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  • Author or Editor: Stephen W. Atwater x
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Summary

Medical records of 23 dogs in which thymoma was diagnosed between Jan 1, 1980 and Dec 31, 1991 were reviewed. All thymomas were located in the cranial mediastinum. Eleven dogs had mega-esophagus, and myasthenia gravis was confirmed in 7 of these 11. One dog developed clinical signs of myasthenia gravis after removal of the thymoma. Concurrent, nonthymic neoplasms were found in 5 dogs, and 2 had hypercalcemia. Three dogs developed third-degree atrioventricular heart block, 1 of which had generalized myositis involving the cardiac muscle.

None of the dogs had evidence of distant metastasis. Histologically, the predominant tumor types were differentiated epithelial type (9/23) and lymphocyte-rich type (6/23). Clear cells (large cells with nonstaining cytoplasm) comprised ≥ 50% of the cell population in tumors from 5 dogs. Mast cells were detected histologically in 85% of the thymomas evaluated. Sixteen dogs were treated, and in 15 of these, surgery was the primary means of treatment. Six of the 9 dogs with megaesophagus that underwent surgery died or were euthanized within 1 week of diagnosis; whereas only 1 of the 4 dogs without megaesophagus that underwent surgery died within 1 week of diagnosis. Two dogs underwent surgery and received adjuvant chemotherapy. One dog died of complications associated with chemotherapy. One dog was treated with chemotherapy alone and survived 14 months. Seven dogs did not undergo treatment; 4 of these were euthanatized immediately after the mass was first discovered.

By means of univariate analysis, age (≤ 8 years old vs > 8 years old), megaesophagus (present vs not present), and histologic type were found to be significantly (P ≤ 0.05) associated with survival time. Only megaesophagus was found to be significantly associated with survival time by multivariate analysis. Dogs with megaesophagus had a Kaplan-Meier median survival time of 4 days. Kaplan-Meier median survival time for dogs without megaesophagus could not be calculated, because most dogs died of causes unrelated to the thymoma and were censored. Kaplan-Meier 1-year survival rate was 83% for dogs without megaesophagus.

Free access
in Journal of the American Veterinary Medical Association

Summary

Forty-four dogs with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of the chemotherapeutic agent mitoxantrone, when administered at dosages higher than what has been previously reported for use in dogs. After each dose was administered, dogs were evaluated for signs of toxicosis for 3 weeks or until the dog developed progressive disease, died, or was euthanatized. Forty dogs had been refractory to 1 or more treatment modalities (surgery, n = 26; chemotherapy other than mitoxantrone, n = 17; radiation, n = 2) prior to entering this study. Ten dogs were given mitoxantrone at a dosage of 5.5 mg/m2 of body surface, IV, every 3 weeks (39 total doses); 11 were given mitoxantrone at a dosage of 6.0 mg/m2, IV, every 3 weeks (26 total doses); and 23 were given mitoxantrone at a dosage of 6.5 mg/m2, IV, every 3 weeks (70 total doses).

The most common signs of toxicosis were vomiting, anorexia, diarrhea, lethargy, and sepsis secondary to myelosuppression. Two dogs, both of which received the highest dosage, died of complications attributable to mitoxantrone administration. The prevalence of toxicoses was not associated with age, breed, sex, tumor type, number of doses, or dosage. Dogs did develop myelosuppression 7 days after they were given mitoxantrone. Median neutrophil count for dogs that received mitoxantrone at a dosage of 6.5 mg/m2 was 2,800 cells/μl (range, 300 to 4,600 cells/μl); median neutrophil count for dogs that received mitoxantrone at a dosage of 6.0 mg/m2 was 3,800 cells/μl (range, 600 to 10,400 cells/μl); and median neutrophil count for dogs that received mitoxantrone at a dosage of 5.5 mg/m2 was 4,500 cells/μl (range, 1,700 to 16,100 cells/μl).

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

A study was undertaken to determine the toxic effects of cisplatin, an antineoplastic agent, when administered immediately after a 1-hour saline diuresis. Four treatments with cisplatin (70 mg/m2 of body surface, q 3 wk) were administered iv to 6 healthy dogs over a 20-minute period after 0.9% NaCl (saline) solution was administered iv for 1 hour at a volume of 132 ml (kg)0.75. Each dog vomited at least once within 8 hours after each treatment was administered. Clinical status, body weight, and food consumption were normal throughout the 12-week study for 5 of the 6 dogs. The sixth dog developed acute renal failure and became acutely blind and deaf within 3 days after the fourth treatment with cisplatin. Serum electrolyte, creatinine, and urea nitrogen values remained within established normal limits in all dogs immediately prior to each treatment, and in 5 of 6 dogs evaluated 3 weeks after the final treatment. The serum creatinine value (3.3 mg/dl) obtained from the Beagle euthanatized 2 weeks after the fourth treatment was above established normal values. Despite normalcy for all but 1 of the creatinine values, serum creatinine concentration obtained 3 weeks after the final treatment with cisplatin was significantly (P = 0.0001) higher than pretreatment values. When compared with data from all other evaluation periods, significant decreases in glomerular filtration rate, as determined by exogenous (P ≤ 0.0001) and endogenous (P ≤ 0.0001) creatinine clearance testing, were identified 3 weeks after the fourth treatment with cisplatin. Neutrophil counts decreased significantly below pretreatment values at the third (P = 0.009), fourth (P < 0.0001), and fifth (P < 0.0001) evaluation period. We concluded that cisplatin can be administered with biochemical evidence, but not necessarily clinical evidence, that renal dysfunction may develop after 4 treatments with cisplatin (70 mg/m2, iv) are administered to dogs, using a 1-hour diuresis protocol.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To examine the biological behavior of ulnar osteosarcoma and evaluate predictors of survival time in dogs.

