Hemoglobin Electrophoresis: Indications and Interpretation | Omicron Clinic<\/title>\n<meta name=\"description\" content=\"Hemoglobin electrophoresis identifies hemoglobinopathies such as sickle cell disease and thalassemia. Indications, technique, and interpretation of results in Quebec.\">\n<meta name=\"keywords\" content=\"\u00e9lectrophor\u00e8se h\u00e9moglobine interpr\u00e9tation, \u00e9lectrophor\u00e8se h\u00e9moglobine dr\u00e9panocytose thalass\u00e9mie, h\u00e9moglobinopathie diagnostic, h\u00e9moglobine S C dr\u00e9panocytose, thalass\u00e9mie \u00e9lectrophor\u00e8se, HPLC h\u00e9moglobine, \u00e9lectrophor\u00e8se h\u00e9moglobine bilan, \u00e9lectrophor\u00e8se h\u00e9moglobine Qu\u00e9bec\">\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>Hemoglobin electrophoresis<\/h1>\n\n <div class=\"co-intro\">\n Hemoglobin electrophoresis is a laboratory technique for separating, identifying and quantifying the different hemoglobin fractions present in circulating erythrocytes, by exploiting the differences in electrical charge of globin chains according to their amino acid composition. Human hemoglobin is a tetrameric protein composed of two pairs of globin chains (two alpha chains and two non-alpha chains), each associated with an iron-carrying heme group. In healthy adults, three hemoglobin fractions normally coexist: hemoglobin A (HbA - \u03b1\u2082\u03b2\u2082 - 96 to 98 % of the total), hemoglobin A2 (HbA2 - \u03b1\u2082\u03b4\u2082 - 2 to 3,5 %) and fetal hemoglobin (HbF - \u03b1\u2082\u03b3\u2082 - <1 % in adults - up to 70 to 90 % in neonates before the switch to globin synthesis at 6 months). Hemoglobinopathies - mutations or deletions of globin genes - constitute the most widespread group of monogenic diseases in the world (over 300 million carriers). They fall into two main categories: structural hemoglobins (substitution of an amino acid on the globin chain - hemoglobin S in sickle cell disease, hemoglobins C, D, E) and thalassemias (quantitative decrease in the synthesis of one or more normal globin chains - alpha-thalassemia and beta-thalassemia). Hemoglobin electrophoresis - or its modern replacement, high-performance liquid chromatography (HPLC) - is the gold standard for diagnosing these diseases, and is an essential tool for neonatal screening, prenatal genetic counseling and follow-up of patients with known hemoglobinopathies. In Quebec, universal newborn screening for hemoglobinopathies using HPLC (Programme qu\u00e9b\u00e9cois de d\u00e9pistage n\u00e9onatal - PQDN) has been in force since 2009 in certain regions, and is gradually being extended.\n <\/div>\n\n <h2>Indications, technique, and normal values<\/h2>\n <ul class=\"co-list\">\n <li><strong>Clinical indications for hemoglobin electrophoresis:<\/strong> hemolytic anemia of undetermined etiology (especially if microcytic hypochromic without iron deficiency - thalassemia); suspicion of sickle cell disease (child or adult from Sub-Saharan Africa, the Caribbean, North Africa, the Middle East, India, or the Mediterranean presenting with vaso-occlusive crises, acute chest syndrome, palpable spleen, or splenic sequestration episodes); pregnancy workup (woman from an endemic area or known carrier partner); prenatal genetic counseling (both parents carrying a hemoglobinopathy trait - 25% % risk of homozygous form); family screening after diagnosis of a hemoglobinopathy; microcytic hypochromic anemia with normal ferritin (minor thalassemia - elevated HbA2); unexplained polycythemia (hemoglobin with high oxygen affinity); universal neonatal screening (PQDN Quebec)<\/li>\n <li><strong>Available techniques:<\/strong> HPLC (high-performance liquid chromatography): the current reference technique - separation of hemoglobin fractions by affinity on a cation-exchange column - precise quantification of all fractions (HbA, HbA2, HbF, HbS, HbC, HbD, HbE, etc.) - results within a few minutes.) - results in 10 to 15 minutes - used for neonatal screening in Quebec (LSPQ); capillary electrophoresis (CE): separation by electric charge in a buffer-filled capillary - excellent precision and reproducibility - complementary to HPLC for rare hemoglobins; cellulose acetate gel electrophoresis (alkaline pH) + citrate agar electrophoresis (acid pH): classic techniques still used in reference laboratories - the combination of the two pH values enables distinction between hemoglobins that co-migrate at a single pH (eg. HbS and HbD co-migrate at alkaline pH but separate at acid pH); falciformation test (sickling test - sodium metabisulfite): rapid screening for the presence of HbS - positive if HbS present (trait or disease) - does not distinguish trait from homozygous form \u2192 always confirm by HPLC or electrophoresis.