eMedicine Specialties > Pediatrics: General Medicine > Hematology

Myelodysplasia

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

Introduction

Background

Myelodysplasia encompasses a heterogenous group of disorders that result in ineffective hematopoiesis. Historically, a wide variety of terms have been used to describe these syndromes, including preleukemia, refractory anemia with excess of myeloblasts, subacute myeloid leukemia, oligoleukemia,1 odoleukemia, and dysmyelopoietic syndromes.

The myelodysplasia syndromes (MDS) are clonal stem cell disorders characterized by progressive cytopenia or cytopenias, usually in the presence of a hypercellular bone marrow and multilineage dysplasia. Usually, all 3 cell lines (myeloid/monocyte, erythroid, megakaryocyte) are involved. Myelodysplasia syndrome is rare in childhood, and most children have a rapidly progressive course. Myelodysplasia disorders have been defined by their predilection to evolve into acute myeloid leukemias (AML), yet not all cases terminate in leukemia.

In 1982, the French-American-British cooperative group classification system (FAB classification) proposed for myelodysplasia syndrome in adults defined 5 categories of disease that represent a transition between myelodysplasia syndrome and AML.2 This classification, along with the related World Health Organization (WHO) classification system, is based on peripheral blood and bone marrow morphology.3 This system has been loosely used to classify myelodysplasia syndrome in children but has recently been challenged by the category, cytology, and cytogenetics (CCC) system, which was specifically designed for children. The CCC system incorporates the category of myelodysplasia syndrome, cytology, and cytogenetics.4 This new classification system is appealing because the predisposing factors, disease pattern, cytogenetics, and disease progression in children differ from those observed in adults.

Pathophysiology

The cellular elements of blood originate from the pluripotent hematopoietic stem cell. Stem cells have extensive regenerative and differentiating capacity and generate lymphoid and myeloid precursors, which then produce lymphocytes, neutrophils, monocytes, eosinophils, basophils, erythrocytes, and platelets.

In myelodysplasia syndrome, a dysregulation occurs in the differentiation process. The point of dysregulation varies with each disorder and with each associated cytogenetic abnormality. Bone marrow failure in myelodysplasia syndrome is due to ineffective hematopoiesis (related to excessive apoptosis) rather than a lack of hematopoiesis. The biologic mechanisms implicated in the pathophysiology of myelodysplasia syndrome to date include genomic instability, epigenetic changes, abnormal apoptosis machinery, abnormal signal-transduction pathways, immune dysregulation, and the role of the bone marrow microenvironment.

Chromosomal abnormalities are frequently found in myelodysplasia syndrome, but their causal relationship to disease remains unclear. The most common chromosome abnormalities involve chromosomes 5, 7, and 8. The association of monosomy 7 or deletion of 7 (del7q) in de novo, secondary, and constitutional forms of myelodysplasia syndrome has implicated chromosome 7 loss as a secondary genetic event in leukemogenesis. Cytogenetic studies and deletion mapping suggest loss of function of a tumor suppressor gene within the deleted segment of chromosome 7. Chromosome loss may occur as a germline mutation or may be acquired as a consequence of cytotoxic therapy. Favorable cytogenetic aberrations in adults involve chromosome Y and chromosome arms 20q- and 5q- but are rare in children.

Mutations in the ras oncogene are observed in 20-30% of childhood myelodysplasia syndrome cases. Increasing evidence suggests that, in the absence of a mutation in Ras protein, dysregulation of Ras by upstream effector proteins could contribute to the development of myelodysplasia syndrome. In patients with neurofibromatosis (NF), NF-1 gene product loss occurs, which results in loss of negative feedback via guanosine 5'triphosphate (GTP) of oncogenic N-ras. This results in unregulated proliferation of an abnormal clone. This is one mechanism thought to be responsible for the increased incidence of myelodysplasia syndrome in children with NF.

Mutations in the telomerase component TERC, which are observed in patients with dyskeratosis congenita, are occasionally seen in pediatric myelodysplasia syndrome without the typical phenotypic features.5  Aberrant methylation of genes has been reported in pediatric myelodysplasia syndrome and is under continued investigation.6  

Clinically, ineffective hematopoiesis manifests as isolated anemia, neutropenia, or thrombocytopenia, or as multiple cytopenias. Often, an isolated cytopenia progresses to pancytopenia over a period of weeks to months.