Design—Retrospective case series.

Animals—30 dogs with primary ulnar osteosarcoma.

Procedures—Medical records were reviewed. Variables recorded and examined to identify predictors of survival time were signalment, tumor location in the ulna, tumor length, serum alkaline phosphatase activity, surgery type, completeness of excision, tumor stage, tumor grade, histologic subtype, development of metastases, and use of chemotherapy.

Results—30 cases were identified from 9 institutions. Eleven dogs were treated with partial ulnar ostectomy and 14 with amputation; in 5 dogs, a resection was not performed. Twenty-two dogs received chemotherapy. Median disease-free interval and survival time were 437 and 463 days, respectively. Negative prognostic factors for survival time determined via univariate analyses were histologic subtype and development of lung metastases. Telangiectatic or telangiectatic-mixed subtype (n = 5) was the only negative prognostic factor identified via multivariate analysis (median survival time, 208 days). Dogs with telangiectatic subtype were 6.99 times as likely to die of the disease.

Conclusions and Clinical Relevance—The prognosis for ulnar osteosarcoma in this population was no worse and may have been better than the prognosis for dogs with osteosarcoma involving other appendicular sites. Partial ulnar ostectomy was associated with a low complication rate and good to excellent function and did not compromise survival time. Telangiectatic or telangiectatic-mixed histologic subtype was a negative prognostic factor for survival time. The efficacy of chemotherapy requires further evaluation.

Full access
in Journal of the American Veterinary Medical Association

Summary:

Eighty-seven cats with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of mitoxantrone, a dihydroxyquinone derivative of anthracene, which was administered at 21-day intervals at dosages ranging from 2.5 to 6.5 mg/m2 of body surface, iv. Eleven of these cats were treated concurrently with radiation but were evaluated separately. Each cat was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the cat developed progressive disease, or until the cat's quality of life diminished to an unacceptable level as determined by the owner or attending veterinarian. Although the primary purpose of this study was to determine a clinically useful dosage and to characterize the toxicoses associated with mitoxantrone administration, each cat was monitored for response to treatment. Forty-nine cats had been refractory to 1 or more treatment modalities prior to inclusion in this study.

The most common signs of toxicosis after treatment with mitoxantrone were vomiting, anorexia, diarrhea, lethargy, sepsis secondary to myelosuppression, and seizures. Two cats died of complications that may have been attributed to mitoxantrone: 1 of cardiomyopathy and the other of pulmonary edema of an undetermined cause. Older cats were more likely to develop signs of toxicosis after the third or fourth mitoxantrone treatment than younger cats (P ≤ 0.05). Cats with signs of toxicosis during the 21-day interval after administration of the first dose of mitoxantrone were significantly (P ≤ 0.05) more likely to develop signs of toxicosis during the 21-day interval between the second and third doses of mitoxantrone. Similarly, cats that became toxic during the 21-day interval between the second and third doses were significantly (P ≤ 0.05) more likely to become toxic during the 21-day interval between the third and fourth doses. Controlling for age, breed, and dose of mitoxantrone, cats that became toxic after the first treatment were 2.4 times more likely to have poor performance status than the non toxic cats. Tumor-bearing cats had some degree of myelosuppression 7 days after they were given mitoxantrone at 6.5 mg/m2, iv (median neutrophil count, 2,440 cells/μl; range, 1,595 to 6,300 cells/μl).

Complete or partial remission (> 50% reduction volume reduction) was obtained in 18.4% (14/76) of cats given mitoxantrone alone. Remission was recorded in 17.6% (9/51) of cats with carcinoma, 11.8% (2/17) of the cats with lymphoma, and 37.5% (3/8) of the cats with sarcoma.

Because the cats with squamous cell carcinoma had a poor response to mitoxantrone, an additional 11 cats with squamous cell carcinoma were treated concurrently with radiation (44 to 65 Gy, 10 to 15 fractions) over a 3-week period beginning at the time the first dose of mitoxantrone (2.5 to 6 mg/m2) was given. None of these 11 cats had any signs of toxicosis attributable to mitoxantrone chemotherapy. Eight cats had a complete remission (median, 170 days; range, 28 to 485 days), and 1 had a partial remission that lasted 60 days.

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate the effectiveness of masitinib for the treatment of nonresectable mast cell tumors (MCTs) in dogs at 12 and 24 months after onset of treatment.

Animals—132 dogs with nonresectable grade 2 or 3 MCTs.

Procedures—Dogs received masitinib (12.5 mg/kg/d, PO; n = 106) or a placebo (26). After 6 months, treatment was extended with tumor assessments at 3-month intervals until detection of disease progression. Endpoints were tumor response and overall survival rate and time.

Results—In dogs with nonresectable MCTs, masitinib significantly improved survival rate, compared with results for the placebo, with 59 of 95 (62.1%) and 9 of 25 (36.0%) dogs alive at 12 months and 33 of 83 (39.8%) and 3 of 20 (15.0%) dogs alive at 24 months, respectively. Median overall survival time was 617 and 322 days, respectively. Tumor control at 6 months had a high predictive value for 24-month survival, with high specificity (88%) and sensitivity (76%), whereas short-term tumor response (within 6 weeks) had a poor predictive value. Complete responses at 24 months were observed in 6 of 67 (9.0%) dogs with nonresectable MCTs treated with masitinib.

Conclusions and Clinical Relevance—Masitinib significantly increased survival rates at 12 and 24 months in dogs with nonresectable MCTs. Control of disease at 6 months, but not best response at 6 weeks, was predictive of long-term survival in dogs treated with masitinib, which suggested that short-term response may be irrelevant for assessing clinical efficacy of tyrosine kinase inhibitors for treatment of MCTs.

Full access
in American Journal of Veterinary Research