<\/li>\n <li><strong>Adult normal values:<\/strong> HbA : 96\u201398 % ; HbA2 : 2,0\u20133,5 % ; HbF : <1,0 % (jusqu'\u00e0 2 % chez certains adultes sains \u2014 persistance h\u00e9r\u00e9ditaire b\u00e9nigne de l'HbF) ; HbS, HbC, HbD, HbE : 0 % (absent chez un adulte normal)<\/li>\n <li><strong>Interferences and limitations:<\/strong> recent transfusion (<3 to 4 months): transfused red blood cells (normal donor HbA) dilute the recipient's HbS or HbF \u2192 underestimation of abnormal fractions \u2014 mention any recent transfusions to the laboratory; infant <6 months old: HbF still predominant \u2014 different interpretation than in adults \u2014 normal neonatal profile: HbF + HbA \u00b1 trace HbA2; severe iron deficiency: underestimates HbA2 (false negative for beta-thalassemia minor) \u2014 correct iron deficit before concluding HbA2 is normal; HbA1c (glycated hemoglobin): fraction visible on HPLC before HbA \u2014 do not confuse with an abnormal fraction<\/li>\n <\/ul>\n\n <h2>Interpretation of Profiles and Clinical Implications<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Profile \/ Diagnostic<\/th><th>HPLC results and mechanism<\/th><th>Clinical implications and management<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Normal adult profile<br><small style=\"font-weight:400;color:#7a8fa0;\">HbA 96\u201398 % \/ HbA2 2\u20133,5 % \/ HbF <1 %<\/small><\/td>\n <td>HbA (\u03b1\u2082\u03b2\u2082): major adult fraction \u2014 physiological carrier of O\u2082 with normal affinity; HbA2 (\u03b1\u2082\u03b4\u2082): minor fraction \u2014 uncertain physiological role \u2014 key biological marker of beta-thalassemia (increased if \u03b2 synthesis deficit); HbF (\u03b1\u2082\u03b3\u2082): minimal physiological persistence (<1 %) in adults \u2014 increases again in certain pathologies (sickle cell disease treated with hydroxyurea, leukemia, aplastic anemias) and in cases of benign hereditary persistence of HbF (HPFH); normal neonatal profile at birth: HbF 70\u201390 %+ HbA 10\u201330 % + HbA2 traces \u2014 \u03b3\u2192\u03b2 switching is completed around 6 months (HbA becomes the majority)<\/td>\n <td>A normal electrophoretic profile in an adult excludes a structural hemoglobinopathy and beta-thalassemia \u2014 however, it does not exclude alpha-thalassemia (mild alpha-thalassemias \u2014 alpha trait \u2212\u03b1\/\u03b1\u03b1 or \u2212\u2212\/\u03b1\u03b1 \u2014 do not alter the adult electrophoretic profile \u2192 diagnosis by molecular biology \u2014 PCR specific for alpha deletions); if persistent microcytic hypochromic anemia with a normal electrophoretic profile and normal ferritin \u2192 consider alpha-thalassemia \u2192 order alpha-globin molecular genetics (LSPQ or reference laboratory); interpretation within the clinical context is always essential \u2014 a normal profile does not exclude all hemoglobinopathies.<\/td>\n <\/tr>\n <tr>\n <td>Sickle cell trait (AS carrier)<br><small style=\"font-weight:400;color:#7a8fa0;\">HbA 55\u201360 % \/ HbS 38\u201345 % \/ HbA2 2\u20133.5 %<\/small><\/td>\n <td>Point mutation \u03b26Glu\u2192Val (GAG\u2192GTG) on an HBB gene allele \u2192 substitution of glutamic acid by valine at position 6 of the beta chain \u2192 HbS; heterozygote (healthy carrier): one normal HBB allele (\u2192 HbA) + one mutated HBB allele (\u2192 HbS) \u2192 majority HbA (55\u201360 %) + minority HbS (38\u201345 %); HbS polymerizes only in conditions of severe hypoxia \u2014 the AS carrier is asymptomatic in daily life but may experience complications at high altitude, during scuba diving, or in case of severe perioperative hypoxia; hemogram: normal or discrete microcytosis (if iron deficiency is associated)<\/td>\n <td>Sickle cell trait (AS) is benign in the vast majority of cases \u2014 AS carriers lead normal lives without major restrictions. Genetic counseling: if both parents are AS carriers \u2192 25% % risk of having an SS child (homozygous sickle cell disease \u2014 illness) with each pregnancy \u2192 prenatal diagnosis possible (chorionic villus sampling or amniocentesis + molecular biology). Rare clinical exceptions: splenic infarction at high altitude (>2,500 m) + recurrent hematuria (renal papillary necrosis) + risk of sudden death during prolonged intense physical exercise in heat and dehydration (case reports) \u2014 advice for caution during intensive competitive sports. Partner screening: systematically recommended if AS carrier and wishing to conceive.