eMedicine Specialties > Pediatrics: General Medicine > Hematology

Myelodysplasia: Differential Diagnoses & Workup

Author: Sharon M Castellino, MD, FAAP, Assistant Professor, Department of Pediatrics, Division of Pediatric Hematology-Oncology, Wake Forest University Health Sciences
Coauthor(s): Timothy P Cripe, MD, PhD, Associate Professor of Pediatric Hematology/Oncology, University of Cincinnati; Director, Translational Research Trials Office, Department of Pediatrics, Cincinnati Children's Hospital Medical Center; Scott C Howard, MD, Associate Professor, University of Tennessee College of Medicine; Associate Member, Department of Oncology, Director of Clinical Trials, International Outreach Program, St Jude Children's Research Hospital
Contributor Information and Disclosures

Updated: Apr 11, 2008

Differential Diagnoses

Acute Lymphoblastic Leukemia
Kostmann Disease
Acute Myelocytic Leukemia
Osteopetrosis
Chromosomal Breakage Syndromes
Parvovirus B19 Infection
Histiocytosis
Transient Erythroblastopenia of Childhood

Other Problems to Be Considered

Nutritional deficiencies
Vitamin B-12 deficiency
Folate deficiency
Pyridoxine-dependent anemia

Viral infections
Epstein-Barr virus (EBV)
Parvovirus infection

Chemical exposure
Cytotoxic chemotherapy
Exposure to antibiotics
Exposure to benzene

Others
Paroxysmal nocturnal hemoglobinuria
Glycogen-storage diseases
Chronic inflammation
Metastatic carcinoma

Workup

Laboratory Studies

  • CBC count (with differential and smear)
    • Peripheral blood count reveals anemia, neutropenia, and/or thrombocytopenia. The anemia is often macrocytic. Cytopenias can evolve and progress over a period of weeks to months.
    • The blood smear commonly reveals macrocytosis, hypogranular granulocytes, pseudo–Pelger-Huet anomaly (hypogranular and hypolobulated granulocytes), and giant platelets. Reticulocyte counts are low despite normal numbers of erythroid progenitors in the marrow. In JMML, marked monocytosis may be present.
  • Bone marrow aspirate and trephine core biopsy (See Procedures.)
  • Quantitative hemoglobin electrophoresis - May reveal elevated hemoglobin F levels, indicating reversion to fetal erythropoiesis
  • Cytogenetic studies (conventional karyotype, fluorescence in situ hybridization (FISH), polymerase chain reaction)
    • These studies reveal chromosomal abnormalities in 40-70% of pediatric cases of myelodysplasia syndrome (MDS).
    • Acquired chromosome abnormalities confirm the diagnosis when myelodysplasia syndrome is suspected.
    • The most commonly known abnormalities include monosomy 7 or 7q-, monosomy 5 or 5q-, or trisomy 8. Myelodysplasia syndrome may also be associated with 20q-, isochromosome 17, and abnormalities of 11q. Reciprocal translocations and inversions are uncommon.
  • Fanconi anemia and paroxysmal nocturnal hemoglobinuria tests
    • Evaluate all patients with suspected myelodysplasia syndrome for Fanconi anemia and for paroxysmal nocturnal hemoglobinuria (PNH).
    • A Fanconi screen using diepoxybutane (DEB) or mitomycin C stimulation reveals abnormal chromosome breakage if this syndrome is present.
    • Measurement of 2 complement regulatory proteins, CD55 (decay accelerating factor [DAF]) and CD59 (membrane inhibitor of reactive lysis [MIRL]) aids in diagnosis of PNH.
  • Human leukocyte antigen (HLA) typing of patient and family members - Should be performed at the outset, in anticipation of allogeneic hematopoietic stem cell transplant
  • Additional laboratory studies
    • In most cases, myelodysplasia syndrome is diagnosed after a history and physical examination, followed by the laboratory workup described above. In some instances, additional tests may be warranted.
    • Viral serologies, especially human immunodeficiency virus (HIV), cytomegalovirus (CMV), EBV, and parvovirus, can be used to exclude viral etiologies of altered hematopoiesis.

Imaging Studies

  • Imaging studies do not contribute to establishing the diagnosis or prognosis of myelodysplasia syndrome.

