Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022575 (keratoconjunctivitis sicca)
772 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 35 year old female with Cushing's syndrome and bilateral adrenal macronodular hyperplasia, in whom a change from ACTH dependency to autonomy was observed, is presented. The diagnosis of Cushing's syndrome was based on the failure of suppression of urinary ketogenic steroids (17 KCS) and free cortisol (uF) with the administration of 2 mg of dexamethasone daily for 2 days. CT scan of the abdomen showed adrenal bilateral multinodular hyperplasia and the sellar CT scan was normal. Initially 8 mg for 2 days of dexamethasone suppressed 17 KCS and uF; however, a few months later this effect was lost as well as the effect of endogenous ACTH on cortisol. Bilateral adrenalectomy was carried out, prior to attainment of normal cortisol levels with Ketoconazole. The adrenal glands has multiple nodules and they weighed 10 and 21 grams. Her postoperative plasmatic cortisol levels were imperceptible. Physiopathologic mechanisms involved in bilateral macronodular adrenal hyperplasia are reviewed.
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PMID:[Cushing's syndrome due to bilateral adrenal macronodular hyperplasia. From ACTH-dependent hypercortisolism to ACTH-independent hypercortisolism]. 166 93

Degenerative myopathy suggestive of glucocorticoid-induced myopathy was diagnosed in a 10-year-old female Poodle X Pekingese dog with a history of progressive lameness. Electromyography revealed bizarre high-frequency discharges. Evidence of adrenal suppression was obtained in response to exogenous ACTH. The predominant source of corticosteroid was an ophthalmic preparation used in the management of keratoconjunctivitis sicca. Considering the apparent adverse effects of the corticosteroid in this case, a study was undertaken to determine the systemic effects, if any, induced by long-term ophthalmic administration of 0.1% dexamethasone suspension in healthy adult dogs. Dogs in one group (n = 5) were treated 4 times daily for 8 weeks, and dogs in another group (n = 5) were treated 4 times daily for 16 weeks. All dogs remained healthy throughout the study, but dexamethasone-treated dogs developed marked adrenal suppression, beginning the second week of treatment and intensifying throughout the treatment period. Histopathologic changes in the liver of dexamethasone-treated dogs included scattered foci of vacuolated hepatocytes, increased hepatocytic glycogen content, and ballooning degeneration of hepatocytes. Muscle specimens were histologically, histochemically, and electromyographically normal.
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PMID:Ophthalmic corticosteroid therapy: systemic effects in the dog. 334 86