<\/td>\n <\/tr>\n <tr>\n <td>Homozygous sickle cell disease (SS)<br><small style=\"font-weight:400;color:#7a8fa0;\">HbS 85\u201395 % \/ HbF 2\u201320 % \/ HbA2 2\u20134 % \/ HbA 0 %<\/small><\/td>\n <td>Two mutated HBB alleles (\u03b26Glu\u2192Val) \u2192 no HbA produced \u2192 almost exclusive HbS; under deoxygenation conditions \u2192 HbS molecule polymerization \u2192 erythrocyte sickling (sickle cells) \u2192 microvascular obstruction (vaso-occlusion) + chronic hemolysis + endothelial inflammation activation; HbF (\u03b1\u2082\u03b3\u2082) inhibits HbS polymerization \u2014 HbF level is a major prognostic factor (HbF >20 %\u2192 fewer crises); hydroxyurea increases HbF synthesis by 15 to 25 % \u2192 reduction in vaso-occlusive crises; typical HPLC profile: HbS 85\u201395 % + variable HbF (2\u201320 % ) + HbA2 2\u20134 % + total absence of HbA<\/td>\n <td>Severe chronic multisystem disease - specialized hematology follow-up mandatory; acute manifestations: painful vaso-occlusive crisis (PVD) + acute chest syndrome (ATS - life-threatening emergency - hypoxemia + pulmonary infiltrate + chest pain) + stroke (CVA - child) + splenic sequestration + aplastic crisis (parvovirus B19); chronic manifestations: splenomegaly + functional asplenia from childhood \u2192 prophylaxis with penicillin V + vaccinations (pneumococcal PCV20 + PPV23, meningococcal, Hib, influenza, COVID); disease-modifying treatments: hydroxyurea (Hydrea) 15-35 mg\/kg\/d \u2192 1st line - HbF \u2191 \u2192 crises \u2193 - reimbursed RAMQ; L-glutamine (Endari); voxelotor (Oxbryta); crizanlizumab (Adakveo); hematopoietic stem cell (HSC) transplantation: only potentially curative treatment - indication in children with severe disease if HLA-identical donor available; gene therapy: advanced clinical trials (Lovo-cel - BLA approved FDA 2023)<\/td>\n <\/tr>\n <tr>\n <td>Beta-thalassemia minor (beta-thal trait)<br><small style=\"font-weight:400;color:#7a8fa0;\">HbA2 >3,5 % \/ HbF 1\u20135 % \/ HbA 92\u201395 %<\/small><\/td>\n <td>A mutated HBB allele (point mutation \u2014 >200 known mutations \u2014 defect in transcription, splicing, or translation of \u03b2-globin mRNA) \u2192 decreased synthesis of \u03b2 chains \u2192 relative excess of \u03b1 chains \u2192 increased HbA2 (compensation by \u03b4-globin overexpression) \u2192 HbA2 >3.5% %(main diagnostic criterion) + slightly increased HbF (1\u20135% % ) + moderate microcytic hypochromic anemia (Hb 10\u201313 g\/dL) + microcytic hypochromic erythrocytes + elevated erythrocyte count (relative polycythemia) + decreased MCV (60\u201370 fL); the carrier is generally asymptomatic or paucisymptomatic (slight fatigue) \u2014 qualified as \u00abminor\u00bb thalassemic or thalassemic trait carrier<\/td>\n <td>Frequent diagnostic trap: beta-thalassemia minor is often confused with iron deficiency (same biological picture \u2014 hypochromic microcytosis); distinguishing features: normal or high ferritin (no iron deficiency) + HbA2 >3.5 % on electrophoresis + high red blood cell count (relative polycythemia) + absence of response to iron supplementation; caution: concomitant iron deficiency lowers HbA2 \u2192 can distort diagnosis (false negative) \u2192 correct iron deficiency before electrophoresis if ferritin is low; genetic counseling: if both parents are carriers \u2192 25 % risk of beta-thalassemia major (Cooley's disease) \u2192 severe transfusion-dependent hemolytic anemia from the first months of life \u2192 prenatal diagnosis recommended; iron supplementation is useless and potentially harmful in thalassemic carriers without confirmed deficiency<\/td>\n <\/tr>\n <tr>\n <td>Other important profiles<br><small style=\"font-weight:400;color:#7a8fa0;\">HbC, HbE, HbD, SC double heterozygotes, and S\u03b2-thal<\/small><\/td>\n <td>HbC (\u03b26Glu\u2192Lys) : fr\u00e9quente en Afrique de l'Ouest \u2014 trait AC asymptomatique \u2014 maladie CC rare (an\u00e9mie h\u00e9molytique mod\u00e9r\u00e9e + spl\u00e9nom\u00e9galie + cristaux d'HbC dans les h\u00e9maties) ; HbSC : double h\u00e9t\u00e9rozygote S\/C \u2014 maladie dr\u00e9panocytaire de s\u00e9v\u00e9rit\u00e9 interm\u00e9diaire \u2014 HbS 50 % + HbC 50 % \u2014 r\u00e9tinopathie prolif\u00e9rative + ost\u00e9on\u00e9crose fr\u00e9quentes \u2014 syndrome thoracique aigu possible ; HbS\u03b2+-thalass\u00e9mie : double h\u00e9t\u00e9rozygote S\/\u03b2+-thal \u2014 HbS 60\u201385 % + HbA 10\u201330 % + HbA2 \u00e9lev\u00e9e + HbF variable \u2014 ph\u00e9notype dr\u00e9panocytaire mod\u00e9r\u00e9 \u00e0 s\u00e9v\u00e8re ; HbS\u03b20-thalass\u00e9mie : double h\u00e9t\u00e9rozygote S\/\u03b20-thal \u2014 HbS 85\u201392 % + HbA 0 % + HbA2 \u00e9lev\u00e9e + HbF variable \u2014 ph\u00e9notype aussi s\u00e9v\u00e8re que la dr\u00e9panocytose SS ; HbE (\u03b226Glu\u2192Lys) : tr\u00e8s fr\u00e9quente en Asie du Sud-Est \u2014 trait AE asymptomatique \u2014 EE l\u00e9g\u00e8re \u2014 HbE\u03b20-thal (double h\u00e9t\u00e9rozygote) : an\u00e9mie s\u00e9v\u00e8re transfuso-d\u00e9pendante dans les formes graves ; HPFH (persistance h\u00e9r\u00e9ditaire de l'HbF) : HbF 15\u201335 % + HbA normale + asymptomatique \u2014 b\u00e9nin<\/td>\n <td>SC sickle cell disease accounts for about 25\u201330 % of sickle cell syndromes in Quebec (in patients originating from West Africa and the Caribbean)\u2014a milder disease than SS but with significant specific complications: proliferative retinopathy (mandatory annual ophthalmological examination from the age of 10\u2014risk of FFA + laser photocoagulation if neovascularization) + osteonecrosis of the femoral head (MRI if hip pain) + priapism + thromboembolism (increased risk compared to SS); HbE is the most widespread globin mutation in the world (100\u2013150 million carriers)\u2014frequent in patients originating from Cambodia, Thailand, Vietnam, and Myanmar\u2014to consider in front of unexplained microcytosis in a patient from Southeast Asia; always interpret electrophoresis based on the patient's geographic origin<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>Alpha-thalassemia - electrophoresis limit:<\/strong> Unlike beta-thalassemia, alpha-thalassemia minor (\u03b1-trait - one or two deletions in the four alpha-globin genes) does not typically alter the adult electrophoretic profile\u2014normal HbA2, normal HbF, no abnormal fraction. It manifests solely as hypochromic microcytosis with normal ferritin. Diagnosis relies on molecular biology (PCR with detection of alpha-globin deletions\u2014\u2212\u03b13.7, \u2212\u03b14.2, \u2212\u2212SEA, \u2212\u2212MED, etc.). This limitation is clinically important: a normal electrophoresis does not rule out alpha-thalassemia in a microcytic patient without iron deficiency, particularly in patients of Asian, African, or Mediterranean origin.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Sickle cell emergencies \u2014 recognize and act fast<\/div>\n <p>In a patient with known sickle cell disease (SS, SC, S\u03b2-thalassemia), consult <strong>immediately to the emergency room<\/strong> if : <strong>Chest pain, cough, fever, hypoxemia<\/strong> Acute chest syndrome (ACS) - a life-threatening emergency - emergency blood transfusions + antibiotics + O\u2082; ; <strong>Sudden focal neurological deficit<\/strong> (hemiplegia, aphasia, visual impairment) \u2192 Sickle cell ischemic stroke \u2014 urgent thrombolysis and\/or transfusion; ; <strong>Abdominal pain + rapidly progressive splenomegaly + sudden pallor<\/strong> (child) \u2192 acute splenic sequestration \u2014 urgent transfusion; ; <strong>Fever >101.3 \u00b0F<\/strong> in a child with sickle cell disease \u2192 pneumococcal sepsis (functional asplenia) \u2014 immediate IV antibiotics.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>The doctors at Clinique Omicron prescribe and interpret hemoglobin electrophoresis, provide genetic counseling for at-risk couples, ensure first-line follow-up for carriers of hemoglobinopathies, and coordinate specialized hematology follow-up for symptomatic cases. The analyses are available from our service points in Quebec and via telemedicine. To make an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The content of this page is for informational purposes only and does not substitute for the advice of a qualified healthcare professional or a laboratory medicine specialist. Any diagnosed hemoglobinopathy requires appropriate medical follow-up and genetic counseling if parental planning is considered.<\/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>\u00c9lectrophor\u00e8se de l’h\u00e9moglobine : indications et interpr\u00e9tation | Clinique Omicron H\u00e9matologie & M\u00e9decine de laboratoire & M\u00e9decine de famille \u00c9lectrophor\u00e8se de l’h\u00e9moglobine L’\u00e9lectrophor\u00e8se de l’h\u00e9moglobine est une technique de laboratoire permettant de s\u00e9parer, d’identifier et de quantifier les diff\u00e9rentes fractions d’h\u00e9moglobine pr\u00e9sentes dans les \u00e9rythrocytes circulants, en exploitant les diff\u00e9rences de charge \u00e9lectrique des cha\u00eenes… <a href=\"https:\/\/cliniqueomicron.ca\/en\/electrophorese-de-lhemoglobine\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Hemoglobin Electrophoresis: Indications 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":"\u00c9lectrophor\u00e8se de l'h\u00e9moglobine | Brossard | Clinique Omicron","_metasync_otto_description":"L'\u00e9lectrophor\u00e8se de l'h\u00e9moglobine identifie les h\u00e9moglobinopathies comme la dr\u00e9panocytose et la thalass\u00e9mie. 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\n\t\t\t\t\t\n\n\n\n\nHemoglobin Electrophoresis: Indications and Interpretation | Omicron Clinic<\/title>\n<meta name=\"description\" content=\"Hemoglobin electrophoresis identifies hemoglobinopathies such as sickle cell disease and thalassemia. Indications, technique, and interpretation of results in Quebec.