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IN the classic experiments of the Russian physiologist Ivan Pavlov, dogs salivated when a bell rang because they had been trained so that their brains associated the sound with the presence of food. Now, American scientists have evoked a …

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Addison’s disease

Addison’s disease, also known as primary adrenal insufficiency and hypocortisolism, is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.[1] Symptoms generally come on slowly and may include abdominal pain, weakness, and weight loss.[1] Darkening of the skin in certain areas may also occur.[1] Under certain circumstances, an adrenal crisis may occur with low blood pressure, vomiting, lower back pain, and loss of consciousness.[1] An adrenal crisis can be triggered by stress, such as from an injury, surgery, or infection.[1]

Addison’s disease arises from problems with the adrenal gland such that not enough of the steroid hormone cortisol and possibly aldosterone are produced,[1] most often due to damage by the body’s own immune system in the developed world and tuberculosis in the developing world.[4] Other causes include certain medications, sepsis, and bleeding into both adrenal glands.[1][4] Secondary adrenal insufficiency is caused by not enough adrenocorticotropic hormone (ACTH) (produced by the pituitary gland) or CRH (produced by the hypothalamus).[1] Despite this distinction, adrenal crises can happen in all forms of adrenal insufficiency.[1] Addison’s disease is generally diagnosed by blood tests, urine tests, and medical imaging.[1]

Treatment involves replacing the absent hormones.[1] This involves taking a corticosteroid such as hydrocortisone and fludrocortisone.[1][2] These medications are usually taken by mouth.[1] Lifelong, continuous steroid replacement therapy is required, with regular follow-up treatment and monitoring for other health problems.[5] A high-salt diet may also be useful in some people.[1] If symptoms worsen, an injection of corticosteroid is recommended and people should carry a dose with them.[1] Often, large amounts of intravenous fluids with the sugar dextrose are also required.[1] Without treatment, an adrenal crisis can result in death.[1]

Addison’s disease affects about 0.9 to 1.4 per 10,000 people in the developed world.[1][3] It occurs most frequently in middle-aged females.[1] Secondary adrenal insufficiency is more common.[3] Long-term outcomes with treatment are typically good.[6] It is named after Thomas Addison, a graduate of the University of Edinburgh Medical School, who first described the condition in 1855.[7] The adjective “addisonian” is used to describe features of the condition, as well as people with Addison’s disease.[8]


  • 1 Signs and symptoms
    • 1.1 Addisonian crisis
  • 2 Causes
    • 2.1 Adrenal destruction
    • 2.2 Adrenal dysgenesis
    • 2.3 Impaired steroidogenesis
  • 3 Diagnosis
    • 3.1 Suggestive features
    • 3.2 Testing
  • 4 Treatment
    • 4.1 Maintenance
    • 4.2 Crisis
  • 5 Epidemiology
  • 6 Prognosis
  • 7 History
    • 7.1 Discovery
  • 8 Other animals
  • 9 References
  • 10 External links

Signs and symptoms[edit]

The symptoms of Addison’s disease develop gradually and may become established before they are recognized. They can be nonspecific and are potentially attributable to other medical conditions.

The signs and symptoms include fatigue; lightheadedness upon standing or difficulty standing, muscle weakness, fever, weight loss, anxiety, nausea, vomiting, diarrhea, headache, sweating, changes in mood or personality, and joint and muscle pains. Some patients have cravings for salt or salty foods due to the loss of sodium through their urine.[8] Hyperpigmentation of the skin may be seen, particularly when the patient lives in a sunny area, as well as darkening of the palmar crease, sites of friction, recent scars, the vermilion border of the lips, and genital skin.[9] These skin changes are not encountered in secondary and tertiary hypoadrenalism.[10]

On physical examination, these clinical signs may be noticed:[8]

  • Low blood pressure with or without orthostatic hypotension (blood pressure that decreases with standing)
  • Darkening (hyperpigmentation) of the skin, including areas not exposed to the sun. Characteristic sites of darkening are skin creases (e.g., of the hands), nipple, and the inside of the cheek (buccal mucosa); also, old scars may darken. This occurs because melanocyte-stimulating hormone (MSH) and ACTH share the same precursor molecule, pro-opiomelanocortin (POMC). After production in the anterior pituitary gland, POMC gets cleaved into gamma-MSH, ACTH, and beta-lipotropin. The subunit ACTH undergoes further cleavage to produce alpha-MSH, the most important MSH for skin pigmentation. In secondary and tertiary forms of adrenal insufficiency, skin darkening does not occur, as ACTH is not overproduced.

