Title: Hypoadrenocorticism in dogs

{{Infobox medical condition (new)
| name            = Hypoadrenocorticism in dogs
| synonyms        = adrenal insufficiency, hypocortisolism
| image           = 
| alt             = 
| caption         = 
| pronounce       = 
| field           = [[Veterinary medicine]]
| symptoms        = 
| complications   = 
| onset           = 
| duration        = 
| types           = 
| causes          = 
| risks           = 
| diagnosis       = 
| differential    = 
| prevention      = 
| treatment       = 
| medication      = 
| prognosis       = 
| frequency       = 
| deaths          = 
}}

'''Hypoadrenocorticism in dogs''', or, as it is known in people, '''[[Addison's disease]]''', is an [[endocrine system]] disorder that occurs when the [[adrenal gland]]s fail to produce enough [[hormone]]s for normal function. The adrenal glands secrete [[glucocorticoid]]s such as [[cortisol]]&lt;ref&gt;{{cite web|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/adrenal/steroids.html|title=Adrenal Steroids|publisher=School of Veterinary Medicine-Colorado State University|access-date=26 January 2011}}&lt;/ref&gt; and [[mineralocorticoid]]s such as [[aldosterone]];&lt;ref&gt;{{cite web|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/adrenal/mineralo.html|title=Mineralocorticoids|publisher=School of Veterinary Medicine-Colorado State University|access-date=26 January 2011}}&lt;/ref&gt; when proper amounts of these are not produced, the metabolic and [[electrolyte]] balance is upset.&lt;ref name=&quot;Electrolytes&quot;&gt;{{Cite web|url=http://www.medicinenet.com/electrolytes/article.htm |title=What Are Electrolytes?|author =Stoeppler, Melissa Conrad|publisher=MedicineNet|access-date=17 April 2010| archive-url= https://web.archive.org/web/20100421092245/http://www.medicinenet.com/electrolytes/article.htm| archive-date= 21 April 2010 &lt;!--DASHBot--&gt;| url-status= live}}&lt;/ref&gt; Mineralocorticoids control the amount of [[Potassium in biology|potassium]], sodium, and water in the body.&lt;ref name=Cortex/&gt;&lt;ref name=peted&gt;{{cite web|url=http://www.peteducation.com/article.cfm?c=2+1597&amp;aid=520|title=Addison's Disease (Hypoadrenocorticism) in Dogs|publisher=Drs. Foster &amp; Smith}}&lt;/ref&gt;{{Citation needed|date=June 2024|reason=The citation that was here (to &quot;The Great Mimic: Canine Addison's Disease&quot;) does not appear to have been real.}} Hypoadrenocorticism is fatal if left untreated.&lt;ref&gt;{{cite web|url=http://www.percorten.novartis.us/pdf/Percorten_V_Monograph.pdf |title=Hypoadrenal gland disease |author =Hardy, RM |work=Textbook of Veterinary Internal Medicine |publisher=WB Saunders |page=1 |access-date=29 September 2012 |url-status=unfit |archive-url=https://web.archive.org/web/20150702013556/http://www.percorten.novartis.us/pdf/Percorten_V_Monograph.pdf |archive-date=July 2, 2015 }} ([[PDF]])&lt;/ref&gt;

The most common cause of inadequate adrenal production is idiopathic adrenocortical atrophy.&lt;ref name=&quot;:0&quot;&gt;{{Cite book|title=Textbook of Veterinary Internal Medicine 5th ed|last=Ettinger|first=Feldman|pages=1488–1499}}&lt;/ref&gt; All causes for hypoadrenocorticism are not yet known. The usual causes are genetic, often related to [[autoimmune]] disorders, where the body attacks and kill its own tissue (&quot;immune mediated destruction&quot;).&lt;ref name=Merck /&gt; Other cases are caused by various disease processes,&lt;ref name=Merck/&gt;&lt;ref name=Canada/&gt;&lt;ref&gt;{{cite web|url=http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2005&amp;PID=10902&amp;Category=1545&amp;O=Generic|title=Acute Adrenocortical Insufficiency|author =Schaer, Michael|year=2005|publisher=30th World Congress of the World Small Animal Veterinary Association|access-date=27 January 2011}}&lt;/ref&gt; including failure of the pituitary gland to secrete [[Adrenocorticotropic hormone|ACTH]], the hormone which stimulates the adrenal production of cortisol.&lt;ref name=peted /&gt;

