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- Author or Editor: Richard W. Nelson x
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Summary
Pheochromocytoma was diagnosed in 4 dogs with pituitary-dependent hyperadrenocorticism and 2 dogs with hyperadrenocorticism caused by adrenocortical tumor. All dogs were examined initially because of clinical signs associated with hyperadrenocorticism. Pheochromocytoma was suspected in 2 dogs with pituitary-dependent hyperadrenocorticism that had ultrasonographic evidence of an adrenal gland mass, and in 1 dog suspected to have hyperadrenocorticism associated with an adrenocortical tumor after complications (systemic hypertension, cardiac arrhythmias) developed during induction of anesthesia. Pheochromocytoma was an unexpected finding at necropsy in the remaining 3 dogs. Two dogs collapsed suddenly and died before diagnostic tests could be performed; the other dog died during anesthesia for cobalt teletherapy of a pituitary macroadenoma. Hypertension, most notable during digital manipulation of the affected adrenal gland, developed during anesthesia and surgery in 3 dogs that underwent exploratory celiotomy.
Summary:
Persistent hypercalcemia attributable to parathyroid gland hyperplasia was identified in 6 dogs with primary hyperparathyroidism. Clinical signs included polydipsia (n = 4), polyuria (n = 4), and signs caused by cystic calculi (n = 3). Abnormal clinical pathologic findings included hypercalcemia (mean, 13.6 mg/dl; range, 12.6 to 14.7 mg/dl; n = 6), hypophosphatemia (mean, 2.2 mg/dl; range, 1.4 to 2.9 mg/dl; n = 6), high serum alkaline phosphatase activity (mean, 222 IU/L; range, 161 to 286 IU/L; n = 3), and isosthenuria (mean, 1.012; range, 1.006 to 1.017; n = 6). Serum parathyroid hormone concentration was within the reference range or high (mean, 23 pmol/L; range, 7 to 119 pmol/L; reference range, 1.5 to 13 pmol/L) in all dogs.
At surgery, the number of large parathyroid glands was variable, being limited to 1 gland in 3 dogs, 2 glands in 2 dogs, and 4 glands in 1 dog. All visibly large parathyroid glands were surgically removed from each dog. Serum calcium concentration decreased into or below the reference range within 72 hours of surgery in all dogs, confirming the diagnosis of primary parathyroid disease. Multiple nodules of adenomatous hyperplasia were identified in each dog. All 6 dogs were treated with vitamin D and calcium carbonate following surgery. The dog from which all 4 parathyroid glands were removed has remained eucalcemic for more than 1 year with vitamin D supplementation. Vitamin D and calcium administration was discontinued within 4 to 12 weeks of surgery in the remaining 5 dogs. These dogs remained eucalcemic without vitamin D supplementation. Two dogs are still alive 12 and 35 months after surgery; 3 dogs died 3 to 4 years after surgery because of unrelated medical causes.
Summary
The effect of orally administered ketoconazole on plasma cortisol concentration in dogs with hyperadrenocorticism was evaluated. Every 30 minutes from 0800 hours through 1600 hours and again at 1800 hours, 2000 hours, and 0800 hours the following morning, 15 clinically normal dogs and 49 dogs with hyperadrenocorticism had plasma samples obtained and analyzed for cortisol concentration. The mean (± sd) plasma cortisol concentration for the initial 8-hour testing period was highest in 18 dogs with adrenocortical tumor (5.3 ±1.6 µg/dl), lowest in 15 control dogs (1.3 ± 0.5 µg/dl), and intermediate in 31 dogs with pituitary-dependent hyperadrenocorticism (pdh; 3.4 ± 1.2 µg/dl). Results in each of the 2 groups of dogs with hyperadrenocorticism were significantly (P < 0.05) different from results in control dogs, but not from each other. The same cortisol secretory experiment was performed, using 8 dogs with hyperadrenocorticism (5 with pdh; 3 with adrenocortical tumor) before and after administration at 0800 hours of 15 mg of ketoconazole/kg of body weight. Significant (P < 0.05) decrease in the 8-hour mean plasma cortisol concentration (0.9 ± 0.2 µg/dl) was observed, with return to baseline plasma cortisol concentration 24 hours later.
