Equis ISSN 2398-2977

Endocrine: hypoadrenocorticism

Synonym(s): Adrenal insufficiency

Contributor(s): Christopher Brown, Ramiro Toribio, Han van der Kolk


  • Deficiency in adrenocortical hormones. Rare in horses.
  • Cause: idiopathic or acquired (iatrogenic); it has been associated with long-term anabolic steroids or long-acting glucocorticoid (triamcinolone   Triamcinolone  ) administration. It may occur in critically ill horses, eg colic, enterocolitis, endotoxemia, sepsis, because the adrenal gland is a shock organ in the horse. Most documented cases of equine hypoadrenocorticism involve discontinuation of chronic administration of glucocorticoids or anabolic steroids.
  • Signs: acute or chronic weakness, depression, diarrhea, bradycardia.
  • Diagnosis: ACTH stimulation test; electrolyte evaluation.
  • Treatment: restore electrolyte balance; replacement of glucocorticoids; supportive therapy.
  • Prognosis: fair with appropriate therapy.



  • Usually idiopathic.
  • Other causes:
    • Long-term administration of anabolic steroids or glucocorticoids (iatrogenic hypoadrenocorticism).
    • Granulomatous disease of adrenal gland(s).
    • Adrenal neoplasia.
    • Hemorrhage or infarction of adrenals.
    • Pituitary gland disease (secondary hypoadrenocorticism).

Predisposing factors

  • Racehorses in training.
  • Severe systemic disease that can compromise adrenal gland function.


  • Inhibition of ACTH secretion due to administration of steroids.


  • Deficiency in the endogenous glucocorticoid, cortisol and the mineralocorticoid aldosterone   →   inadequate energy metabolism and electrolyte imbalances.
Primary hypoadrenocorticism
  • Damage to adrenal gland (usually idiopathic)   →   deficiency of glucocorticoid secretion   →   impaired gluconeogenesis and fat metabolism; depletion of liver glycogen stores   →   depression, gastrointestinal disturbances.
  • Deficiency of mineralocorticoid (aldosterone)   →   loss of sodium chloride in urine; retention of potassium and hydrogen by distal convoluted tubule of kidney   →   water and electrolyte imbalance (hyperkalemia)   →   bradycardia, hypovolemia, muscle weakness   →   hypovolemic shock.
  • May be able to function adequately early in course of disease, but may not be able to respond to stress.

Secondary hypoadrenocorticism

  • Any condition that decreases the function of the hypothalamus-pituitary component of the hypothalamus-pituitary-adrenal axis and   →    decreased secretion of ACTH or ACTH-releasing factors (corticotropin-releasing factor-CRF or arginine vasopressin-AVP).
  • The decreased secretion of ACTH   →    decreased stimulation of the adrenal cortex to release glucocorticoids.

Iatrogenic hypoadrenocorticism

  • Perhaps the most common cause of hypoadrenocorticism.
  • The long-term administration of glucocorticoids or anabolic steroids   →    inhibit secretion of adrenocorticotrophic hormone (ACTH) from the pituitary gland   →    decreased stimulation of adrenal gland cortex.


  • Acute or chronic.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Orsini A J, Donaldson M T, Koch C & Boswell R (2007) Iatrogenic secondary hypoadrenocorticism in a horse with pituitary pars intermedia dysfunction (equine Cushing's disease). Equine Vet Educ 19 (2), 81-87.
  • Couetil L L & Hoffman A M (1998) Adrenal insufficiency in a neonatal foal. JAVMA 212 (10), 1594-1596 PubMed.
  • Dowling P M, Williams M A & Clark T P (1993) Adrenal insufficiency associated with long-term anabolic steroid administration in a horse. JAVMA 203 (8), 1166-1169 PubMed.
  • Slone D E et al (1983) Cortisol disappearance rate and pathophysiologic changes after bilateral adrenalectomy in equids. Am J Vet Res 44, 276-279 PubMed.
  • Slone D E et al (1980)Vascular anatomy and surgical technique for bilateral adrenalectomy in the equid.Am J Vet Res 41, 829-832 PubMed.

Other sources of information

  • Toribio R E (2004) The Adrenal Glands. In: Equine Internal Medicine. Eds: Reed S M, Bayly W M & Sellon D C. 2nd edn. Saunders, USA. pp 1357-1361.