Hypoadrenocorticism is more frequent in dogs than in humans; in fact, it may occur one hundred times more often in the canine population. It mostly affects young to middle-aged female dogs,&lt;ref name=Canada/&gt; as the average age at diagnosis being four years old (although it has been found in puppies and dogs up to twelve years old). About seventy percent of dogs that are diagnosed with hypoadrenocorticism are female.&lt;ref name=Canada/&gt; Hypoadrenocorticism is still relatively uncommon or underdiagnosed in dogs. Statistics gathered from a large veterinary hospital placed the number at 0.36 dogs per 1000. For an average veterinary practice with two veterinarians and 1500 canine patients, this would mean an average of one diagnosis of the disease each year.&lt;ref name=Canada/&gt;&lt;ref name=Percortenpdf&gt;{{cite web|url=http://www.percorten.novartis.us/pdf/Percorten_V_Monograph.pdf |author =Kelch, WJ |work=The Compendium |title=Canine hypoadrenocorticism (Addison's Disease) |date=June 1998 |page=4 |access-date=29 September 2012 |url-status=unfit |archive-url=https://web.archive.org/web/20150702013556/http://www.percorten.novartis.us/pdf/Percorten_V_Monograph.pdf |archive-date=July 2, 2015 }}([[PDF]])&lt;/ref&gt;

== Signs and symptoms ==
The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, [[bradycardia]], weak femoral pulses, [[abdominal pain]], lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, and pain in the hindquarters.&lt;ref name=&quot;Merck&quot; /&gt;&lt;ref name=&quot;petplace&quot; /&gt; [[Polyuria]] and [[polydipsia]], diarrhea, and shivering are occasionally reported.

[[Hypoglycemia]] can also be present, and initially may be confused with a seizure disorder or an insulin-secreting pancreatic tumor ([[insulinoma]]).  Hypoadrenocorticism may also be misdiagnosed as food poisoning, parvovirus [[enteritis]], [[gastric volvulus]], or spinal/joint problems, earning this disease nicknames like &quot;the Great Mimic&quot; and &quot;the Great Imitator&quot;.&lt;ref name=Brooks/&gt; It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.&lt;ref name=Southpaws/&gt;

===Addisonian crisis===

If hyponatremia (low sodium) and hyperkalemia (high potassium) are severe, the resulting hypovolemia, prerenal azotemia, and [[cardiac arrhythmia]]s may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as [[diabetic ketoacidosis]], necrotizing pancreatitis, and septic peritonitis.&lt;ref&gt;Gough, Alex (2007). Differential diagnosis in Small Animal Medicine. Blackwell Publishing: Carlton, Victoria.&lt;/ref&gt;

== Causes ==
[[Image:Gray1185.png|thumb|right|200px|Layers of the adrenal cortex (the outer portion of the adrenal gland)]]
The adrenal glands are located above the [[kidney]]s. The [[Adrenal gland#Cortex|adrenal outer layer]], or cortex, has three layers; each produces a specific type of steroid.&lt;ref name=Cortex&gt;{{cite web|url=http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/40202.htm|title=Adrenal Cortex|publisher=Merck Veterinary Manual|year=2008|access-date=26 January 2011}}&lt;/ref&gt;&lt;ref name=Brooks/&gt;
{| class=&quot;wikitable&quot;
|+ Layers of the adrenal cortex&lt;ref name=Adrenal/&gt;{{Citation needed|date=June 2024|reason=The citation that was here (&quot; Peterson, Mark E.; Kintzer, Peter P. (2006). &quot;Hypoadrenocorticism in Dogs&quot;. Ohio State University Endocrinology Symposium&quot;) does not seem to actually exist, though many similar pieces do...}}
|-
! Layer !! Type of steroid produced !! Example
|-
|Zona glomerulosa ||Mineralocorticoids || aldosterone
|-
|Zona fasciculata ||Glucocorticoids || cortisol
|-
|Zona reticularis || Sex steroids (androgens) ||
|}

