The efficacy and safety of the antithyroid drug methimazole were evaluated over a 3-year period in 262 cats with hyperthyroidism. In 181 of the cats, methimazole was administered for 7 to 130 days (mean, 27.7 days) as a preoperative preparation for thyroidectomy. The remaining 81 cats were given methimazole for 30 to 1,000 days (mean, 228 days) as sole treatment for the hyperthyroid state. After 2 to 3 weeks of methimazole therapy (10 to 15 mg/d), the mean serum thyroxine (T4) concentration decreased significantly (P < 0.001) from a pretreatment value of 12.1 Kg/dl to 2.1 Wg/dl. The final maintenance dose needed to maintain euthyroidism in the 81 cats that were given methimazole as sole treatment for hyperthyroidism ranged from 2.5 to 20 mg/d (mean, 11.9 mg/d). Clinical side effects developed in 48 (18.3%) cats (usually within the first month of therapy), which included anorexia, vomiting, lethargy, self-induced excoriation of the face and neck, bleeding diathesis, and icterus caused by hepatopathy. Mild hematolvgic abnormalities developed in 43 (16.4%) cats (usually within the first 2 months of treatment), which included eosinophilia, lymphocytosis, and slight leukopenia. In ten (3.8%) cats, more serious hematologic reactions developed including agranulocytosis and thrombocytopenia (associated with bleeding). These hematologic abnormalities resolved within 1 week after cessation of methimazole treatment. Immunologic abnormalities associated with methimazole treatment included the development of antinuclear antibodies in 52 of 238 (21.8%) cats tested and red cell autoantibodies (as evidenced by positive direct antiglobulin tests) in three of 160 (1.9%) cats tested. These immunologic reactions were not associated with evidence of immune-mediated hemolytic anemia or lupus-like syndrome in any of the cats. Tlie results of this study indicate that methimazole is effective in blocking excess thyroid hormone secretion in cats with hyperthyroidism. In addition, although not entirely free of adverse side effects, methimazole is a relatively safe antithyroid drug for use in the cat. (Journal of Veterinary Internal Medicine 1988; 2:150-157) IN RECENT YEARS, hyperthyroidism has become a common and well-recognized disorder of middle-aged to older cats.'-3 Medical treatment with antithyroid drugs of the thionamide class, which act to block thyroid hormone synthesis and thereby lower high circulating thyroid hormone concentrations, can be of great value in the long-term control of the hyperthyroid Antithyroid drugs also play an important role in preop- erative preparation for successful thyroide~tomy.~-~ Advantages of long-term antithyroid drug treatment over other available treatment modalities (surgery and radioactive iodine) include absence of certain complications such as permanent hypothyroidism and postsurgical hyp~parathyroidism.~ In addition, unlike surgery or radioiodine, use of antithyroid drugs requires no advanced skills, training, or special licensing. Therefore, it is a practical treatment choice for most practi...

The efficacy and toxicity of CCNU (1-[2-chloroethyl]3-cyclohexyl-1-nitrosourea) were evaluated in 23 dogs with measurable mast cell tumors (MCT). Twenty-two dogs had cutaneous MCT and 1 dog had an intranasal MCT Nineteen (83%) dogs had biopsy of their original mass performed and 4 (17%) had aspiration cytology of masses. Of the 19 tumors histologically graded, 1 (5%) neoplasm was classified as grade I, 10 (53%) were grade II, and the remaining 8 (42%) were grade III. Dogs were treated with CCNU at a dosage of 90 mg/m2 body surface area every 3 weeks. Response could be evaluated in 19 dogs. Eight of the 19 dogs (42%) had a measurable response to CCNU. One dog had a durable complete response for 440 days. Seven dogs (37%) had a partial response for a median and mean duration of 77 days and 109 days, respectively (range, 21-254 days). Treatment with CCNU resulted in stable disease in 6 dogs (32%) for a median and mean duration of 78 days and 122 days, respectively (range, 42-347 days). The acute dose-limiting toxicity was neutropenia 7 days after administration of CCNU. The median and mean neutrophil counts 7 days after CCNU were 1,452 cells/microL and 1,683 cells/microL, respectively (n = 17). Other toxicoses were uncommon. CCNU should be considered an active agent in the treatment of MCT in dogs.