Procedures

  • Bone marrow aspiration and biopsy are essential to establish the diagnosis and to classify the myelodysplasia syndrome.
  • Biopsy findings are needed to ascertain cellular architecture, cellularity, percentage of blasts, and the presence of fibrosis. These studies may need to be repeated as cytopenias evolve.
  • Bone marrow findings are reviewed under Histologic Findings.

Histologic Findings

  • Bone marrow aspiration and biopsy are essential diagnostic tools. The bone marrow of patients with myelodysplasia syndrome can be normocellular or hypocellular.12 As many as 10% of patients present with hypocellular bone marrow. Bone marrow biopsy should also be preformed to assess cellularity and architecture because fibrosis can be a component of disease.
  • Typically, cytopenia is seen in more than one hematopoietic lineage. Myeloid abnormalities, especially an increased percentage of blasts, are characteristic of myelodysplasia syndrome but are not pathognomonic. Other myeloid alterations include hypogranular or agranular cells, abnormal granulation, Auer rods, or the pseudo–Pelger-Huet anomaly. Erythroid abnormalities are the most common feature and can include megaloblastoid changes, dyserythropoiesis, multinuclearity, nuclear budding, increased ringed sideroblasts, and internuclear bridging. Megakaryopoiesis is commonly altered and manifests as an increased proportion of megakaryoblasts, micromegakaryocytes, or cells with nuclear cytoplasmic dyssynchrony.
  • Because the diagnosis of myelodysplasia syndrome relies heavily on marrow morphology, interobserver and intraobserver differences complicate disease classification. This led to a universal morphologic classification by the FAB, defined by a consensus of hematologists and hematopathologists. The FAB system attempts to classify myelodysplasia syndrome and acute nonlymphocytic leukemia (ANLL) subtypes based on morphologic features in the marrow. Five myelodysplasia subtypes were described in adults based on blood and marrow blast percentage, the presence of Auer rods, the absolute blood monocyte count, and the frequency of ring sideroblasts. The FAB classification subtypes are as follows:
    • Refractory anemia
    • Refractory anemia with ringed sideroblasts (RARS)
    • Refractory anemia with excess blasts (RAEB)
    • Chronic myelomonocytic leukemia (CMML)
    • Refractory anemia with excess blasts in transformation (RAEBT)
  • Although this system is helpful, it does not adequately account for the clinical features of pediatric myelodysplasia syndrome.13 The current FAB system is strictly based on morphology and, therefore, does not take into account cytogenetics or predisposing abnormalities. However, both are significant to classification and, possibly, to prognosis in children. Furthermore, RARS almost never develops in children. Finally, no provision for isolated cytopenias other than anemia is recognized in the current FAB system.
  • In an attempt to include some cytogenetic information, the WHO recently proposed an alternate classification scheme for MDS. The WHO classification is as follows:3
    • Refractory anemia with or without ringed sideroblasts (erythroid dysplasia only, marrow blasts <5%)
    • RA with multilineage dysplasia (blasts <5%)
    • 5q- syndrome (blasts <5%, no other genetic abnormalities)
    • RAEB (blasts 5-20%)
    • Myelodysplasia syndrome unclassified (does not fit into the above groups)
  • The changing classification schemes and continuing controversies underscore the fact that the understanding of myelodysplasia is evolving.
  • A working group of the Society of International Pediatric Oncology (SIOP) recently attempted to reach a consensus on the above issues. Mandel et al have proposed a system that would account for disease category (ie, de novo, syndrome related, treatment/toxin related), morphology, and cytogenetics.14 In addition, suggestions have been made for a dysplasia score for each lineage in order to compare morphologic features more consistently in this heterogeneic group of diseases.
  • JMML is unique to the pediatric age group and has been categorized separately from myelodysplasia syndrome. This disease is characterized by the absence of t(9;22), an absolute peripheral monocyte count of higher than 450, elevated hemoglobin F levels, selective in vitro hypersensitivity to granulocyte-macrophage colony-stimulating factor (GM-CSF), and excessive proliferation of monocyte-macrophage colonies in clonogenic culture.