\">\n<meta name=\"keywords\" content=\"\u00e9lectrophor\u00e8se h\u00e9moglobine interpr\u00e9tation, \u00e9lectrophor\u00e8se h\u00e9moglobine dr\u00e9panocytose thalass\u00e9mie, h\u00e9moglobinopathie diagnostic, h\u00e9moglobine S C dr\u00e9panocytose, thalass\u00e9mie \u00e9lectrophor\u00e8se, HPLC h\u00e9moglobine, \u00e9lectrophor\u00e8se h\u00e9moglobine bilan, \u00e9lectrophor\u00e8se h\u00e9moglobine Qu\u00e9bec\">\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>Hemoglobin electrophoresis<\/h1>\n\n <div class=\"co-intro\">\n Hemoglobin electrophoresis is a laboratory technique for separating, identifying and quantifying the different hemoglobin fractions present in circulating erythrocytes, by exploiting the differences in electrical charge of globin chains according to their amino acid composition. Human hemoglobin is a tetrameric protein composed of two pairs of globin chains (two alpha chains and two non-alpha chains), each associated with an iron-carrying heme group. In healthy adults, three hemoglobin fractions normally coexist: hemoglobin A (HbA - \u03b1\u2082\u03b2\u2082 - 96 to 98 % of the total), hemoglobin A2 (HbA2 - \u03b1\u2082\u03b4\u2082 - 2 to 3,5 %) and fetal hemoglobin (HbF - \u03b1\u2082\u03b3\u2082 - <1 % in adults - up to 70 to 90 % in neonates before the switch to globin synthesis at 6 months). Hemoglobinopathies - mutations or deletions of globin genes - constitute the most widespread group of monogenic diseases in the world (over 300 million carriers). They fall into two main categories: structural hemoglobins (substitution of an amino acid on the globin chain - hemoglobin S in sickle cell disease, hemoglobins C, D, E) and thalassemias (quantitative decrease in the synthesis of one or more normal globin chains - alpha-thalassemia and beta-thalassemia). Hemoglobin electrophoresis - or its modern replacement, high-performance liquid chromatography (HPLC) - is the gold standard for diagnosing these diseases, and is an essential tool for neonatal screening, prenatal genetic counseling and follow-up of patients with known hemoglobinopathies. In Quebec, universal newborn screening for hemoglobinopathies using HPLC (Programme qu\u00e9b\u00e9cois de d\u00e9pistage n\u00e9onatal - PQDN) has been in force since 2009 in certain regions, and is gradually being extended.\n <\/div>\n\n <h2>Indications, technique, and normal values<\/h2>\n <ul class=\"co-list\">\n <li><strong>Clinical indications for hemoglobin electrophoresis:<\/strong> hemolytic anemia of undetermined etiology (especially if microcytic hypochromic without iron deficiency - thalassemia); suspicion of sickle cell disease (child or adult from Sub-Saharan Africa, the Caribbean, North Africa, the Middle East, India, or the Mediterranean presenting with vaso-occlusive crises, acute chest syndrome, palpable spleen, or splenic sequestration episodes); pregnancy workup (woman from an endemic area or known carrier partner); prenatal genetic counseling (both parents carrying a hemoglobinopathy trait - 25% % risk of homozygous form); family screening after diagnosis of a hemoglobinopathy; microcytic hypochromic anemia with normal ferritin (minor thalassemia - elevated HbA2); unexplained polycythemia (hemoglobin with high oxygen affinity); universal neonatal screening (PQDN Quebec)<\/li>\n <li><strong>Available techniques:<\/strong> HPLC (high-performance liquid chromatography): the current reference technique - separation of hemoglobin fractions by affinity on a cation-exchange column - precise quantification of all fractions (HbA, HbA2, HbF, HbS, HbC, HbD, HbE, etc.) - results within a few minutes.) - results in 10 to 15 minutes - used for neonatal screening in Quebec (LSPQ); capillary electrophoresis (CE): separation by electric charge in a buffer-filled capillary - excellent precision and reproducibility - complementary to HPLC for rare hemoglobins; cellulose acetate gel electrophoresis (alkaline pH) + citrate agar electrophoresis (acid pH): classic techniques still used in reference laboratories - the combination of the two pH values enables distinction between hemoglobins that co-migrate at a single pH (eg. HbS and HbD co-migrate at alkaline pH but separate at acid pH); falciformation test (sickling test - sodium metabisulfite): rapid screening for the presence of HbS - positive if HbS present (trait or disease) - does not distinguish trait from homozygous form \u2192 always confirm by HPLC or electrophoresis.