-70 g\/L + dyspnea at rest + tachycardia + hypotension + angina<\/strong> \u2192 severe symptomatic anemia \u2192 urgent transfusion of packed red blood cells (O- if grouping not available) \u2192 simultaneous etiological workup \u2192 CBC + reticulocytes + group + IAR + coagulation.<\/p>\n <p><strong>Slate-gray central cyanosis + SpO\u2082 ~85 % fixed regardless of O\u2082 administered + exposure to an oxidizing drug (dapsone + benzocaine + nitrates).<\/strong> \u2192 methemoglobinemia \u2192 co-oximetry on blood gas \u2192 methylene blue 1-2 mg\/kg IV if MetHb >20 % and symptomatic patient \u2192 urgent.<\/p>\n <p><strong>Intense headache + confusion + nausea in an enclosed space or after exposure to incomplete combustion + normal SpO\u2082 on pulse oximeter<\/strong> \u2192 CO intoxication \u2192 COHb by co-oxymetry \u2192 immediate O\u2082 100 % \u2192 evaluation for hyperbaric oxygen therapy if COHb >25 % or loss of consciousness \u2192 immediate evacuation of source.<\/p>\n <p><strong>Acute anemia + chest pain + fever + hypoxemia in a known sickle cell patient<\/strong> \u2192 acute chest syndrome \u2192 hematological emergency \u2192 transfusion (single or erythrocyte exchange depending on baseline Hb) + ceftriaxone + azithromycin + O\u2082 \u2192 hospitalization.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron doctors prescribe and interpret hemoglobin assays as part of blood counts, prenatal check-ups, periodic check-ups and assessment of symptoms of fatigue or shortness of breath. The initial assessment of anemia - including ferritin, vitamin B12, folate and TSH - as well as the management of mild to moderate iron-deficiency anemia, can be performed at several points of service in Quebec, or by teleconsultation. For complex situations - hemoglobinopathies, hemolytic anemias, prenatal screening - coordination with hematology or medical genetics is organized. 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. Any hemoglobin abnormality must be evaluated in its full clinical context before concluding a diagnosis or initiating treatment.<\/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>H\u00e9moglobine (Hb) : valeurs normales, an\u00e9mie et interpr\u00e9tation | Clinique Omicron H\u00e9matologie & M\u00e9decine de famille & M\u00e9decine interne H\u00e9moglobine (Hb) L’h\u00e9moglobine (Hb) est la prot\u00e9ine t\u00e9tram\u00e9rique contenue dans les globules rouges (\u00e9rythrocytes) dont la fonction principale est le transport de l’oxyg\u00e8ne des poumons vers les tissus, et le retour du dioxyde de carbone vers… <a href=\"https:\/\/cliniqueomicron.ca\/en\/hemoglobine-hb\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Hemoglobin (Hb): normal values, anemia and interpretation | Omicron Clinic<\/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":"H\u00e9moglobine (Hb) : valeurs | Brossard | Clinique Omicron","_metasync_otto_description":"L'h\u00e9moglobine transporte l'oxyg\u00e8ne dans le sang. H\u00e9moglobine basse (an\u00e9mie), \u00e9lev\u00e9e (polyglobulie), \u00e9lectrophor\u00e8se, dr\u00e9panocytose et prise en charge au Qu\u00e9bec.","_metasync_otto_keywords":"","_metasync_otto_og_title":"H\u00e9moglobine (Hb) : valeurs | Brossard | Clinique Omicron","_metasync_otto_og_description":"D\u00e9couvrez l'importance de l'h\u00e9moglobine. Analysez vos niveaux avec Clinique Omicron.","_metasync_otto_twitter_title":"H\u00e9moglobine (Hb) : valeurs | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"L'h\u00e9moglobine transporte l'oxyg\u00e8ne dans le sang. H\u00e9moglobine basse (an\u00e9mie), \u00e9lev\u00e9e (polyglobulie), \u00e9lectrophor\u00e8se, dr\u00e9panocytose et prise en charge au Qu\u00e9bec.","rank_math_title":"","rank_math_description":"","_yoast_wpseo_title":"","_yoast_wpseo_metadesc":"","_aioseo_title":"H\u00e9moglobine (Hb) : valeurs normales, an\u00e9mie et interpr\u00e9tation | Clinique Omicron","_aioseo_description":"L'h\u00e9moglobine transporte l'oxyg\u00e8ne dans le sang. 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\n\t\t\t\t\t\n\n\n\n\nHemoglobin (Hb): normal values, anemia and interpretation | Omicron Clinic<\/title>\n<meta name=\"description\" content=\"Hemoglobin transports oxygen in the blood. Low hemoglobin (anemia), high hemoglobin (polycythemia), electrophoresis, sickle cell disease and management in Quebec.