Addison's Disease in Great Danes

Addison’s disease (hypoadrenocortism) is the result of a failure of the cortex of the adrenal glands to produce hormones vital for life. The body has two adrenal glands which are situated at the top end of both kidneys , deep in the abdomen. The two hormones produced by the adrenal glands are glucocorticoids ( corticosteroids) and mineralocorticoids . Both hormones are produced in the cortex or outer shell of the gland under the influence of a releasing hormone produced in the brain. This hormone production is the same as with the thyroid gland. When the body signals its need for more adrenal gland hormones the brain receives the message to manufacture more hormones. This signal is then sent to the adrenal gland via blood messages to produce increased amounts of the required hormone.

Glucocorticoid hormones main effect is on carbohydrate, protein and fat metabolism and to promote the production of glucose by the liver from specialised enzymes. It also has an important effect on muscles, bone, skin, blood, kidneys, fatty tissue and the immune system. Its affect on the immune system and inflammatory process are suppressive hence reducing fever, inflammation and pain. Mineralocorticoids are important in controlling low blood pressure and excessive build up of an important electrolyte called potassium. This is achieved by balancing sodium and chloride ( these electrolytes make up common table salt) and water in the body.

Addison’s disease is a syndrome that results from a deficiency of both glucocorticoids (corticosteroids) and mineralocorticoids secretion from the adrenal gland cortex. Destruction of more than 90% of both adrenal glands causes a clinical deficiency of both hormones and is termed primary hypoadrenocortism or Addison’s disease. Secondary hypoadrenocortism is caused by a deficiency of the brain hormone that is used to send the message to the adrenal glands to increase hormone production.

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Addison’s disease occurs more frequently in dogs than other species. There are many causes of this disease but the most common are;

  • the self destruction of the adrenal gland where it is literally attacked by the bodies own defence mechanism
  • medication used to treat other diseases
  • destruction of the adrenal glands due to tumours
  • haemorrhage or a clot in the blood supply to the gland
  • fungal infections
  • tumours of the adrenal gland

Anyone of the above causes would lead to a deficiency of mineralocorticoids and glucocorticoids. There is no breed preference to this disease and all dogs are equally susceptible of developing the disease. The disease does however seem to occur in dogs from 3 months to 9 years with the average age being about 4 – 5 years. 70% of all cases reported in dogs have been seen to occur in bitches.

The clinical signs are varied and may be either acute or chronic. The chronic form of the disease is far more common.

The appearance of the acute form is sudden collapse or collapsing when stressed. Other signs include a weak pulse, a slow heart rate, abdominal pain, vomiting and diarrhoea. This is the severest form of the disease and is treated as an emergency.

The clinical signs of the chronic form are vague and non-specific, with symptoms of a ‘waxing-waning type of illness’. The severity of each sign can vary and is usually interspersed with periods of apparent good health. This disease can easily be mistaken for kidney disease, neuromuscular disorders and various other illnesses resulting in weakness, weight loss, vomiting and diarrhoea. The most common findings on a clinical examination are depression and weakness, a slow heart rate and a weak pulse. This disease can only be diagnosed from laboratory tests of blood and urine samples an ECG ( electrocardiogram – a graphic picture of the heart beat) and radiography ( xray pictures of the body).

Initial treatment of this disease involves intravenous fluid drips and glucocorticoid therapy if the dog is presented in a collapsed state. Once the dog is stable then maintenance treatment consisting of synthetic glucocorticoids and mineralocorticoids to replace the body’s deficiency. This also needs to be administered with table salt to balance the electrolytes the body is having a problem with trying to control.

The prognosis of this disease is good provided the cause is not a tumour or some irreversible condition. It is very important that the owner understands the disease and is able to administer treatment if a crisis situation develops.

Guy Liebenberg BSc BVSc MRCVS Cert Vet Acu

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