===Primary===
[[Image:Anatomy and physiology of animals Adrenal glands.jpg|thumb|Primary disease: problem with the adrenal glands.]]
[[Adrenal insufficiency|Primary adrenocortical insufficiency]] is the more common form of hypoadrenocorticism. All layers of the adrenal gland stop functioning; the problem is with the adrenal gland.&lt;ref name=Merck/&gt; This causes a deficiency of both mineralocorticoid and glucocorticoid secretion. Most cases are classified as idiopathic, although immune-mediated adrenocortical destruction is a likely cause. Bilateral destruction of the [[adrenal cortex]] by neoplasia (e.g. lymphosarcoma), granulomatous disease, or [[Thrombosis|arterial thrombosis]] can also cause primary adrenocortical insufficiency. The destruction is progressive, although variable in rate, ultimately leading to complete loss of adrenocorotical function. A partial deficiency syndrome may occur initially, with signs manifested only during times of [[Stress (biological)|stress]] (e.g., boarding, travel, surgery).

===Secondary===
[[Image:Pituitary gland representation.PNG|thumb|Secondary disease: problem with the anterior pituitary.]]
In secondary hypoadrenocorticism the problem is not in the adrenal gland but in the [[pituitary gland]]. Usually, the [[Anterior pituitary|anterior portion]] of the pituitary gland produces a hormone, [[adrenocorticotropic hormone]] (ACTH), that signals the [[zona fasciculata]] and [[zona reticularis]] to produce their steroids. When the pituitary is unable to produce ACTH, these zones stop production of their hormones. The [[zona glomerulosa]] is not controlled by ACTH, and remains able to produce a normal amount of mineralocorticoids.&lt;ref name=Merck/&gt; A dog with secondary hypoadrenocorticism only needs to have medication to replace the glucocorticoid steroid cortisol.&lt;ref name=Canada/&gt;&lt;ref name=Brooks/&gt;&lt;ref name=Canadian/&gt; One dog in every 42 diagnosed with hypoadrenocorticism has the secondary form of the disease where mineralocorticoid production remains intact.&lt;ref name=Brooks/&gt;

Secondary adrenocortical insufficiency involves only a deficiency of glucocorticoid secretion. Destructive lesions (e.g. neoplasia, inflammation) in the [[pituitary gland]] or hypothalamus and chronic administration of exogenous glucocorticoids or megestrol acetate (cats) are the most common causes.&lt;ref&gt;Nelson and Couto (2005). Manual of Small Animal [[Internal medicine|Internal Medicine]]. 2nd Edition. Elsevier Mosby: St. Louis, Missouri. p.503-507&lt;/ref&gt;

===Drug induced===
Drug induced ([[Iatrogenesis|iatrogenic]]) hypoadrenocorticism is caused during abrupt cessation of a [[corticosteroid|steroid]] medication.&lt;ref name=Adrenal&gt;{{cite web|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/adrenal/histo_overview.html|title=Overview of Adrenal Histology|publisher=School of Veterinary Medicine-Colorado State University|access-date=26 January 2011}}&lt;/ref&gt;&lt;ref&gt;{{cite web|url=http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2009&amp;Category=8069&amp;PID=53472&amp;O=Generic|title=Corticosteroids: Friend or Foe?|author =Maddison, Jill|year=2009|publisher=Proceedings of the 34th World Congress of the World Small Animal Veterinary Association|access-date=11 February 2011}}&lt;/ref&gt; During steroid treatment, the adrenal glands do not function fully. The body senses the levels of the [[exogenous]] steroids in the system and therefore does not signal for additional production.&lt;ref name=Brooks/&gt; The usual protocol for stopping steroid medications is not to eliminate them suddenly, but to withdraw from them gradually in a &quot;tapering off&quot; process, which allows the production to adjust to normal. If steroids are abruptly withdrawn, the dormant adrenal glands may not able to reactivate, and the body will need to have its adrenal glucocorticoid hormones replaced by medication.&lt;ref name=Brooks/&gt;
{{clear|right}}