Twenty dogs with hyperadrenocorticism (11 with pdh, 9 with adrenocortical tumor) were treated with ketoconazole at a dosage of 15 mg/kg given every 12 hours for a half month to 12 months. The disease in 2 dogs with pdh failed to respond to treatment, but 18 dogs had complete resolution of clinical signs of hyperadrenocorticism and significant (P < 0.05) reduction in plasma cortisol responsiveness to exogenous adrenocorticotropin (acth). The healthy control dogs had a mean baseline plasma cortisol concentration of 1.4 ± 0.4 µg/dl and a post-acth cortisol concentration of 10.6 ± 3.1 µg/dl. Before ketoconazole administration, all 11 dogs with pdh had a mean baseline plasma cortisol concentration of 4.4 ± l.9 µg/dl and a post-acth cortisol concentration of 33.6 ± 17.6 µg/dl. The 9 dogs with adrenocortical tumor had a mean baseline plasma cortisol concentration of 4.4 ± 1.3 µg/dl and post-acth cortisol concentration of 28.1 ± 14.1 µg/dl. After 5 days of ketoconazole administration, the post-acth plasma cortisol concentration for dogs with pdh or adrenocortical tumor was 4.0 ± 5.4 µg/dl and 6.0 ± 3.3 µg/dl, respectively. Similar responses were observed after 60, 180, and 360 days of ketoconazole treatment.
Summary
The purpose of this study was to determine the sensitivity of dogs with hyperadrenocorticism to treatment with the adrenocorticolytic agent mitotane. Specifically, we looked for differences in response to treatment using this drug in dogs with adrenocortical tumors (adrenal tumor hyperadrenocorticism, ath) vs those with pituitary-dependent hyperadrenocorticism (pdh). For inclusion in this study, each dog must have had clinical signs, data base laboratory abnormalities, and endocrine screening test results consistent with the diagnosis of hyperadrenocorticism. Further, each dog had to have been treated for at least 6 months with mitotane and have histologic evidence for adrenocortical or pituitary neoplasia (all dogs were necropsied). Thirteen dogs with ath (8 carcinomas, 5 adenomas) were identified. The ages and body weights of these 13 dogs were computer-matched to 13 dogs with pdh. All dogs were initially treated with approximately 50 mg of mitotane/kg/d of body weight. Reexaminations were performed after 7, 30, 90, and 180 days of treatment.
Individual dosages varied widely after the initial 5 to 12 days of treatment. The mean (± sd) dose of mitotane (mg/kg/d) for the first 7 days of treatment was 47.5 ± 9.4 for dogs with ath vs 45.7 ± 11.9 for dogs with pdh. The mean plasma cortisol concentrations 1 hour after acth administration at the 7-day recheck were significantly higher in dogs with ath (502 ± 386 nmol/L) than in dogs with pdh (88 ± 94 nmol/L). At 30 days, the mean daily dose of mitotane and post-acth cortisol concentration were significantly greater in dogs with ath (28.8 ± 15.4 mg/kg/d; 392 ± 356 nmol/L, respectively) than in dogs with pdh (10.5 ± 7.5 mg/kg/d; 99 ± 72 nmol/L, respectively). After 90 days of treatment, these values were larger (25.3 ± 16.8 mg/kg/d; 340 ±193 nmol/L in dogs with ath vs those in dogs with pdh (5.4 ± 2.5 mg/kg/d, 110 ± 94 nmol/L) and again after 180 days (26.0 ± 22.1 mg/kg/d, 268 ± 152 nmol/L in dogs with ath vs 6.3 ± 3.4 mg/kg/d, 80 ± 116 nmol/L in dogs with pdh). Clinical signs were consistent with laboratory values, that is, cortisol control was not as good in dogs with ath as in the dogs with pdh. On the basis of these findings, we suggest that dogs with hyperadrenocorticism caused by ath are more resistant to mitotane than are dogs with pdh.
Abstract
Objective—To determine the efficacy and safety of percutaneous ethanol injection (PEI) for the treatment of hyperthyroidism caused by bilateral hyperplastic thyroid nodules in cats.
Design—Prospective study.
Animals—7 cats.
Procedure—Hyperthyroidism was diagnosed on the basis of clinical signs and increased serum total thyroxine (TT4) concentrations. The presence of 2 cervical thyroid nodules was confirmed by use of ultrasonography and technetium Tc 99m albumin thyroid scans. After the death of 1 cat that received PEI in both thyroid nodules at the same time, the protocol was changed to injecting ethanol into 1 nodule at a time, with at least 1 month between injections. Clinical signs, serum TT4 concentrations, serum ionized calcium concentrations, laryngeal function, findings on ultrasonographic examinations of the ventral cervical region, and results of thyroid scans were monitored.
Results—Serum TT4 concentrations transiently decreased in all 6 cats (into the reference range in 5 of 6 cats) within 4 days of the first staged ethanol injection. Each subsequent injection resulted in a transient decrease in serum TT4 concentration. The longest period of euthyroidism was 27 weeks. Adverse effects included Horner's syndrome, dysphonia, and laryngeal paralysis. One cat died of unrelated causes. One cat underwent bilateral thyroidectomy, 2 cats were treated with methimazole, and 2 cats that had increased serum TT4 concentrations were not treated further, because they remained clinically normal.
