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     CANINE ADDISONS DISEASE     

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Addison's is an uncommon disease yet it can cause incapacitating illness or death, though many dogs respond well to treatment.  The disease, also known as hypoadrenocorticism, results from a deficiency of the bod's steroids.  Steroids are vital to many of the body's control mechanisms, including electrolyte levels, heart function and blood pressure.  As a result, symptoms of disease can be wide ranging and vary from mild to severe.

Middle-aged female dogs are most commonly affected.  The average patient is five years old, but Addison's can occur in dogs less than one year to greater than 12 years.  In addition to spontaneous disease, Addison's can occur following veterinary medication and then withdrawal of steroid treatment  given for a wide range of conditions.  Most dogs suffer no ill-effects following steroid treatment, thouigh some remain Addisonian for life.

The worst form of the disease is the potentially fatal Addisonian crisis.  Patients are collapsed and generally have diarrhoea, vomiting and slow heart rates.  Weakness, dehydration and hypothermia are common.  In contrast, most affected dogs suffer mild "waxing and waning" disease over many years, with occasional diarrhoea and vomiting, and periods of lethargy.  Digested blood may be passed in faeces that appear dark and tar-like.

Acutely affected dogs need life-saving intravenous fluids and steroids.  Lonf term treatment requires replacement of one or more of the steroids which the dog lacks.  Dogs require periodic blood tests to check the adequacy of treatment.  In periods of stress such as hospitalisation or travel, increased doses of steroids may be needed to control symptoms.  Treatment is lifelong, and is started at low doses which are gradually increased if necessary.
Harvey Caruthers

reprinted with kind permission from Alastair Balmain
Deputy Editor:Shooting Times & Country Magazine
Blue Fin Building, 110 Southwark Street SE1 0SU
Tel: 020 3148 4750

 
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Canine Addison's Disease
Addison's Disease

Addison's Disease or Hypoadrenocortiscm

So your Dog has Addison's Disease

Diagnosis Kidney Disease - or is it?


CANINE ADDISON'S DISEASE

http://www.petwellness.com
 
Lack of energy, vomiting and weight loss in dogs may be symptoms of a number of common disorders; however, they can also be early signs of a relatively rare disorder called Canine Addison's Disease (hypoadrenocorticism). Because it is so easily confused with many other diseases and frequently remains undiagnosed until the dog collapses from weight loss, weakness or dehydration, Canine Addison's Disease is often referred to as "The Great Pretender." If left untreated, the disease can be critical, even fatal. 

Canine Addison's Disease occurs when a dog's adrenal glands do not produce enough hormones and other chemicals that help regulate many bodily functions, such as metabolism, blood pressure and stress response. While it is not contagious, it is not fully understood why dogs develop Addison's. The most likely cause is genetic; however, other possible causes include infections, immune system disorders and trauma. 

Studies have found that 70% to 85% of dogs with Canine Addison's Disease are female1 and that the dogs most often affected are between 4 and 7 years old. Some breeds seem to be affected more commonly than others. These breeds include Great Danes, Portuguese Water Spaniels, Rottweilers, Standard Poodles, West Highland White Terriers and Wheaten Terriers. 

Some of the most common signs a pet owner may observe in a dog with Canine Addison's Disease include:

Most Common Signs
Less Frequent Signs
Anorexia
Lack of energy
Weakness
Vomiting
Diarrhea
Weight loss
Dehydration 

Bloody vomit or stool
Excessive thirst or urination
Loss of appetite
Hair loss
Shaking and tremors 


If your dog shows any of these signs, consult a veterinarian at once. Chances are, your dog does not have Addison's, but any discomfort or irregularity should always be evaluated by a veterinarian. 

Although abnormalities may be noted in EKGs and X-rays, veterinarians generally use laboratory tests to confirm the diagnosis of Canine Addison's Disease. These may include various blood and urine tests. Even then, Canine Addison's Disease may escape diagnosis because the results of the laboratory tests may be similar to those in dogs with kidney failure. 

The ACTH stimulation test provides one of the most accurate and reliable tests for diagnosing Canine Addison's Disease. For this test, the veterinarian collects blood samples before and after giving the patient an injection of a hormone to see how the dog's body responds. 

Most veterinarians will treat Canine Addison's Disease with a medication that replaces the hormones that the adrenal glands can no longer produce. Today, the only medication approved by the FDA* for treating Canine Addison's Disease is PERCORTEN®-V (desoxycorticosterone pivalate). 

It has been demonstrated that PERCORTEN-V is well tolerated with a low incidence of side effects. In a small percentage of treated dogs, depression, excessive thirst and urination, digestive, skin and coat changes, weakness and injection site reactions (pain, abscesses) may occur. Some of these effects may resolve with adjustments in dose or interval of PERCORTEN-V or concomitant glucocorticoid administration. 

Do not use in pregnant dogs or in dogs that are suffering from congestive heart disease, severe renal disease or edema. Dogs with renal failure must be stabilized before receiving PERCORTEN-V.
 