\">\n<meta name=\"keywords\" content=\"h\u00e9moglobine valeurs normales, h\u00e9moglobine basse an\u00e9mie, h\u00e9moglobine \u00e9lev\u00e9e, \u00e9lectrophor\u00e8se h\u00e9moglobine, h\u00e9moglobine A1c, dr\u00e9panocytose thalass\u00e9mie, h\u00e9moglobine grossesse Qu\u00e9bec, an\u00e9mie traitement\">\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 & Family Medicine & Internal Medicine<\/span>\n <h1>Hemoglobin (Hb)<\/h1>\n\n <div class=\"co-intro\">\n Hemoglobin (Hb) is the tetrameric protein found in red blood cells (erythrocytes), whose main function is to transport oxygen from the lungs to the tissues, and return carbon dioxide to the lungs. It represents around 33 % of the red blood cell's weight, and is made up of four polypeptide subunits (globins), each bearing a heme prosthetic group containing a ferrous iron atom (Fe\u00b2\u207a) capable of reversibly binding to an oxygen molecule. Hemoglobin concentration in blood is expressed in grams per liter (g\/L) or per deciliter (g\/dL) - 1 g\/dL = 10 g\/L. Normal adult values are 130 to 175 g\/L for men and 120 to 160 g\/L for women, according to Canadian laboratories. Hemoglobin is the reference parameter for diagnosing and classifying the severity of anemia (Hb below normal values, depending on age and sex) and polycythemia (Hb above normal values). It differs from hematocrit in that it measures the hemoglobin concentration itself - and not the volume occupied by red blood cells - making it a more stable parameter, less influenced by variations in mean corpuscular volume (MCV). Hemoglobin electrophoresis can be used to identify pathological structural variants (HbS in sickle cell disease, HbC, HbE) and abnormalities in globin chain synthesis (thalassemias), with major implications for preventive medicine and medical genetics.\n <\/div>\n\n <h2>Hemoglobin structure, function and variants<\/h2>\n <ul class=\"co-list\">\n <li><strong>Molecular structure and types of hemoglobin :<\/strong> structure of normal adult Hb (HbA): tetramer of two alpha (\u03b1) and two beta (\u03b2) chains \u2192 formula \u03b1\u2082\u03b2\u2082 \u2192 molecular weight: 64,500 Da \u2192 each chain carries a heme group (protoporphyrin IX + Fe\u00b2\u207a) \u2192 binding capacity: 1 molecule of O\u2082 per iron atom \u2192 4 molecules of O\u2082 per Hb molecule \u2192 allosteric cooperativity: binding of one O\u2082 molecule increases the affinity of the other three sites (sigmoid dissociation curve for oxyhemoglobin) \u2192 regulators of affinity for O\u2082: 2,3-diphosphoglycerate (2,3-DPG): binds to deoxyhemoglobin \u2192 decreases affinity for O\u2082 \u2192 promotes release of O\u2082 to tissues + pH (Bohr effect): low pH + high CO\u2082 (active tissues) \u2192 decreases affinity \u2192 release of O\u2082 + high temperature \u2192 decreases affinity \u2192 release of O\u2082; normal age-dependent hemoglobin types: fetal hemoglobin (HbF = \u03b1\u2082\u03b3\u2082): predominant in utero and in the first weeks of life \u2192 high affinity for O\u2082 (captures O\u2082 at placenta from maternal circulation) \u2192 gradually replaced by HbA after birth: HbF 70-90 % at birth \u2192 1 % in adulthood) under certain conditions: hemoglobinopathies + leukemias + aplasia + normal adult hemoglobin: HbA (\u03b1\u2082\u03b2\u2082): 96-98 % + HbA\u2082 (\u03b1\u2082\u03b4\u2082): 2-3.5 % \u2192 increased level in beta-thalassemia minor (trait): HbA\u2082 >3.5 % = diagnostic criterion + HbF: <1 %; pathological forms of hemoglobin: HbS (sickle cell disease): glutamate \u2192 valine substitution in position 6 of \u03b2 chain (\u03b26Glu\u2192Val) + GAG\u2192GTG mutation \u2192 deoxygenated HbS polymerizes \u2192 RBC sickling + HbC: \u03b26Glu\u2192Lys substitution \u2192 crystallizes \u2192 moderate hemolysis + HbE: \u03b226Glu\u2192Lys substitution + splicing mutations \u2192 microcytosis + frequent in Southeast Asia + other variants: HbD-Punjab + HbO-Arab + Hb Constant Spring (\u03b1-chain extension); hemoglobin measurement on modern automatons: cyanmhemoglobin method (ICSH - reference method): RBC lysis + oxidation of Fe\u00b2\u207a to Fe\u00b3\u207a (methemoglobin) + transformation to cyanmethemoglobin + spectrophotometric reading at 540 nm \u2192 but most modern automata (Sysmex XN + Beckman-Coulter