Twenty-one dogs with spontaneous hyperadrenocorticism presented a clinical picture characterized by an insidious onset of abdominal enlargement, muscular weakness, obesity and alopecia. Slight diabetes mellitus was present in some. In the bitches usually there was absence of oestrus for a long time. In addition to polydipsia and polyphagia, features indicative of heat intolerance were observed frequently. The signs and symptoms found are compared to those of human Cushing's syndrome.Determinations of the excretion of 17-hydroxycorticosteroids in 24-hr. urines were of great diagnostic significance. There was a considerable overlap of levels of plasma 11\g=b\-hydroxycorticosteroids in normal dogs and those with hyperadrenocorticism. Results of dexamethasone suppression tests are given.In the sera of four exophthalmic animals and in one pituitary obtained by necropsy, elevated levels of exophthalmos-producing substance were found. Pathological findings have become available in a number of cases.Preliminary results with hypophysectomy in four dogs are encouraging.

The mechanism of thyroid action on bone was studied in 15 patients with thyrotoxicosis and 14 patients with hypothyroidism. The patients were studied twice: when they were thyrotoxic or hypothyroid and when they had returned to a euthyroid state. Parameters of bone turnover showed a decrease when hyperthyroid patients became euthyroid: serum calcium (2.51 \m=+-\0.04 vs 2.38 \m=+-\0.03 mmol/1, P< 0.05), acid phosphatase (11.7 \ m=+-\0.7 vs 8.3 \ m=+-\0.4 U/l, P < 0.01), alkaline phosphatase (124 \m=+-\11 vs 98 \m=+-\8 U/l, P <0.05), the calcium/creatinine ratio (1.03 \m=+-\0.31 vs 0.43 \m=+-\0.07, P <0.01) and the hydroxyproline/creatinine ratio in the urine (69.9 \m=+-\12 vs 20.7 \ m=+-\2.4, P < 0.01). These parameters showed an increase when hypothyroid patients became euthyroid: serum calcium (2.36 \ m=+-\ 0.03 vs 2.48 \ m=+-\ 0.04 mmol/l, P < 0.01), alkaline phosphatase (60 \ m=+-\ 4 vs 84 \ m=+-\ 8 U/l, P < 0.05) and the hydroxyproline/creatinine ratio in the urine (15.9 \ m=+-\4.3 vs 25.3 \m=+-\3.2, P < 0.05). Changes in the calcium regulating hormones, parathyroid hormone, calcitonin and vitamin D metabolites, were not observed when hyperthyroid patients became euthyroid. When hypothyroid patients were treated a decrease in serum levels of 1.25-dihydroxyvitamin D (32.6 \ m=+-\4.6 vs 17.9 \ m=+-\ 2.5 ng/l, P <0.01) was observed. Serum growth hormone levels decreased when hypothyroid patients became euthyroid (4.3 \ m=+-\ 0.5 vs 2.6 \ m=+-\0.4 mU/l, P < 0.01). The possible mechanisms of thyroid action on bone are discussed. The presented findings are in accordance with a direct effect of thyroid hormones on bone in thyrotoxicosis. An additional factor could be somatomedin, that might also be involved in changes in bone turnover in hyper-and hypothyroidism.

Hexokinase (ADP: D‐hexose‐6‐phosphotransferase, EC 2.7.1.1) was studied in human thyroid carcinomas (n = 11), follicular adenomas (n = 32), and normal thyroid tissue (n = 21). The specific activity was significantly increased in carcinoma (0.163 ± 0.083 U/mg protein) compared with normal tissue (0.030 ± 0.010 U/mg protein) (P < 0.001). Specific activities of follicular adenomas are rather heterogeneous, but when subdivided into three groups according to histopathologic criteria, a significant difference was found between follicular adenomas group I and II and follicular adenomas group III. A lesser cellular differentiation of adenomas is indicated by the lower degree or even absence of colloid production and follicle formation. A higher proliferation rate may be assumed on the grounds of the irregularities in outline, the often defective pseudocapsule, and signs of compression of the surrounding tissue. The highest specific activity in adenomas was found in the group with the highest proliferative activity, i.e., group III, whereas the lowest specific activities were found in adenomas with the lowest grade of proliferation, i.e., group I; the former was comparable with values found in carcinomas and the latter was comparable with values found in normal thyroid tissue. An interesting difference was found when the compartmentation of hexokinase was compared in carcinomas of different degree of differentiation. In papillary carcinomas a significantly lower proportion of hexokinase (HK) is present in the cytosol in comparison to follicular and undifferentiated carcinomas. In carcinomas more HK II and less HK I was found in comparison with normal thyroid tissue. In contrast hexokinase isozyme composition and compartmentation in adenomas were not different from normal thyroid tissue.

SUMMARY The median urinary excretion of 17-oxosteroids in 22 normal unanaesthetized dogs was 0·06 (range: 0·02–0·24) mg./kg. body weight/24 hr. 17-Oxosteroid excretion increased markedly after the administration of dehydroepiandrosterone and androstenedione, while testosterone caused only a very small increase. The median urinary excretion of total 17-hydroxycorticosteroids (17-OHCS) in 21 dogs was 0·16 (range: 0·06–0·320 mg./kg. body weight/24 hr. This was calculated to amount to about 50–60% of the cortisol produced. Stimulation with corticotrophin (ACTH) resulted in an increase of urinary 17-OHCS and of plasma 11β-OHCS levels, but 17-oxosteroid excretion was only slightly increased. In 27 dogs the median plasma 11β-OHCS level was 4·0 (range: 1·3–9·7) μg./100 ml. at 8.00 hr. and 3·6 (range: 0·4–7·0) μg./100 ml. at 17.00 hr. In eight dogs 3-hourly plasma 11β-OHCS estimations were done; six of these animals showed a diurnal variation comparable to that in man.

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