Page 1288 - Clinical Small Animal Internal Medicine

1226 Section 11 Oncologic Disease

an arduous process due to the large number and mor­
Box 133.1 Classification of leukemias in animals
VetBooks.ir as proposed by the Animal Leukemia Study Group phologic similarities of chromosomes and their resist­
ance to banding. Recently, however, advancements in
Lymphoid leukemias
molecular cytogenetic analysis have aided in the discov­
ery of canine chromosomal abnormalities that are simi­
Chronic lymphocytic leukemia (CLL) lar to human AML which may serve not only as diagnostic
Acute lymphoblastic leukemia (ALL)
and prognostic factors but also as therapeutic targets.
Myeloid neoplasia
Epidemiology
Acute myeloid leukemias (AML) A lack of veterinary studies examining myeloid neoplasms
Acute myeloblastic leukemia with minimal differentia- has led to a deficiency of uniform diagnostic criteria,
tion (LMA‐M0) nomenclature, and ultimately accurate diagnosis. Because
Acute myeloblastic leukemia without differentiation of this, correct information regarding incidence and other
(LMA‐M1) epidemiologic information cannot be verified until a
Acute myeloblastic leukemia with maturation (LMA‐M2) more uniform classification system is standardized.
Acute promyelocytic leukemia (LMA‐M3) (not recog-
nized in animals) Signalment
Acute myelomonocytic leukemia (LMA‐M4) Acute myeloid leukemia is rare with a variable patient
Acute monocytic leukemia (LMA‐M5) age at diagnosis. Males are more commonly affected
Acute erythroleukemia (LMA‐M6) than females and large‐breed dogs seem to be predis­
Acute erythroleukemia with erythroid predominance posed. Retrospective studies suggest an increased inci­
(LMA‐M6Er) dence in German shepherds, golden retrievers, and
Megakaryoblastic leukemia (LMA‐M7) Labrador retrievers. Small‐breed dogs have been
represented in single‐case reports. The majority of feline
Chronic myeloid leukemia (CML) AML patients are FeLV positive.
Chronic myelomonocytic leukemia History and Clinical Signs
Chronic monocytic leukemia The clinical course of AML is rapid. Common clinical
Eosinophilic leukemia signs include extreme lethargy, secondary infection, and
Basophilic leukemia hemorrhage. Hematologic abnormalities can be severe
Polycythemia vera with a WBC count as high as 150,000 μ/L. Anemia, neu­
Essential thrombocythemia
tropenia, and thrombocytopenia are also common.
Spleen, lymph nodes, and liver are frequently involved
Myelodysplastic syndromes (MDSs)
but other sites such as heart, kidney or central nervous
Myelodysplastic syndrome with excessive blasts (MDS‐EB) system (CNS) may be infiltrated as well.
Myelodysplastic syndrome with refractory cytopenia
(MDS‐RC) Diagnosis
Myelodysplastic syndrome with erythroid predominance It is important to understand that AML is a disorder
(MDS‐ER) resulting from uncontrolled proliferation or decreased
apoptosis of cells incapable of maturation, leading to the
accumulation of poorly differentiated or “blast” cells.
This is different from other myeloid neoplasms which
code of M‐#, with the M standing for myeloid. The most result from unregulated proliferation of cells that exhibit
commonly reported forms in the dog are acute myelo­ incomplete/defective maturation, leading to the accu­
blastic leukemia (M1 and M2) and acute myelomo­ mulation of well differentiated cells. The diagnosis of
nocytic leukemia (M4). Monocytic leukemia (M5), AML is generally made by evaluation of peripheral blood
erythroleukemia (M6), and megakaryoblastic leukemia or bone marrow. Confirmation of AML should include
(M7) are also recognized in dogs but promyelocytic leu­ consistent hematologic and morphologic criteria,
kemia (M3) has not been reported. positive staining for myeloperoxidase which is a heme
In dogs, the etiology of AML along with the other mye­ protein synthesized during myeloid differentiation that
loid neoplasms is unknown. Genetic and environmental constitutes the major component of neutrophil azuro­
factors such as exposure to radiation, drugs or toxic philic granules, a consistent pattern of beta‐2 integrin
chemicals are thought to play a role. Defining genetic expression and absence of lymphoid antigens by immu­
factors in dogs is difficult because canine karyotyping is nocytochemistry or flow cytometry (Figure 133.3).