Hematology & Internal Medicine
Dacryocytes (teardrop cells)
Tear ducts — from the Greek tears (teardrop) - are abnormally deformed red blood cells with a characteristic unipolar elongation in the shape of a teardrop or teardrop, with a rounded tip and a pointed, tapering apex. They belong to the poikilocyte group (abnormally shaped red blood cells) and are distinguished from ovalocytes (elliptocytes) by their marked asymmetry and pointed apex. The presence of dacryocytes on a peripheral blood smear, even in small numbers, is a morphological signal of major clinical importance: it almost always indicates a severe disturbance of medullary architecture, or mechanical stress exerted on erythrocytes as they are forced to pass through fibrous or infiltrated tissue. The mechanism of dacryocyte formation is twofold. On the one hand, during extramedullary erythropoiesis (hematopoiesis outside the normal bone marrow - spleen, liver - occurring when the marrow is fibrotic or invaded), erythroblasts release immature red blood cells which are deformed as they pass through the splenic sinusoids, cross-linking their membrane. On the other hand, in states of medullary fibrosis, mature red blood cells are irreversibly stretched and deformed as they pass through the network of reticulin and collagen fibers that obstruct the medullary sinusoids - they retain this teardrop shape once in the circulation. The presence of numerous dacryocytes on the smear, associated with leukoerythroblastosis (circulating erythroblasts + immature granulocytes in the peripheral blood), constitutes the myelo-phthisic picture - an almost pathognomonic sign of severe bone marrow invasion or fibrosis requiring urgent hematological investigation.
Formation mechanism and morphology
- Mechanical mechanism (medullary fibrosis): Bone marrow fibrosis (deposition of reticulin fibers, WHO classification grade MF-2 to MF-3) creates a rigid network that deforms red blood cells as they pass through the medullary sinusoids; the erythrocyte membrane, stretched in one direction, retains this anisotropic deformation through irreversible reorganization of the cytoskeleton (spectrin, actin, protein 4.1); the dacryocytes thus formed are more rigid and have a shortened lifespan in circulation (moderate hemolysis) – they are progressively eliminated by splenic macrophages.
- Splenic mechanism (extramedullary erythropoiesis): in myelofibrosis or medullary infiltration, hematopoiesis shifts to the spleen (myeloid splenomegaly) and liver (hepatomegaly); erythroblasts produced outside the marrow release red blood cells with incomplete membrane maturation; these cells are deformed by the forced passage through the Billroth cords and splenic sinusoids → irreversible teardrop shape; the association of splenomegaly + dacryocytes + circulating erythroblasts is highly suggestive of primary myelofibrosis
- Morphology on the smear: the dacryocyte is larger than a normal red blood cell (elongated macrocyte); its rounded end contains the main hemoglobin; the tapered end is pale and thinner; true dacryocytes (point oriented in a variable direction from one cell to another) must be distinguished from pseudo-dacryocytes caused by artifacts (points oriented in the same direction - artifact of smear preparation, particularly at the tail of the smear); semi-quantitative scoring on the smear: rare (1+), present (2+), numerous (3+), abundant (4+); even 1+ of true dacryocytes on a well-prepared smear warrants investigation
Causes of Dacryocytes - Differential Diagnosis
| Cause | Mechanism and clinical context | Diagnostic elements associated |
|---|---|---|
| Primary Myelofibrosis (PMF) Primary cause - abundant dacryocytes |
