Hypoadrenocorticism

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Small adrenal glands from a dog that developed hypoadrenocorticism following treatment for Cushing's disease with o,p'DDD.
Lateral thoracic radiographs of a dog with microcardia (a small cardiac shadow) secondary to hypoadrenocorticism and severe hypovolemia
Histologic section of an adrenal gland from a dog with hypoadrenocorticism. The adrenal cortex is diminished in width and contains a lymphocytic infiltrate. Hematoxylin and eosin stain, 40x magnification.

Hypoadrenocorticism (Addison's disease) has been referred to as 'the great pretender,' due to its ability to mimic other common diseases in the dog and thereby represent a diagnostic challenge.

Naturally occurring hypoadrenocorticism is an uncommon canine disease, with a predisposition in young to middle-aged female dogs.

The disease is usually caused by an immune-mediated destruction of all adrenocortical layers of the adrenal glands (adrenalitis)[1], resulting in deficiencies of mineralocorticoids (aldosterone) and glucocorticoids (cortisol). A small number of dogs suffer from glucocorticoid deficiency only.

Rare causes of primary adrenal cortex destruction include infiltration by fungus (Histoplasma spp, Blastomyces spp, Coccidioides spp, Cryptococcus spp)[2], neoplasia, amyloidosis, trauma, or coagulopathy.

Autoimmune polyglandular syndrome has rarely been described in the dog[3] with concurrent hypothyroidism, diabetes mellitus, hypoparathyroidism or infertility.

Iatrogenic primary hypoadrenocorticism is relatively common cause due to treatment of hyperadrenocorticism with drugs such as mitotane[4][5]. Somer dogs may develop permanent hypocortisolism from mitotane and require lifelong glucocorticoid supplementation[6].

Clinical signs of hypoadrenocorticism are associated with deficiency in aldosterone and cortisol. Dogs suffering from hypoadrenocorticism may present in a variety of conditions, from a mild gastroenteritis to acute shock[7].

These are usually nonspecific signs including dehydration, anorexia, lethargy and weakness, vomiting, diarrhea (hematochezia and melena are common), and weight loss.

Diagnosis is based on clinical signs supported by evidence of hyponatremia and hyperkalemia. A reduced sodium: potassium ratio (<25:1) raises the index of suspicion for hypoadrenocorticism. [8]. Other features of hematology include a stress leukogram, anemia, hypercalcemia, azotemia, hypoglycemia, hypoalbuminemia and hypocholesterolemia. Mild elevations in liver enzymes (ALT, AST and GGT) are common observed.

A definitive diagnosis is based on a subnormal ACTH stimulation test (pre- and post-ACTH cortisols) and adrenal ultrasonography. Approximately 85% of dogs with hypoadrenocorticism have basal and post-ACTH cortisol concentrations of <1.0ug/dL and more than 90% have cortisol concentrations <2.0ug/dL. Very rarely, ACTH stimulation cortisol levels are not abnormally low, but serum aldosterone levels are[9].

Treatment of acute Addisonian crisis involves addressing the hypovolemic shock, correcting electrolyte imbalances and treating the glucocorticoid deficit with dexamethasone.

Life-long daily mineralocorticoid (fludrocortisone or desoxycorticosterone pivalate) and glucocorticoid supplementation (prednisolone) are required[10].

The prognosis for hypoadrenocorticism is usually good with appropriate maintenance therapy and appropriate owner education.

References

  1. Frank CB et al (2013) Correlation of Inflammation with Adrenocortical Atrophy in Canine Adrenalitis. J Comp Pathol Jan 21
  2. LaPerle KMD, Capen CC. (2007) Endocrine system. In: McGavin MD, Zachary JF, editors. Pathologic Basis of Veterinary Disease. 4th ed. St. Louis, Missouri: Mosby; pp:693–741
  3. Reusch CE. (2000) Hypoadrenocorticism. In: Ettinger SJ, Feldman EC, editors. Textbook of Veterinary Internal Medicine. 5th ed. Philadelphia: WB Saunders; pp:1488–1499
  4. Peterson ME, Kintzer PP. (1997) Medical treatment of pituitary-dependent hyperadrenocorticism. Vet Clin North Am: Small Anim Pract 27:255–272
  5. Peterson ME (2001) Medical treatment of canine pituitary-dependent hyperadrenocorticism (Cushing’s Disease). Vet Clin North Am: Small Anim Pract 31:1005–1014
  6. Ettinger S.J., Feldman E.C. (2005) Textbook of Veterinary Internal Medicine, Sixth Edition. Elsevier Saunders. pp:1612-1622
  7. Klein, Sc & Peterson, ME (2010) Canine hypoadrenocorticism: Part I. Can Vet J 51(1):63–69
  8. Seth M et al (2011) White blood cell count and the sodium to potassium ratio to screen for hypoadrenocorticism in dogs. J Vet Intern Med 25(6):1351-1356
  9. Ferguson DC, Hoenig M (2003) Endocrine system. In: Latimer KS, EA Mahaffey, KW Prasse. Duncan and Prasse's Veterinary Laboratory Medicine: Clinical Pathology, 4th ed. Iowa State Press, Ames, pp:295-300
  10. Kintzer PP, Peterson ME (1997) Primary and secondary canine hypoadrenocorticism. Vet Clin N Am Small Anim Pract 27:349-357