The Soft-Coated Wheaten Terrier is one of the breeds listed in veterinary literature as having a predisposition for Addison’s disease. The purpose of this article is to provide Wheaten owners and breeders with information about the disease. Increased awareness will lead to early diagnosis and treatment before the crisis stage of the disease.

Addison’s disease is the common name and Hypoadrenocorticism the commonly used scientific name. Adrenal insufficiency and adrenocortical hypofunction are less commonly used terms. Addison’s disease is the insufficient production and secretion of hormones (glucocorticoids, mineralocorticoids and androgens) by the adrenal gland cortex. This is a disease that if left untreated, leads to death.

Dr. Thomas Addison first described the disease in humans in 1849. In 1856 it was demonstrated that removal of both adrenal glands resulted in the death of experimental animals. This proved that these glands are necessary for the maintenance of life. Addison’s disease in dogs was not reported until 1953.

What causes Addison’s disease? To date no one has discovered the cause or any specific risk factors for this disease. About 80% of human hypoadrenocorticism is immune-mediated destruction of the adrenal cortices. Many of the features of canine Addison’s disease resemble those in humans and it is likely that dogs also have this immune-mediated destruction.

What is Autoimmune disease? Autoimmunity is a misdirected immune response, in which the body’s defenses become self-destructive. Under normal conditions the body’s immune mechanism is able to recognize its own tissues and chemicals. This recognition of self is called immunologic tolerance. When tolerance breaks down the body fails to interpret its own cells as self. Autoimmunity may result from a combination of factors such as; genetic predisposition, hormonal factors and environmental triggers such as viral infections and vaccinations. Autoantibodies reactive to the adrenal cortex are diagnostic of autoimmune Addison’s disease and have been identified in dogs with this disease.

When immune-mediated disease affects the adrenal glands; it may also affect other glands. Up to 5% of Addisonian dogs have endocrine failure in the thyroid gland (hypothyroidism), the pancreas (diabetes), parathyroid gland (hypoparathyroidism) and reproductive disorders (primary gonadal failure). Addison’s disease does not cause other disorders; it is just that the immune disorder may affect more than one tissue.

Who gets Addison’s disease? Addison’s disease can occur in dogs of any age, sex or breed. Current research has shown this to be primarily a disease of young to middle-aged females as is the case for most immune-mediated disorders in the dog. Up to 70% of dogs diagnosed are female. 80% are 7 years of age or younger with the average age being 4.6 years. Dogs of all breeds are affected, including mixed breeds. Recent publications describe an increased familial or genetic predisposition with a possible contribution of triggers as a cause for the disease in some breeds.

Two examples of familial predisposition are; (1) a group of related Standard Poodles was studied and ten were found to have Addison’s disease. This group had no pattern of inheritance, but the prevalence of disease was extremely high compared to the general canine population. (2) The 1996 Autoimmune Endocrine Health Survey for Bearded Collies also concluded there was a hereditary Addison’s disease that exists in the Bearded Collie population.

Dr. Margaret Slater has just completed a health survey for the SCWTCA. There were 1246 dogs in the final survey, a total of 4 Wheatens with Addison’s. This is 0.6% of the 1246 dogs. She states it doesn’t appear to be very common in the breed.

Dr. Meryl Littman states that the prevalence of Addison’s in SCWT’s is really not known. She estimates she knows of over 350 Wheatens with PLE/PLN, but only a dozen or so with Addison’s. "So although there is a predisposition in the SCWT breed, Addison’s is still not that common". She does not know of any pedigrees with a higher incidence of Addison’s, but this needs more study. It appears to be a sporadic problem within the breed.

There are two types of Addison’s disease. Primary hypoadrenocorticism constitutes the majority of canine cases. This type originates within the adrenal glands and is an atrophy or destruction of all layers of the adrenal cortex. Secondary hypoadrenocorticism is caused by decreased secretion of hormones by the hypothalamus or the pituitary glands. Their hormones stimulate the adrenal cortex to release its hormones. Without these triggering hormones the adrenal glands fail to function

The adrenal glands are small structures located above each kidney. They have two main sections: the center or medulla and the outer area or cortex. Addison’s disease concerns hormones called corticosteroids produced by the cortex. There are two main types of corticosteroid - glucocorticoids and mineralocorticoids. They are needed to adapt to stressful situations and without them, even small stresses can lead to disaster.

