Page 1290 - Clinical Small Animal Internal Medicine

1228 Section 11 Oncologic Disease

occurs. If clinical signs are present, they are often non­ Signalment
VetBooks.ir specific and may include lethargy, inappetence, organo­ and cats with no breed or sex predilection.
Polycythemia vera generally affects middle‐aged dogs
megaly, pale mucous membranes, and hemorrhage
caused by severe thrombocytopenia.
History and Clinical Signs
Diagnosis The majority of clinical signs occur secondary to hyper­
At diagnosis, the peripheral white blood cell count viscosity syndrome which is the sludging of blood due to
(WBC) count is commonly >100 000/μL. Neutrophils increased red blood cell mass. These signs may include
and neutrophilic precursors accumulate in bone mar­ hemorrhage, exercise intolerance, neurologic signs such
row, peripheral blood and other organs such as the as seizures or ataxia, splenomegaly, hyperemic mucous
spleen, liver, and lymph nodes. Eosinophils and baso­ membranes, injected sclera/retinal vessels, and weak­
phils may also be increased. CML must be distinguished ness. Cardiac or renal disease may also occur.
from a leukemoid reaction caused by inflammation,
immune‐mediated diseases, and/or a paraneoplastic Diagnosis
syndrome. Staging tests such as three‐view thoracic radi­ Recommended diagnostic tests to rule out relative or
ographs, abdominal ultrasound, and bone marrow cytol­ secondary polycythemia include thoracic radiographs,
ogy can be helpful in making this distinction. Biopsy of abdominal ultrasound, bone marrow aspiration, arterial
the liver or spleen may also be helpful in distinguishing blood gas measurements, and serum EP levels if possible.
CML from a leukemoid reaction due to its invasiveness. The diagnosis of PV is made by the demonstration of sig­
nificant erythrocytosis (hematocrit of 60–75%) with
Therapy normal to decreased serum EP levels. Bone marrow
Treatment of CML consists of the chemotherapy agent cytology in PV is consistent with erythroid hyperplasia
hydroxyurea at 20–25 mg/kg PO twice daily until the leu­ with normal patterns of maturation.
kocyte count drops to 15 000–20 000 cells/μL. The dos­
age of hydroxyurea can then be reduced by 50% on a Therapy
daily basis or to 50 mg/kg given biweekly or triweekly. Treatment of PV consists of decreasing the red blood cell
(RBC) volume and, ideally, suppression of erythroid pro­
Prognosis duction in the bone marrow. Phlebotomy with reinfusion
Although responders can be managed for several months of the patient’s plasma after removal of the RBCs or
with chemotherapy, most CML patients will enter a ter­ administering colloid and crystalloid solutions to replace
minal phase of their disease. HSCT offers the only pos­ lost electrolytes is recommended. The PCV should be
sibility of cure for dogs but may not be feasible or reduced to 50–60% or by one‐sixth of its starting value
practical. Death is either due to infection or hemorrhage (15–20 mL/kg body weight can be removed at one time).
caused by neutrophil dysfunction and thrombocytopenia The drug of choice to suppress erythroid production is
or secondary to a “blast crisis.” Response rates in patients hydroxyurea which works by inhibiting DNA synthesis.
in a blast crisis are low and the prognosis is very poor. Hydroxyurea is instituted at 20–25 mg/kg PO given twice
It is unknown whether the subset of canine CML patients daily in dogs (10–15 mg/kg in cats orally once daily).
that have a BCR‐ABL chromosome will respond to Once the hematocrit is below 60%, hydroxyurea is main­
BCR‐ABL kinase inhibitors which have become the tained at every other day dosing with the goal of main­
standard of care for human CML patients. taining a normal or close to normal packed cell volume
(PCV).
Polycythemia Vera
Etiology/Pathophysiology Prognosis
Polycythemia vera (PV) is a clonal disorder of erythroid The prognosis of PV is good with a high response rate
precursors in the bone marrow, which leads to the over­ and survival times of longer than a year for responders.
production of red blood cells independent of erythropoi­
etin. PV is rare in the dog and must be differentiated Basophilic and Eosinophilic Leukemia
from more common causes of polycythemia such as rela­ and Essential Thrombocythemia
tive polycythemia which is a result of hemoconcentra­ Etiology/Pathophysiology
tion or secondary polycythemia which is driven by Basophilic leukemia has rarely been reported in dogs and
erythropoietin. Conditions associated with secondary is diagnosed by an increased WBC count with a high
polycythemia include chronic pulmonary disease, con­ proportion of basophils in bone marrow and/or periph­
gestive heart failure, renal disease, renal neoplasia, and/ eral blood. The etiology is unknown. It is unclear whether
or right‐to‐left cardiac shunts. dogs and cats develop eosinophilic leukemia. At this