Philadelphia-negative myeloproliferative neoplasm (MPN) — JAK2 V617F mutation (50–60%), CALR exon 9 mutation (25–30%), or MPL mutation (5–8%) → constitutive activation of the JAK-STAT pathway → clonal proliferation of dysplastic megakaryocytes → release of TGF-β, PDGF, bFGF → progressive bone marrow fibrosis (grades MF-0 to MF-3); incidence 0.5–1/100,000/year — peak 65–70 years; massive splenomegaly (sometimes >20 cm — left abdominal mass sensation, early satiety); constitutional symptoms (fever, night sweats, weight loss — MPN-SAF score); abundant dacryocytes (3+–4+) + characteristic leukoerythroblastosis; complete myelophthisic picture | NFS: anemia (Hb often <10 g/dL) + leukocytosis or leukopenia + initial thrombocytosis then thrombocytopenia; smear: abundant dacryocytes + erythroblasts + myelocytes/metamyelocytes (leukoerythroblastosis) + macrocytes + hypochromia; very high LDH (cell lysis); high uric acid (cell turnover); bone marrow biopsy (BMB) - gold standard: reticulin fibrosis (grade MF-2 or MF-3) + dysplastic megakaryocytes clustered together; JAK2/CALR/MPL mutation (myeloproliferative NGS panel); DIPSS-Plus score (prognosis); treatment: ruxolitinib (JAK1/2 inhibitor - reduces splenomegaly and symptoms - standard of care); fedratinib, pacritinib, momelotinib (alternative JAK inhibitors); allogeneic hematopoietic stem cell transplant (HSCT) if eligible - only potentially curative treatment |
| Myelofibrosis secondary Evolution of pre-existing NMP |
Évolution en myélofibrose de la polyglobulie de Vera (PV → MF post-PV dans 10–20 % à 20 ans) ou de la thrombocytémie essentielle (TE → MF post-TE dans 5–10 % à 15 ans) ; même tableau morphologique que la MFP avec dacryocytes + leucoérythroblastose ; antécédent de NMP documenté ; mutation JAK2 quasi constante dans les post-PV | Smear + BOM + JAK2 mutation; WHO 2022 criteria for post-PV (Barosi) or post-ET (Barosi) transformation to MF; treatment similar to PMF: ruxolitinib, allogeneic HSCT if eligible |
| Spinal cord invasion (tuberculous myelitis) Bone metastases, hematologic disorders |
Replacement of normal hematopoietic tissue by extrinsic tumor cells → myelophthisic picture: dacryocytes + leucoerythroblastosis + thrombocytopenia; most common metastatic cancers responsible: breast carcinoma (most frequent—especially lobular), prostate carcinoma, lung carcinoma, renal carcinoma, gastric carcinoma, melanoma; hematological diseases: lymphoma (Hodgkin and non-Hodgkin—bone marrow involvement in 30–80 % depending on the type); acute leukemia (blast infiltration); multiple myeloma (extensive plasmacytic replacement); myelofibrosis (rare) | Smear: dacryocytes (often 1+–2+) + erythroblasts + occasionally visible abnormal cells (blasts, tumor cells — rare); elevated LDH, elevated alkaline phosphatase (osteoblastic metastases — prostate); CA 15-3, PSA, CEA depending on suspected primary site; thoraco-abdomino-pelvic CT + FDG-PET; BM Bx — gold standard: metastatic cells on pathological examination + immunohistochemistry (CK, TTF-1, PSA depending on primary site); bone marrow biopsy distant from the usual puncture site (iliac crest) if first biopsy is non-contributory |
| Severe megaloblastic anemia B12 or folate deficiency |
Small dacryocytes + ovalocytes + macrocytes + hypersegmentation of neutrophils (PMNs — >5 lobes in >5 % of PMNs) on smear; mechanism: intra-medullary dyserythropoiesis due to DNA synthesis defect → giant erythroblasts (megaloblasts) → abnormally shaped red blood cells; classic association with pancytopenia (macrocytosis + leukopenia + mild thrombocytopenia); fewer and less typical dacryocytes than in myelofibrosis | Vitamine B12 sérique <150 pmol/L + acide méthylmalonique et homocystéine élevés (marqueurs fonctionnels plus sensibles) ; folates érythrocytaires ; anti-facteur intrinsèque (maladie de Biermer — 50–70 % de sensibilité) ; anti-cellules pariétales (70–90 % mais peu spécifiques) ; traitement : B12 IM (cyanocobalamine ou hydroxocobalamine) si maladie de Biermer ou malabsorption ; B12 orale 1 000 µg/jour si déficit alimentaire |
| Thalassemia (severe forms) | Precipitation of excess alpha chains (beta-thalassemia) in erythroblasts → severe ineffective erythropoiesis + marked poikilocytosis including dacryocytes, target cells, ovalocytes, fragments; beta-thalassemia major (Cooley) and beta-thalassemia intermedia; hemolysis + splenomegaly + hemosiderosis | NFS: severe hypochromic microcytic anemia; smear: major poikilocytosis (dacryocytes + target cells + ovalocytes + basophilic stippling); hemoglobin electrophoresis (high HbF, absent HbA in thalassemia major); high ferritin (hemolysis + iron overload); globin gene genotyping |
| Rare causes and artifacts | Reactive myelofibrosis secondary to miliary tuberculosis, histoplasmosis, visceral leishmaniasis (Kala-azar); hemoglobin C (sickle cell disease); pyruvate kinase deficiency; splenectomy (transient post-splenectomy dacryocytes); smear artifact (pseudo-dacryocytes oriented in the same direction - tail artifact cells) | Clinical context + infectious serologies if reactive myelofibrosis is suspected; careful examination of the smear (tip orientation—if all point in the same direction → artifact); hemoglobin electrophoresis + enzyme assay if unexplained hemolysis |