Cortisol is the major adrenal glucocorticoid. It affects every tissue in the body and is responsible for carbohydrate, lipid and protein metabolism, maintenance of normal blood pressure, and counteraction of the effects of stress. To counteract stress cortisol increases glucose levels in the blood, providing a source of energy for all the body’s activities. Abnormal adrenal glands do not secrete any cortisol causing decreased levels of glucose to deal with stress. Aldosterone is the major mineralocorticoid and is responsible for maintaining the levels of minerals, sodium, potassium and chloride in the body. Aldosterone’s affect on the kidneys results in the maintenance of fluid levels and mineral balance in the body.

The onset of Addison’s disease is a gradual process with 85 to 90% of adrenal cells being destroyed before signs of deficient secretion become obvious. Individual variation exists among dogs so some dogs show symptoms earlier or later than others. A partial deficiency syndrome may occur, where the adrenal glands secrete adequate amounts to maintain a near-normal state. Symptoms only occur during periods of stress when there are inadequate levels of corticosteroids to deal with the stressful situation. As destruction progresses secretion is inadequate even under non-stressful conditions.

This illness appears to affect some dogs episodically. These dogs fluctuate between appearing normal and quite ill. This waxing-waning course of illness is not always obvious to owners of affected dogs. Vague symptoms such as; occasional anorexia, vomiting, and/or diarrhea, muscle weakness, lethargy and depression are common. The vague symptoms often have the owner talking him or herself out of a veterinary visit. Signs of illness are often nonspecific and similar to more common diseases such as kidney, gastrointestinal and infectious diseases. The mimicking of other diseases is why Addison’s disease is often called the "great pretender".

A hallmark symptom of Addison’s disease is impaired tolerance to stress. Even mild physical or emotional stress can cause an Addisonian crisis. A healthy dog responds to stress by releasing cortisol. Dogs with Addison’s disease can’t do this. Therefore, the physiologic defense provided by cortisol does not operate. Absence of Aldosterone compounds the problem with depletion of fluids and impairment of cardiac function. This leads to eventual circulatory collapse.

What constitutes stress and the amount of stress a dog can tolerate varies with each dog. Examples of stressors are: elective surgery such as spaying/neutering, traumatic injuries, infection, vaccinations, cold weather, or psychological distress such as trips to the veterinarian, the family packing up for a vacation, being placed in a boarding kennel, traveling or summer thunderstorms. Stress can be fun things too such as agility or obedience classes.

Commonly reported symptoms. Severity can vary dramatically from dog to dog.

• Anorexia

• Thin/Weight Loss
• Depression/Lethargy
• Vomiting/Diarrhea
• Weakness
• Collapse
• Shaking and Shivering
• Excessive urination with or without excessive thirst
• Waxing and Waning Course of Illness
• Painful/Sensitive Abdomen
• Fatigue/exercise intolerance
• The dog may also appear clumsy and unable to climb stairs or jump on the bed. This may be due to muscle loss or weakness. The dog does not have the strength to do normal activities.

On examination by the veterinarian the dogs were noted to have;

• Mental Depression
• Thin/emaciated
• Muscular Weakness
• Dehydration
• Slow weak pulse
• Blood in feces
• Gastrointestinal hemorrhage
• Collapse
• Abdominal pain
• Pale mucous membranes/anemia
• Low temperature
• Low blood pressure
• Grand Mal Seizure

Addisonian Crisis the Endocrine Emergency. Addisonian crisis occurs when the dog is in circulatory collapse and shock. The deficiency of Aldosterone leads to severe depletion of sodium (hyponatremia) resulting in depletion of body fluids (hypovolemia) and potassium retention (hyperkalemia). This progresses to collapse, bradycardia (slow heart rate), hypotension (low blood pressure). and associated cardiac arrhythmias (abnormal heart beats). In Addison’s hypovolemia and shock cause bradycardia but in other diseases this condition causes tachycardia (fast heart rate). Deficiency of cortisol causes low blood sugar levels (hypoglycemia). Hypoglycemic seizures have been reported in dogs with Addison’s. Decreased secretion of gastrointestinal enzymes causes anorexia, nausea, vomiting, flatulence and diarrhea. These symptoms as well as anxiety, mental depression, and loss of mental acuity, may also be related to the absence of cyclic peaks of cortisol.