== Diagnosis ==
Hypoadrenocorticism is often tentatively diagnosed on the basis of history, physical findings, [[clinical pathology]], and, for primary adrenal insufficiency, characteristic electrolyte abnormalities.&lt;ref&gt;{{cite news|last1=Gallagher|first1=Alex|title=Demystifying Tests for Hyperadrenocorticism|url=http://www.cliniciansbrief.com/sites/default/files/attachments/ASK_Demystifying%20Tests%20for%20HAC.pdf|work=Clinicians' Brief|date=November 2014|access-date=2017-01-23|archive-url=https://web.archive.org/web/20141222040116/http://www.cliniciansbrief.com/sites/default/files/attachments/ASK_Demystifying%20Tests%20for%20HAC.pdf|archive-date=2014-12-22}}&lt;/ref&gt;

*Clinical pathology - Abnormalities may be identified on hematology, biochemistry and urinalysis. Elevated concentrations of potassium ([[hyperkalemia]]), and low sodium and chloride values ([[hyponatremia]] and [[hypochloremia]]) are the classic electrolyte alterations. The sodium/potassium ratio often is &lt;27 (normal is between 27:1 and 40:1) and maybe &lt;20 in animals with primary adrenal insufficiency.&lt;ref name=&quot;:0&quot; /&gt; However, not all dogs have an abnormal [[electrolyte]] ratio during an Addisonian episode.&lt;ref name=Canada/&gt;
*ECG - The severity of the [[ECG]] abnormalities correlates with the severity of the hyperkalemia. Therefore, the ECG can be used to identify and estimate the severity of hyperkalemia and to monitor changes in serum potassium during therapy.
*Diagnostic imaging - Abdominal ultrasound may reveal small [[adrenal gland]]s, suggesting adrenocortical atrophy. However, finding normal-sized adrenal glands does not rule out hypoadrenocorticism. Rarely, megaesophagus is evident on radiographs.
*[[ACTH stimulation test]] - Confirmation requires evaluation of an ACTH stimulation test. Baseline plasma cortisol and urine cortisol/Cr ratios are unreliable for confirming the diagnosis. One major diagnostic criterion is abnormally decreased post-ACTH plasma cortisol. Normal plasma cortisol after ACTH stimulation rules out adrenal insufficiency.&lt;ref&gt;{{cite journal|last1=Lathan|first1=P|last2=Moore|first2=GE|last3=Zambon|first3=S|last4=Scott-Moncrieff|first4=JC|title=Use of a low-dose ACTH stimulation test for diagnosis of hypoadrenocorticism in dogs.|journal=Journal of Veterinary Internal Medicine|date=2008|volume=22|issue=4|pages=1070–3|doi=10.1111/j.1939-1676.2008.0118.x|pmid=18537878|doi-access=free}}&lt;/ref&gt;&lt;ref&gt;{{cite news|last1=ACVIM|first1=Ronald Lyman DVM Dipl.|title=Consider ACTH stimulation test when you suspect canine hyperadrenocorticism|url=http://veterinarynews.dvm360.com/consider-acth-stimulation-test-when-you-suspect-canine-hyperadrenocorticism|work=dvm360.com|date=November 1, 2008|access-date=January 23, 2017|archive-date=July 4, 2018|archive-url=https://web.archive.org/web/20180704182712/http://veterinarynews.dvm360.com/consider-acth-stimulation-test-when-you-suspect-canine-hyperadrenocorticism|url-status=dead}}&lt;/ref&gt;&lt;ref&gt;{{cite web|title=ACTH Stimulation Test|url=http://www.idexx.com.tw/pdf/zh_tw/smallanimal/snap/cortisol/cortisol-acth-stimulation-protocol.pdf|archive-url=https://web.archive.org/web/20170202020508/http://www.idexx.com.tw/pdf/zh_tw/smallanimal/snap/cortisol/cortisol-acth-stimulation-protocol.pdf|archive-date=2 February 2017|publisher=Idexx|access-date=23 January 2017}}&lt;/ref&gt; The only accurate test for hypoadrenocorticism is an [[ACTH stimulation test]]; however, any administration of a steroid other than [[dexamethasone]] will invalidate this test.&lt;ref name=Merck/&gt;&lt;ref name=Canadian/&gt; Carry out test by:&lt;ref name=&quot;:0&quot; /&gt;
**Measuring serum cortisol before and after administration of ACTH gel or synthetic ACTH
***Normal dogs generally have post stimulation cortisol levels &gt; 10&amp;nbsp;ug/dl. 
***Post stimulation levels &lt; 2&amp;nbsp;ug/dl is considered diagnostic and most Addison's patients are &lt; 1&amp;nbsp;ug/dl.