*NADA #141-029, Approved by FDA.
1. Hardy RM: Hypoadreanal gland disease. In Ettinger SJ, Feldman EC, editors. Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders; 1995. p 1579-1593.
2. Kelch WJ. Canine hypoadrenocorticism (Addision's Disease). The Compendium, June 1998.
3. Grooters AM. Addision's Disease: Diagnosis and Treatment. In: North American Veterinary Conference 1998 Proceedings. Gainesville, FL: Eastern States Veterinary Association; 1998. p 238-242.
4. Tilley LP, Smith FWK: Hypoadrenocorticism (Addison's Disease). In Tilley LP, Smith FWK, editors. The 5-minute Veterinary Consult. Philadelphia: Williams & Wilkins, 1997. p 716-717.
5. Peterson ME, Kintzer PP, Kass PH. Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). Journal of the American Veterinary Medical Association 1996; 208: p 85-91.

 
© 2006 Novartis Animal Health US, Inc.  
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   Addison's Disease

http://www.vetstop.com.au

The adrenal glands are essential for life. They are two small glands which sit next to the kidneys. Their size does not correlate with their importance. They secrete a number of hormones essential for normal functioning as well as survival in stressful situations. Addison’s Disease (named after it’s discoverer in 1855) means there is insufficient production of these hormones. It is also called hypoadrenocorticism. Addison’s disease can be primary: atrophy (dying off) of the adrenal gland or secondary: a problem with the pituitary gland which secretes hormones that control growth and activity of the adrenal glands.

Causes
Primary: It is believed that most cases of primary Addison’s Disease are due to the body’s immune system destroying the adrenal tissue. The reasons for this are unknown. Other less common causes include infections, cancer, trauma, drug side effects and various types of inflammation.

Secondary
 This is due to problems with the pituitary gland which include inflammation, trauma or tumours.

Physiology
The hormones produce by the adrenals can be grouped as follows:

Mineralocorticoids - aldosterone

Glucocorticoids - cortisol

Primary Sex Hormones - androgens, oestrogens

Stress Hormones - adrenalin (note: the production of these hormones seems to be unaffected in primary Addison’s Disease)

The main groups we are concerned with are the mineralocorticoids and the glucocorticoids. The areas of the body that these hormones influence area as follows:

Mineralocorticoids: control the ability to maintain electrolyte and water balance in the body

Glucocorticoids: affect nearly every tissue in the body - promote a sense of well being & stimulate appetite; help control blood glucose levels; help the kidneys control water & calcium levels in the blood, help with control of red & white blood cell numbers.

As you see, without these hormones we have a very sick animal which will not survive long without treatment.

History
Addison’s is seen mainly in middle aged female dogs. There seems to be no obvious breed prevalence. The disease usually follows a waxing and waning course and may be confused with other diseases as the clinical signs are very non-specific.

Physical signs
The physical signs tend to relate to the lack of these important hormones. These will include:

weakness, depression, lethargy

anorexia, weight loss

vomiting, diarrhoea

excess drinking or urinating

slow heart rates

abdominal pain

hypothermia

Laboratory Signs
The laboratory signs are more useful in diagnosing Addison’s and will help to explain the physical signs

Increased Lymphocyte (a type of white blood cell) numbers

Anaemia

Increase serum potassium

Decreased serum sodium

Altered sodium/potassium ratio (Na:K): <27

Increased serum phosphorus

Increased serum calcium

Decreased blood glucose

Increased BUN & Creatinine (indicators of kidney function)

Acidosis (upset in body’s acid/base balance)

Low blood cortisol levels

Xrays may also be done which may reveal a smaller than normal heart due to the reduction in volume of circulating fluid in the body as part of Addison’s disease.

If the pet is not too sick, a test called an ACTH stimulation is performed. As this test takes several hours to complete and sometimes days for results, treatment for Addison’s Disease can usually be instituted on other laboratory results.

Treatment
Treatment is normally in two stage:

1. Adrenal Crisis Management

Adrenal Crisis Management is required when we have a very sick animal with abnormalities as those listed above. Your Vet will decide what the best course of action is to follow according to each individual case. This may involve fluid therapy and drugs to help reverse the changes. Once the animal has recovered to a normal state we can go onto Maintenance Therapy

2. Maintenance therapy
Maintenance Therapy is usually lifelong and involves tablets to replace the hormone that are deficient: ie glucocorticoids & mineralocorticoids. Your Vet will decide which medications are best for each case.

Monitoring
Careful monitoring of electrolytes is important throughout he early stages of Addison's disease management. Your Vet is likely to give you a list of dates when further blood tests will be needed. These will usually be quite frequent at first with the intervals between blood tests gradually increasing.

Reprinted with kind permission from Michael at VetStop Admin http://www.vetstop.com.au

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ADDISON'S DISEASE OR HYPOADRENOCORTICISM

by Helen Larson, Oakbank, Manitoba, Benchmarks, vol. 28 (4)
http://www.scwtca.org

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.

Wheatens and Addison's
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".

