eMedicine Specialties > Hematology > Stem Cells and Disorders

Agnogenic Myeloid Metaplasia With Myelofibrosis

Author: Asheesh Lal, MBBS, MD, Physician, Department of Internal Medicine, Lexington Medical Center
Contributor Information and Disclosures

Updated: Oct 8, 2008

Introduction

Background

Agnogenic myeloid metaplasia (AMM), first described by Heuck in 1879, is a clonal disorder arising from the neoplastic transformation of early hematopoietic stem cells.1,2,3,4 Agnogenic myeloid metaplasia is categorized as a chronic myeloproliferative disorder, along with chronic myelogenous leukemia (CML), polycythemia vera, and essential thrombocytosis.5 The disorder is characterized by anemia, bone marrow fibrosis, extramedullary hematopoiesis, leukoerythroblastosis, teardrop-shaped red blood cells (RBCs) in peripheral blood, and hepatosplenomegaly.

For excellent patient education resources, visit eMedicine's Blood and Lymphatic System Center and Cancer and Tumors Center. Also, see eMedicine's patient education article Anemia.

Pathophysiology

In patients with agnogenic myeloid metaplasia, the hematopoietic system is most affected. Other organ systems may be involved by extramedullary hematopoiesis.

Clonality studies in patients with agnogenic myeloid metaplasia demonstrate that myeloid cells arise from clonal stem cells; however, bone marrow fibroblasts and, sometimes, T cells are polyclonal. The cause of the excessive marrow fibrosis observed in agnogenic myeloid metaplasia remains unclear. Platelets, megakaryocytes, and monocytes are thought to secrete several cytokines, such as transforming growth factor beta (TGF-β), platelet-derived growth factor (PDGF), interleukin-1 (IL-1), epidermal growth factor (EGF), and basic fibroblast growth factor (bFGF), which may result in fibroblast formation and extracellular matrix proliferation. In addition, endothelial proliferation and growth of capillary blood vessels in the bone marrow are observed and may be a result of TGF-β and bFGF production.

Neoangiogenesis is a hallmark feature of chronic myeloproliferative disorders. Approximately 70% of patients with agnogenic myeloid metaplasia have substantial increases in bone marrow microvessel density. Neoangiogenesis in agnogenic myeloid metaplasia is noted in both medullary and extramedullary hematopoiesis. Increased serum vascular endothelial growth factor levels have been postulated as the underlying mechanism for increased angiogenesis.

Frequency

United States

Agnogenic myeloid metaplasia is an uncommon disease, with an annual incidence of approximately 0.5-1.5 cases per 100,000 individuals.

International

The worldwide incidence of agnogenic myeloid metaplasia is unknown.

Mortality/Morbidity

The main causes of death in patients with agnogenic myeloid metaplasia are infection, hemorrhage, cardiac failure, postsplenectomy complications, and transformation to acute leukemia.

  • Leukemic transformation occurs in approximately 20% of patients with agnogenic myeloid metaplasia within the first 10 years. Renal failure, hepatic failure, and thrombosis have also been reported as causes of death.
  • The median length of survival is approximately 3.5-5.5 years from diagnosis, with a range of 1-15 years.
  • The 5-year survival rate is approximately half that expected for age- and sex-matched controls. Less than 20% of patients are expected to be alive at 10 years.6

Race

  • Agnogenic myeloid metaplasia appears to be more common in white people than in individuals of other races.
  • An increased prevalence rate of agnogenic myeloid metaplasia has been noted in Ashkenazi Jews.

Sex

A slight male preponderance appears to exist for agnogenic myeloid metaplasia; however, in younger children, girls are affected twice as frequently as boys.

Age

  • Agnogenic myeloid metaplasia characteristically occurs in individuals older than 50 years. The median age at diagnosis is approximately 65 years.
  • Agnogenic myeloid metaplasia has been reported in persons in all phases of life, from neonates to octogenarians.
  • Approximately 22% of affected patients are younger than 56 years. Agnogenic myeloid metaplasia usually occurs in children in the first 3 years of life.

Clinical

History

One fourth of patients with agnogenic myeloid metaplasia are asymptomatic, and the diagnosis is made as a result of detecting splenomegaly or checking blood cell counts for an unrelated cause. Symptoms may occur as a result of anemia, splenomegaly, hypermetabolic states, extramedullary hematopoiesis, bleeding, bone changes, portal hypertension, and immune abnormalities.