The ACTH stimulation test does not distinguish between primary and secondary hypoadrenocorticism, or adrenocortical destruction caused by mitotane overdose. Differentiation between primary and secondary hypoadrenocorticism can be made by periodically measuring serum electrolytes, baseline endogenous ACTH, or possibly serum or plasma aldosterone during the ACTH stimulation test. While most [[corticosteroid]] drugs will invalidate the results of an ACTH test, [[dexamethasone]] may be used in the event of an Addison's emergency without fear of compromising the results of the test.&lt;ref&gt;{{cite web |url=http://www.axiomvetlab.com/GUIDE%20TO%20ENDOCRINOLOGY.pdf |archive-url=https://web.archive.org/web/20110904195357/http://www.axiomvetlab.com/GUIDE%20TO%20ENDOCRINOLOGY.pdf |archive-date=2011-09-04 |title=Guide to Endocrinology|website=Axiom Vet Lab|pages=7|access-date=16 May 2011}}&lt;/ref&gt;

In general, hypoadrenocorticism is underdiagnosed in dogs,
{{Citation needed|date=June 2024|reason=This citation also does not appear, after a quick search, to exist. &quot;Glucocortoid Deficient Hypoadrenocorticism More Prevalent than Previously Believed-Abstract #69&quot;}} and one must have a clinical suspicion of it as an underlying disorder for many presenting complaints. Females are overrepresented (~70% of cases),&lt;ref name=Brooks&gt;{{cite web|url=http://www.veterinarypartner.com/Content.plx?A=608|title=Addison's Disease (Hypoadrenocorticism)|author =Brooks, Wendy C.|publisher=Veterinary Partner|access-date=26 January 2011}}&lt;/ref&gt; and the disease often appears in middle age (four to seven years), although any age or gender may be affected.&lt;ref name=dogdays&gt;{{cite web|url=http://grants.nih.gov/grants/policy/air/dog_days.htm |title=Dog Days of Science |publisher=National Institutes of Health |access-date=1 September 2008 |url-status=unfit |archive-url=https://web.archive.org/web/20160328175350/http://grants.nih.gov/grants/policy/air/dog_days.htm |archive-date=March 28, 2016 }}&lt;/ref&gt; Dogs with hypoadrenocorticism may also have one of several [[autoimmune disorder]]s.&lt;ref name=&quot;dogdays&quot;/&gt; Because it is an [[endocrine]] disorder, they may also have [[Peripheral neuropathy|neuropathy]] and some endocrine-related eye diseases.&lt;ref name=Eye&gt;{{cite journal|title=Ocular Manifestations of Endocrine Disease |author=Plummer, Caryn E. |author2=Specht, Andrew |author3=Gelatt, Kirk N. |journal=Compendium (Yardley, Pa) |publisher=Compendium |date=December 2007 |volume=29 |issue=12 |pages=733–43 |pmid=18225637 }}&lt;/ref&gt;

===Addisonian crisis===
If deterioration of the adrenal glands progresses far enough, a dog may experience an Addisonian crisis, an acute episode during which [[potassium]] levels increase ([[hyperkalemia]]), disrupting normal functions of the [[heart]].&lt;ref name=MarVista/&gt; [[Heart arrhythmia|Arrhythmia]] can result and [[blood pressure]] may drop to dangerously low levels, while the dog's kidneys may cease to function properly.&lt;ref name=Cortex/&gt;&lt;ref name=peted/&gt;&lt;ref name=NewHope&gt;{{cite web|url=http://www.nhahonline.com/k9endocrinology.htm|title=Addison's Disease|publisher=New Hope Animal Hospital|access-date=25 January 2011|archive-url=https://web.archive.org/web/20061113214741/http://www.nhahonline.com/k9endocrinology.htm|archive-date=13 November 2006}}&lt;/ref&gt;&lt;ref&gt;{{cite web|url=https://www.ncbi.nlm.nih.gov/books/NBK26/|title= Endocrinology-an Integrated Approach-Aldosterone|author =Nussey, SS. |author2=Whitehead, SA.|publisher=National Institutes of Health (US)|year=2001|access-date=25 January 2011}}&lt;/ref&gt; Some 35% of canine Addison's cases are diagnosed as the result of an [[Addisonian crisis#Addisonian crisis|Addisonian crisis]]. It is a medical emergency.&lt;ref name=Merck/&gt;&lt;ref name=Southpaws/&gt;&lt;ref name=Canadian&gt;{{cite journal |first1=Susan C. |last1=Klein |first2=Mark E. |title=Canine hypoadrenocorticism: part II |journal=The Canadian Veterinary Journal |volume=51 |issue=2 |pages=179–84 |year=2010 |last2=Peterson |pmid=20436864 |pmc=2808283}}&lt;/ref&gt;&lt;ref name=Durkan&gt;{{cite web|url=http://veterinarycalendar.dvm360.com/endocrine-emergencies-proceedings-0?id=&amp;sk=&amp;date=&amp;pageID=2 |title=Endocrine Emergencies|author =Durkan, Samuel|pages=2–3|date=January 2008|publisher= DVM 360|access-date=25 January 2011}}&lt;/ref&gt;