Comparisons of Diseases to which SCWT are Predisposed (4)

RD
PLN
PLE
ADDISON'S
Age of Onset
< 1-3 yrs
Mean ~ 6 yrs
Mean ~ 4.5 yrs
Average 4.3-5.4 yrs
Sex Predilection
None noted
Female: male 1.6
Female: male 1.7
Female (in general)
PU/PD
Yes
Yes
Yes
Yes
Vomiting/Diarrhea
Yes
Yes
Yes
Yes
Azotemia
Yes
Eventually
No
Possibly (pre-renal)
Low albumin
No
Yes
Yes
Possibly (melena)
Low globulin
 No
No
Yes
Possibly (melena)
Low Na:K ratio
 Not noted
Rarely (-7.0%)
Rarely (-7.0%)
Yes
 

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.

Addison's Disease Reference List
I used 46 articles/textbooks and many personal correspondences to research this topic. Listed are the key references:
Feldman, Edward C. D.V.M. and Nelson, Richard W. D.V.M. (1996). Canine and Feline Endocrinology and Reproduction (2nd ed.). Philadelphia: W.B. Saunders Co.
Novartis Animal Health Professional Services. Canine Hypoadrenocorticism: Diagnosis and Treatment of an Emerging Disease. Greensboro, NC. Novartis Animal Health US Inc..
Canine Addison's Disease Awareness Collaborative (May 1999). Addisonian Dog Owners Survey. k9 Addison's Internet Support Group k9Addisons@egroups.com
Littman, Meryl P., (1999). ACIVM Proceedings Wheaten Terrier PLE-PLN. Proceedings of the 17TH Annual Veterinary Forum, ACIVM 1999, 554-556.
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.
Levy, J.K., (1994). Hypoglycemic seizures attributable to hypoadrenocorticism in a dog. Journal American Veterinary Medicine Association 204(4), 526-530.
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.
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.
Login, Joyce A., (1998). Diagnosis and Treatment of Hypoadrenocorticism (Addison's Disease). Veterinary Medical Bulletin. Novartis Animal Health US, Inc.
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.
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.
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.

Copyright © 1997-2003 Helen Larson
Reprinted with kind permission from Helen Moreland, President, SCWTCA
The Soft Coated Wheaten Terrier Club of America
All rights reserved

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 So Your Dog Has Addison’s Disease

Shannon Wilkinson

http://www.addisondogs.com

The diagnosis is in; it’s Addison’s disease. All of us here at AddisonDogs.com remember hearing those words from our vet.  Sometimes they brought up feelings of sadness, or fear, occasionally relief to know what’s going on.  Then the vet starts talking about mineralo-somethings and prednisone and DOCP and daily this and monthly that and soon your head is swimming.  You just want your dog back.  That’s how AddisonDogs.com came to be.




addisonsdog1
the adrenal glands are
located above the
kidneys

What is Addison’s disease anyway?
Let’s start with a brief overview of Addison’s disease.  It is the common name for hypoadrenocorticism, or adrenal insufficiency.  It is a disease with symptoms that are common to many other ailments, making diagnosis difficult and sometimes a process of elimination.  But once Addison’s is correctly diagnosed, a properly treated dog can live a normal, active life.

The adrenal, one on each kidney, is made up of two layers, the cortex and the medulla.  The outer area, or cortex, secretes corticosteroid hormones such as cortisol and aldosterone.  The medulla, part of the sympathetic nervous system, secretes epinephrine (adrenaline), which is generally not affected by Addison’s.

There are three forms of Addison’s disease:  primary, secondary and atypical.  Primary and atypical Addison’s are usually the result of immune mediated damage to the glands. Secondary hypoadrenocorticism is from failure of the pituitary to stimulate the adrenals with adrenocorticotropic hormone (ACTH).  It is important for you to know which type of Addison’s disease your dog is being treated for.





addisonsdog2
SYMPTOMS

Vomiting
Diarrhea
Lethargy
Depression
Lack of appetite
Tremors or shaking
Muscle weakness
Pain in hind quarters


 I don’t have a diagnosis – what are the symptoms?
The symptoms of Addison’s disease can be vague.  More importantly, they are similar to the symptoms of many different problems.  Initially, the dog may be listless, or seem depressed.  Many dogs are described as just seeming off, or losing the normal sparkle in their eye.  Lack of appetite is a good indicator.  Other symptoms include gastro-intestinal problems like vomiting and diarrhea.  Pain in the hindquarters, or generalized muscle weakness such as a dog that can’t jump onto the bed or couch as he has done in the past is not uncommon.  Shivering or muscle tremors may also be present.  The most important thing to remember is that you know your dog better than anyone.  If something seems amiss, have it checked out.

These symptoms may wax and wane over months or years making diagnosis difficult.  If the adrenals continue deteriorating, ultimately the dog will have an acute episode called an Addisonian crisis.  Potassium levels elevate and disrupt normal function of the heart.  Arrhythmias can result and blood pressure drops to dangerously low levels.  BUN and creatinine levels, generally indicators of kidney function, are often elevated.  At this point many animals are diagnosed with renal failure, as the kidneys are unable to function properly.  Typically animals are given IV solutions for rehydration, which may produce an almost miraculous recovery.  This too, is a great indication that failure of the adrenals rather than of the kidneys is creating the symptoms.





addisondogs3
Electrolyte levels are important,
but not a definitive test for Addisons.
____________________
 
Primary Addison's involves changes
 in electrolytes while Atypical and
Secondary do not.
____________________
 
An ACTH Stim test is the only definitive 
test for diagnosing Addison's.


