Hematology & Internal Medicine & Family Medicine
Polycytes (target cells - codocytes)
Polycytes - also known as target cells, codocytes (from the Latin codex = target cells - are erythrocytes with a characteristic archery-target appearance on the May-Grünwald-Giemsa (MGG) stained blood smear: a hemoglobin-dense central zone (pink-red central pellet), surrounded by an annular pale halo (zone of low hemoglobin concentration), then a densely-colored peripheral edge - giving the image of a concentric three-circle target. This peculiar appearance results from an abnormally high membrane surface-to-cell volume ratio: either the erythrocyte membrane surface is increased (excess cholesterol and membrane phospholipids, as in hepatopathies), or the intracellular volume is reduced (hemoglobin deficiency due to hypochromia - as in thalassemia and severe iron-deficiency anemia), or both mechanisms coexist. The presence of polycytes on the blood smear is never an isolated sign to be ignored: although no polycyte is specific to a single disease, their proportion and association with other erythrocyte morphological abnormalities (hypochromia, microcytosis, anemia) point to specific etiologies requiring appropriate workup. The four main etiological categories to be considered in the presence of codocytes on the smear are hemoglobinopathies and thalassemias (the main cause worldwide), chronic hepatopathies (the most frequent cause in Western countries), severe iron-deficiency anemia, and functional or post-surgical asplenia. The term «polycyte» used in French-speaking hematology is sometimes a source of confusion, as it can also refer to hypersegmented polynuclear cells in certain contexts - clarification by the term «target cell» or «codocyte» is preferable in medical communications.
Mechanisms of target cell formation
- Excess membrane due to lipid accumulation (hepatic mechanism): in chronic hepatopathies (cirrhosis + chronic hepatitis + cholestasis) → disturbance of hepatic lipid metabolism → accumulation of free cholesterol and lecithin in the erythrocyte membrane → increased membrane surface area without increased cell volume → increased surface/volume ratio surface/volume ratio → excess membrane folds into target shape when spread on slide + hepatic codocytes are normocytic or slightly macrocytic + normochromic or slightly hypochromic + often associated with stomatocytes and acanthocytes in advanced forms
- Volume reduction due to hemoglobin deficiency (hypochromic mechanism): in thalassemias + sickle cell disease (HbS + HbC + HbE) + severe iron deficiency anemia → hemoglobin content insufficient to fill the red cell normally → intracellular volume reduced without proportional reduction in membrane surface → flaccid, excess membrane takes on target shape + hypochromic codocytes are microcytic + hypochromic + with a broad, well-defined pale halo
- Asplenia - different mechanism: the spleen normally filters out abnormal erythrocytes and intracytoplasmic inclusions + in the absence of a spleen (surgical or functional asplenia) → target red blood cells or those carrying inclusions that would have been eliminated by the spleen persist in the circulation + codocytes in the context of asplenia are often associated with Howell-Jolly bodies (resident nuclear inclusions normally eliminated by the spleen) + the presence of Howell-Jolly bodies on a smear is quasi-pathognomonic of asplenia
Main etiologies and diagnostic associations
| Etiology | Proportion of codocytes and morphological appearance | Other associated anomalies and balance sheet |
|---|---|---|
| Thalassemia beta (thalassemic trait and thalassemia major) | Abundant codocytes (10-80 %) + microcytic + hypochromic + with large central pale zone + often associated with teardrop cells (dacryocytes) + circulating erythroblasts in major forms + basophilic punctations | Marked microcytosis (VGM 3.5 %) in beta-thalassemic trait + variable HbF + genetic work-up if in doubt. |
| Hemoglobinosis C (HbC) and HbSC | Very high proportion of codocytes (30-90 % of RBCs in homozygous HbCC) + often the most numerous and characteristic codocytes in all hematological pathology + intracellular HbC crystals possible (hexagonal) | Mild to moderate hemolytic anemia + splenomegaly + hemoglobin electrophoresis: HbC predominant + HbA absent in HbCC + systematic electrophoresis if very numerous codocytes with no other obvious cause |
