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  • Author or Editor: R. C. Straw x
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Summary

Of 82 dogs with thyroid carcinoma seen between January 1981 and October 1989, 20 had freely movable tumors without evidence of metastasis and were treated with surgical excision alone. Uncensored mean and median survival times for these 20 dogs were both 20.5 months. Kaplan-Meier survival analysis, which censors for nontumor-related deaths and dogs lost to follow-up, indicated that median survival time was greater than 36 months. Seven dogs died of tumor-related causes: 2 died because of metastasis or local recurrence of the tumor, 5 died of treatment-related complications (eg, laryngeal paralysis, hypocalcemia, tracheostomy complications). Eight dogs died of unrelated causes; 1 dog was lost to follow-up at 26 months after surgery; 3 dogs were alive 19, 24, and 26 months after surgery. Cause of death could not be determined in the remaining dog. Long-term survival is possible following surgical removal of mobile thyroid carcinomas in dogs.

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in Journal of the American Veterinary Medical Association

Summary

One hundred twenty-nine dogs with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of the new dihydroxyquinone derivative of anthracene, mitoxantrone, which was administered iv at 21-day intervals at dosages ranging from 2.5 to 5 mg/m2 body surface area. Each dog was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the dog died, whichever came first. The number of dogs in each evaluation period were as follows: 1 dose (n = 129), 2 doses (n = 82), 3 doses (n = 43), 4 doses (n = 26), 5 doses (n = 19), 6 doses (n = 9), 7 doses (n = 6), 8 doses (n = 5), 9 doses (n = 3), and 10 doses (n = 1). The most common signs of toxicosis were vomiting, diarrhea, anorexia, and sepsis secondary to myelosuppression. None of the dogs died of complications resulting from mitoxantrone treatment. Dogs with signs of toxicosis during the 21-day interval from administration of the first dose of mitoxantrone were 95 times (P = 0.003) more likely to develop signs of toxicosis during the 21-day interval from the second dose of mitoxantrone. Similarly, dogs that developed signs of toxicosis during the 21-day interval from the administration of the second dose were 34 times (P < 0.001) more likely to develop signs of toxicosis during the 21-day interval from the administration of the third dose. With each 1 mg/m2 increase in mitoxantrone, the odds of developing signs of toxicosis increased by 5.9 fold (P < 0.001). The performance status (modified Karnofsky performance scheme) of each dog was not adversely affected to a significant extent by mitoxantrone-induced toxicosis until the fifth dose (P = 0.0008). Cardiac toxicosis was not detected. Mitoxantrone was also administered iv to 4 clinically normal dogs, at a dosage of 5 mg/m2 of body surface area, a decrease in the neutrophil count was seen, with the nadir occurring on day 10 (mean ± sem: 1,159 ± 253 cells/μl; range, 480 to 1,680 cells/μl). Tumor-bearing dogs did not seem to have the same degree of myelosuppression (mean ± sem, 6,263 ± 1,230 cells/μl; range, 228 to 18,600 cells/μl).

Free access
in Journal of the American Veterinary Medical Association