Objective—To determine the maximum tolerated dose (MTD) of cisplatin administered with piroxicam, the antitumor activity and toxicity of cisplatin combined with piroxicam in dogs with oral malignant melanoma (OMM) and oral squamous cell carcinoma (SCC), and the effects of piroxicam on the pharmacokinetics of cisplatin in dogs with tumors. Design—Prospective nonrandomized clinical trial. Animals—25 dogs. Procedure—Dogs were treated with a combination of cisplatin (escalating dose with 6 hours of diuresis with saline [0.9% NaCl] solution) and piroxicam (0.3 mg/kg [0.14 mg/lb], PO, q 24 h). The initial cisplatin dose (50 mg/m2) was increased by 5 mg/m2 until the MTD was reached. Tumor stage and size were determined at 6-week intervals during treatment. The pharmacokinetics of cisplatin were determined in dogs receiving a combination of cisplatin and piroxicam during the clinical trial and dogs that were treated with cisplatin alone. Results—11 dogs with OMM and 9 dogs with SCC were included in the clinical trial. The MTD of cisplatin when administered in combination with piroxicam was 50 mg/m2. Tumor remission occurred in 5 of 9 dogs with SCC and 2 of 11 dogs with OMM. The most common abnormality observed was renal toxicosis. Clearance of cisplatin in dogs that were treated with cisplatin alone was not significantly different from that in dogs treated with a combination of cisplatin and piroxicam. Conclusions and Clinical Relevance—Cisplatin administered in combination with piroxicam had antitumor activity against OMM and SCC. The level of toxicity was acceptable, although renal function must be monitored carefully. ( J Am Vet Med Assoc 2004;224:388–394)

Invasive transitional cell carcinoma (TCC) of the urinary bladder responds poorly to medical therapy. Combining platinum chemotherapy with a cyclooxygenase (cox) inhibitor has shown promise against canine TCC, where the disease closely mimics the human condition. A phase II clinical trial of carboplatin combined with the cox inhibitor, piroxicam, was performed in 31 dogs with naturally occurring, histopathologically confirmed, measurable TCC. Complete tumour staging was performed before and at 6-week intervals during therapy. Tumour responses in 29 dogs included 11 partial remissions, 13 stable disease and five progressive disease. Two of the 31 dogs were withdrawn prior to the re-staging of the tumour. Gastrointestinal toxicity was observed in 23 dogs. Hematologic toxicity was noted in 11 dogs. The median survival was 161 days from first carboplatin treatment to death. In conclusion, carboplatin/piroxicam induced remission in 40% of dogs providing evidence that a cox inhibitor enhances the antitumour activity of carboplatin. The frequent toxicity and limited survival, however, do not support the use of this specific protocol against TCC.

OBJECTIVE-To evaluate the antitumor activity and toxic effects of deracoxib, a selective cyclooxygenase-2 inhibitor, in dogs with transitional cell carcinoma (TCC) of the urinary bladder. DESIGN-Clinical trial. Animals-26 client-owned dogs with naturally occurring, histologically confirmed, measurableTCC of the urinary bladder. PROCEDURES-Dogs were treated PO with deracoxib at a dosage of 3 mg/kg/d (1.36 mg/lb/d) as a single-agent treatment for TCC. Tumor response was assessed via radiography, abdominal ultrasonography, and ultrasonographic mapping of urinary bladder masses. Toxic effects of deracoxib administration in dogs were assessed through clinical observations and hematologic and biochemical analyses. RESULTS-Of 24 dogs for which tumor response was assessed, 4 (17%) had partial remission, 17 (71%) had stable disease, and 3 (13%) had progressive disease; initial response could not be assessed in 2 of 26 dogs. The median survival time was 323 days. Median time to progressive disease was 133 days. Renal, hepatic, and gastrointestinal abnormalities attributed to deracoxib administration were noted in 4% (1/26), 4% (1/26), and 19% (5/26) of dogs, respectively. CONCLUSIONS AND CLINICAL RELEVANCE-Results indicated that deracoxib was generally well tolerated by dogs and had antitumor activity against TCC.

Dogs with histologically confirmed lymphoma were treated with a 14-week induction chemotherapy protocol that included dexamethasone. A phase II clinical trial was done using a standard two-stage design. Complete remission occurred in 21 (88%) dogs, with a median initial progression-free interval of 186 days. Toxicity was mild and self-limiting in the majority of dogs.

A 25.3 kg, 4-year-old spayed female Labrador Retriever was referred to the Purdue University Veterinary Teaching Hospital (PUVTH) emergency service for progressively worsening inappetance, lethargy, polyuria, and polydipsia for a duration of 1 week. Intermittent regurgitation and diarrhea began the day before presentation. The referring veterinarian treated the dog with fluids IV and antibiotics without response.The dog was alert and responsive at presentation. Physical abnormalities included a body condition score of 2/5, pallor, tacky mucous membranes, bilateral enlargement of popliteal and mandibular lymph nodes, splenomegaly, and a grade 2/5 lameness of the right pelvic limb. Body temperature, pulse rate, and respiration rate were normal.A complete blood count (CBC) revealed hyperproteinemia (10.7 g/dL; reference range, 6.0-8.0 g/dL), and a moderate normocytic normochromic anemia (HCT, 26%; reference range, 37-55%). Marked rouleaux, rare immature lymphocytes, and lymphoblasts were apparent on the blood smear. These intermediatesized plasmacytoid cells had round nuclei with moderately coarse chromatin, occasional small nucleoli, and scant cytoplasm with occasional punctuate vacuoles. The immature lymphocytes suggested the presence of a lymphoid neoplasm. Platelet clumping prevented an automated count, but they appeared decreased on blood smear evaluation. Serum biochemistry revealed mild hypercalcemia (13.0 mg/dL; reference range 9.7-12.3 mg/ dL), hypernatremia (153 mg/dL; reference range 138-148 mg/dL), and hyperproteinemia (13.3 g/dL; reference range, 4.8-6.9 g/dL) characterized by hyperglobulinemia (10.9 g/dL; reference range, 1.7-3.8 g/dL). Urinalysis revealed a specific gravity of 1.012 with proteinuria (41,000 mg/dL). The dog was admitted to the hospital and treated with lactated Ringer's solution and doxycycline a (5 mg/kg IV q24h). The following day, a CBC revealed persistent hyperproteinemia (10.3 g/dL), a severe nonregenerative anemia (HCT, 18%; reticulocytes, 7,890/mL; o 60,000/mL although this ''nonregenerative'' refers to the reference range, it is a bit confusing) neutropenia (2,370/mL; reference range, 3,000-12,000/mL), and thrombocytopenia (51,900/mL; reference range 200,000-500,000/mL). Rouleaux formation, immature lymphoid cells, and lymphoblasts were repeatable findings. Serum biochemistry revealed a decreasing hypercalcemia (12.6 mg/dL) and persistent hypernatremia (153 mmol/L). Reductions were noted in hyperproteinemia (12.0 g/dL) and hyperglobulinemia (9.0 g/dL)Thoracic radiographs showed diffuse interstitial pulmonary infiltrates throughout all lung fields. Abdominal radiographs showed marked splenomegaly and remodeling of the right femoral head and neck, consistent with arthritis. Abdominal ultrasonography revealed an enlarged spleen with a coarse echotexture, and multiple enlarged mesenteric lymph nodes. Fundoscopic examination revealed tortuous vessels with retinal hemorrhages bilaterally, and evidence of retinal detachment in the right eye.Aspiration cytology of the popliteal lymph ...

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