Robert Douglas, PhD Equine Cushing's Syndrome was first described in the literature 40 years ago as caused by dysfunction of the pars intermedia (PI) of the pituitary gland. The initial lesion in the horse is not in the pituitary gland but likely nearby in the hypothalamus. By some as yet unknown mechanism, a loss of dopamine innervation in the PI results in a toss of negative control or feedback on the PI and ultimately hyperplasia and enlargement of the PI occurs. At the onset of this cascade of events resuiting in Cushing' s-like disease, there is an increase in the PI secretion of the proopiomelancortin(POMC) derived peptides. This increase in POMC peptides decreases the sensitivity of the negative feedback effects of glucocorticoids on ACTH production. These peptide hormones also increase the effects of ACTH on adrenal steroidogenesis. The result is a decrease in circadian rhythmicity of cortisol secretion (below 30% ?). There is a concomitant increase in the secretion of opiate-active Beta endorphin which may explain the lethargy seen in many horses thought to have Cushing' slike disease. Moreover, it is well accepted that the most common clinical signs in horses with confirmed PI adenomas include: hirsuitism, weight
Journal of Equine Veterinary Science – Elsevier
Published: Nov 1, 1999
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