This crisis may be the first time the owner suspects anything is wrong and may be fatal if not treated promptly. The goal of emergency treatment is stabilization with aggressive therapy. Virtually every dog treated with IV therapy, glucocorticoids, and mineralocorticoids have shown rapid improvement. There may be a need for intensive monitoring and therapy for several days to stabilize the dog. Studies have found that between 33 to 51% of dogs with Addison’s were diagnosed during a crisis. The dog owners stated their dog had signs and symptoms of being unwell, but they had a difficult time getting a definitive diagnosis. The emotional trauma to both the dog and its owners, combined with expense are the primary reasons for early diagnosis before crisis occurs.

Diagnostic Testing: Blood Chemistry Profile: Electrolyte profiles (Sodium, Potassium, Chloride) are extremely valuable. They support a tentative diagnosis and are useful in modifying therapy. Balance of these chemicals is vital to health and abnormal levels can be life threatening. The diagnostic chemistry profile will have a low sodium (<135 meq/L) and elevated potassium (>6.0 meq/L). Sodium potassium ratios are used to identify adrenal insufficiency. Normal ratios are between 27:1 and 40:1. In primary hypoadrenocorticism the sodium: potassium ratio will be below 25:1. However, these changes are not present in all dogs. EKG abnormalities are associated with high potassium and low sodium. Untreated high potassium can lead to cardiac arrest and death. Other diseases can cause elevated potassium and/or low sodium. The definitive test for Addison’s disease is the ACTH stimulation test. This test directly assesses the capacity of the adrenal gland to secrete cortisol and indirectly assesses Aldosterone secretion. An ACTH stimulation test should be considered in dogs with signs of weight loss, decreased appetite, and intermittent vomiting and diarrhea.

Long-term Management of Dogs with Primary Hypoadrenocorticism. In every case, medications must be administered to maintain the life of the animal. Treatment is replacement of the hormones with synthetic glucocorticoids (i.e. Prednisone) and mineralocorticoids (i.e. Florinef or Percorten V). Therapy usually brings about a rapid recovery, and involves life-long medications. Steroids do not cure disorders; they just treat the symptoms. Prednisone may be needed on a regular basis, or at times when the dog will be in a stressful situation. These medications come in multiple potencies and forms and have no set or consistent dosage. They need to be individualized to the severity of the condition and the patient response. When given in the minimum dose that maintains a therapeutic response side effects can be kept to a minimum. Key is to remember every dog is different. Once achieved improvements in the dog’s health are usually maintained.

Florinef (fludrocortisone) is in pill form and has been used for treatment of dogs with Addison’s for over 20 years. Advantages of this medication are; dosage can be quickly changed to adjust incorrect doses, most owners can administer tablets and the drug is readily available at most human pharmacies. Disadvantages are; extremely high doses may be required which increases the side effects, owner compliance in giving the medication on a regular basis is often a problem and at high doses this therapy is expensive.

Percorten V or DOCP (desoxycorticosterone pivalate) is an injection that is given once every 21 to 30 days. The dog on this medication may also require low doses of Prednisone. The most common cause of Percorten treatment failure is insufficient supplemental glucocorticoid administration. Advantages of this form of treatment are; infrequent doses of the drug (every 21 to 30 days) improves compliance, most owners can be taught to administer injections to their dogs and expense is similar or less in larger dogs. Disadvantages are; the need for supplemental Prednisone, if the owner is unable to give injections it must be done at a veterinarian’s office at an added expense, pain on injection and the drug is not as readily available as Florinef and must be purchased at the veterinarian’s office.

Most often the veterinarian will try to stabilize the dog on Florinef. If this is not possible a change to Percorten V (DOCP) is indicated. The goal is to use the medication that produces the desired effect - a healthy and happy dog.

One side effect that requires caution is immune system suppression. Synthetic glucocorticoids produce suppression of the immune system by suppressing antibody formation. This can lead to compromised resistance and susceptibility to infection. When vaccinating Addisonian dogs avoid giving combinations by using separate injections at spaced intervals to prevent overwhelming the immune system.

The owner has to pay close attention to a dog with this disease by watching for signs and symptoms and changes in the dog’s behavior. These dogs crash quickly! Okay in evening but by morning all signs and symptoms present. Symptoms that can alert owners to a problem are; dehydration (touch the dogs gums, if they feel tacky this is a sign of dehydration, a well hydrated dog has wet slippery gums), changes in appetite, vomiting and/or diarrhea, appear tired and there is no tail wagging.