===Whipworms===

Dogs with infected with the whipworm ''[[Trichuris trichiura]]'' can exhibit low sodium and high potassium values, as is seen in hypoadrenocorticism; however, their ACTH values are normal.&lt;ref name=Brooks/&gt;&lt;ref name=MarVista&gt;{{cite web|url=http://www.marvistavet.com/html/body_addison_s_disease.html|title=What Is Addison's Disease?|publisher=MarVista Vet|access-date=29 April 2011|archive-url=https://web.archive.org/web/20110516063341/http://www.marvistavet.com/html/body_addison_s_disease.html|archive-date=16 May 2011}}&lt;/ref&gt;

===Pacific Rim===

Breeds that began in the Pacific Rim, among them [[American Akita|Akita]]s and [[Shiba Inu]]s, tend to have higher potassium values in laboratory test, and elevated levels are not abnormal. Dogs who do not have hypoadrenocorticism have normal values on ACTH tests.&lt;ref name=Brooks/&gt;&lt;ref name=MarVista/&gt;

== Treatment ==
Aggressiveness of therapy depends on the clinical status of the patient and the nature of the insufficiency (glucocorticoid, mineralocorticoid, or both). Many dogs and cats with primary adrenal insufficiency are presented in Addisonian crisis and require immediate, aggressive therapy. In contrast, secondary insufficiency often has a chronic course.

Hypoadrenocorticism is treated with oral daily administration of [[fludrocortisone]] (trade name Florinef)&lt;ref&gt;{{cite web|url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000710/ |title=Fludrocortisone Acetate |publisher=National Institutes of Health |access-date=26 January 2011 |url-status=unfit |archive-url=https://web.archive.org/web/20120925073043/http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000710/ |archive-date=September 25, 2012 }}&lt;/ref&gt;&lt;ref&gt;{{cite web|url=http://www.veterinarypartner.com/Content.plx?P=A&amp;C=31&amp;A=536&amp;S=0|title=Fludrocortisone Acetate (Florinef)|author =Brooks, Wendy C.|publisher=Veterinary Partner|access-date=26 January 2011}}&lt;/ref&gt; or a monthly injection of [[11-Deoxycorticosterone|desoxycorticosterone pivalate]], DOCP (Percorten-V or Zycortal) &lt;ref&gt;{{cite web|url=http://www.percorten.novartis.us/about/about.htm |title=About Percorten-V-Treatment for Canine Addison's Disease |publisher=Novartis Animal Health |access-date=26 January 2011 |url-status=unfit |archive-url=https://web.archive.org/web/20150222065821/http://www.percorten.novartis.us/about/about.htm |archive-date=February 22, 2015 }}&lt;/ref&gt;&lt;ref&gt;{{cite web|url=http://www.percorten.novartis.us/pdf/PercortenV-product-info.pdf |title=Percorten-V Product Information |publisher=Novartis Animal Health |access-date=26 January 2011 |url-status=unfit |archive-url=https://web.archive.org/web/20150226110713/http://www.percorten.novartis.us/pdf/PercortenV-product-info.pdf |archive-date=February 26, 2015 }}([[PDF]])&lt;/ref&gt;&lt;ref&gt;{{cite web|url=http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2009&amp;Category=&amp;PID=53636&amp;O=Generic |title=Management of Hypoadrenocorticism|author =Church, David B.|publisher=Proceedings of the 34th World Congress of the World Small Animal Veterinary Association|year=2009|access-date=25 January 2011}}&lt;/ref&gt;&lt;ref&gt;{{cite web|url=http://www.dechra-us.com/products/dog/zycortal|title=Zycortal|publisher=Dechra|access-date=March 7, 2017}}&lt;/ref&gt; and daily [[prednisone]] or [[prednisolone]]. One drug is needed to supplement mineralcortidoids and the other to supplement corticosteroids. This effectively replaces what the adrenal cortex is failing to produce. Routine blood work is necessary in the initial stages until a maintenance dose is established.&lt;ref name=Merck&gt;{{cite web|title=Hypoadrenocorticism |work=The Merck Veterinary Manual |year=2008 |url=http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/40204.htm |access-date=9 January 2007 |archive-url=https://web.archive.org/web/20070117101126/http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm%2Fbc%2F40204.htm |archive-date=17 January 2007 |url-status=live}}&lt;/ref&gt; Most of the medications used in the therapy of hypoadrenocorticism cause excessive thirst and urination. It is absolutely vital to provide fresh drinking water for a canine with this disorder.&lt;ref name=petplace&gt;{{Cite web |url=http://www.petplace.com/dogs/hypoadrenocorticism-addison-s-disease-in-dogs/page1.aspx |title=Hypoadrenocorticism (Addison's Disease) in Dogs |author =Spielman, Bari |work=PetPlace.com |access-date=28 October 2009}}&lt;/ref&gt;