<\/li>\n <li><strong>Adult normal values:<\/strong> HbA : 96\u201398 % ; HbA2 : 2,0\u20133,5 % ; HbF : <1,0 % (jusqu'\u00e0 2 % chez certains adultes sains \u2014 persistance h\u00e9r\u00e9ditaire b\u00e9nigne de l'HbF) ; HbS, HbC, HbD, HbE : 0 % (absent chez un adulte normal)<\/li>\n <li><strong>Interferences and limitations:<\/strong> recent transfusion (<3 to 4 months): transfused red blood cells (normal donor HbA) dilute the recipient's HbS or HbF \u2192 underestimation of abnormal fractions \u2014 mention any recent transfusions to the laboratory; infant <6 months old: HbF still predominant \u2014 different interpretation than in adults \u2014 normal neonatal profile: HbF + HbA \u00b1 trace HbA2; severe iron deficiency: underestimates HbA2 (false negative for beta-thalassemia minor) \u2014 correct iron deficit before concluding HbA2 is normal; HbA1c (glycated hemoglobin): fraction visible on HPLC before HbA \u2014 do not confuse with an abnormal fraction<\/li>\n <\/ul>\n\n <h2>Interpretation of Profiles and Clinical Implications<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Profile \/ Diagnostic<\/th><th>HPLC results and mechanism<\/th><th>Clinical implications and management<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Normal adult profile<br><small style=\"font-weight:400;color:#7a8fa0;\">HbA 96\u201398 % \/ HbA2 2\u20133,5 % \/ HbF <1 %<\/small><\/td>\n <td>HbA (\u03b1\u2082\u03b2\u2082): major adult fraction \u2014 physiological carrier of O\u2082 with normal affinity; HbA2 (\u03b1\u2082\u03b4\u2082): minor fraction \u2014 uncertain physiological role \u2014 key biological marker of beta-thalassemia (increased if \u03b2 synthesis deficit); HbF (\u03b1\u2082\u03b3\u2082): minimal physiological persistence (<1 %) in adults \u2014 increases again in certain pathologies (sickle cell disease treated with hydroxyurea, leukemia, aplastic anemias) and in cases of benign hereditary persistence of HbF (HPFH); normal neonatal profile at birth: HbF 70\u201390 %+ HbA 10\u201330 % + HbA2 traces \u2014 \u03b3\u2192\u03b2 switching is completed around 6 months (HbA becomes the majority)<\/td>\n <td>A normal electrophoretic profile in an adult excludes a structural hemoglobinopathy and beta-thalassemia \u2014 however, it does not exclude alpha-thalassemia (mild alpha-thalassemias \u2014 alpha trait \u2212\u03b1\/\u03b1\u03b1 or \u2212\u2212\/\u03b1\u03b1 \u2014 do not alter the adult electrophoretic profile \u2192 diagnosis by molecular biology \u2014 PCR specific for alpha deletions); if persistent microcytic hypochromic anemia with a normal electrophoretic profile and normal ferritin \u2192 consider alpha-thalassemia \u2192 order alpha-globin molecular genetics (LSPQ or reference laboratory); interpretation within the clinical context is always essential \u2014 a normal profile does not exclude all hemoglobinopathies.<\/td>\n <\/tr>\n <tr>\n <td>Sickle cell trait (AS carrier)<br><small style=\"font-weight:400;color:#7a8fa0;\">HbA 55\u201360 % \/ HbS 38\u201345 % \/ HbA2 2\u20133.5 %<\/small><\/td>\n <td>Point mutation \u03b26Glu\u2192Val (GAG\u2192GTG) on an HBB gene allele \u2192 substitution of glutamic acid by valine at position 6 of the beta chain \u2192 HbS; heterozygote (healthy carrier): one normal HBB allele (\u2192 HbA) + one mutated HBB allele (\u2192 HbS) \u2192 majority HbA (55\u201360 %) + minority HbS (38\u201345 %); HbS polymerizes only in conditions of severe hypoxia \u2014 the AS carrier is asymptomatic in daily life but may experience complications at high altitude, during scuba diving, or in case of severe perioperative hypoxia; hemogram: normal or discrete microcytosis (if iron deficiency is associated)<\/td>\n <td>Sickle cell trait (AS) is benign in the vast majority of cases \u2014 AS carriers lead normal lives without major restrictions. Genetic counseling: if both parents are AS carriers \u2192 25% % risk of having an SS child (homozygous sickle cell disease \u2014 illness) with each pregnancy \u2192 prenatal diagnosis possible (chorionic villus sampling or amniocentesis + molecular biology). Rare clinical exceptions: splenic infarction at high altitude (>2,500 m) + recurrent hematuria (renal papillary necrosis) + risk of sudden death during prolonged intense physical exercise in heat and dehydration (case reports) \u2014 advice for caution during intensive competitive sports. Partner screening: systematically recommended if AS carrier and wishing to conceive.