Two hundred dogs with pituitary dependent hyperadrenocorticism (PDH) were treated with mitotane a t an initial daily dosage of 21 to 69 mg/kg (mean = 45.2 mg/kg) for 5 to 14 days. During the induction period, 194 of the dogs also were given daily maintenance dosages of a glucocorticoid. Fifty of the dogs exhibited one or more adverse effects during initial induction, including weakness, vomiting, anorexia, diarrhea, and ataxia. After completion of the induction period, repeat ACTH stimulation testing revealed significant decreases in mean serum cortisol concentrations when compared with initial values. Twentyfive dogs, however, still responded to exogenous ACTH with serum cortisol concentrations above normal resting range, necessitating daily treatment for an additional 5 to 55 days. In contrast, 70 of the 200 dogs had low post-ACTH serum cortisol concentrations after the induction period. These subnormal serum cortisol concentrations generally increased spontaneously to within normal resting range 2 to 6 weeks after cessation of mitotane. In 184 dogs, mitotane was continued at an initial mean maintenance dosage of 49 mg/kg administered weekly in two to three divided doses. Of these dogs, 107 had one or more relapses of hyperadrenocorticism during treatment. In the 75 dogs that had one relapse, the median maintenance dosage was increased by approximately 35%, whereas the median maintenance dosage in the 32 dogs having two or more relapses was eventually increased by 225% over the initial dosage. After a mean maintenance treatment time of 2.0 years, the final maintenance dosage required in the 184 dogs ranged from 26.8 to 330 mg/kg/week. Concurrent glucocorticoid and mineralocorticoid deficiency (Addison's disease) developed in I1 dogs after 27 days to 3.5 years (median = 4.6 months) of maintenance mitotane. The mean survival time of the 200 dogs was 2.2 years (range = 10 days to 8.2 years). Of the 34 dogs that died or were euthanatized within the initial 6 months, 18 died because of complications of hyperadrenocorticism. In contrast, dogs usually did not die of complications associated with hyperadrenocorticism after the first few months of treatment, when the signs of disease were in remission. Eleven dogs died or were euthanatized as a result of the compressive effects of an expanding pituitary tumor. The results of this study indicate that mitotane is effective and relatively safe for the treatment of dogs with PDH. Of the dogs treated for longer than 3 months, over 80% were considered to have a good to excellent response to treatment. Adverse effects, although they did occur with some frequency, were generally not lifethreatening, were related to the development of low serum cortisol concentrations, and usually resolved PITUITARY-DEPENDENT hyperadrenocorticism (PDH), a syndrome characterized by excessive corticosteroid production secondary to oversecretion of ACTH by the pituitary gland with resultant bilateral adrenocortical

The efficacy and toxicity of CCNU (1-[2-chloroethyl]3-cyclohexyl-1-nitrosourea) were evaluated in 23 dogs with measurable mast cell tumors (MCT). Twenty-two dogs had cutaneous MCT and 1 dog had an intranasal MCT Nineteen (83%) dogs had biopsy of their original mass performed and 4 (17%) had aspiration cytology of masses. Of the 19 tumors histologically graded, 1 (5%) neoplasm was classified as grade I, 10 (53%) were grade II, and the remaining 8 (42%) were grade III. Dogs were treated with CCNU at a dosage of 90 mg/m2 body surface area every 3 weeks. Response could be evaluated in 19 dogs. Eight of the 19 dogs (42%) had a measurable response to CCNU. One dog had a durable complete response for 440 days. Seven dogs (37%) had a partial response for a median and mean duration of 77 days and 109 days, respectively (range, 21-254 days). Treatment with CCNU resulted in stable disease in 6 dogs (32%) for a median and mean duration of 78 days and 122 days, respectively (range, 42-347 days). The acute dose-limiting toxicity was neutropenia 7 days after administration of CCNU. The median and mean neutrophil counts 7 days after CCNU were 1,452 cells/microL and 1,683 cells/microL, respectively (n = 17). Other toxicoses were uncommon. CCNU should be considered an active agent in the treatment of MCT in dogs.