Conclusions and Clinical Relevance—Percutaneous ethanol ablation of bilateral thyroid nodules as a treatment for cats with hyperthyroidism is not recommended. This treatment is not as efficacious as the medical and surgical treatments presently used. (J Am Vet Med Assoc 2001;218:1293–1297)
Abstract
Objective—To determine ultrasonographic characteristics of the thyroid gland in healthy small-, medium-, and large-breed dogs and evaluate the relationships of thyroid gland size and volume with body weight and body surface area (BSA).
Animals—72 dogs of small (6 Toy and 6 Miniature Poodles), medium (12 Beagles), and large breeds (12 Akitas and 36 Golden Retrievers).
Procedure—Each dog's thyroid gland was examined ultrasonographically with a 10- to 5-MHz multifrequency linear-array transducer. Size, shape, echogenicity, and homogeneity of thyroid lobes were evaluated on longitudinal and transverse images. Thyroid lobe volume was estimated by use of the equation for an ellipsoid (π/6 [length × height × width]).
Results—Thyroid lobes appeared fusiform or elliptical on longitudinal images and triangular or round to oval on transverse images. In most dogs, thyroid lobes were hyperechoic or isoechoic, compared with surrounding musculature, and had a homogeneous echogenic pattern. Mean length, width, height, and volume of thyroid lobes were significantly greater in Akitas and Golden Retrievers, compared with findings in Beagles or Poodles; mean length, width, and height were significantly greater in Beagles, compared with findings in Poodles. Total thyroid gland volume correlated with body weight (r = 0.73) and BSA (r = 0.74).
Conclusions and Clinical Relevance—Among the dog breeds examined ultrasonographically, thyroid lobe size and volume were more variable than shape, echogenicity, and homogeneity. The correlation of thyroid gland volume with BSA suggests that size of the dog, rather than breed, should be considered when assessing thyroid glands ultrasonographically.
Abstract
Objective—To evaluate accuracy of 6 portable blood glucose meters (PBGMs) by comparing results of these meters with results obtained with a reference chemistry analyzer.
Design—Evaluation study.
Animals—49 dogs (158 blood samples).
Procedures—Venous blood samples were tested with the 6 PBGMs, and results were compared with results of a commercially available analyzer that used a reference method based on the hexokinase reaction.
Results—Plasma glucose concentrations obtained with the reference analyzer ranged from 41 to 639 mg/dL. There were significant correlations between blood glucose concentrations obtained with the 6 PBGMs and plasma glucose concentrations obtained with the reference analyzer (r ≥ 0.96). However, for all 6 PBGMs, results differed from results for the reference analyzer, with the difference increasing as plasma glucose concentration increased. Significant differences in bias were found among meters. For 142 samples classified as hypoglycemic, euglycemic, or hyperglycemic on the basis of results of the reference analyzer, the percentage of samples that were misclassified on the basis of results of the PBGMs ranged from 2.1% to 38.7%.
Conclusions and Clinical Relevance—Results of the present study suggested that there were substantial differences in the accuracy of currently available PBGMs when used to determine blood glucose concentration in dogs.
Abstract
Objective—To compare the sensitivity and specificity of serologic evaluation and fungal culture of tissue for diagnosis of nasal aspergillosis in dogs.
Design—Prospective study.
Animals—58 dogs with nasal discharge and 26 healthy dogs.
Procedures—Dogs with nasal discharge were anesthetized and underwent computed tomography and rhinoscopy; nasal tissues were collected for histologic examination and fungal culture. Sera were assessed for antibodies against Aspergillus spp (healthy dog sera were used as negative control specimens). Nasal aspergillosis was diagnosed in dogs that had at least 2 of the following findings: computed tomographic characteristics consistent with aspergillosis, fungal plaques detected during rhinoscopy, and histologically detectable fungal hyphae in nasal tissue. Histologic characteristics of malignancy were diagnostic for neoplasia. Without evidence of neoplasia or fungal disease, nonfungal rhinitis was diagnosed.
Results—Among the 58 dogs, 21 had nasal aspergillosis, 25 had nonfungal rhinitis, and 12 had nasal neoplasia. Fourteen aspergillosis-affected dogs and 1 dog with nonfungal rhinitis had serum antibodies against Aspergillus spp. Fungal culture results were positive for Aspergillus spp only for 17 dogs with aspergillosis. With regard to aspergillosis diagnosis, sensitivity, specificity, and positive and negative predictive values were 67%, 98%, 93%, and 84%, respectively, for serum anti-Aspergillus antibody determination and 81%, 100%, 100%, and 90%, respectively, for fungal culture.
Conclusions and Clinical Relevance—Results suggest that seropositivity for Aspergillus spp and identification of Aspergillus spp in cultures of nasal tissue are highly suggestive of nasal aspergillosis in dogs; however, negative test results do not rule out nasal aspergillosis.
