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A 5-year-old, 27 kg, castrated male American Pit Bull Terrier was referred to the internal medicine service at Louisiana State University, School of Veterinary Medicine for further evaluation and treatment of acute tumor lysis syndrome (ATLS). Four weeks before presentation, the owner noted a submandibular swelling. At this time, the dog was examined at a local emergency clinic where it received a steroid injection. The dog improved clinically, but the swelling reoccurred approximately 2 weeks later. At this time, the dog also developed anorexia and hematochezia. Two weeks before referral to Louisiana State University, the dog was examined and found to have generalized lymphadenopathy and melena. A CBC disclosed a leukocytosis with a total white blood cell count (WBC) of 26,960/mL (reference range, 5,500-16,900/mL), a lymphocyte count of 15,030/mL (reference range, 500-4,900/mL), a normal hematocrit of 42% (reference range, 37-55%), and thrombocytopenia with a platelet count of 66,000/mL (reference range, 175,000-500,000/mL). Neither a manual platelet count nor a microscopic examination of a blood smear was performed. Serum biochemistry results were unremarkable. Fine needle aspirates of the submandibular, prescapular, and popliteal lymph nodes were performed and submitted to a veterinary clinical pathology laboratory.a Cytology results were consistent with a diagnosis of lymphoma. The dog was referred to a private practice veterinary oncologist for additional diagnostics and treatment.One day before to referral to Louisiana State University, the patient presented to the oncologist. Physical examination findings were unremarkable with the exception of generalized lymphadenopathy. A repeated CBC before chemotherapy disclosed persistent leukocytosis predominantly composed of lymphocytes (WBC 36,680/ mL [reference range, 5,500-16,9000/mL]; lymphocyte count 12,730/mL [reference range, 500-4,900/mL]) regenerative anemia also was present with a hematocrit of 27 and 4.7% reticulocytes. Platelet count had normalized at 264,000/mL (reference range, 175,000-500,000/mL). Serum biochemistry analysis was unremarkable. No additional staging was performed. The dog was started on a L-asparaginase, cyclophosphamide, doxorubicin, vincristine, and prednisone (L-CHOP)-based protocol. The dog was premedicated with 25 mg of diphenhydramine, and induced with L-asparaginase 10,000 IU IM and prednisone 50 mg PO. Approximately 8 hours after induction, it became listless and started vomiting. Antiemetics (maropitant citrate 27 mg SC and dolasetron 17 mg IV) were administered. The patient failed to improve and repeated serum biochemistry, performed approximately 22 hours after administration of chemotherapy, disclosed moderate azotemia (BUN concentration 104 mg/dL, serum creatinine concentration 3.8 mg/dL), severe hyperphosphotemia (24 mg/dL), severe hyperkalemia (8.7 mEq/L), and hypocalcemia (6.3 mg/dL; reference range, 8.6-11.8 mg/dL). Results were confirmed by repeat analysis and a tentative diagnoses of acute kidney injury (AKI) and AT...
This prospective study was designed to determine the urinary concentrations of purine metabolites in healthy and diseased dogs. The goals were to test the hypothesis that urine concentrations of terminal purine metabolites will identify dogs with diseases that disturb purine degradation. Five hundred and sixty-three client-owned dogs admitted sequentially to the veterinary medical centre were included. Dogs were divided into groups on the basis of their disease. Urine concentrations of xanthine, uric acid, allantoin and creatinine were measured by high-pressure liquid chromatography. Xanthine and uric acid to creatinine ratios were significantly increased in dogs with chronic kidney disease (p = 0.01). The uric acid to creatinine ratio was significantly increased in dogs with cancer compared with clinically healthy dogs (p = 0.04), and significantly increased in dogs receiving chemotherapy for their disease (p < 0.01). Compared to clinically healthy dogs, xanthine and uric acid to creatinine ratios were significantly increased in dogs with hyperadrenocorticism (p < 0.01, and 0.04, respectively). Therefore, the results of this study found that the urinary concentrations of purine metabolites in dogs are significantly impacted by systemic disease. Cancer, chronic kidney disease, and hyperadrenocorticism are associated with altered concentrations of urinary purine metabolites in dogs.
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