 How can you be sure it’s Addison’s?
One of the first things to look at when Addison’s disease is suspected are the electrolyte levels.  The two that are of greatest concern are sodium (Na) and potassium (K).  In addition to looking at these values, it is important to look at the ratio between the two.  This number is derived by dividing K into Na and should be between 27 and 40.  For example, a dog with a Na level of 145 and a K level of 4.5 would have a ratio of 32.  A dog in an Addisonian crisis will typically have a low Na level, elevated K and low ratio. (see laboratory results for more info)

While electrolyte levels are important indicators, they are not the definitive test to determine Addison’s disease.  In fact, with secondary and atypical hypoadrenocorticism, electrolyte levels may not be affected.  For definitive diagnosis the dog is given the ACTH stimulation or response test.  This tests the ability of the adrenal glands to produce the corticosteroid hormone cortisol.

To perform the ACTH stimulation test, an initial blood sample is drawn and the cortisol level is measured.  The dog is injected with a form of the pituitary hormone ACTH that tells the adrenals to produce cortisol.  After an hour, blood is drawn again, and the cortisol level measured.  Resting cortisol should range from 1-4 μg/dl in the average dog, and should be significantly higher, in the range of 6-20 μg/dl, post-stimulation. (These numbers may vary depending on the lab.) If resting cortisol is low and the dog has no or a low response to the stimulation, the diagnosis is Addison’s disease.  Be aware that some glucocorticoids, such as prednisone, can affect the results of the ACTH test, while dexamethasone does not.

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Primary Addisons requires the
replacement medications
 of mineralocortioids. ____________________

 
Atypical and Secondary require 
the replacement of 
glucocorticoids only.
____________________
 
Atypical Addison's 
can become Primary and requires 
careful monitoring of your dog.
____________________
 
Addison's dogs require additional
 glucocorticods during periods of stress,
 injury or surgery.


 Keeping on top of it
There are several medications used to treat Addison’s.  The first type acts as a mineralocorticoid and replaces the aldosterone – the hormone responsible for maintaining electrolyte levels.  It is replaced with either an oral medication called Florinef ™ (fludrocortisone acetate) or the injectable Percorten-V™ (desoxycorticosterone pivalate or DOCP). For dogs that have atypical or secondary Addison’s neither of these medications are used because the production of aldosterone isn’t effected and electrolytes remain in balance.

In addition to replacing the aldosterone, the cortisol, or glucocorticoids, normally secreted by the adrenals must also be replaced.  This is typically done with an oral form of prednisone or hydrocortisone.  With atypical and secondary Addison’s the glucocorticoid is the only medication given.   

The bottom line
While your dog with Addison’s disease will need medications and monitoring for the rest of his life, most dogs with Addison’s can return to their favorite activities.  You will learn to read your dog, understand what his stress triggers are and follow your instincts in his care.  Together, you will overcome ADversity and learn from this experience.  You will help your dog lead a normal, active and fun-filled life.

Treatment and Medications

There are several medications used to treat Addison’s disease.  The first type acts as a mineralocorticoid and replaces aldosterone – the hormone responsible for maintaining electrolyte levels.  It is replaced with either an oral medication called Florinef ™ (fludrocortisone acetate) or the injectable Percorten-V™ (desoxycorticosterone pivalate or DOCP). For dogs that have atypical or secondary Addison’s neither of these medications are used because the production of aldosterone isn’t effected and electrolytes remain in balance.
   
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Florinef ™
 (fludrocortisone acetate)
All about Florinef
What is compounded Florinef?
Where to purchase compounded Florinef 
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Percorten-V™ 
(desoxycorticosterone pivalate or DOCP)
All about Percorten-V
Where to purchase
DOCP Calculator
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In addition to aldosterone, the cortisol, or glucocorticoids, normally secreted by the adrenals must also be replaced.  This is typically done with an oral form of prednisone or hydrocortisone.  During a crisis, the dog may receive an injection of dexamethasone, a potent and fast-acting glucocorticoid.  The dog may be started initially on high doses of prednisone to facilitate a return to health.  On an on-going basis, the glucocorticoid dose can be reduced and in some cases eliminated except on an as-needed basis.  With atypical and secondary Addison’s the glucocorticoid is the only medication given. 

Mineralocorticoids:
Primary Addison’s disease is treated by replacing the mineralocorticoid, Aldosterone, with either tablets of Florinef or the injectable Percorten-V.  These medications help maintain the balance of the electrolytes Sodium (Na) and Potassium (K).

Florinef is the brand name for fludrocortisone acetate.  This medication is also available in its generic form, fludrocortisone acetate, from compounding pharmacists.  It is primarily a mineralocorticoid, but also has some glucocorticoid activity.  The starting dose recommended by the Merck Veterinary Manual is 0.05 – 0.1 mgs per 10 lbs of bodyweight.  Some dogs require significantly higher doses to maintain normal electrolytes.