DxH) use the cyanide-free method (SLS - sodium lauryl sulfate) \u2192 coefficient of variation <1 % \u2192 interference: severe lipemia + massive hyperleukocytosis + carboxyhemoglobin \u2192 false high Hb if uncorrected<\/li>\n <li><strong>Normal values, physiological variations and definition of anemia :<\/strong> hemoglobin reference values (Canadian laboratories - venous plasma - calibrated automatons): adult male (18-70 years): 130-175 g\/L + adult female (18-70 years): 120-160 g\/L + pregnancy: Hb <110 g\/L = anemia (WHO) in 1st and 3rd trimester + Hb 70 years): slight physiological decline expected but any Hb <120 g\/L (H) or <110 g\/L (F) merits investigation + altitude: +10 g\/L for 1,000 m altitude above 1,500 m (hypoxia-stimulated EPO) + smoking: slightly higher Hb (carboxyhemoglobin \u2192 shift in dissociation curve \u2192 relative hypoxia \u2192 EPO stimulation) \u2192 correct Hb for smoking in population; WHO definition of anemia (2001): adult male: Hb <130 g\/L + adult non-pregnant female: Hb <120 g\/L + pregnant female 1st + 3rd trimester: Hb <110 g\/L + pregnant female 2nd trimester: Hb <105 g\/L + child 6 months-5 years: Hb <110 g\/L + child 5-11 years: Hb <115 g\/L + child 12-14 years: Hb <120 g\/L; classification of anemia severity: mild: Hb 100-130 g\/L (H) or 100-120 g\/L (F) \u2192 mild symptoms on exertion + moderate: Hb 70-100 g\/L \u2192 fatigue + dyspnea on exertion + palpitations + severe: Hb <70 g\/L \u2192 rest dyspnea + rest tachycardia + high output heart failure + angina + very severe (critical): Hb <50 g\/L \u2192 life-threatening \u2192 indication for near-absolute transfusion<\/li>\n <li><strong>Hemoglobin electrophoresis and neonatal screening :<\/strong> hemoglobin electrophoresis: method: separation of Hb variants according to their electrical charge in agarose or cellulose acetate gel (alkaline pH 8.6 and\/or acid pH 6.2) \u2192 HPLC (High Performance Liquid Chromatography): current reference method \u2192 separation + quantification of Hb fractions (HbA + HbA\u2082 + HbF + variants) on cation exchange column \u2192 automatic detection \u2192 highly sensitive and reproducible \u2192 interpretation of fractions: HbA\u2082 >3.5 %: beta-thalassemic trait (\u03b2TA or \u03b2TB) \u2192 HbA\u2082 4-7 % in beta-thalassemia minor \u2192 if >7 %: associated hemoglobin D + HbF >5 % in adults: thalassemic syndrome + hereditary persistence of HbF (PHHF) + sickle cell anemia treated with hydroxyurea + hemopathies \u2192 presence of an HbS fraction: sickle cell anemia (SS if HbA absent + SA if HbA present = sickle cell trait) + presence of HbC: HbCC (moderate chronic hemolytic anemia) or HbSC (major sickle cell syndrome with moderate phenotype); neonatal screening in Quebec: provincial neonatal screening program (Quebec) \u2192 screening for sickle cell disease + major sickle cell syndromes by HPLC on dried blood (blotting paper - \u00abGuthrie test\u00bb) at D2-J5 of life \u2192 indication: high-risk population (sub-Saharan Africa + Caribbean + Mediterranean + India + Southeast Asia) \u2192 Programme Qu\u00e9b\u00e9cois de D\u00e9pistage N\u00e9onatal (PQDN - MSSS) \u2192 if screening positive \u2192 confirmation by HPLC on venous sample + genotyping \u2192 genetic consultation + pediatric hematological follow-up \u2192 genetic counseling: if both parents are carriers (trait) \u2192 risk 1\/4 homozygous form (disease) + 1\/2 trait + 1\/4 non-carrier child<\/li>\n <\/ul>\n\n <h2>Anemia, hemoglobinopathies and special clinical situations<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Clinical situation<\/th><th>Assessment and diagnosis<\/th><th>Treatment and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Diagnostic approach to low Hb - etiological algorithm<br><small style=\"font-weight:400;color:#7a8fa0;\">VGM - reticulocytes - ferritin - B12 - hemolysis<\/small><\/td>\n <td>Low hemoglobin requires a structured diagnostic approach based on erythrocyte indices, reticulocytosis and biochemical tests; first step - VGM as a morphological orientation tool: microcytic anemia (VGM <80 fL) : martial deficiency (most frequent cause - low ferritin + CST 100 fL) : vitamin B12 deficiency (autoimmune gastric atrophy - Biermer's disease - anti-FI positive + gastrostomy + strict veganism) + folate deficiency (pregnancy + alcoholism + drugs: MTX + carbamazepine + trimethoprim) + alcoholism (direct macrocytosis independent of deficiencies) + hypothyroidism + MDS (myelodysplastic syndrome - macrocytosis + dysplasia on CBC + pancytopenia) + drugs (hydroxyurea + zidovudine + capecitabine); second stage - reticulocytes : regenerative anemia (high reticulocytes - RPN >2) \u2192 marrow actively producing \u2192 look for hemolysis or bleeding + aregenerative anemia (low reticulocytes - RPN <2) \u2192 insufficient production \u2192 nutritional deficiency + marrow insufficiency + chronic disease<\/td>\n <td>Biological work-up oriented according to the type of anemia: systematic 1st-line work-up: complete CBC with blood smear (RBC morphology: microcytes + hypochromia + elliptocytes + spherocytes + schizocytes + sickle cells + targets + Howell-Jolly bodies + nucleated RBCs) + reticulocytes + ferritin + CRP (ferritin = acute-phase reactant \u2192 interpret with CRP) + vitamin B12 + serum folate + TSH + creatinine + GFR; if regenerative anemia (elevated reticulocytes) \u2192 hemolysis workup: LDH (elevated if intravascular or intracorpuscular hemolysis) + haptoglobin (collapsed if intravascular hemolysis - haptoglobin binds to free Hb \u2192 complex catabolized by liver) + total bilirubin + indirect (elevated if hemolysis \u2192 hemolytic jaundice) + direct antiglobulin test (DAT or direct Coombs): positive if autoantibodies (IgG) or complement (C3d) on RBCs \u2192 autoimmune hemolytic anemia (AHAI) \u2192 GS Rh + phenotyping + hematology opinion + smear : spherocytes (AHAI + hereditary spherocytosis) + schizocytes (MAT - thrombotic microangiopathy - PTT + SHU + CIVD) + sickle cells + Heinz bodies (after special staining - G6PD deficiency + methemoglobinemia); if aregenerative anemia + macrocytosis: B12 (<148 pmol\/L \u2192 deficiency) + methylmalonic acid (AMM) + homocysteine : functional markers of B12 deficiency (more sensitive than serum B12 levels) + antiintrinsic factor (Biermer's disease - specificity 95-99 % but sensitivity 50-70 %) + anti-gastric parietal cells (APC - sensitivity 85 % but not very specific) + gastroscopy + gastric biopsy if Biermer's suspected \u2192 atrophic fundic gastritis<\/td>\n <\/tr>\n <tr>\n <td>Sickle cell disease - HbSS and major sickle cell syndromes<br><small style=\"font-weight:400;color:#7a8fa0;\">Vaso-occlusive crisis - hydroxyurea - transfusion - transplantation<\/small><\/td>\n <td>Sickle cell disease is the most common monogenic disease in the world - its management has been transformed by hydroxyurea, erythrocyte exchange and new targeted therapies; pathophysiology: deoxygenated HbS polymerizes into rigid fibers \u2192 sickling of RBCs \u2192 3 major consequences: chronic hemolysis (lifespan of sickled RBCs : 10-20 days vs 120 days for normal RBCs \u2192 severe chronic hemolytic anemia - baseline Hb 60-90 g\/L) + vaso-occlusion (sickle + rigid RBCs block capillaries \u2192 tissue ischemia \u2192 intense pain + organ necrosis) + endothelial dysfunction (intravascular hemolysis \u2192 free Hb \u2192 NO scavenging \u2192 vasoconstriction + hypercoagulability); major sickle cell syndromes: HbSS (homozygous sickle cell disease): most severe \u2192 70-80 % sickle cell RBCs + HbSC (HbS + HbC in trans): moderate phenotype \u2192 proliferative retinopathy + thromboembolic complications + Hb often 90-110 g\/L + HbS\u03b2\u2070-thalassemia: HbS + no \u03b2 chain \u2192 picture close to SS + HbS\u03b2\u207a-thalassemia: HbS + little \u03b2 chain \u2192 moderate phenotype; major clinical manifestations: painful vaso-occlusive crisis (CVO): intense osteoarticular pain (back + hips + limbs) \u2192 management: level 3 immediately if VAS >7 (morphine IV or SC) + NSAIDs + ketorolac + NaCl 0.9 % (hyperhydration) + local heat \u2192 hospitalization if VAS >7 or duration >4h + acute chest syndrome (ACS): pulmonary infiltrate + chest pain + fever + hypoxemia \u2192 main cause of sickle cell mortality \u2192 treatment: urgent transfusion (single or exchange) + antibiotic (ceftriaxone + azithromycin) + bronchodilators + O\u2082 + ischemic stroke (20 % of HbSS before age 20 without prevention) + splenic sequestration (especially child <5 years) + priapism + sickle cell nephropathy<\/td>\n <td>Treatment of sickle cell disease - therapeutic options: hydroxyurea (HU): mechanism: increase in