If the owner knows about an upcoming stressful situation (shows, traveling etc.), the animals generally need an increased dose of prednisone (2-4 times maintenance) to help deal with the added stress. Avoidance of stress is important for dogs with hypoadrenocorticism. Physical illness also stresses the body and may mean that the medication(s) need to be adjusted during this time.&lt;ref&gt;{{cite web|url=http://endocrine.niddk.nih.gov/pubs/addison/addison.htm|title=Adrenal Insufficiency and Addison's Disease|publisher=National Endocrine and Metabolic Diseases Information Service|access-date=16 May 2011|archive-url=https://web.archive.org/web/20110426030100/http://www.endocrine.niddk.nih.gov/pubs/addison/addison.htm|archive-date=26 April 2011}}&lt;/ref&gt; Most dogs with hypoadrenocorticism have an excellent prognosis after proper stabilization and treatment.&lt;ref name=Southpaws&gt;{{cite web|url=http://www.southpaws.com/topics-of-interest/addisons-disease/ |title=Addison's Disease |publisher=Southpaws Veterinary Center |access-date=26 January 2011 |url-status=unfit |archive-url=https://web.archive.org/web/20110716112620/http://www.southpaws.com/topics-of-interest/addisons-disease/ |archive-date=July 16, 2011 }}&lt;/ref&gt;&lt;ref name=Canadian/&gt;

===Addisonian crisis===

Treatment is directed towards (1) correcting hypotension, hypovolemia, electrolyte imbalances, and [[metabolic acidosis]]; (2) improving vascular integrity, and (3) providing an immediate source of glucocorticoids. Rapid correction of hypovolemia is the first priority.

Restoring blood volume is vital to correcting hypotension, hypovolemia, and addressing electrolyte and metabolic imbalances. This is achieved by the rapid administration of fluids. This helps to correct hyponatremia, restore perfusion to organs, and reduce hyperkalemia through increased GFR and dilution effects. Further treatment of hyperkalemia is addressed if necessary. Often, the fluid therapy can sufficiently address hyperkalemia, but in the presence of significant cardiac abnormalities, the addition of [[calcium gluconate]] may be necessary in addition to glucose, insulin, or bicarb to promote intracellular shift of potassium.&lt;ref name=&quot;:0&quot; /&gt;

Most patients show dramatic improvement within 24 to 48 hours of appropriate fluid and glucocorticoid therapy. Over the ensuing 2 to 4 days, a gradual transition from [[Intravenous therapy|IV fluids]] to oral water and food is undertaken, and maintenance mineralocorticoid and glucocorticoid therapy is initiated. Failure to make this transition smoothly should raise suspicion of insufficient glucocorticoid supplementation, concurrent endocrinopathy (e.g. [[hypothyroidism]]), or concurrent illness (especially renal damage).