Management of dacryocytes on a blood smear
- First step—confirm and quantify: ensure that dacryocytes are genuine (tips pointing in multiple directions, typical morphological appearance) and not artifacts from the tail of a smear (pseudo-dacryocytes uniformly oriented); note the presence and quantity of circulating erythroblasts (nucleated cells—abnormal outside of pregnancy and severe hypoxia), young granulocyte forms (myelocytes, metamyelocytes—leukoerythroblastic picture), giant platelets, or platelet clumps
- Second step - First-line biological assessment: Complete blood count with manual differential + reticulocytes; LDH and uric acid (tumor and cellular lysis); complete liver function tests (hepatomegaly due to extramedullary erythropoiesis); ferritin (often very high in MF - inflammatory marker + iron overload); vitamin B12 and folate (rule out megaloblastosis); peripheral blood smear re-examined by a hematologist.
- Third step — imaging and specialized investigation: abdominal ultrasound (splenomegaly — size, volume in cm³) or abdomino-pelvic CT scan; JAK2 V617F + CALR exon 9 + MPL W515 mutation panel (MPN) on peripheral blood; oncological staging if primary cancer is suspected (CT scan + FDG-PET scan + tumor markers); referral to hematologist for bone marrow biopsy (BMB) — gold standard for diagnosis of myelofibrosis and bone marrow infiltration
- Bone Marrow Biopsy (BMB): performed under local anesthesia at the posterior superior iliac crest; provides: histology (reticulin and collagen fibrosis - WHO classification MF-0 to MF-3), bone marrow cellularity, immunohistochemistry (characterization of metastatic tumor cells), cytogenetics (del(13q), del(20q), +8, +9 - frequent abnormalities in MPN); severe myelofibrosis often makes bone marrow aspiration (bone marrow puncture-aspiration - BMA) impossible (dry tap - pathognomonic of advanced myelofibrosis)
ℹ️
The discovery of dacryocytes on a blood smear should systematically lead to a search for Leucoerythroblastosis (simultaneous presence of erythroblasts + immature granulocyte precursors in peripheral blood). This association— Tableau myélo-physique — indicates a profound disruption of bone marrow architecture and must lead to urgent hematological investigation (JAK2/CALR/MPL mutations + bone marrow biopsy) to primarily rule out primary myelofibrosis or metastatic bone marrow infiltration. The isolated presence of 1-2 dacryocytes without leucoerythroblastosis or splenomegaly can sometimes be observed in benign anemias — their clinical significance is then less but always to be considered in the clinical context.
Signs requiring urgent hematological consultation
Consult a doctor or hematologist immediately if the blood smear reveals numerous dacryocytes (2+ or more) associated with: circulating erythroblasts, immature granulocytes (leukoerythroblastosis); significant splenomegaly on clinical examination or imaging; unexplained pancytopenia or cytopenia; constitutional symptoms (prolonged fever, heavy night sweats, unexplained weight loss >10 % in 6 months); very high LDH without an obvious cause.
These combined elements constitute a myelo-phthisical picture that justifies a bone marrow biopsy on a semi-urgent basis (within 1 to 4 weeks) to rule out progressive primary myelofibrosis or neoplastic marrow infiltration.
Consult at Clinique Omicron
Clinique Omicron physicians interpret blood smear results, prescribe first-line investigations for the discovery of dacryocytes (CBC, LDH, ferritin, JAK2/CALR/MPL mutations, oncological workup if indicated), and refer to a hematologist for bone marrow biopsy based on the clinical presentation. Consultations are available at our service points in Quebec as well as via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is provided for informational purposes only and does not substitute for the advice of a qualified healthcare professional. The presence of teardrop cells on a blood smear should always be correlated with the clinical context and interpreted by a physician.
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