Addison’s disease is associated with the development of other autoimmune diseases, such as type I diabetes, thyroid disease (Hashimoto’s thyroiditis), celiac disease, or vitiligo.[11][12] Addison’s disease may be the only manifestation of undiagnosed celiac disease.[11] Both diseases share the same genetic risk factors (HLA-DQ2 and HLA-DQ8 haplotypes).[13]

The presence of Addison’s in addition to mucocutaneous candidiasis, hypoparathyroidism, or both, is called autoimmune polyendocrine syndrome type 1.[14] The presence of Addison’s in addition to autoimmune thyroid disease, type 1 diabetes, or both, is called autoimmune polyendocrine syndrome type 2.[15]

Addisonian crisis[edit]

Main article: Adrenal crisis

An “Addisonian crisis” or “adrenal crisis” is a constellation of symptoms that indicates severe adrenal insufficiency. This may be the result of either previously undiagnosed Addison’s disease, a disease process suddenly affecting adrenal function (such as adrenal hemorrhage), or an intercurrent problem (e.g., infection, trauma) in someone known to have Addison’s disease. It is a medical emergency and potentially life-threatening situation requiring immediate emergency treatment.

Characteristic symptoms are:[16]

  • Sudden penetrating pain in the legs, lower back, or abdomen
  • Severe vomiting and diarrhea, resulting in dehydration
  • Low blood pressure
  • Syncope (loss of consciousness and ability to stand)
  • Hypoglycemia (reduced level of blood glucose)
  • Confusion, psychosis, slurred speech
  • Severe lethargy
  • Hyponatremia (low sodium level in the blood)
  • Hyperkalemia (elevated potassium level in the blood)
  • Hypercalcemia (elevated calcium level in the blood)
  • Convulsions
  • Fever


The negative feedback loop for glucocorticoids

Causes of adrenal insufficiency can be categorized by the mechanism through which they cause the adrenal glands to produce insufficient cortisol. These are adrenal dysgenesis (the gland has not formed adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol) or adrenal destruction (disease processes leading to glandular damage).[8]

Adrenal destruction[edit]

Autoimmune adrenalitis is the most common cause of Addison’s disease in the industrialized world. Autoimmune destruction of the adrenal cortex is caused by an immune reaction against the enzyme 21-hydroxylase (a phenomenon first described in 1992).[17] This may be isolated or in the context of autoimmune polyendocrine syndrome (APS type 1 or 2), in which other hormone-producing organs, such as the thyroid and pancreas, may also be affected.[18]

Adrenal destruction is also a feature of adrenoleukodystrophy, and when the adrenal glands are involved in metastasis (seeding of cancer cells from elsewhere in the body, especially lung), hemorrhage (e.g., in Waterhouse-Friderichsen syndrome or antiphospholipid syndrome), particular infections (tuberculosis, histoplasmosis, coccidioidomycosis), or the deposition of abnormal protein in amyloidosis.[19]

Adrenal dysgenesis[edit]

All causes in this category are genetic, and generally very rare. These include mutations to the SF1 transcription factor, congenital adrenal hypoplasia due to DAX-1 gene mutations and mutations to the ACTH receptor gene (or related genes, such as in the Triple A or Allgrove syndrome). DAX-1 mutations may cluster in a syndrome with glycerol kinase deficiency with a number of other symptoms when DAX-1 is deleted together with a number of other genes.[8]

Impaired steroidogenesis[edit]

To form cortisol, the adrenal gland requires cholesterol, which is then converted biochemically into steroid hormones. Interruptions in the delivery of cholesterol include Smith-Lemli-Opitz syndrome and abetalipoproteinemia.

Of the synthesis problems, congenital adrenal hyperplasia is the most common (in various forms: 21-hydroxylase, 17α-hydroxylase, 11β-hydroxylase and 3β-hydroxysteroid dehydrogenase), lipoid CAH due to deficiency of StAR and mitochondrial DNA mutations.[8] Some medications interfere with steroid synthesis enzymes (e.g., ketoconazole), while others accelerate the normal breakdown of hormones by the liver (e.g., rifampicin, phenytoin).[8]


Suggestive features[edit]

Routine laboratory investigations may show:[8]

  • Hypoglycemia, low blood sugar (worse in children due to loss of glucocorticoid’s glucogenic effects)
  • Hyponatremia (low blood sodium levels), due to loss of production of the hormone aldosterone, to the kidney’s inability to excrete free water in the absence of sufficient cortisol, and also the effect of corticotropin-releasing hormone to stimulate secretion of ADH.
  • Hyperkalemia (raised blood potassium levels), due to loss of production of the hormone aldosterone.
  • Eosinophilia and lymphocytosis (increased number of eosinophils or lymphocytes, two types of white blood cells)
  • Metabolic acidosis (increased blood acidity), also is due to loss of the hormone aldosterone because sodium reabsorption in the distal tubule is linked with acid/hydrogen ion (H+) secretion. Absent or insufficient levels of aldosterone stimulation of the renal distal tubule leads to sodium wasting in the urine and H+ retention in the serum.




In suspected cases of Addison’s disease, demonstration of low adrenal hormone levels even after appropriate stimulation (called the ACTH stimulation test or synacthen test) with synthetic pituitary ACTH hormone tetracosactide is needed for the diagnosis. Two tests are performed, the short and the long test. Dexamethasone does not cross-react with the assay and can be administered concomitantly during testing.

