Addison’s Disease in Dogs

Introduction

Addison’s disease (AD) is also called primary adrenal insufficiency or hypoadrenocorticism (HA).1 It is a disorder of the adrenal glands, which are located near the kidneys. The glands are responsible for producing hormones – aldosterone and cortisol.1 The hormones’ purpose is to control the water balance of the body, as well as its salt and sugar levels. Cortisol also helps dogs deal with stressful situations. In animals, the condition is usually referred to as HA, although its common name (AD) can be used as well.

It is a disease that is hard to diagnose as most of its symptoms are vague.2 In fact, the state of dogs with HA may worsen if they experience stress, which complicates the diagnosis further. These situations may lead to Addisonian crises as the production of cortisol stays low, limiting the animal’s ability to deal with stress.2 Therefore, it is necessary to learn about AD’s symptoms and presentation to diagnose the condition on time and provide patients with treatment that is sufficient for them to live a healthy life. The analysis of this disorder’s etiology and pathology is also crucial as it allows one to see how AD can be developed in dogs of different breeds.

Etiology and Pathology

HA is commonly divided into two types – primary and secondary. In both variations, the adrenal glands are damaged or suppressed. They do not produce enough hormones for the dog to cope with stress and maintain a healthy water and electrolytes balance. Primary AD occurs in the majority of dogs with this condition.2 It is usually further divided into typical and atypical disorders. The typical HA is an autoimmune condition where the dog’s body destroys its adrenal tissue.1 Environmental causes, toxins, concurrent diseases, cancer, or medications, can trigger the development of the atypical variety.2 Cushing’s syndrome – the condition where the production of cortisol surpasses normal levels, can also become a foundation for the animal to develop HA.1 If the treatment of the syndrome ends in the destruction of the adrenal tissue, the dog’s hormone levels decrease drastically, leading to HA.

Secondary AD occurs in dogs that have issues with their pituitary gland, for example, if it grows a tumor or is damaged in another way.2 As this gland is responsible for the regulation of hormones in the brain; the tumor interferes with its normal functioning and damages the adrenal glands in the process. Other reasons include previous medical treatment with steroids that have been stopped abruptly after prolonged use.1 This condition can be temporary or persistent, depending on the specific case.

Epidemiology

While the condition is not common, some data about its distribution exists in scholarly research. The majority of all canine HA cases are of the primary type in which an autoimmune reaction affects the adrenal cortex and destroys it as a result.1 Secondary HA occurs much less frequently, which can be explained by its connection to other diseases and health-related issues. In the first case, the most common factors that influence the autoimmune system are not transparent, and the disorder is usually described as idiopathic. The prevalence of HA in dogs also differs in regards to their age, sex, and breed. According to some studies, there is a predominance of HA among female dogs, with some reporting that it is rather significant.1 However, other research does not find a strong correlation between sex and AD development, noting that some breeds do not show any signs of such distribution.1 Thus, this aspect needs to be investigated further to support or contradict the existing findings. As for the patients’ age, dogs develop AD while they are young or middle-aged.

A separate sphere of research is devoted to breed-specific manifestations and the prevalence of HA. The condition is said to appear more often in a number of breeds, including poodles, Portuguese water dogs, collies, Labrador retrievers, and Nova Scotia duck tolling retrievers.3 In standard poodles, the predominance of autoimmune diseases can be exceptionally high because of the breeding process – dogs are chosen and inbred to adhere to the contest-winning form.3 The list of such disorders includes a variety of conditions such as thrombocytopenia, pancytopenia, and thyroiditis. Therefore, genetic bottleneck inbreeding of poodles may be a reason for AD occurring at such a frequent rate. Nevertheless, it remains unclear whether this breed has any difference in numbers between male and female dogs.

Clinical Presentation and Diagnosis

During the development of AD, the animal’s adrenal glands are destroyed or decreased in size. The clinical presentation has a set of symptoms that can easily be attributed to a number of other conditions.2 Some characteristics and signs of the general HA include weakness, lethargy, dehydration, vomiting, loss of appetite, and depression.2 All mentioned above symptoms can be associated with many conditions such as stomach problems or the flu.1 Other common symptoms of AD are more severe than others. Diarrhea, excessive thirst, shaking, unstable and slow heart rate can increase the dog’s stress, contributing to the development of the condition. If left untreated, the animal can have an Addisonian crisis defined by the mentioned above symptoms becoming severe and debilitating.2 A dog with HA can collapse after experiencing a stressful situation. Some patients can also be cool to touch, although this sign is not as universal.

To diagnose AD, healthcare professionals have to perform a number of diagnostic tests on the patient. The history of previous lab test results can show if any changes are rapid or significant. Analyses that evaluate the condition of the dog’s kidneys and liver, electrolyte levels, and urine contents can provide one with some insights into the animal’s health. For example, sugar levels can be measured to find an inconsistency with the previous results.1. Another way to diagnose AD can include antibody diagnostics, although the conclusions may be indefinite.4 Finally, an ACTH-stimulation test will show how low the levels of cortisol in the blood are.2

Treatment and Prevention

Dogs have to be treated for other diseases, regularly monitored to detect any changes in hormonal levels, and medications should not be stopped abruptly. The basic treatment of AD is the reduction of stress and replacement of missing hormones with prednisolone or gluco- and mineralocorticoids.2 They can be administered in the form of tablets and injections.1 The first method may suit some dogs, while the second can be more comfortable for others because injections are stressful but less frequent.2 For example, a 3 kg patient can be given prednisolone with a dose of 0.5 mg/kg every 6 hours for the duration of one day with the continuous reduction of the dosage to 0.1 mg/kg per day.2 Thus, during the first day of treatment, the dog would receive 6 mg of the drug.

References

Hanson JM, Tengvall K, Bonnett BN, Hedhammar Å. Naturally occurring adrenocortical insufficiency – an epidemiological study based on a Swedish‐insured dog population of 525,028 dogs. J Vet Intern Med. 2016;30(1):76-84.

Reusch CE, Fracassi F, Sieber‐Ruckstuhl NS, Burkhardt WA, Hofer‐Inteeworn N, Schuppisser C, Stirn M, Hofmann‐Lehmann R, Boretti FS. Altered serum thyrotropin concentrations in dogs with primary hypoadrenocorticism before and during treatment. J Vet Intern Med. 2017;31(6):1643-8.

Pedersen NC, Brucker L, Tessier NG, Liu H, Penedo MC, Hughes S, Oberbauer A, Sacks B. The effect of genetic bottlenecks and inbreeding on the incidence of two major autoimmune diseases in standard poodles, sebaceous adenitis and Addison’s disease. Canine Genet Epidemiol [Internet]. 2015;2(1):14. Web.

Baumstark ME, Sieber‐Ruckstuhl NS, Müller C, Wenger M, Boretti FS, Reusch CE. Evaluation of aldosterone concentrations in dogs with hypoadrenocorticism. J Vet Intern Med. 2014;28(1):154-9.