Cushing’s Disease (Pituitary Pars Intermedia Dysfunction)
Basic Information 
Clinical Presentation
Physical Exam Findings
• Chronic laminitis is a consistent finding in these horses.
• PU and PD have been reported in up to 75% of horses.
• Failure to shed hair coat in spring or summer is a consistent finding.
• Weight loss, lethargy, increased docility
• Secondary infections (dermatitis, sinusitis, pneumonia), dental disease
• Excessive sweating (hyperhidrosis) and lack of sweating (anhidrosis)
• Redistribution of fat deposits
• Pendulous abdomen, sway back, and loss of muscle mass
• Other clinical signs include abnormal estrus cycles and neurologic signs (seizures, narcolepsy).
Etiology and Pathophysiology
• The hypothalamus, via dopamine, inhibits cells (melanotropes) of the pars intermedia of the pituitary gland.
• Hypothalamic neuronal oxidative damage results in loss of dopaminergic inhibition of melanotropes, which leads to hyperplasia, adenoma formation, and excessive production of adrenocorticotropic hormone (ACTH), α-melanocyte-stimulation hormone (α-MSH), and β-endorphin
• Excessive ACTH leads to increased cortisol concentrations (hyperadrenocorticism) and clinical signs of the disease.
• Increased α-MSH concentrations may be responsible for abnormal hair shedding.
• Increased β-endorphin concentrations appear to be responsible for the calm behavior of these horses.
• High cortisol concentrations lead to hyperglycemia, insulin resistance, laminitis, immunosuppression, and secondary infections.
• Adenoma enlargement may result in additional hypothalamic damage.
• Neuronal degeneration may be responsible for seizures.
• PPID is a better term for this disease because unlike humans and dogs with Cushing’s disease in which the adenoma is in the pars distalis (anterior lobe), the adenoma is in the pars intermedia in horses.
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