The dose may be divided and given twice per day or given all at once, usually in the morning.  A 50-pound dog would take between 0.25 and 0.5 mgs to start.  The brand name Florinef tablets may be purchased directly from your vet or from a pharmacy.  Some people find it more cost effective and efficient to have the proper dose of the medication prepared by a compounding pharmacist in capsule, liquid, or chewable form.

Percorten-V is the brand name for desoxycorticosterone pivalate.  It is an injectable medication with only mineralocorticoid activity.  It does not have any glucocorticoid activity.  The dose recommended by Novartis, the manufacturer, is 0.75 – 1.0 mgs per one lbs. of bodyweight, given every 21 – 30 days.  There are 25 mgs in each ml (or cc) of the medication.

A 50-pound dog would receive between 37.5 – 50 mgs or 1.5 – 2.0 mls.  Some dogs are adequately maintained on lower doses, while some dogs require lower doses to minimize rare side effects.  Percorten-V is available only through a licensed veterinarian, although some veterinary pharmacies may carry the medication.


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Glucocorticoids

 


 

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 Glucocorticoids:
The adrenal glands produce cortisol, a glucocorticoid.  It is the hormone measured by the ACTH Stimulation test used to diagnose Addison’s disease.

All dogs with Addison’s require the supplementation of glucocorticoids in times of stress.  Many need glucocorticoids on a more regular basis, particularly those on DOCP.  Dogs with atypical or secondary Addison’s only take glucocorticoids.

The most common glucocorticoids are prednisone, hydrocortisone and dexamethasone.  There are additional glucocorticoids such as prednisolone and methylprednisolone.  The Merck Veterinary manual recommends a prednisone dose of 0.1 – 0.2 mgs/lb. per day.  This is equivalent to 0.4 – 0.8 mgs/lb. per day of hydrocortisone.

However, some dogs show symptoms of excess glucocorticoids on these doses.  These problems may include excessive drinking and urination, increased appetite, recurring infections, elevated liver enzymes, panting, restlessness and even behavioral changes.  Because these dogs will be on medications for the rest of their lives, it is important to fine-tune the dosages to maximize benefits, while minimizing unwanted side effects.  If you are working to reduce your dogs dose of glucocorticoids, be sure to work with your vet and lower the amount slowly.

Determining what constitutes stress for your dog, when additional glucocorticoids are necessary, is very individual.  Like people, dogs find different situations stressful.  Stress can be in many forms, both good and bad, from physical to emotional.  For some dogs a trip to the vet requires extra medication, while for others it could be houseguests or extra active playtime. Knowing your dog’s triggers is crucial.  It is essential to monitor the dog closely and be prepared to give extra medication when the need arises







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More about ACTH test

Reading your dogs blood work

Determining Electrolyte Ratio

Electrolyte ratio is determined by dividing the "NA" number by the "K" number.

145÷ 4.5 = 32

Electrolyte Calculator
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Laboratory Results

Blood tests:
Addison’s disease is diagnosed through a blood test called the ACTH Stimulation or Response test.  This test is typically only done once to diagnose the condition.  To perform the ACTH stimulation test, an initial blood sample is drawn and the cortisol level is measured.  The dog is injected with a synthetic form of the pituitary hormone ACTH that tells the adrenals to produce cortisol.  After an hour, blood is drawn again, and the cortisol level measured.  Resting cortisol should range from 1-4 μg/dl in the average dog, and should be significantly higher, in the range of 6-20 μg/dl, post-stimulation.  If resting cortisol is low and the dog has no or a low response to the stimulation, the diagnosis is Addison’s disease.  Be aware that some glucocorticoids, such as prednisone, can affect the results of the ACTH test, while dexamethasone does not.

At diagnosis, your dog will probably have what’s referred to as a Super Chem or Chem Panel and CBC (Complete Blood Count) to look at other important blood values.  The results from these blood tests help to determine if organs such as the kidneys, liver and pancreas are functioning properly, as well as if any signs of infection are present.  A complete blood test should be completed every 6 months to one year for a dog with Addison’s disease.

There are two blood test results that are of particularly interest in Addison’s disease.  They are Sodium (Na) and Potassium (K).  The hormone Aldosterone regulates these electrolytes.  In primary Addison’s disease, the adrenal glands don’t produce (enough) Aldosterone, so it must be replaced with Florinef or DOCP.  This is information that you and your vet will use to monitor the effectiveness of the mineralocorticoid (DOCP or fludrocortisone). The electrolytes are checked frequently at the beginning to determine correct medication levels.