HbF (inhibits polymerization of HbS) + reduction in reticulocytes and leukocytes + improvement in RBC hydration \u2192 dose: 15-35 mg\/kg\/d PO + titration to maximum tolerated dose (nadir Platelets >80,000 + PNN >2,000) \u2192 proven efficacy: 1995 MSH trial (Charache - NEJM): reduction of CVO by 44 % + of STA by 50 % + of transfusions by 50 % + recommended from 9 months (child) by NHLBI 2014 guidelines + adverse effects: myelosuppression (CBC monitoring every 4-8 weeks) + macrocytosis (benign - compliance marker) + theoretical mutagen but no clinically documented leukemic surrisk + reimbursed RAMQ on drug list + voxelotor (Oxbryta): HbS polymerization inhibitor (increases HbS affinity for O\u2082) \u2192 HOPE 2019 trial (Vichinsky - NEJM): Hb improvement +1.5 g\/dL + hemolysis reduction + FDA approval 2019 \u2192 under INESSS evaluation in Quebec + crizanlizumab (Adakveo): anti-P-selectin (inhibits sickle cell RBC adhesion to endothelium) \u2192 SUSTAIN 2017 trial (Ataga - NEJM): CVO reduction of 45 % vs placebo \u2192 FDA approval 2019 + Health Canada 2021 + L-glutamine (Endari): reduces oxidative stress in sickle cell RBCs \u2192 FDA approval 2017 + hematopoietic stem cell transplantation (allograft): only curative treatment available \u2192 indication: HbSS + recurrent APS + stroke + frequent CVO \u00b1 comorbidities + HLA-compatible donor (ideally sibling) \u2192 cure rate: 85-95 % if genotypic donor \u2192 gene therapy (LentiGlobin bb1111 - Bluebird Bio + CRISPR-Cas9 - Vertex\/CRISPR Therapeutics): BCL11A gene editing or direct correction of HbS mutation \u2192 FDA approval December 2023 (exagamglogene autotemcel - Casgevy - world's first approved CRISPR therapy) \u2192 availability in Canada: under evaluation Health Canada \/ INESSS 2024-2025<\/td>\n <\/tr>\n <tr>\n <td>Thalassemias - alpha and beta<br><small style=\"font-weight:400;color:#7a8fa0;\">Thalassemia trait - thalassemia major - iron - Desferal<\/small><\/td>\n <td>Thalassemias are quantitative abnormalities of globin chain synthesis - reduction or absence of production of one or more chains \u2192 imbalance \u2192 precipitation of excess chains \u2192 intramedullary destruction + peripheral hemolysis; beta-thalassemia: mutations in the HBB gene (chromosome 11) \u2192 reduction (\u03b2\u207a) or absence (\u03b2\u2070) of \u03b2-chain synthesis + clinical classification: beta-thalassemia trait (\u03b2Thal minor or \u00abthalassemia minor\u00bb): heterozygous \u03b2\u2070 or \u03b2\u207a \u2192 slightly low Hb (100-120 g\/L in F) + very low VGM (3.5 % on HPLC \u2192 no treatment \u2192 important for genetic counseling + thalassemia intermediate (\u03b2Thal intermediate): genotype \u03b2\u207a\/\u03b2\u207a or \u03b2\u2070\/\u03b2\u207a + moderate mutations \u2192 Hb 70-100 g\/L \u2192 intermittent transfusion + iron overload possible + thalassemia major (Cooley - \u03b2Thal major - \u03b2\u2070\/\u03b2\u2070): Hb <70 g\/L requiring regular transfusions + extramedullary erythropoiesis + hepatosplenomegaly + bone deformities (thalassemic facies) \u2192 management in specialized center; alpha-thalassemia: deletions of the HBA1\/HBA2 gene (chromosome 16) - 4 alleles: 1 deletion (\u03b1\u03b1\/\u03b1-): silent carrier \u2192 asymptomatic \u2192 normal Hb + VGM \u2192 2 deletions (\u03b1-\/\u03b1- or \u03b1\u03b1\/--): alpha-thalassemic trait \u2192 low VGM + normal or slightly low Hb + normal HbA\u2082 (different from beta!) \u2192 diagnosis by PCR\/genotyping \u2192 3 deletions (--\/\u03b1-): HbH (\u03b2\u2084) - HbH disease \u2192 moderate chronic haemolytic anaemia + haemoglobin H precipitates + Heinz bodies \u2192 Hb 80-110 g\/L \u2192 4 deletions (--\/--): Hb Bart (\u03b3\u2084) - hydrops fetalis \u2192 incompatible with ectopic life \u2192 immediate fetal death in utero or neonatal.