It is important that after the crisis is corrected that the patient is put on a maintenance therapy of corticosteroids and mineralocorticoids.

==Epidemiology==
Hypoadrenocorticism is typically a disease of young to middle-aged female dogs, although Standard Poodles and Bearded Collies of both sexes are prone to the condition.&lt;ref name=&quot;Lathan 2005&quot;&gt;{{cite journal|last1=Lathan|first1=P|last2=Tyler|first2=JW|title=Canine Hypoadrenocorticism: Pathogenesis and Clinical Features|journal=Compendium|date=February 2005|volume=27|issue=2|pages=110–120|url=http://www.vetfolio.com/internal-medicine/canine-hypoadrenocorticism-pathogenesis-and-clinical-features|access-date=2017-08-20|publisher=VetFolio}}&lt;/ref&gt;

Hypoadrenocorticism is an inherited disease in the following breeds (and therefore a higher proportion of dogs within these breeds are affected, compared to other breeds):&lt;ref name=&quot;Scott-M 2014&quot;&gt;{{cite book|last1=Scott-Moncrieff|first1=JC|editor1-last=Feldman|editor1-first=EC|editor2-last=Nelson|editor2-first=RW|editor3-last=Reusch|editor3-first=CE|editor4-last=Scott-Moncrieff|editor4-first=JCR|title=Canine and feline endocrinology|date=2014|publisher=Saunders Elsevier|isbn=978-1-4557-4456-5|pages=485–520|edition=4th|chapter=Chapter 12: Hypoadrenocorticism}}&lt;/ref&gt; 
* [[Bearded Collie]] 
* [[Nova Scotia Duck Tolling Retriever]]
* [[Portuguese Water Dog]]
* [[Standard Poodle]]

Some breeds are at increased [[relative risk|risk]] of hypoadrenocorticism:
* [[Airedale Terrier]]&lt;ref name=&quot;Scott-M 2014&quot;/&gt;
* [[Basset Hound]]&lt;ref name=&quot;Scott-M 2014&quot;/&gt;
* [[Bearded Collie]]&lt;ref name=&quot;Scott-M 2014&quot;/&gt;
* [[Great Dane]]&lt;ref name=&quot;Canada&quot;/&gt;
* [[Rottweiler]]&lt;ref name=&quot;Scott-M 2014&quot;/&gt;
* Springer Spaniels:&lt;ref name=&quot;Scott-M 2014&quot;/&gt; [[English Springer Spaniel]] and [[Welsh Springer Spaniel]]
* [[St. Bernard (dog)|Saint Bernard]]&lt;ref name=&quot;Scott-M 2014&quot;/&gt;
* [[Soft-Coated Wheaten Terrier]]&lt;ref name=Canada&gt;{{cite journal |first1=Susan C. |last1=Klein |first2=Mark E. |title=Canine hypoadrenocorticism: part I |journal=The Canadian Veterinary Journal |volume=51 |issue=1 |pages=63–9 |year=2010 |last2=Peterson |pmid=20357943 |pmc=2797351}}&lt;/ref&gt;
* [[West Highland white terrier]]&lt;ref name=Canada/&gt;

Some breeds have a reduced [[relative risk|risk]] of hypoadrenocorticism:&lt;ref name=&quot;Scott-M 2014&quot;/&gt;
* [[Boxer (dog)|Boxer]]
* [[Cocker Spaniel]]
* [[Golden Retriever]]
* [[Pit Bull Terrier]]
* [[Lhasa Apso]]
* [[Yorkshire Terrier]]

==History==
The first case of hypoadrenocorticism in dogs was recorded in 1953, over 100 years after it was described in humans by [[Thomas Addison]].&lt;ref&gt;{{cite journal|last1=Little|first1=C|last2=Marshall|first2=C|last3=Downs|first3=J|title=Addison's disease in the dog.|journal=The Veterinary Record|date=29 April 1989|volume=124|issue=17|pages=469–70|doi=10.1136/vr.124.17.469|pmid=2728304|s2cid=37536148}}&lt;/ref&gt;

==References==
{{Reflist}}

{{DEFAULTSORT:Hypoadrenocorticism in dogs}}
[[Category:Dog diseases]]