I was fortunate to communicate with four Wheaten owners whose dogs have Addison’s disease. They provided me with detailed information about their experiences and the health of their dogs. The course of their disease followed the clinical picture described in much of the literature I read.

If the diagnosis of Addison’s disease is made early, it is controllable with an excellent prognosis. After therapy stabilizes the condition, the dog can usually lead a normal life with few if any restrictions. The most important factors are long-term response to medications and diligent owners and veterinarians. Recognition of the disease and the cost of treatment seem to be the biggest obstacles to a successful outcome.

With the health focus for Wheaten breeders and owners on PLE and PLN we must not forget there are other diseases affecting our breed. Many of the signs and symptoms are the same. Let us be vigilant and not overlook other causes of illness as this leads to delayed diagnosis and treatment of those diseases. This in turn leads to prolonged illness of our dogs. Addison’s disease is another reason to send the dog’s information to the open registry. If there is a hereditary link we need to find and understand it.

I would like to acknowledge the following for their help in my research: Kathleen Strauser, Exec Director, Canine Addison’s Disease Awareness Collaborative, for information, articles and suggestions; the owners who submitted information about their dogs and experiences, Dr. Margaret Slater for correspondence on preliminary data from 1999 SCWT Health Survey and Dr. Meryl Littman for her correspondence.

I used 46 articles/textbooks and many personal correspondences to research this topic. Listed are the key references:

1. Feldman, Edward C. D.V.M. and Nelson, Richard W. D.V.M. (1996). Canine and Feline Endocrinology and Reproduction (2^nd ed.). Philadelphia: W.B. Saunders Co.

2. Novartis Animal Health Professional Services. Canine Hypoadrenocorticism: Diagnosis and Treatment of an Emerging Disease. Greensboro, NC. Novartis Animal Health US Inc..

3. Canine Addison’s Disease Awareness Collaborative (May 1999). Addisonian Dog Owners Survey. k9 Addison’s Internet Support Group k9Addisons@egroups.com

4. Littman, Meryl P., (1999). ACIVM Proceedings Wheaten Terrier PLE-PLN. Proceedings of the 17^TH Annual Veterinary Forum, ACIVM 1999, 554-556.

5. Littman, Meryl P., Dambach, D.M., Vaden, Shelley L. and Giger, U., (2000). Familial Protein-Losing Enteropathy and Protein-Losing Nephropathy in Soft Coated Wheaten Terriers: 222 Cases (1983-1997). Journal Veterinary Internal Medicine 14, 68-80.

6. Levy, J.K., (1994). Hypoglycemic seizures attributable to hypoadrenocorticism in a dog. Journal American Veterinary Medicine Association 204(4), 526-530.

7. Melian, C. and Peterson, M.E., (1996). Diagnosis and treatment of naturally occurring hypoadrenocorticism in 42 dogs. Journal Small Animal Practice (37) 6, 268-275.

8. Peterson, M.E., Kintzer, P.P. and Kass, P.H., (1996). Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). Journal American Veterinary Medical Association 208(1), 85-91.

9. Login, Joyce A., (1998). Diagnosis and Treatment of Hypoadrenocorticism (Addison’s Disease). Veterinary Medical Bulletin. Novartis Animal Health US, Inc.

10. Kelch, W.J., Lynn, R.C., Smith, C.A. and New, J.C.Jr., (1998). Canine Hypoadrenocorticism (Addison’s Disease). Compendium of Continuing Education for the Practicing Veterinarian 20(8), 921-935.

11. Schaer, M., Riley, W.J., Buergelt, C.D., Bowen, D.J., Senior, D.F., Burrows, C.F. and Campbell, G.A., (1986). Autoimmunity and Addison’s Disease in the Dog. Journal American Animal Hospital Association 22, 789-794.

12. Report on the 1996 Autoimmune Endocrine Health Survey. Beardie Bulletin, November 1997. and Sell, Elsa, MD Health Committee Chairperson (1998). Addison’s Update, Beardie Bulletin, May 1998.

About the author: I have a degree in nursing and no veterinary training. I presented information on Addison’s disease for the health seminar at the Soft-Coated Wheaten Terrier Association of Canada’s National Specialty in June 2000. This article is a small portion of the information presented. I have tried to make the article informative without getting too technical. Please contact me if you would like more information or the complete reference listing.

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