Absolute polycythemia is an infrequent clinical finding characterized by an increased mature erythrocyte count, hematocrit, and hemoglobin concentrations. It is classified as primary or secondary. Primary polycythemia, or polycythemia vera, is a rare, idiopathic myeloproliferative disorder manifested by abnormal proliferation of the hematopoietic bone marrow elements, with an absolute increase in red blood cell mass and total blood volume in the absence of increased erythropoietin levels. Secondary polycythemias are further classified as either appropriate or inappropriate depending on their etiology, and arise due to increased circulating levels of erythropoietin or erythropoietin-like substances, which cause an increase in circulating mature erythrocytes.1,3,4
Polycythemia was diagnosed in a 13-yr-old female black lemur (Eulemur macaco macaco) that was examined for progressive lethargy, anorexia and visible weight loss. Further diagnostic tests, utilizing established algorithms for differentiating between polycythemia vera and secondary polycythemias, implicated a membranous glomerulopathy as the probable cause for inappropriate secondary polycythemia.2,3 Intermittent phlebotomies based on the rise in hematocrit were initially used to control the disease. Aspirin was administered orally at 10 mg/kg three times weekly for the prevention of thrombotic events that are often associated with polycythemia. When monthly phlebotomies failed to prevent the hematocrit from rising above 60 L/L, alternative therapeutic options were explored. Hydroxyurea (Hydrea®, Bristol-Myers Squibb Company, New York, New York) is a non-alkylating, reversible myelosuppressive agent that specifically inhibits cells in the synthetic phase of the cell cycle. This drug was initiated at a dosage of 50 mg/kg p.o. once weekly in addition to monthly phlebotomy. The anabolic steroid stanozolol (Winstrol®, Abbott Laboratories, North Chicago, Illinois) was later added to the treatment regime at 2 mg p.o. daily due to progressive weight loss. The hydroxyurea treatment was also increased to twice weekly at this time. Additional medical complications, including hypoalbuminemia and hypoferremia, which can be associated with the long-term medical management of polycythemia were addressed in this lemur.
The lemur has been on therapy with hydroxyurea for over 14 mo, and the hematocrit has been maintained below 60 L/L. No drug-specific adverse reactions have been observed. To the authors’ knowledge this is the first report of hydroxyurea usage in a nonhuman primate species. In this case, we conclude that hydroxyurea in combination with phlebotomy is an effective treatment modality for controlling the clinical and peripheral blood abnormalities associated with polycythemia.
The authors gratefully acknowledge the invaluable assistance of the veterinary technicians Virginia Crossett and Judy Tucker, the veterinary and veterinary technician preceptors, and the animal care staff at the Louisville Zoo. In addition, we thank Dr. Alan Hammer for his expertise, and his staff at Kentucky Veterinary Specialists in Louisville, Kentucky.
1. Brain, M.C. and S. Couban. 1995. Polycythemia. In: Brain, M.C. and P.P. Carbone (ed.). Current Therapy in Hematology-Oncology. Mosby-Year Book, Inc., St. Louis. 94–99.
2. Harmening, D.M. 1997. The Polycythemias. In: Clinical Hematology and Fundamentals of Hemostasis, 3rd ed. F.A. Davis Co., Philadelphia. 386–395.
3. Wasserman, L.R., P.L. Berk and, and N.I. Berlin (eds.). 1995. Polycythemia Vera and the Myeloproliferative Disorders. W.B. Saunders Co., Philadelphia.
4. Withrow S.J. and E.G. MacEwen. 1996. Small Animal Clinical Oncology, 2nd ed. W.B. Saunders Co., Philadelphia.