<\/td>\n <td>Treatment of severe thalassemias: regular transfusions (thalassemia major): goal: maintain pre-transfusion Hb >95-100 g\/L \u2192 suppression of inefficient erythropoiesis (main source of iron overload) \u2192 pheno-compatible RBCs (Rh + Kell at least) \u2192 leukodepleted \u2192 interval: every 2-4 weeks according to regimen + iron chelation: necessary in all polytransfused patients (iron overload \u2192 cardiac + hepatic + endocrine hemosiderosis): deferasirox (Exjade - Jadenu): 10-20 mg\/kg\/d PO \u2192 1st line \u2192 well tolerated \u2192 monitor creatinine + hepatic workup + deferoxamine (Desferal): 20-40 mg\/kg\/d SC nightly infusion \u00d7 8-10h \u2192 effective but restrictive (nightly SC injection) \u2192 reserved if deferasirox CI + deferiprone (Ferriprox): 75-100 mg\/kg\/d PO \u00d7 3\/d \u2192 useful for cardiac chelation + in combination with deferoxamine if advanced cardiac fibrosis \u2192 chelation goal: serum ferritin 20 ms (cardiac siderosis monitoring - CMR method); hematopoietic stem cell transplantation: curative treatment of thalassemia major \u2192 cure rate: 85-90 % if genoidentical HLA donor + patient in Pesaro class I (absence of hepatomegaly + no portal fibrosis + regular chelation before transplantation) \u2192 betibeglogene autotemcel gene therapy (Zynteglo - Bluebird Bio): lentiviral vector \u2192 insertion of a functional copy of the \u03b2-globin gene \u2192 FDA 2022 approval + Health Canada under evaluation; luspatercept (Reblozyl): traps TGF-\u03b2 ligands \u2192 reduces inefficient erythropoiesis \u2192 FDA + EMA approval for transfusion-dependent beta-thalassemia \u2192 BELIEVE 2020 trial (Cappellini - NEJM): reduction in transfusion requirement of \u226533 % in 21.4 % vs. 4.5 % on placebo \u2192 Health Canada approval 2021<\/td>\n <\/tr>\n <tr>\n <td>Methemoglobinemia and carboxyhemoglobin - Dysfunctional Hb<br><small style=\"font-weight:400;color:#7a8fa0;\">Methylene blue - CO - co-oximetry - intoxication<\/small><\/td>\n <td>Some forms of hemoglobin are unable to transport oxygen - their accumulation leads to tissue hypoxia despite sometimes normal total Hb; methemoglobinemia: mechanism: oxidation of Fe\u00b2\u207a to Fe\u00b3\u207a in the heme moiety \u2192 methemoglobin (MetHb) unable to bind O\u2082 + left Bohr effect on the curve of remaining Hb \u2192 worsening hypoxia \u2192 clinical thresholds: MetHb >10 %: central cyanosis (grey-slate hue) + low SpO\u2082 pulse saturation (~85 % regardless of actual O\u2082 level) \u2192 \u00absaturation set at 85 % by pulse oximeter\u00bb \u2192 major diagnostic pitfall as pulse oximeter does not distinguish MetHb from OxyHb + MetHb >20-30 %: headache + dizziness + dyspnoea + confusion + MetHb >50 %: convulsions + coma + life-threatening + MetHb >70 %: potentially fatal; causes of acquired methemoglobinemia: drugs: dapsone ++ + primaquine + nitrates + nitrites (contaminated water + excess nitrite-treated deli meats) + benzocaine + topical lidocaine + chloroquine + metoclopramide + nitrofurantoin + rasburicase \u2192 at-risk populations: G6PD deficiency (reduced NADPH oxidase pathway \u2192 less reducing power) + infants (50 % + mechanical ventilation; co-oxymetry: reference method for measuring Hb fractions: OxyHb + DeoxyHb + MetHb + COHb + SulfHb \u2192 available on blood gas co-oximeters (ABL from Radiometer + EPOC) \u2192 do not rely on pulse-oximeter alone if CO intoxication or methemoglobinemia suspected<\/td>\n <td>Carbon monoxide (CO) intoxication and carboxyhemoglobin: CO binds to hemoglobin with 240\u00d7 higher affinity than O\u2082 \u2192 carboxyhemoglobin (COHb) \u2192 displaces O\u2082 \u2192 tissue hypoxia \u2192 also blocks mitochondrial cytochrome c oxidase (direct cellular toxicity) \u2192 left-shifted dissociation curve (less O\u2082 delivered to tissues); CO sources: incomplete combustion (gas + fuel oil + wood + coal + propane + gasoline) + fire + engine in enclosed space + motor-driven electric generator; clinical picture according to COHb: COHb 50 %: coma + convulsions + cardiorespiratory arrest + COHb >70 %: fatal; diagnostic pitfall: SpO\u2082 on pulse-oximeter normal or subnormal (COHb absorbs light like OxyHb at 660 nm \u2192 false high saturation) \u2192 always assay COHb by co-oximetry if CO intoxication suspected; treatment: O\u2082 normobaric at 100 % (reservoir mask or intubation) \u2192 COHb half-life: ambient air 5-6h \u2192 O\u2082 100 % 60-90 min \u2192 O\u2082 hyperbaric (HBOT) 2.5-3 ATA \u2192 20-30 min \u2192 HBOT indications (Weaver 2002 NEJM): COHb >25 % + pregnancy + loss of consciousness + neurological symptoms + cardiac ischemia \u2192 available in Quebec: CHU de Qu\u00e9bec + IUCPQ hyperbaric center + SMOH (Service M\u00e9dical d'Oxyg\u00e9noth\u00e9rapie Hyperbare) \u2192 neurological sequelae: lucid post-interval syndrome (dementia + personality disorders + parkinsonism) \u2192 10-30 % of severe forms \u2192 brain MRI: lesions of the pallidums + periventricular white matter. <\/tr>\n <tr>\n <td>Hemoglobin and pregnancy - Gestational anemia and screening<br><small style=\"font-weight:400;color:#7a8fa0;\">Iron - folates - B12 - screening for hemoglobinopathies - thalassemia<\/small><\/td>\n <td>Pregnancy profoundly modifies hemoglobin and exposes to specific risks that justify systematic screening; physiological modifications of pregnancy on Hb: hemodilution: expansion of plasma volume by 40-50 % in 2nd trimester + increase in erythrocyte mass by 20-30 % \u2192 Hb dilutes \u2192 \u00abphysiological anemia\u00bb \u2192 minimum acceptable Hb in pregnancy according to WHO: 110 g\/L (1st + 3rd trimester) + 105 g\/L (2nd trimester) \u2192 caution: the 'physiological anemia\u00ab of pregnancy should not lead to overlooking a true iron deficiency anemia \u2192 ferritin <30 \u00b5g\/L \u2192 martial deficiency \u2192 treat + increase needs: iron: iron needs increase from 1 mg\/d (outside pregnancy) to 6-7 mg\/d at the end of pregnancy \u2192 needs covered by a varied diet + systematic supplementation if ferritin <30 \u00b5g\/L + folates: needs double in pregnancy \u2192 systematic pre-conceptional supplementation: folic acid 0.4-5 mg\/d (0.4 mg if no particular risk + 4 mg if history of AFTN + valproate + morbid obesity + diabetes) \u2192 recommendation Society of Obstetricians and Gynaecologists of Canada (SOGC) 2015 + MSSS Quebec \u2192 reduces the risk of neural tube defects by 70 % + vitamin B12: supplementation recommended if strict vegan diet (risk of maternal + neonatal deficiency) \u2192 B12 1,000 \u00b5g\/d PO; screening for hemoglobinopathies in pregnancy in Quebec: SOGC 2008 recommendation (J Obstet Gynaecol Can): Hb electrophoresis recommended for all high-risk pregnant women (African + Caribbean + Mediterranean + Middle Eastern + Asian origin) \u2192 in Quebec: universal screening recommended by several pediatric associations \u2192 if maternal sickle cell trait (HbAS) \u2192 paternal screening \u2192 if both parents carriers \u2192 genetic counseling + prenatal diagnosis (amniocentesis + villocentesis \u2192 HBB + HBA genotyping) \u2192 universal neonatal screening available in Quebec if at-risk origin.<\/td>\n <td>Management of anemia in pregnancy: iron-deficiency anemia in pregnancy: 1st-line oral iron: ferrous sulfate 300 mg\/d or ferrous fumarate (Palafer) + ascorbic acid \u2192 Hb monitoring + ferritin at 4 weeks \u2192 if severe anemia (Hb <90 g\/L in 2nd-3rd trimester) or intolerance to oral iron + urgent need for correction: IV iron : carboxymaltose iron (Ferinject) \u2192 reassuring safety data after 1st trimester (no sufficient data in 1st trimester) \u2192 superior efficacy to oral iron for rapid correction of Hb + avoid transfusion in pregnancy unless life-threatening emergency (risk of maternal-fetal erythrocyte alloimmunization); megaloblastic anemia in pregnancy: folate deficiency: folic acid 5 mg\/d \u00d7 4-6 weeks + B12 deficiency: B12 1,000 \u00b5g\/d PO or 1,000 \u00b5g IM \u00d7 7 days (cyanocobalamin or hydroxocobalamin) if malabsorption; prenatal screening for sickle cell risk: if two parents carry a sickle cell trait (HbAS + HbAS) or another risk combination (HbAS + HbAC + HbAS + \u03b2Thal) \u2192 risk: 1\/4 affected child \u2192 prenatal diagnosis possible: villocentesis (SA 10-13) or amniocentesis (SA 15-18) \u2192 HBB genotyping \u2192 couple's informed decision \u2192 medical genetics consultation (Cliniques de g\u00e9n\u00e9tique m\u00e9dicale at CHU de Qu\u00e9bec + CHUM + CHU Ste-Justine + McGill University Health Centre); postpartum transfusion: postpartum hemorrhage (PPH): major cause of maternal mortality \u2192 Hb <70 g\/L + hemodynamic instability \u2192 packed red blood cells + PFC + cryoprecipitate + tranexamic acid (1 g IV \u00d7 2\/d - WOMAN Trial 2017 Lancet) \u2192 oxytocin + uterotonics \u2192 interventional radiology (uterine artery embolization) if possible before surgery <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>The pulse oximeter does not measure hemoglobin:<\/strong> SpO\u2082 measured by the digital sensor reflects the oxygen saturation of available hemoglobin - but detects neither anemia (low Hb), nor methemoglobinemia, nor CO intoxication. A SpO\u2082 at 98 % with Hb at 60 g\/L represents severe tissue hypoxemia despite normal saturation. Blood gas co-oximetry is the only method for determining OxyHb, DeoxyHb, COHb and MetHb fractions.