<\/td>\n <\/tr>\n <tr>\n <td>Homozygous sickle cell disease (SS)<br><small style=\"font-weight:400;color:#7a8fa0;\">HbS 85\u201395 % \/ HbF 2\u201320 % \/ HbA2 2\u20134 % \/ HbA 0 %<\/small><\/td>\n <td>Two mutated HBB alleles (\u03b26Glu\u2192Val) \u2192 no HbA produced \u2192 almost exclusive HbS; under deoxygenation conditions \u2192 HbS molecule polymerization \u2192 erythrocyte sickling (sickle cells) \u2192 microvascular obstruction (vaso-occlusion) + chronic hemolysis + endothelial inflammation activation; HbF (\u03b1\u2082\u03b3\u2082) inhibits HbS polymerization \u2014 HbF level is a major prognostic factor (HbF >20 %\u2192 fewer crises); hydroxyurea increases HbF synthesis by 15 to 25 % \u2192 reduction in vaso-occlusive crises; typical HPLC profile: HbS 85\u201395 % + variable HbF (2\u201320 % ) + HbA2 2\u20134 % + total absence of HbA<\/td>\n <td>Severe chronic multisystem disease - specialized hematology follow-up mandatory; acute manifestations: painful vaso-occlusive crisis (PVD) + acute chest syndrome (ATS - life-threatening emergency - hypoxemia + pulmonary infiltrate + chest pain) + stroke (CVA - child) + splenic sequestration + aplastic crisis (parvovirus B19); chronic manifestations: splenomegaly + functional asplenia from childhood \u2192 prophylaxis with penicillin V + vaccinations (pneumococcal PCV20 + PPV23, meningococcal, Hib, influenza, COVID); disease-modifying treatments: hydroxyurea (Hydrea) 15-35 mg\/kg\/d \u2192 1st line - HbF \u2191 \u2192 crises \u2193 - reimbursed RAMQ; L-glutamine (Endari); voxelotor (Oxbryta); crizanlizumab (Adakveo); hematopoietic stem cell (HSC) transplantation: only potentially curative treatment - indication in children with severe disease if HLA-identical donor available; gene therapy: advanced clinical trials (Lovo-cel - BLA approved FDA 2023)<\/td>\n <\/tr>\n <tr>\n <td>Beta-thalassemia minor (beta-thal trait)<br><small style=\"font-weight:400;color:#7a8fa0;\">HbA2 >3,5 % \/ HbF 1\u20135 % \/ HbA 92\u201395 %<\/small><\/td>\n <td>A mutated HBB allele (point mutation \u2014 >200 known mutations \u2014 defect in transcription, splicing, or translation of \u03b2-globin mRNA) \u2192 decreased synthesis of \u03b2 chains \u2192 relative excess of \u03b1 chains \u2192 increased HbA2 (compensation by \u03b4-globin overexpression) \u2192 HbA2 >3.5% %(main diagnostic criterion) + slightly increased HbF (1\u20135% % ) + moderate microcytic hypochromic anemia (Hb 10\u201313 g\/dL) + microcytic hypochromic erythrocytes + elevated erythrocyte count (relative polycythemia) + decreased MCV (60\u201370 fL); the carrier is generally asymptomatic or paucisymptomatic (slight fatigue) \u2014 qualified as \u00abminor\u00bb thalassemic or thalassemic trait carrier<\/td>\n <td>Frequent diagnostic trap: beta-thalassemia minor is often confused with iron deficiency (same biological picture \u2014 hypochromic microcytosis); distinguishing features: normal or high ferritin (no iron deficiency) + HbA2 >3.5 % on electrophoresis + high red blood cell count (relative polycythemia) + absence of response to iron supplementation; caution: concomitant iron deficiency lowers HbA2 \u2192 can distort diagnosis (false negative) \u2192 correct iron deficiency before electrophoresis if ferritin is low; genetic counseling: if both parents are carriers \u2192 25 % risk of beta-thalassemia major (Cooley's disease) \u2192 severe transfusion-dependent hemolytic anemia from the first months of life \u2192 prenatal diagnosis recommended; iron supplementation is useless and potentially harmful in thalassemic carriers without confirmed deficiency<\/td>\n <\/tr>\n <tr>\n <td>Other important profiles<br><small style=\"font-weight:400;color:#7a8fa0;\">HbC, HbE, HbD, SC double heterozygotes, and S\u03b2-thal<\/small><\/td>\n <td>HbC (\u03b26Glu\u2192Lys) : fr\u00e9quente en Afrique de l'Ouest \u2014 trait AC asymptomatique \u2014 maladie CC rare (an\u00e9mie h\u00e9molytique mod\u00e9r\u00e9e + spl\u00e9nom\u00e9galie + cristaux d'HbC dans les h\u00e9maties) ; HbSC : double h\u00e9t\u00e9rozygote S\/C \u2014 maladie dr\u00e9panocytaire de s\u00e9v\u00e9rit\u00e9 interm\u00e9diaire \u2014 HbS 50 % + HbC 50 % \u2014 r\u00e9tinopathie prolif\u00e9rative + ost\u00e9on\u00e9crose fr\u00e9quentes \u2014 syndrome thoracique aigu possible ; HbS\u03b2+-thalass\u00e9mie : double h\u00e9t\u00e9rozygote S\/\u03b2+-thal \u2014 HbS 60\u201385 % + HbA 10\u201330 % + HbA2 \u00e9lev\u00e9e + HbF variable \u2014 ph\u00e9notype dr\u00e9panocytaire mod\u00e9r\u00e9 \u00e0 s\u00e9v\u00e8re ; HbS\u03b20-thalass\u00e9mie : double h\u00e9t\u00e9rozygote S\/\u03b20-thal \u2014 HbS 85\u201392 % + HbA 0 % + HbA2 \u00e9lev\u00e9e + HbF variable \u2014 ph\u00e9notype aussi s\u00e9v\u00e8re que la dr\u00e9panocytose SS ; HbE (\u03b226Glu\u2192Lys) : tr\u00e8s fr\u00e9quente en Asie du Sud-Est \u2014 trait AE asymptomatique \u2014 EE l\u00e9g\u00e8re \u2014 HbE\u03b20-thal (double h\u00e9t\u00e9rozygote) : an\u00e9mie s\u00e9v\u00e8re transfuso-d\u00e9pendante dans les formes graves ; HPFH (persistance h\u00e9r\u00e9ditaire de l'HbF) : HbF 15\u201335 % + HbA normale + asymptomatique \u2014 b\u00e9nin<\/td>\n <td>SC sickle cell disease accounts for about 25\u201330 % of sickle cell syndromes in Quebec (in patients originating from West Africa and the Caribbean)\u2014a milder disease than SS but with significant specific complications: proliferative retinopathy (mandatory annual ophthalmological examination from the age of 10\u2014risk of FFA + laser