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Encyclopedia |
Equine Pituitary Pars Intermedia Dysfunction (PPID) (aka Equine Cushing’s Disease) In horses, PPID is attributed to an adenoma (a small benign tumor) in the pars intermedia of the pituitary gland. The cells that make up the tumor produce excessive amounts propriomelanocortin (POMC) and adrenocorticotropic hormone (ACTH). One unanswered question in horses is what exactly causes PPID in horses – is it a spontaneous pituitary disease (primary) or is it a consequence of loss of dopaminergic innervation (secondary)? Dopamine is a hormone secreted by the hypothalamus which regulates secretion of POMC and ACTH by the pars intermedia of the pituitary. The excessive secretion of these peptides leads to perpetually increased adrenal secretion of cortisol (hyperadrenocorticism). Cortisol is the physiological glucocorticoid in the equine species. Excessive cortisol circulating in the body potentiates catecholamine (adrenaline) release and accounts for the myriad of clinical signs associated with the disease. The classic sign of Equine PPID is the long hair coat that fails to shed (hirsuitism). Up to 2/3 of cushinoid patients develop the tendency for excessive sweating due to the thermoregulatory response of a long coat. Some horses exhibit increased water intake and urination. Weight loss and lethargy and/or poor performance have also been noted in the horses with PPID. Equids with PPID also may exhibit signs of delayed wound healing and have a tendency towards developing secondary infections, including skin infections, foot abscesses, conjunctivitis, sinusitis, gingivitis, pneumonia, etc. Chronic, insidious onset laminitis is the most significant clinical complication of PPID in horses (50%). PPID as a risk factor for laminitis is two fold: 1) impaired perfusion of the hoof by excess catecholamines acting directly on vascular smooth muscle (vasoconstriction and limited blood flow) and 2)indirectly by excess cortisol circulation causing insulin resistance (inhibiting glucose uptake by the cells in the hoof = no energy). The structural components of the equine hoof (lamellar keratinocytes) have an exceptionally high glucose requirement. Maintenance of the structural integrity of the hoof may rely on glucose delivery to and uptake by these cells. Excess cortisol production can also cause insulin resistance by inhibiting the action of insulin on cells. This promotes the availability of glucose for cells that do not depend on insulin for glucose uptake (nervous system). Glucose toxicity can occur with these cells and cause the release of additional enzymes that cause further constriction of the blood vessels and also impair perfusion in the hoof, possibly leading to the development of laminitis. The most effective ways to manage equine PPID and its associated side effects is through diet and administration of an oral medication one to two times daily for life. The medication of choice is a dopamine agonist called pergolide mesylate. This medication acts like dopamine and suppresses the excessive secretion of ACTH and POMC. It is supplied as a liquid (1mg/ml). There is a broad dosage for horses and usually they are started at the lowest dose for management. Transient anorexia may be observed but usually passes in the first week. Dietary management consists of a low sugar/low starch diet (low glycemic index) supplemented with adequate vitamins and minerals. Additionally, limiting grain meals and pasture access, especially during spring and fall, and providing high quality forage is recommended. If additional calories are needed to maintain adequate body weight after 4-6 weeks, vegetable oil may be added to the diet in the form of corn or canola oil. Start by adding ¼ to ½ cup once to twice daily and increase as needed, not to exceed 1 cup twice daily. Low Starch, Low sugar feeds
Complete feed brands:
** grain intake should be limited if not totally restricted Additional supplements:
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