Frequency

International

The exact incidence of myelodysplasia syndrome in childhood has been difficult to estimate because of controversies regarding its classification, the heterogeneity of presentation, and the heterogeneity of risk factors in the population. The annual incidence is 0.5-4 per million population,7 and myelodysplasia syndrome accounts for about 2% of hematologic malignancies in children.

Mortality/Morbidity

Mortality in myelodysplasia syndrome results from bleeding, recurrent infection, and leukemic transformation. In the absence of treatment, myelodysplasia syndrome can be rapidly fatal, with or without the transformation to AML. An estimated 20-40% of adults with myelodysplasia syndrome develop leukemia, and 30-40% of patients with myelodysplasia syndrome experience infection, bleeding, or both.

Treatment-related morbidity and mortality in childhood myelodysplasia syndrome are related to complications of bone marrow transplantation. This includes graft failure with subsequent aplasia, transfusion-related diseases, infection, iatrogenic immunosuppression, graft versus host disease, and graft rejection.

Race

No racial predilection has been observed in myelodysplasia syndrome.

Sex

The male-to-female ratio varies from 1.7-4.8:1 in different series.8 The significance of this male predominance is unclear but is attributed, in part, to the increased prevalence of juvenile myelomonocytic leukemia (JMML), which was previously termed juvenile chronic myelogenous leukemia (JCML), in boys and monosomy 7 syndrome in children.9

Age

Myelodysplasia syndrome is uncommon in childhood, with 50% of cases occurring in persons older than 60 years.8 Monosomy 7 syndrome and JMML occur almost exclusively in children younger than 4 years. Children treated with radiation or intensive chemotherapy for another malignancy are more likely to develop myelodysplasia syndrome as a secondary adverse event.

Clinical

History

Patients with myelodysplasia (MDS) may present with symptoms of hematopoietic failure, including infection, bleeding, bruising, fatigue, weight loss, and dyspnea upon exertion. Alternatively, asymptomatic children may have unexplained cytopenias or isolated splenomegaly discovered during routine evaluation for an unrelated symptom. The interval between onset of symptoms and diagnosis ranges from 0-23 months, with a median of 2 months.

Eliciting a prior history of malignancy is important to distinguish between de novo versus secondary myelodysplasia syndrome when possible. Specifically, a history of previous exposure to alkylating agent chemotherapy, radiation therapy, or hematopoietic stem cell transplant is important because these are risk factors for therapy-related myelodysplasia syndrome. A history of constitutional bone marrow failure syndrome (eg, Fanconi syndrome, Diamond-Blackfan anemia, Kostmann syndrome, Schwachman-Diamond syndrome) or aplastic anemia can also precede secondary myelodysplasia syndrome. Familial cases of MDS have also been reported; the history is usually that of a first-degree relative with myelodysplasia syndrome, AML, or both.

Physical

The physical examination often reveals the degree of cytopenia (eg, with symptoms of pallor, bruising, petechiae). Splenomegaly and hepatomegaly are more common in childhood myelodysplasia syndrome and are predominate in JMML. A pathognomonic erythematous maculopapular rash is seen in one third of patients with JMML. Congenital anomalies and syndromic features are significant because of the association of myelodysplasia syndrome with several constitutional disorders, as described in Causes.

Causes

About 25% of children with myelodysplasia syndrome have an associated syndrome or congenital abnormality; these are uncommon in adults. Known inherited predispositions to the development of myelodysplasia syndrome include NF type 1 (NF-1), Fanconi anemia, severe congenital neutropenia (Kostmann syndrome), Down syndrome, Noonan syndrome, Shwachman-Diamond disease, Diamond-Blackfan anemia, and Dubowitz syndrome. Bloom syndrome, Poland syndrome, and ataxia telangiectasia have also been associated with preleukemia. 

The most recent pediatric classification systems for myelodysplasia syndrome have designated Down syndrome–related diseases (eg, transient myeloproliferative disorder, myeloid leukemia of Down syndrome) as unique and separate from myelodysplasia syndrome classification in other children.10  This is based on the unique mutations, molecular phenotype, and therapy response seen in this population.

Treatment-related myelodysplasia syndrome following cytotoxic chemotherapy is of more concern in the pediatric population as more childhood malignancies are cured.11 The most common association is with prior alkylator therapy, with or without concomitant radiation. The risk of myelodysplasia syndrome peaks 5-7 years after alkylator treatment and is related to cumulative dose. A strong association with monosomy 7 or del7q is recognized.

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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