  • Anemia may occur as a result of ineffective erythropoiesis, erythroid hypoplasia, and hypersplenism. Anemia may cause easy fatigability, weakness, dyspnea, and palpitations.
  • Splenomegaly may result in early satiety and left upper quadrant discomfort. Splenic infarcts, perisplenitis, or subcapsular hematoma may occur, causing severe left upper quadrant or left shoulder pain. Occasionally, patients may have diarrhea related to pressure on the colon.
  • A hypermetabolic state occurs and can result in weight loss, night sweats, and low-grade fever. Gout and urate kidney stones may develop.
  • Bleeding is observed in one fourth of patients with agnogenic myeloid metaplasia and varies in severity from insignificant cutaneous petechiae to severe, life-threatening gastrointestinal (GI) tract bleeding. Platelet dysfunction, acquired factor V deficiency, thrombocytopenia, disseminated intravascular coagulation (DIC), esophageal varices, and peptic ulcer disease may occur, contributing to bleeding.
  • Extramedullary hematopoiesis may cause symptoms, depending on the organ or site of involvement. The condition may result in GI tract hemorrhage, spinal cord compression, focal seizures, symptoms related to brain tumors, ascites, hematuria, pericardial effusion, pleural effusion, hemoptysis, and respiratory failure.
  • Portal hypertension may occur as a result of markedly increased splenoportal blood flow and decreased hepatic vascular compliance. Ascites, esophageal and gastric varices, GI tract bleeding, and hepatic encephalopathy may occur. Hepatic or portal vein thrombosis may also arise as complications.
  • Patients with agnogenic myeloid metaplasia develop osteosclerosis. This may cause severe joint and bone pain.
  • One half of patients with agnogenic myeloid metaplasia have abnormalities of humoral immunity. A variety of autoantibodies and circulating immune complexes may be detected, and amyloidosis may develop. Infections, commonly pneumonia, may occur as a result of immune deficiency.

Physical

  • Splenomegaly is the most common finding in patients with agnogenic myeloid metaplasia, and it is present in approximately 90% of patients. Spleen size may vary from barely palpable to massive (observed in 35% of patients).
  • Hepatomegaly is also observed in 60-70% of patients with agnogenic myeloid metaplasia.
  • Pallor is observed in 60% of patients.
  • Other physical findings include petechiae and ecchymosis (20%), lymphadenopathy (10-20%), signs of portal hypertension (10-18%), and gout (6%).

Causes

No specific risk factors can be identified in most patients with agnogenic myeloid metaplasia, although exposure to radiation, Thorotrast contrast agents, and industrial solvents (eg, benzene, toluene) have been associated with an increased risk.7,8,9,10

More on Agnogenic Myeloid Metaplasia With Myelofibrosis

Overview: Agnogenic Myeloid Metaplasia With Myelofibrosis
Differential Diagnoses & Workup: Agnogenic Myeloid Metaplasia With Myelofibrosis
Treatment & Medication: Agnogenic Myeloid Metaplasia With Myelofibrosis
Follow-up: Agnogenic Myeloid Metaplasia With Myelofibrosis
Multimedia: Agnogenic Myeloid Metaplasia With Myelofibrosis
References
Further Reading
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References

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Further Reading

Related eMedicine Topics

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Keywords

agnogenic myeloid metaplasia with myelofibrosis, AMM, agnogenic myeloid metaplasia, myeloid metaplasia, idiopathic myelofibrosis, aleukemic myelosis, nonleukemic myelosis, myelosclerosis, leukoerythroblastic anemia with diffuse osteosclerosis, megakaryocytic splenomegaly, anemia, bone marrow fibrosis, extramedullary hematopoiesis, leukoerythroblastosis, hepatosplenomegaly, hematopoietic system, chronic myeloid leukemia, CML, chronic myelogenous leukemia, chronic myelocytic leukemia, polycythemia vera, essential thrombocytosis

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Contributor Information and Disclosures

Author

Asheesh Lal, MBBS, MD, Physician, Department of Internal Medicine, Lexington Medical Center
Asheesh Lal, MBBS, MD is a member of the following medical societies: American Society of Clinical Oncology and American Society of Hematology
Disclosure: Nothing to disclose.

Medical Editor

Karen Seiter, MD, Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College
Karen Seiter, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, and American Society of Hematology
Disclosure: Novartis Honoraria Speaking and teaching; Schering Honoraria Speaking and teaching; Cephalon Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Troy H Guthrie, Jr, MD, Director of Cancer Institute, Baptist Medical Center
Troy H Guthrie, Jr, MD is a member of the following medical societies: American Federation for Medical Research, American Medical Association, American Society of Hematology, Florida Medical Association, Medical Association of Georgia, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Rajalaxmi McKenna, MD, FACP, Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Emmanuel C Besa, MD, Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Thomas Jefferson University
Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, and New York Academy of Sciences
Disclosure: Nothing to disclose.

 
 
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