Normal ranges for these values may vary based on the lab and equipment used.  Typically, the normal level for Sodium is between 139 to 154 mEq/L and Potassium should be between 3.6 to 5.5 mEq/L.  In addition to looking at these values, it can be helpful to look at the ratio between the two.  This number is derived by dividing K into Na and should be between 27 and 40.  For example, a dog with a Na level of 145 and a K level of 4.5 would have a ratio of 32.  A dog in an Addisonian crisis will typically have a low Na level, elevated K and low ratio. It is important to learn at what levels your dog feels his best.
   
mailto:shannon@shannonwilkinson.com
© 2003-2006 AddisonDogs.com
Common Sense Disclaimer: AddisonDogs.com does not have a vet on staff nor does it through its board, list-owners
or list-members provide medical advice. All information is for educational purposes and is not intended to diagnose or treat.
 You are encouraged to visit your vet if you have any concerns about the health of your animals.

 Reprinted with kind permission from Susan Long
No material from this website — graphics, photographics, or written material— may be used without express written permission from AddisonDogs.com.
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Diagnosis: Kidney Disease

Or is it?

Josephine Tucker

The difference between the clinical signs and blood analysis of kidney disease (causing renal failure) and Addison’s disease is very subtle, that is unless you are aware of what you are looking for, and then the possibility of primary Addison’s disease can become so obvious it stares you in the face!  

Vets could be forgiven for not recognising the vague, non-specific clinical signs of Addison’s disease if the consequences of a misdiagnosis were not so dire.  It will most certainly result in the premature and unnecessary death of your dog.

In just three months, two Addisonian cases I have been involved in were originally misdiagnosed as definite cases of kidney disease. The dogs were put on a KD diet (a special veterinary diet for dogs with kidney disease) and no improvement was seen. Both dogs were deteriorating, and when Addison’s disease was mentioned to the vets’ they dismissed it. After the owners were made aware of the clinical signs and typical blood results of dogs with Addison’s disease, it seemed very possible to them that their vets had misdiagnosed their dog’s condition. The information gave them enough courage to challenge their vet’s diagnosis and in both cases this resulted in a confirmed diagnosis of Addison’s disease, which undoubtedly saved the dogs’ lives.

These two cases were almost identical, so how many other dogs are being misdiagnosed and dying needlessly?  Many years ago when I had to take one of my dogs to the Royal Veterinary College, the vet looking after him told me that in the previous three days, four dogs had been admitted to the hospital with Addison’s disease.  He said if veterinary surgeons only looked at their text books it would not be necessary for these dogs to be referred to the vet college!  No one is saying that Addison’s is an easy diagnosis to make, as it shares so many similarities with kidney disease (and other diseases), but there are tell-tale signs that not only should the vet be aware of but also the owners, and if these signs are apparent it should be enough reason to suspect Addison’s disease.

Although Addison’s disease has been diagnosed in a dog as old as 14, it is more likely for an aged dog to have degenerative kidney disease than Addison’s disease. This article is more relevant to dogs of young to middle age, as this is when Addison’s disease is more likely to occur, especially in a breed known to be genetically predisposed to this disease. 

Much has been written about Addison’s in the past.  This article is intended to give a brief outline of the disease, concentrate mainly on the common factors, and more importantly the subtle differences between kidney disease and Addison’s disease, and how the tell-tale signs can be identified from the blood results. You don’t have to be a vet or scientifically minded, just look at the overall picture and be brave enough to challenge your vet’s diagnosis and ask for an ACTH stimulation test, if for no other reason than to rule it out and give you peace of mind.

Primary Addison’s disease (hypoadrenocorticism) is the result of an autoimmune destruction of the adrenal glands.  The adrenal glands produce several hormones; the most important of these are aldosterone (a mineralocorticoid) and cortisol (a glucocorticoid).  Insufficient production of these hormones alters the electrolyte balance in the body, in particular the sodium and potassium levels, and can produce clinical signs such as:

Lethargy, depression, nervousness, weight loss, anorexia (no appetite), vomiting, weakness (particularly of the back legs), shaking or muscle tremors, limping, diarrhoea (with or without traces of blood), abdominal pain, dehydration, excessive thirst and urination, weak pulse, slow heart rate and abnormal heart rhythm, anaemia (pale gums) and collapse. One important difference between acute/chronic renal failure and Addison’s disease is, the heart rate in renal failure is more likely to be fast (Tachycardia) and in Addison’s disease it is more likely to be slow (Bradycardia).  Signs of the disease are most apparent when the dog is physiologically or psychologically stressed.

Addison’s disease is progressive and it can take many months before clinical signs are seen. Sadly, in some cases - if subtle changes are missed - the first sign can be death.  Clinical signs are often vague to start with and can seem insignificant, but this is a common observation of the disease. Outward signs wax and wane and respond to fluid therapy or can worsen with stress. As the autoimmune destruction continues the adrenal glands will reduce in size until they are unable to produce enough adrenal hormones to sustain the dog. At this point the clinical signs, and abnormalities in the blood, are increasing and the dog is at risk of collapse, and subsequent death.  It then becomes a serious veterinary emergency, and it is very desirable to achieve a diagnosis before this occurs.  Unfortunately, it can become a fight against time to get the vet to even consider that the dog may have Addison’s disease. A common remark is ‘Oh, it won’t be Addison’s, we never see it’.  Never see it, or never diagnose it?

