{"id":1435427,"date":"2017-06-01T12:00:11","date_gmt":"2017-06-01T10:00:11","guid":{"rendered":"https:\/\/staging-wp-int.laboklin.com\/the-diagnosis-of-canine-hyperadrenocorticism\/"},"modified":"2024-07-24T12:49:12","modified_gmt":"2024-07-24T10:49:12","slug":"the-diagnosis-of-canine-hyperadrenocorticism","status":"publish","type":"post","link":"https:\/\/laboklin.com\/no\/the-diagnosis-of-canine-hyperadrenocorticism\/","title":{"rendered":"The Diagnosis of Canine Hyperadrenocorticism"},"content":{"rendered":"

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Physiology<\/span><\/h2>\n

Cortisol, which is produced in the adrenal glands, is absolutely essential in physiological concentrations. Cortisol regulates the metabolism by increasing glyconeogenesis, increases the reactivity of blood vessels, influences osmoregulation and electrolyte balance and has anti-inflammatory properties. <\/span><\/p>\n

In order to ensure that the body does not produce too much cortisol, its production is regulated by the hypothalamic-pituitary-adrenal axis. The hypothalamus secretes CRH (corticotropinreleasing hormone), which stimulates the hypothalamus to secrete ACTH (adrenocorticotropic hormone). ACTH causes an increase in corticol secretion in the adrenal glands. The hypothalamic-pituitary-adrenal axis is controlled by a negative feedback loop, which prevents the production of too much cortisol. Cortisol therefore inhibits the secretion of CRH and ACTH. <\/span><\/p>\n

Pathophysiology<\/span><\/h2>\n

Overproduction of cortisol leads to hyperadrenocorticism, which is also known as Cushing\u2019s syndrome. It is primarily caused by pituitary tumours (80-85%), whereby micro (85%) or macroadenomas (15%) secrete ACTH uncontrollably, which then leads to cortisol secretion in the adrenal glands. In these animals, cortisol levels are increased and ACTH is normal or increased:<\/span><\/p>\n

The remaining 15-20% are generally caused by unilateral benign or malignant adrenal tumours, which uncontrollably secrete cortisol. In these animals, cortisol levels are increased, while ACTH is reduced.<\/p>\n

Dogs with pituitary hyperadrenocorticism are 2-16 years old (average 7-9) and can be any sex or breed, although smaller dogs and poodles, dachshunds, and terriers (Yorkshire, Jack Russell, Staffordshire, Bull) are most commonly affected.
\nDogs with adrenal hyperadrenocorticism are older: 6-16 years old (11-12). Large breeds (>20 kg) are most often affected.<\/span><\/p>\n

The typical clinical signs in both cases are caused by increased cortisol levels in the blood. The same clinical signs can also be found in dogs that havebeen treated with exogenous steroids.<\/span><\/p>\n

Diagnosis<\/span><\/h2>\n

Cushing\u2019s syndrom is a clinical diagnosis in dogs. The following clinical signs are observed in dogs with hyperadrenocorticism (Peterson, 300 dogs):<\/p>\n

\u2022 Polyuria\/polydipsia 82%
\n\u2022 Pot belly 67%
\n\u2022 Hepatomegaly 67%
\n\u2022 Alopecia 63%
\n\u2022 Lethargy 62%
\n\u2022 Polyphagia 57%
\n\u2022 Muscle weakness 57%
\n\u2022 Anoestrus 54%
\n\u2022 Obesity 47%
\n\u2022 Muscular atrophy 35%
\n\u2022 Comedones 34%
\n\u2022 Panting 31%
\n\u2022 Testicular atrophy 29%
\n\u2022 Hyperpigmentation 23%
\n\u2022 Calcinosis cutis (pathognomonic) 8%
\n\u2022 Facial paresis 7%<\/p>\n

Unspecific tests should be carried out at first if Cushing\u2019s syndrome is suspected in a patient. Blood chemistry, haematology, and urinalysis are helpful. The following results are expected (Peterson, 300 dogs):<\/p>\n

\u2022 ALP (AP)\u2191 86%
\n\u2022 Eosinopenia 84%
\n\u2022 ALT\u2191 53%
\n\u2022 Hypercholesterinaemia 48%
\n\u2022 Hypophosphataemia 38%
\n\u2022 Total CO2<\/sub>\u2191 33%
\n\u2022 Leukocytosis 32%
\n\u2022 Erythrocytosis 17%
\n\u2022 Lymphopenia 14%<\/p>\n

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