More on Myelodysplasia

Overview: Myelodysplasia
Differential Diagnoses & Workup: Myelodysplasia
Treatment & Medication: Myelodysplasia
Follow-up: Myelodysplasia
References
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Further Reading

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Keywords

myelodysplasia, myelodysplasia syndromes, MDS, myelodysplastic syndromes, MDSs, preleukemia syndromes, dysmyelopoietic syndromes, hematopoietic dysplasia, refractory dysmyelopoietic anemia, monosomy 7 syndrome, refractory anemia, juvenile chronic myelogenous leukemia, JCML, hematopoiesis, refractory anemia with excess of myeloblasts, subacute myeloid leukemia, oligoleukemia, odoleukemia, stem cell disorder
 
cytopenia, acute nonlymphocytic leukemia, ANLL, neurofibromatosis, NF, neutropenia, thrombocytopenia, juvenile myelomonocytic leukemia, JMML, Fanconi anemia, severe congenital neutropenia, Kostmann syndrome, Down syndrome, Noonan syndrome, Shwachman-Diamond disease, Diamond-Blackfan anemia, Dubowitz syndrome, Bloom syndrome, Poland syndrome, ataxia telangiectasia, bone marrow failure, dyskeratosis congenita, bone marrow transplantation, graft versus host disease, graft rejection, juvenile chronic myelogenous leukemia, JCML, splenomegaly

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Contributor Information and Disclosures

Author

Sharon M Castellino, MD, FAAP, Assistant Professor, Department of Pediatrics, Division of Pediatric Hematology-Oncology, Wake Forest University Health Sciences
Sharon M Castellino, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Society of Hematology, and American Society of Pediatric Hematology/Oncology
Disclosure: Nothing to disclose.

Coauthor(s)

Timothy P Cripe, MD, PhD, Associate Professor of Pediatric Hematology/Oncology, University of Cincinnati; Director, Translational Research Trials Office, Department of Pediatrics, Cincinnati Children's Hospital Medical Center
Timothy P Cripe, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American Society of Hematology, and American Society of Pediatric Hematology/Oncology
Disclosure: Nothing to disclose.

Scott C Howard, MD, Associate Professor, University of Tennessee College of Medicine; Associate Member, Department of Oncology, Director of Clinical Trials, International Outreach Program, St Jude Children's Research Hospital
Scott C Howard, MD is a member of the following medical societies: American Society of Clinical Oncology and American Society of Pediatric Hematology/Oncology
Disclosure: Nothing to disclose.

Medical Editor

Sharada A Sarnaik, MB, BS, Professor of Pediatrics, Wayne State University School of Medicine; Director, Sickle Cell Center, Attending Hematologist/Oncologist, Children's Hospital of Michigan
Sharada A Sarnaik, MB, BS is a member of the following medical societies: American Association of Blood Banks, American Association of University Professors, American Society of Hematology, American Society of Pediatric Hematology/Oncology, New York Academy of Sciences, and Society for Pediatric Research
Disclosure: Nothing to disclose.

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Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

James L Harper, MD, Associate Professor, Department of Pediatrics, Division of Hematology/Oncology and Bone Marrow Transplantation, Associate Chairman for Education, Department of Pediatrics, University of Nebraska Medical Center; Assistant Clinical Professor, Department of Pediatrics, Creighton University; Director, Continuing Medical Education, Children's Memorial Hospital; Pediatric Director, Nebraska Regional Hemophilia Treatment Center
James L Harper, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for Cancer Research, American Federation for Clinical Research, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Council on Medical Student Education in Pediatrics, and Hemophilia and Thrombosis Research Society
Disclosure: Nothing to disclose.

CME Editor

Samuel Gross, MD, Professor Emeritus, Department of Pediatrics, University of Florida, Clinical Professor, Department of Pediatrics, UNC, Adjunct Professor, Department of Pediatrics, Duke University
Samuel Gross, MD is a member of the following medical societies: American Association for Cancer Research, American Society for Blood and Marrow Transplantation, American Society of Clinical Oncology, American Society of Hematology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Robert J Arceci, MD, PhD, King Fahd Professor of Pediatric Oncology, Department of Oncology, Division of Pediatric Oncology, Johns Hopkins University School of Medicine
Robert J Arceci, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Pediatric Society, American Society of Clinical Oncology, American Society of Hematology, and American Society of Pediatric Hematology/Oncology
Disclosure: Nothing to disclose.

 
 
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