Hypoadrenocorticism (Addison’s Disease): A Great Pretender

One of my favorite diseases to diagnose and treat is Addison’s disease. The medical name for this disease is hypoadrenocorticism, an adrenal gland disorder that predominantly affects dogs and rarely cats. The opposite of Cushing’s disease, this disease can manifest in a myriad of ways. This week I spend some time introducing this interesting disease in an effort to raise awareness. Happy reading!

Hypoadrenocorticism (Addison’s Disease) – What is it?

Addison’s disease or hypoadrenocorticism is the result of abnormally low hormone production by a part of the adrenal glands called the cortex. Think of the adrenal glands as peanut M&Ms™ – there is the peanut center and a chocolate coating. Addison’s disease is caused by a problem in the chocolate coating. Specifically, one or more important hormones, most notably cortisol and aldosterone, are not produced in adequate volumes. These hormones are essential for regulating water balance, salt, and sugar in the body.

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The normal basic anatomy of the adrenal glands

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The adrenal cortex of the adrenal glands can be thought of as the chocolate coating of a peanut M&M(™)

 

When animals are stressed, their adrenal glands synthesize the hormone cortisol to help them cope with various stressors. Addisonian patients can’t make enough cortisol, and thus are not able to adequately deal with stress. Stressors are quite individual, and vary widely based on a patient’s temperament. For many patients living with Addison’s disease, any change in normal routine (e.g.: having house guests, boarding in a kennel, etc.) is stressful and can precipitate signs of disease.

Hypoadrenocorticism most commonly occurs in young to middle-aged female dogs, but can occur in males too. Addison’s disease rarely occurs naturally in cats. Some breeds are over-represented, particularly Standard Poodles, West Highland White Terriers, Great Danes, Bearded Collies, Portuguese Water Dogs, and Wheaten Terriers.

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Standard Poodles are over-representing for living with Addison’s disease

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Wheaten Terriers are over-represented for living with Addison’s disease

 

Common clinical signs of Addison’s disease include:

  • Weakness
  • Collapse
  • Reduced (or loss of) appetite
  • Vomiting
  • Diarrhea
  • Weight loss
  • Blood in feces
  • Abdominal pain
  • Shaking
  • Dehydration
  • Abnormal heart rhythm
  • Increased thirst (called polydipsia)
  • Increased frequency of urination (called polyuria)

Clinical signs of Addison’s disease may occur suddenly and can be life-threatening – such a manifestation is called an Addisonian crisis. However, signs of illness may also occur intermittently and vary in severity. As you can see, many of the common clinical signs are very general ones, and are often associated with other illnesses. For this reason, Addison’s disease is called a “great pretender.”

Hypoadrenocorticism (Addison’s Disease) – How is it diagnosed?

As I have discussed in previous blog posts, the two most important initial tests a veterinarian will perform for sick pets is obtaining a thorough patient history and performing a complete physical examination. Based on the information from them, additional blood and urine screening will be recommended, typically:

  • Complete blood count or CBC: This is a non-invasive blood test that tells veterinarians about a pet’s red blood cells, white blood cells, and platelets (initial clot-forming cells). When animals are stressed, there are expected changes in some types of white blood cells that occur due to the release of cortisol by the adrenal glands – these changes are cumulatively called a “stress leukogram.” Remember Addisonian patients can’t make enough cortisol, so these expected changes are not documented. This phenomenon is referred to as “a lack of a stress leukogram.”
  • Serum biochemical profile or CHEM: This is a non-invasive blood test that evaluates liver and kidney values, and as well as some digestive enzymes and electrolyes (e.g.: sodium, potassium, and chloride). Classic or typical Addisonian patients commonly have elevated kidney values, as well as elevated potassium, low sodium, low chloride, elevated calcium, low blood glucose/sugar, and low cholesterol levels. Mild-to-moderate liver enzymes changes are also possible. Elevated potassium levels can be associated with life-threateningly abnormal heart rhythms. Electrolyte derangements are chiefly caused by an inadequate production of a hormone called aldosterone, while the other changes are predominantly caused by a lack of cortisol. Typical Addisonian patients have deficiencies in both aldosterone and cortisol, but some have issues only with cortisol. Such patients are said to be living with atypical Addison’s disease, and are not expected to have the classic electrolyte abnormalities.
  • Urinalysis or UA: The vast majority of patients with Addison’s disease have dilute urine due to a lack of aldosterone that prevents adequate urine concentration.

Upon review of these results, an additional non-invasive blood test called an adrenocorticotropic hormone (ACTH) stimulation test may be recommended.

The ACTH stimulation test is the definitive diagnostic test for Addison’s disease.

To perform this test, a baseline blood cortisol level is collected from a vein. Subsequently a patient is injected in a vein with ACTH in an attempt to stimulate the adrenal glands to secrete cortisol. Another blood sample is collected one (1) hour after ACTH injection. Patients living with Addison’s disease can’t produce more cortisol in response to the injected ACTH, and thus the second blood cortisol sample is essentially unchanged from the baseline value.

Hypoadrenocorticism (Addison’s Disease) – How it is treated?

Patients with severe clinical signs – an Addisonian crisis – require immediate hospitalization and aggressive critical care. Stabilization with intravenous fluids, nutritional support, and supplementation of cortisol-like and aldosterone-like hormones the body can no longer adequately produce is of paramount important to treatment success. Partnering with a board-certified veterinary emergency and critical care specialist or board-certified veterinary internal medicine specialist can be instrumental in maximizing the likelihood of a positive outcome.

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Patients with Addison’s disease often initially require hospitalization for intensive therapies, including intravenous fluids

 

Addison’s disease is not curable, but it is entirely and readily treatable. Chronic treatment involves supplementing patients with cortisol-like and possibly aldosterone-like medications for life because their adrenal glands can’t adequately perform these functions. Those who are diagnosed and managed appropriately can lead a normal, high-quality life. I often say if I have to diagnose a life-long disease in one of my patients, I want to diagnose Addison’s disease because these fur babies generally respond quickly and wonderfully!

The take-away message about hypoadrenocorticism (Addison’s disease)…

Addison’s disease or hypoadrenocorticism is an adrenal gland disorder characterized by inadequate production of some important hormones, most notably cortisol and aldosterone. Recognizing the possibility of this disease in patients is not always straightforward, and consultation with a board-certified veterinary internal medicine specialist can be invaluable for obtaining an efficient diagnosis. With timely life-long treatment, patients with Addison’s disease can lead happy and full lives.

To find a board-certified veterinary internal medicine specialist, please visit the American College of Veterinary Internal Medicine.

To find a board-certified veterinary emergency and critical care specialist, please visit the American College of Veterinary Emergency and Critical Care.

Wishing you wet-nosed kisses,

cgb

Dr. Christopher G. Byers is a board-certified veterinary emergency/critical care and small animal internal medicine specialist, and is a contributing author to multiple veterinary textbooks. He is the founder and editor of CriticalCareDVM.com, and can be found on all social media sites (Facebook, Twitter, LinkedIn, Instagram, Tumblr, Pinterest).