| Chronic liver disease (cirrhosis + hepatitis + cholestasis) | Codocytes of variable proportion (5-30 %) + normocytic to macrocytic + normochromic + often associated with acanthocytes (spur cells) in advanced alcoholic cirrhosis + stomatocytes possible | Macrocytosis possible + disturbed liver function tests (transaminases + GGT + bilirubin + PT) + thrombocytopenia (hypersplenism) + anemia often multifactorial (digestive bleeding + folic acid deficiency + alcohol) |
| Severe iron-deficiency anemia | Codocytes in moderate proportion (5-15 %) + microcytic + strongly hypochromic + large central pale zone + often associated with hypochromic ovalocytes (pencil cells) and very hypochromic small erythrocytes (anulocytes) | Microcytosis + marked hypochromia + very low ferritin + low serum iron + high TIBC + high RDW (anisocytosis) + response to martial supplementation |
| Asplenia (post-splenectomy or functional) | Codocytes in variable proportions + often few in number + associated with Howell-Jolly bodies (round intracytoplasmic basophilic inclusions = nuclear remnants) + frequent reactive thrombocytosis | Howell-Jolly body = most characteristic sign of asplenia + thrombocytosis + CBC with normal or slightly disturbed formula except for poikilocytosis + post-splenectomy or sickle cell context (progressive functional asplenia) |
| Hemoglobin S (sickle cell disease) | Codocytes present (5-20 %) in SS homozygotes or composite heterozygotes (HbSC) + sickle cells + Pappenheimer bodies (iron granules) + circulating erythroblasts | Chronic hemolytic anemia + pathognomionic hemoglobin electrophoresis (predominantly HbS) + positive falciform test + elevated LDH + collapsed haptoglobin |
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In clinical practice, the presence of numerous target cells (more than 10-15 % of erythrocytes) on a blood smear from an adult patient with no known history should lead to a hemoglobin electrophoretic test to rule out a hemoglobinopathy (thalassemia, HbC, HbS) - particularly in patients of Mediterranean, African, Near Eastern or Asian origin, where these conditions are endemic. An ethnic and family history is essential to orient the diagnosis.
Diagnostic approach to codocytes on the smear
- Step 1 - Quantify and contextualize : proportion of codocytes (> 10 % = significant) + appearance: microcytic and hypochromic (hemoglobinopathy + iron-deficiency anemia) or normochromic-macrocytic-normocytic (hepatopathy + asplenia) + number of codocytes in relation to total poikilocytosis
- Step 2 - Search for associated anomalies : Howell-Jolly bodies (asplenia) + sickle cells (HbS) + basophilic punctata (thalassemia + lead poisoning) + acanthocytes + stomatocytes (hepatopathy) + hypochromic ovalocytes (iron deficiency) + erythroblasts (thalassemia major + severe hemolysis)
- Step 3 - Targeted biological work-up according to hypothesis : if microcytosis + hypochromia → ferritin + serum iron + TIBC + hemoglobin electrophoresis + if normocytosis-macrocytosis → liver workup + GGT + bilirubin + PT + if Howell-Jolly body → confirm asplenia (abdominal ultrasound) + if very numerous codocytes (HbC suspected) → hemoglobin electrophoresis + HPLC chromatography
Medical consultation recommended
A medical consultation is recommended when target cells are found in significant proportion on a blood smear, particularly if associated with anemia or microcytosis - the etiological work-up is necessary to distinguish benign, treatable causes (iron-deficiency anemia) from genetic conditions requiring genetic counseling (thalassemia, HbC, sickle cell anemia) or chronic liver disease requiring hepatological management. For blood smear interpretation with codocytes and diagnostic orientation, Clinique Omicron offers medical consultations at its points of service in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
Consult at Clinique Omicron
Clinique Omicron's specialized physicians and nurse practitioners (SPNs) interpret blood smears containing codocytes or target cells, prescribe the appropriate etiological work-up (ferritin + hemoglobin electrophoresis + hepatic work-up) depending on the morphological and clinical context, and refer to hematology for hemoglobinopathies or to hepatology for confirmed chronic hepatopathies. Consultations are available at several points of service in Quebec, as well as via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The contents of this page are provided for information purposes only and do not replace the advice of a physician or hematologist. Codocyte interpretation must always be performed in the full clinical and biological context, with knowledge of the patient's ethnic origin to guide towards endemic hemoglobinopathies.
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