ISSN 2398-2950      

Hyperadrenocorticism

ffelis

Synonym(s): Cushing's disease, Cushing's syndrome, HAC


Introduction

  • Syndrome resulting from excessive production of glucocorticoids.
  • Rare endocrine disease in cats (cf dogs).
  • Cause:
    • Pituitary dependent: excessive ACTH production in pituitary gland - 75% of cases.
    • Adrenal dependent: autonomous excessive corticosteroid production in adrenal gland - 25% of cases.
  • Signs: polydipsia, polyuria, polyphagia, alopecia, insulin-resistant diabetes mellitus, skin thinning and tearing.
  • Diagnosis: screening lab tests and dynamic tests of adrenal function.
  • Treatment: medical (trilostane) or surgery (adrenalectomy).
  • Prognosis: poor without treatment.
    Print out the Owner factsheet on Cushing's Disease (hyperadrenocorticism) Cushing's disease (hyperadrenocorticism)  to give to your client.

Pathogenesis

Etiology

Either Failure of negative feedback on ACTH release  →  pituitary dependent.
Or Failure of response to reduced ACTH release  →  adrenal dependent.
  • Functional pituitary tumor.
  • Functional adrenal tumor - usually unilateral with 60% adenomas and 40% carcinomas.
  • Iatrogenic HAC, because of prolonged progestogen or corticosteroid therapy reported but rare.

Pathophysiology

  • Often clinical signs at presentation, eg polydipsia/polyuria and polyphagia relate to diabetes mellitus rather than glucocorticoid excess per se.
  • Glucocorticoids profoundly affect carbohydrate, protein and fat metabolism.
  • Glucocorticoids also modify inflammatory and immune responses.
  • Excessive glucocorticoids cause:

Liver

  • Increased gluconeogenesis.
  • Increased glycogen stores.

Pancreas

  • Peripheral insulin resistance   →   increased insulin production initially   →   subsequent beta-cell exhaustion and cell death   →   diabetes mellitus.
  • Alternatively, glucose toxicity   →   decreased insulin secretion   →   diabetes mellitus.

Muscle

  • Increased protein catabolism   →   muscle wasting and weakness.

Bone

  • Direct catabolic effect on bone matrix   →   increased urinary calcium excretion and inhibition of vitamin D action.
  • Glucocorticoids   →   negative calcium balance   →   increased PTH   →   osteoporosis.

Skin

  • Hyperkeratosis, loss of collagen, atrophy of hair follicles, disturbed protein metabolism   →   thin skin   Hyperadrenocorticism: thinning skin  , poor wound healing, poor scar formation, cessation of hair growth.

Blood

  • Leucocytosis.
  • Decrease in circulating lymphocytes and eosinophils.
  • Increase in circulating neutrophils and monocytes.

Kidney

  • Interference with ADH release or action   →   polyuria   →   polydipsia.
  • Osmotic diuresis because of hyperglycemia.
  • Increased calcium excretion.

Immune system

  • Reduced inflammatory response.
  • Reduced immune response.

Fat

  • Increased lipolysis.
  • Redistributed fat deposits.

Timecourse

  • Many months   →   years.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Boland L A & Barrs V R (2017) Peculiarities of feline hyperadrenocorticism: update on diagnosis and treatment. J Feline Med Surg 19 (9), 933-947 PubMed.
  • Neiger R, Witt A L, Noble A et al (2004) Trilostane therapy for treatment of pituitary-dependent hyperadrenocorticism in 5 cats. J Vet Intern Med 18 (2), 160-164 PubMed.
  • Hoenig M (2002) Feline hyperadrenocorticism - where are we now? J Feline Med Surg (3), 171-174 PubMed.
  • Ferasin L (2001) Iatrogenic hyperadrenocorticism in a cat following a short therapeutic course of methylprednisolone acetate. JFMS (2), 87-93 PubMed.
  • Feldman E C & Nelson R W (2000) Acromegaly and hyperadrenocorticism in cats - a clinical perspective. JFMS (3), 153-158 PubMed.
  • Rossmeisl J H Jr., Scott-Moncrieff J C, Siems J et al (2000) Hyperadrenocorticism and hyperprogesteronemia in a cat with an adrenocortical adenocarcinoma. JAAHA 36 (6), 512-517 PubMed.
  • Zimmer C, Hörauf A & Reusch C (2000) Ultrasonographic examination of the adrenal gland and evaluation of the hypophyseal-adrenal axis in 20 cats. JSAP 41 (4), 156-160 PubMed.
  • Zerbe C A (1999) The Hypothalamic-Pituitary-Adrenal Axis and Pathophysiology of Hyperadrenocorticism. Comp Contin Educ Pract Vet 21 (12), 1134-1137 VetMedResource.
  • Watson P J & Herrtage M E (1998) Hyperadrenocorticism in 6 cats. JSAP 39 (4), 175-84 PubMed.
  • Schwedes C S (1997) Mitotane (O,p'-DDD) treatment in a cat with hyperadrenocorticism. JSAP 38 (11), 520-524 PubMed.
  • Henry C J, Clark T P, Young D W et al (1996) Urine cortisol:creatinine ratio in healthy and sick cats. J Vet Intern Med 10 (3), 123-126 PubMed.
  • Duesberg C A, Nelson R W, Feldman E C et al (1995) Adrenalectomy for treatment of hyperadrenocorticism in - cats 10 cases (1988-1992). JAVMA 207 (8), 1066-1070 PubMed.
  • Nelson R W, Feldman E C & Smith M C (1988) Hyperadrenocorticism in cats - seven cases (1978-1987). JAVMA 193 (2), 245-250 PubMed.

Other sources of information

  • Helton-Rhodes K (1997) Cutaneous manifestations of hyperadrenocorticism. In: August J R (Ed)Consultations in Feline Internal Medicine 3. pp 191-198. Philadelphia, PA: W B Saunders. ISBN 0-7216-5814-8. (very good and concise discussion of specific dermatology).
  • Feldman E C & Nelson R W (1996) Hyperadrenocorticism in cats. In: Canine and Feline Endocrinology and Reproduction2nd edn. Philadelphia: W B Saunders. pp 256-261.
  • Feldman E C & Nelson R W (1991) Hyperadrenocorticism. In: August, J.R. (Ed) Consultations in Feline Internal Medicine. pp 267-270. Philadelphia, PA: W B Saunders. ISBN 0-7216-2226-7. (good review, very good discussion of therapy management).

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