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Results of surgical treatment for hyperadrenocorticism caused by adrenocortical neoplasia in the dog: 25 cases (1980-1984).

Results of surgical treatment for neoplasia of the adrenal cortex that caused hyperadrenocorticism were evaluated in 25 dogs. Surgical examination of the adrenal glands was performed by use of a ventral midline approach in 24 dogs and a retroperitoneal approach in 1 dog. All 25 dogs had a unilateral, adrenocortical tumor. Histologic examination identified 14 adrenocortical carcinomas and 11 adenomas. Seven dogs with carcinoma had visible metastasis to the liver, 3 had local invasion into the caudal vena cava, and 1 had extension into the adjacent renal vein. Seven of the 9 dogs with metastasis were euthanatized at time of surgery. Of the remaining 18 dogs that survived surgery, 9 (4 with carcinoma and 5 with adenoma) developed serious postoperative complications including acute renal failure, pneumonia, and pulmonary artery thromboembolism; 8 of these dogs died or were euthanatized. Of the remaining 10 dogs, clinical signs associated with hyperadrenocorticism resolved in the 7 dogs that had adrenocortical adenoma and in 1 of the 3 dogs that had carcinoma. The remaining 2 dogs with carcinoma had persistent hyperadrenocorticism and were treated with high doses of mitotane. Although no response was observed in 1 dog with visible hepatic metastasis, a decrease in serum cortisol concentrations and resolution of clinical signs were detected in the other dog during prolonged daily administration of mitotane.

Adenoma↗

[Study of plasma androstenedione and testosterone levels in hypercorticism syndromes].

Plasma T and A were studied in 10 patients with hypercorticism. In the female patients, plasma A and T were elevated in 4 cases of Cushing's disease, slightly decreased in 2 cases of adrenal adenoma and greatly increased in I case of adrenal carcinoma. In 3 male patients, A plasma levels followed ACTH levels, but T was subnormal, irrespective of the cause of hypercorticism. Furthermore, in 8 normal men, the decrease of plasma T, observed after ACTH administration, was not directly related to ACTH, but rather to cortisol, as it was not observed after metyrapone induced ACTH increase. As no change in LH secretion was shown and as dexamethasone reduced the testosterone response to HCG, it seems likely that glucocorticoids act directly on testosterone biosynthesis.

Adrenal Cortex Neoplasms↗

[Hyperlipemia].

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Adrenal Cortex Hormones↗