photocoagulation if neovascularization) + osteonecrosis of the femoral head (MRI if hip pain) + priapism + thromboembolism (increased risk compared to SS); HbE is the most widespread globin mutation in the world (100\u2013150 million carriers)\u2014frequent in patients originating from Cambodia, Thailand, Vietnam, and Myanmar\u2014to consider in front of unexplained microcytosis in a patient from Southeast Asia; always interpret electrophoresis based on the patient's geographic origin<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>Alpha-thalassemia - electrophoresis limit:<\/strong> Unlike beta-thalassemia, alpha-thalassemia minor (\u03b1-trait - one or two deletions in the four alpha-globin genes) does not typically alter the adult electrophoretic profile\u2014normal HbA2, normal HbF, no abnormal fraction. It manifests solely as hypochromic microcytosis with normal ferritin. Diagnosis relies on molecular biology (PCR with detection of alpha-globin deletions\u2014\u2212\u03b13.7, \u2212\u03b14.2, \u2212\u2212SEA, \u2212\u2212MED, etc.). This limitation is clinically important: a normal electrophoresis does not rule out alpha-thalassemia in a microcytic patient without iron deficiency, particularly in patients of Asian, African, or Mediterranean origin.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Sickle cell emergencies \u2014 recognize and act fast<\/div>\n <p>In a patient with known sickle cell disease (SS, SC, S\u03b2-thalassemia), consult <strong>immediately to the emergency room<\/strong> if : <strong>Chest pain, cough, fever, hypoxemia<\/strong> Acute chest syndrome (ACS) - a life-threatening emergency - emergency blood transfusions + antibiotics + O\u2082; ; <strong>Sudden focal neurological deficit<\/strong> (hemiplegia, aphasia, visual impairment) \u2192 Sickle cell ischemic stroke \u2014 urgent thrombolysis and\/or transfusion; ; <strong>Abdominal pain + rapidly progressive splenomegaly + sudden pallor<\/strong> (child) \u2192 acute splenic sequestration \u2014 urgent transfusion; ; <strong>Fever >101.3 \u00b0F<\/strong> in a child with sickle cell disease \u2192 pneumococcal sepsis (functional asplenia) \u2014 immediate IV antibiotics.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>The doctors at Clinique Omicron prescribe and interpret hemoglobin electrophoresis, provide genetic counseling for at-risk couples, ensure first-line follow-up for carriers of hemoglobinopathies, and coordinate specialized hematology follow-up for symptomatic cases. The analyses are available from our service points in Quebec and via telemedicine. To make an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The content of this page is for informational purposes only and does not substitute for the advice of a qualified healthcare professional or a laboratory medicine specialist. Any diagnosed hemoglobinopathy requires appropriate medical follow-up and genetic counseling if parental planning is considered.<\/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>\u00c9lectrophor\u00e8se de l’h\u00e9moglobine : indications et interpr\u00e9tation | Clinique Omicron H\u00e9matologie & M\u00e9decine de laboratoire & M\u00e9decine de famille \u00c9lectrophor\u00e8se de l’h\u00e9moglobine L’\u00e9lectrophor\u00e8se de l’h\u00e9moglobine est une technique de laboratoire permettant de s\u00e9parer, d’identifier et de quantifier les diff\u00e9rentes fractions d’h\u00e9moglobine pr\u00e9sentes dans les \u00e9rythrocytes circulants, en exploitant les diff\u00e9rences de charge \u00e9lectrique des cha\u00eenes… <a href=\"https:\/\/cliniqueomicron.ca\/en\/electrophorese-de-lhemoglobine\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Hemoglobin Electrophoresis: Indications 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":"\u00c9lectrophor\u00e8se de l'h\u00e9moglobine | Brossard | Clinique Omicron","_metasync_otto_description":"L'\u00e9lectrophor\u00e8se de l'h\u00e9moglobine identifie les h\u00e9moglobinopathies comme la dr\u00e9panocytose et la thalass\u00e9mie. Indications, technique et interpr\u00e9tation des r\u00e9s...","_metasync_otto_keywords":"","_metasync_otto_og_title":"\u00c9lectrophor\u00e8se de l'h\u00e9moglobine : | Brossard | Clinique Omicron","_metasync_otto_og_description":"L'\u00e9lectrophor\u00e8se de l'h\u00e9moglobine identifie les h\u00e9moglobinopathies comme la dr\u00e9panocytose et la thalass\u00e9mie. Indications, technique et interpr\u00e9tation des r\u00e9s...","_metasync_otto_twitter_title":"\u00c9lectrophor\u00e8se de l'h\u00e9moglobine : | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"L'\u00e9lectrophor\u00e8se de l'h\u00e9moglobine identifie les h\u00e9moglobinopathies comme la dr\u00e9panocytose et la thalass\u00e9mie. 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