It is most commonly seen in older animals,[1] and is classically associated with the formation of a long, wavy coat (hirsutism) and chronic laminitis.
[3] Without regulation from dopamine, the pars intermedia develops hyperplasia and adenoma formation, leading to gross enlargement and excessive production of POMC.
[1][2] POMC produced from the melanotropes of the pars intermedia is cleaved into adrenocorticotropic hormone (ACTH) and β-lipotropin (β-LPH).
In a horse with PPID, ACTH levels are high as a result of pars intermedia production, but it is not subject to negative feedback regulation.
[1] Other abnormalities associated with the disease include mild anemia, neurophilia, lymphopenia, eosinopenia, and increased liver enzymes.
[2] PPID shares similarities to equine metabolic syndrome (EMS), which also causes regional adiposity, laminitis, and insulin resistance.
[8] Failure to use a seasonally adjusted reference range may lead to false-positive results in normal horses if they are sampled in the fall.
[5][13] Basal plasma ACTH levels may increase if the horse is severely ill or under great stress or pain, such as if it has laminitis.
[8] Additionally, ACTH levels may not be significantly increased early on in the disease, leading to false negatives.
The administration of exogenous TRH causes an increase in ACTH and α-MSH in plasma of both normal horses and those with PPID.
In both cases, plasma ACTH peaks 2–10 minutes after administration, before slowly dropping to normal levels over the course of an hour.
[14][13] TRH is currently not licensed for use in horses, and can cause various side effects, including yawning, flehmen, muscle trembling, and coughing.
Additionally, elevations may occur secondary to stress, concurrent disease, and due to individual variation.
[17] The fasting insulin concentration involves giving a horse a single flake of hay at 10 pm the night before testing, with blood being drawn the following morning.
The following morning, karo corn syrup is given orally, and glucose and insulin levels are measured at 60 and 90 minutes after administration.
Obese animals are often best maintained on a diet consisting of ration balancer and hay, fed at 1.5% body weight and decreased if needed.
Animals resistant to weight loss, despite diet and exercise changes, can be placed on levothyroxine to increase metabolism.
[18] The primary treatment of PPID is pergolide, a dopamine agonist that provides suppression to the pars intermedia in place of the dysfunctional hypothalamus.
Horses should be reassessed in 30 days following the start of treatment, through evaluation of clinical signs and by baseline diagnostic testing, to ensure the appropriate dose is being prescribed.
[14] Attitude, activity levels, hyperglycemia, and increased drinking and urination are usually improved within 30 days of initiating treatment.
Other clinical signs, such as hirsutism, potbellied appearance, muscle wasting, laminitic episodes, and increased predisposition to infection, usually take between 30 days and a year to improve.