If your dog is visiting the vet regularly because of continuing symptoms, ask for a Complete Blood Count (CBC) and a full biochemistry blood test to be done, and don’t forget to ask for a printout of the results for your own records. The printout will show you a list of different chemical values, some of which are mentioned below.  The most important ones to look at in a case of Addison’s disease are the sodium and potassium levels.  However, not all cases of Primary Addison’s disease will have all the clinical signs and blood abnormalities, and this has to be borne in mind.  Also, there is a less common condition called Atypical Addison’s disease, in which the dog is deficient in cortisol only. Cortisol enables the body to cope with stress, and clinical signs relating to a deficiency may include: depression, nervousness, anorexia, weak pulse and collapse, particularly in stressful situations.  The adrenal mineralocorticoid hormone regulates the conservation of sodium and excretion of potassium from the body.  In atypical Addison’s this is less severely affected therefore the sodium and potassium levels may be within normal range.

Greater than 90% of Primary Addisonian cases will have high potassium and low sodium values, with a ratio of less than 27.  Prior to diagnosis, Addisonian dogs often show a ratio of less than 23. However, the ratio alone is only suggestive, and not diagnostic, of Addison’s disease. Individual electrolyte concentrations can be more reliable. As the disease progresses, the ratio will drop even further and the dog may collapse and become critically ill. ¹

Routine Laboratory Abnormalities  -  Haematology & Biochemistry
INCREASED: 
High Potassium (K)
High Creatinine,
High Urea, (BUN – blood urea nitrogen; or SUN - serum urea nitrogen)
High Urea/creatinine ratio (Azotaemia)
Increased Eosinophils
Increased Lymphocytes
High Bilirubin -  in some patients
High Calcium (mild to moderate) – in some patients
ALT- ALP - AST (Mild to moderate increase of liver enzymes) – in some patients

DECREASED:
Low Sodium  (Na)
Low Sodium/potassium ratio (K:Na ratio -  less than 27) Addisonian dogs often have a ratio of <23.
Low Chloride  (80% of Addisonian dogs will have low chloride values)
Low Glucose – in some patients
Low Albumin (moderate to severe) – in some patients
Total white blood cell count (WBC) – in some patients
Red blood cell count (RBC or HCT)

Another possible difference between kidney disease and Addison’s may be seen in the white blood cells (eg., neutrophils, eosinophils, lymphocytes). When a dog is poorly he becomes stressed and this is reflected in the white cells. The neutrophil numbers would be expected to be high/normal or increased, and the eosinophils and lymphocytes would be decreased or low/normal numbers. This is called ‘stress leucogram’ and is seen in both chronic and acute renal failure, but not in Addison’s disease. A dog with Addison’s disease may show a much lower white cell reading than would be expected in such a poorly dog.  In fact there may even be reverse of what would normally be expected, eg., low/normal values of neutrophils and a higher value of lymphocytes and eosinophills (called a ‘reverse stress leucogram’). ¹ ²

The terms used above might sound a bit too scientific but all of these values are clearly written on the laboratory report with the reference range, so it is not difficult to see if something is high or low and you may be able to build up a picture that may lead to a possible diagnosis. One point to remember, as Addison’s is a progressive disease, remarkable values may not be present in the earlier stages.  If the problems are ongoing regularly recheck the subsequent blood results for any of the above abnormalities.

Points to consider:
Is your dog young / middle aged?

Over a period of time, has your dog experienced several of the symptoms listed above and has he/she responded well to fluid therapy?

Has your young to middle aged dog been diagnosed with kidney disease?  Is he/she improving on the treatment/diet provided by your vet? If the answer is no, then consider Addison’s disease.

Do you have a dog whose breed is known to be genetically predisposed to Addison’s disease?

Do you know of any relatives of your dog who may have been diagnosed with Addison’s disease or kidney failure at a young age, or other autoimmune disease? Speak to your dog’s breeder; he/she may be able to give you valuable information.

Have a Full Serum Biochemistry panel and a Complete Blood Count test done and ask your vet for a copy of the results for your own records.  Study the results yourself and check for the abnormalities listed above. If symptoms persist, have a further blood test done to see if there are any changes, but don’t leave it too long in between (a week or less) as deterioration seems to quicken in the last stages.  Keep each laboratory report for comparison. Blood testing is never a waste of money (in the long term it can save you money), and it provides a ‘bench mark’ on which to base further tests).

What to do if you if your dog continues to deteriorate and you suspect that he/she may have Addison’s disease.
If your dog is extremely poorly, eg. very lethargic, call your vet straight away, regardless of the time, or if it is a weekend or Bank holiday. 

Tell your vet of your concerns and suspicions. Relay clinical signs and draw attention to any significant blood results. It is surprising how many vets miss the significant sodium/potassium clue.

If the breed is genetically predisposed to Addison’s, stress this to your vet.