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Hb <65-70 g\/L + dyspnea at rest + tachycardia + hypotension + angina<\/strong> \u2192 severe symptomatic anemia \u2192 urgent transfusion of packed red blood cells (O- if grouping not available) \u2192 simultaneous etiological workup \u2192 CBC + reticulocytes + group + IAR + coagulation.<\/p>\n <p><strong>Slate-gray central cyanosis + SpO\u2082 ~85 % fixed regardless of O\u2082 administered + exposure to an oxidizing drug (dapsone + benzocaine + nitrates).<\/strong> \u2192 methemoglobinemia \u2192 co-oximetry on blood gas \u2192 methylene blue 1-2 mg\/kg IV if MetHb >20 % and symptomatic patient \u2192 urgent.<\/p>\n <p><strong>Intense headache + confusion + nausea in an enclosed space or after exposure to incomplete combustion + normal SpO\u2082 on pulse oximeter<\/strong> \u2192 CO intoxication \u2192 COHb by co-oxymetry \u2192 immediate O\u2082 100 % \u2192 evaluation for hyperbaric oxygen therapy if COHb >25 % or loss of consciousness \u2192 immediate evacuation of source.<\/p>\n <p><strong>Acute anemia + chest pain + fever + hypoxemia in a known sickle cell patient<\/strong> \u2192 acute chest syndrome \u2192 hematological emergency \u2192 transfusion (single or erythrocyte exchange depending on baseline Hb) + ceftriaxone + azithromycin + O\u2082 \u2192 hospitalization.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron doctors prescribe and interpret hemoglobin assays as part of blood counts, prenatal check-ups, periodic check-ups and assessment of symptoms of fatigue or shortness of breath. The initial assessment of anemia - including ferritin, vitamin B12, folate and TSH - as well as the management of mild to moderate iron-deficiency anemia, can be performed at several points of service in Quebec, or by teleconsultation. For complex situations - hemoglobinopathies, hemolytic anemias, prenatal screening - coordination with hematology or medical genetics is organized. 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. Any hemoglobin abnormality must be evaluated in its full clinical context before concluding a diagnosis or initiating treatment.<\/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>H\u00e9moglobine (Hb) : valeurs normales, an\u00e9mie et interpr\u00e9tation | Clinique Omicron H\u00e9matologie & M\u00e9decine de famille & M\u00e9decine interne H\u00e9moglobine (Hb) L’h\u00e9moglobine (Hb) est la prot\u00e9ine t\u00e9tram\u00e9rique contenue dans les globules rouges (\u00e9rythrocytes) dont la fonction principale est le transport de l’oxyg\u00e8ne des poumons vers les tissus, et le retour du dioxyde de carbone vers… <a href=\"https:\/\/cliniqueomicron.ca\/en\/hemoglobine-hb\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Hemoglobin (Hb): normal values, anemia and interpretation | Omicron Clinic<\/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":"H\u00e9moglobine (Hb) : valeurs | Brossard | Clinique Omicron","_metasync_otto_description":"L'h\u00e9moglobine transporte l'oxyg\u00e8ne dans le sang. H\u00e9moglobine basse (an\u00e9mie), \u00e9lev\u00e9e (polyglobulie), \u00e9lectrophor\u00e8se, dr\u00e9panocytose et prise en charge au Qu\u00e9bec.","_metasync_otto_keywords":"","_metasync_otto_og_title":"H\u00e9moglobine (Hb) : valeurs | Brossard | Clinique Omicron","_metasync_otto_og_description":"D\u00e9couvrez l'importance de l'h\u00e9moglobine. Analysez vos niveaux avec Clinique Omicron.","_metasync_otto_twitter_title":"H\u00e9moglobine (Hb) : valeurs | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"L'h\u00e9moglobine transporte l'oxyg\u00e8ne dans le sang. H\u00e9moglobine basse (an\u00e9mie), \u00e9lev\u00e9e (polyglobulie), \u00e9lectrophor\u00e8se, dr\u00e9panocytose et prise en charge au Qu\u00e9bec.","rank_math_title":"","rank_math_description":"","_yoast_wpseo_title":"","_yoast_wpseo_metadesc":"","_aioseo_title":"H\u00e9moglobine (Hb) : valeurs normales, an\u00e9mie et interpr\u00e9tation | Clinique Omicron","_aioseo_description":"L'h\u00e9moglobine transporte l'oxyg\u00e8ne dans le sang. 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