Hypokalaemia in a hyperthyroid domestic shorthair cat with adrenal hyperplasia.

A 13-year-old female domestic shorthair cat presented with polyphagia and weight loss. Marked systolic hypertension was found on examination. Elevated total thyroxine levels confirmed hyperthyroidism, and hypokalaemia was also documented. A euthyroid state and normotension were achieved following 4 weeks of treatment with carbimazole and amlodipine. Despite potassium supplementation, the hypokalaemia worsened. Abdominal ultrasonography revealed left adrenomegaly. Plasma aldosterone concentrations were initially in the lower half of the reference interval and, when repeated 2 months later, were undetectable. Urea and creatinine remained in the lower half of the reference interval throughout treatment, and urine specific gravity suggested good urine concentrating ability. The fractional excretion of potassium confirmed a renal source of potassium loss. Blood gas analysis was unremarkable. It was theorised that an aldosterone precursor was causing signs of mineralocorticoid excess and undetectable plasma aldosterone levels. Treatment with an aldosterone receptor antagonist successfully increased the serum potassium concentration. Owing to difficulties administering medication and associated effects on life quality the cat was euthanased. Adrenal hyperplasia was apparent on post-mortem histopathology.

Intravesicular administration of clotrimazole for treatment of candiduria in a cat with diabetes mellitus.

A 12-year-old spayed female domestic longhair cat developed fungal cystitis (Candida sp). The cat had a history of chronic diabetes mellitus, hyperadrenocorticism, and bacterial cystitis caused by Escherichia coli. Antifungal agents (itraconazole and fluconazole) were administered orally without noticeable effect on the candiduria. Because of the ineffectiveness of these treatments, intravesicular administration of 1% clotrimazole solution was performed weekly for 3 treatments. Complete resolution of urinary candidiasis was detected after the third infusion. Intravesicular administration of clotrimazole solution appears to be a safe and effective treatment of fungal cystitis in cats.

[Glucocorticoid-induced osteoporosis: recent findings]. / Osteoporosi indotta da glicocorticoidi: recenti acquisizioni.

The clinical features, pathogenesis and management of bone involvement in Cushing's syndrome are briefly reviewed. Personal data on bone mineral density and markers of bone turnover in Cushing's syndrome and adrenal incidentalomas are also reported. As long ago as 1932, Harvey Cushing recognized osteoporosis as a serious consequence of endogenous hypercortisolism. The introduction of cortisone in the therapy of autoimmune, rheumatic, allergic or dermatologic disorders was followed by several reports of detrimental effects on bone of patients who had undergone prolonged glucocorticoid treatment. Due to the rarity of Cushing's syndrome, most of the studies in the literature on glucocorticoid-induced osteoporosis refer to exogenous over-exposure to cortisone and its synthetic derivatives. Only a small number of works concern endogenous hypercortisolism, even if the characteristics of bone damage seem qualitatively the same. Finally, very few data are reported on the hypothetical detrimental effect on bone in the condition of the silent hypercortisolism of adrenal incidentalomas. Glucocorticoid-induced osteoporosis in Cushing's syndrome often results in vertebral fractures, and bone loss is more evident in trabecular than in cortical bone. Notwithstanding some distinctive features in osteoporosis induced by endogenous and exogenous glucocorticoid excess, the common eventual picture is notable bone damage that involves mainly the trabecular bone. Prompt and effective therapy is mandatory to reduce the risk of fractures. The present options include calcium and vitamin D supplementation, estrogen replacement therapy, bisphosphonates, either oral or parenteral. A novel approach to the clinical problem of glucocorticoid-induced osteoporosis might, in the future, be based on studies on selective glucocorticoid receptor modulators, a new class of synthetic glucocorticoids that exhibit significant anti-inflammatory and immunosuppressive activities, with reduced side effects on bone.

[Calcium-regulating hormones in endogenous hypercorticism]. / Kal'tsiireguliruiushchie gormony pri éndogennom giperkortitsizme.

Investigation of 44 patients with endogenous hypercorticism (EH) of various degrees of severity showed that the development of osteoporosis was accompanied by changes in the indices of calcium-phosphorus metabolism and calcium regulating hormones. Marked variations in the level of parathyroidin, calcitonin, vitamin D3 were observed in a severe type of EH. All the examinees were characterized by a decrease in the transport form of vitamin D3, which was most noticeable in a mild form of EH. A significant decrease in the concentration of the transport form of vitamin D3 against a background of hypercalcemia and hypercalciuria in mild EH can be regarded as the most informative indicators in early diagnosis of initial symptoms of osteoporosis.

[Phosphorus-calcium metabolism and calcium-regulating hormones in endogenous hypercorticism]. / Fosforno-kal'tsievyi obmen i kal'tsiireguliruiushchie gormony pri éndogennom giperkortitsizme.

The authors presented the results of a study of the indices of phosphorocalcium homeostasis, metabolism of osseous tissue and calcium regulating hormones in 44 patients with Icenko-Cushing's syndrome with regard to severity of disease and expression of osteoporosis. It was shown that disturbances of phosphorocalcium homeostasis and an increase in the level of the parathyroid hormone were characteristic for the active stage of Icenko-Cushing's disease and were most noticeable in a severe course of disease accompanied by sharply marked osteoporosis. Hypocalcemia, hypophosphatemia, hypercalciuria, a decrease in phosphate maximum resorption and an increase in AP activity in the blood serum were revealed in this form of disease. Patients with the average gravity of disease and weakly pronounced osteoporosis were characterized by hypercalcemia and an increase in calcium intestinal absorption. Patients with the active stage of hypercorticism were characterized by hypermagnesemia. Secondary hyperparathyrosis was found in 25% of patients with the active stage of Icenko-Cushing's disease.

Cushing's syndrome with bilateral multinodular adrenal hyperplasia. Ultrastructural, histochemical, and immunohistochemical study.

An unusual case of Cushing's syndrome of a 59-year-old man with bilateral multinodular adrenal hyperplasia and microadenoma of the pituitary gland is presented. Failure to suppress plasma cortisol with large doses of dexamethasone may suggest autonomous growth of hyperplastic nodules of the adrenals, which were at first induced by prolonged stimuli of ACTH from the microadenoma of the pituitary gland. ACTH could not be detected in the microadenoma cells on paraffin sections, while Crooke's cells were strongly positive for ACTH. The interrelation between bilateral multinodular adrenal hyperplasia and pituitary microadenoma is discussed.

[Bartter's disease associated with hypercorticism, phosphate and magnesium deficiencies and familial renal tubular disease]. / Un syndrome de bartter associant un hypercortisolisme, un diabete phosphore et magnesien et une tubulopathie d'origine familiale

A new case of Bartter's syndrome is described. There is a context of other cases of familial renal tubular disease with a sex-linked heredity. In this case, the Bartter's syndrome is associated with magnesium deficiency and hypomagnesemia, with a ricket and severe phosphate deficiency, and finally with an hypercorticism. The basal secretion rate of cortisol agree with a Cushing's syndrome. This hypercorticism is corrected by aminogluthetimide. The influence of the hyperreninism on the hypercorticism is discussed.