The vet should respond by asking you to take your dog to the surgery immediately.  If your vet shares your suspicions he may carry out an ACTH stimulation blood test. (Unfortunately this is not possible over a weekend).  If your vet does not respond to your concerns then start making telephone calls until you find one who does. Don’t worry about offending your existing vet; your dog may be in extreme and immediate danger.
If your dog is too poorly for an ACTH stim test and has typical electrolyte imbalance usually seen in primary Addison’s disease, then your vet will need to give life saving treatment, eg., saline (sodium) intravenous fluids to re-hydrate, and bring down the dangerously high potassium levels and raise the sodium levels in the blood, and an intravenous injection of dexamethasone to enable your dog to cope with the stress.  ²

NOTE:  Dexamethasone is a glucocorticoid but unlike prednisolone it does not interfere with the ACTH stim test. 

Giving intravenous fluids and dexamethasone will hopefully support your dog until the result of the ACTH stim test is known.  Do not leave your dog without supportive treatment at this critical time.  It wouldn’t be the first time that a dog has died waiting for the results of the ACTH stim test to come through.

If the result is positive, your dog will be prescribed a mineralocorticoid hormone called Florine-f.  The initial dose is usually on the low side, and is gradually increased until the sodium and potassium levels are within normal range and clinical signs have resolved. The treatment must be given every day for life (usually the dose is split and given twice a day).  For the first few weeks or so your dog will also be on prednisolone (a glucocorticoid). Once stabilised, there is usually enough glucocorticoid in Florine-f to control everyday stress levels, so the prednisolone can be withdrawn. At times of added stress, however, (caused by fireworks or even going to the groomers etc.,) the owner must give additional prednisolone to enable the dog to cope with the trauma.  These are replacement doses and are vital to an Addisonian dog’s survival and should not be confused with higher treatment doses of steroids used to treat inflammatory conditions.  The body is designed to produce these hormones on a supply and demand basis.  An Addisonian dog no longer has the ability to do this and they rely on the owner to anticipate stressful situations and administer the appropriate medication. It is not a difficult regime to follow once the dog is stabilised and you are familiar with the condition.

Initially, blood tests to check electrolytes should be every 5-7 days and as clinical signs improve and blood results return to within normal limits the tests can become less frequent.  Electrolyte blood tests should still be carried out every 6 months when the dog is stable.  

In the United States dogs with Addison’s disease are more often treated with intramuscular or subcutaneous injections of desoxycorticosterone pivalate (DOCP – trade name Percorten-V.)  Dogs seem to do better with these injections than with Florine-f.  The dosage must be balanced by effect, both in the amount of the drug given and the interval between injections.  This can range from every 20 to 35 days, but usually is every 26-28th day.  After the initial injection sodium and potassium levels will be evaluated at 12 and 25 days to determine the size and timing of the next injection.  DOCP has purely mineralocorticoid activity, and so it is necessary to give a small dose of prednisolone – usually 2.5mg to 5.0mg every 24 or 48 hours. 

Many dogs with Addison’s disease also are hypothyroid, and treating their thyroid problem tends to make treating the Addison’s easier.  Usually the dog will require less Florine-f or DOCP, and will handle stress better too. 

The resolution of both clinical signs and blood results must be taken into consideration when evaluating the dog’s progress and should not be used in isolation. Remember in Addison’s disease especially, clinical signs usually reflect blood results and vice versa, but one may lag behind the other. If your dog is receiving an appropriate dose of Florine-f (this can vary from dog to dog) and his/her clinical signs or blood results do not stabilise after a few months, a full biochemistry blood test to check kidney/liver function etc., may be useful, or ask your vet for a referral to an endocrinologist, just in case there is an unidentified, underlying problem. 
If the ACTH stim test does not confirm Addison’s disease, it may have to be repeated at a later date if clinical signs and blood abnormalities persist.  The result of the ACTH stim test reflects the ‘current’ adrenal function status and may not show a ‘flat line response’- which is diagnostic of Addison‘s disease - until much later in the disease process. 

The good news is that the prognosis for Addison’s disease is usually excellent. Dogs can go on to live a happy, normal life on daily medication for many years, living well into old age, 15 or 16 years. It is certainly a much better prognosis than kidney disease.

There is plenty of general and practical information on Addison’s disease on the internet, however, if anyone would like further, specific, information please email  jo@cimda.fsnet.co.uk  Reliable information can be obtained by visiting BeaCon’s website on www.beaconforheath.org

Jo Tucker
References:
1. BSAVA Manual of Canine & Feline Clinical Pathology
2. BSAVA Manual of Small Animal Endocrinology
Additional information from Linda Aronson DVM
reprinted with kind permission from Josephine Tucker

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There is a newsgroup for owners of pets with Addison’s disease. To subscribe visit: http://groups.yahoo.com/group/k9Addisons/

Canine Hypoadrenocorticiscm
Addisons Disease
Addisons-Uncommon or Under-Diagnosed
Addisons Disease
Percorten-V
Hypoadrenocorticism
DOCP
Percorten-V information

Addisons Disease
Florinef Information
Addison's Disease & ACTH Testing Procedures
FAQ's
Canine Addisons Info.com


chloebutton  talabutton  

The above information is simply informational. It's intent is not to replace the advice of a veterinarian nor to assist you in making a diagnosis of your pet. Please consult with your own veterinarian for confirmation of any diagnosis. Your pets life may depend on it.