The short test compares blood cortisol levels before and after 250 micrograms of tetracosactide (intramuscular or intravenous) is given. If, one hour later, plasma cortisol exceeds 170 nmol/l and has risen by at least 330 nmol/l to at least 690 nmol/l, adrenal failure is excluded. If the short test is abnormal, the long test is used to differentiate between primary adrenal insufficiency and secondary adrenocortical insufficiency.

The long test uses 1 mg tetracosactide (intramuscular). Blood is taken 1, 4, 8, and 24 hr later. Normal plasma cortisol level should reach 1000 nmol/l by 4 hr. In primary Addison’s disease, the cortisol level is reduced at all stages, whereas in secondary corticoadrenal insufficiency, a delayed but normal response is seen.

Other tests may be performed to distinguish between various causes of hypoadrenalism, including renin and adrenocorticotropic hormone levels, as well as medical imaging – usually in the form of ultrasound, computed tomography or magnetic resonance imaging.

Adrenoleukodystrophy, and the milder form, adrenomyeloneuropathy, cause adrenal insufficiency combined with neurological symptoms. These diseases are estimated to be the cause of adrenal insufficiency in about 35% of male patients with idiopathic Addison’s disease, and should be considered in the differential diagnosis of any male with adrenal insufficiency. Diagnosis is made by a blood test to detect very long chain fatty acids.[20]



Treatment for Addison’s disease involves replacing the missing cortisol, sometimes in the form of hydrocortisone tablets, or prednisone tablets in a dosing regimen that mimics the physiological concentrations of cortisol. Alternatively, one-quarter as much prednisolone may be used for equal glucocorticoid effect as hydrocortisone. Treatment is usually lifelong. In addition, many patients require fludrocortisone as replacement for the missing aldosterone.

People with Addison’s are often advised to carry information on them (e.g., in the form of a MedicAlert bracelet or information card) for the attention of emergency medical services personnel who might need to attend to their needs.[21][22] It is also recommended that a needle, syringe, and injectable form of cortisol be carried for emergencies.[22] People with Addison’s disease are advised to increase their medication during periods of illness or when undergoing surgery or dental treatment.[22] Immediate medical attention is needed when severe infections, vomiting, or diarrhea occur, as these conditions can precipitate an Addisonian crisis. A patient who is vomiting may require injections of hydrocortisone instead.[23]


Standard therapy involves intravenous injections of glucocorticoids and large volumes of intravenous saline solution with dextrose (glucose). This treatment usually brings rapid improvement. If intravenous access is not immediately available, intramuscular injection of glucocorticoids can be used. When the patient can take fluids and medications by mouth, the amount of glucocorticoids is decreased until a maintenance dose is reached. If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate.[24]


The frequency rate of Addison’s disease in the human population is sometimes estimated at roughly one in 100,000.[25] Some put the number closer to 40–144 cases per million population (1/25,000–1/7,000).[1][26] Addison’s can affect persons of any age, sex, or ethnicity, but it typically presents in adults between 30 and 50 years of age.[27] Research has shown no significant predispositions based on ethnicity.[26]


Outcomes are typically good when treated. Most can expect to live relatively normal lives. Someone with the disease should be observant of symptoms of an “Addison’s crisis” while the body is strained, as in rigorous exercise or being sick, the latter often needing emergency treatment with intravenous injections to treat the crisis.[28]

Individuals with Addison’s disease have more than a doubled mortality rate.[29] Furthermore, individuals with Addison’s disease and diabetes mellitus have an almost 4 time increase in mortality compared to individuals with only diabetes.[30]



Addison’s disease is named after Thomas Addison, the British physician who first described the condition in On the Constitutional and Local Effects of Disease of the Suprarenal Capsules (1855).[31] All of Addison’s six original patients had tuberculosis of the adrenal glands.[32] While Addison’s six patients in 1855 all had adrenal tuberculosis, the term “Addison’s disease” does not imply an underlying disease process.

The condition was initially considered a form of anemia associated with the adrenal glands. Because little was known at the time about the adrenal glands (then called “Supra-Renal Capsules”), Addison’s monograph describing the condition was an isolated insight. As the adrenal function became better known, Addison’s monograph became known as an important medical contribution and a classic example of careful medical observation.[33]

Other animals[edit]

Main article: Hypoadrenocorticism in dogs

Hypoadrenocotricism has been diagnosed in several other species, including dogs, cats[34], a Grey seal [35], a Red Panda [36], a flying fox [37] and a sloth [38]

The condition has been diagnosed in all breeds of dogs. In general, it is underdiagnosed, and one must clinically suspect it as an underlying disorder for many presenting complaints. Females are overrepresented, and the disease often appears in middle age (4–7 yr), although any age or either gender may be affected.[citation needed]

Hypoadrenocorticism is treated with fludrocortisone or with monthly injections of desoxycorticosterone pivlate (DOCP) and daily prednisone. Routine blood work is necessary in the initial stages until a maintenance dose is established. Most of the medications used in the therapy of hypoadrenocorticism can cause excessive thirst and urination if not prescribed at the lowest effective dose, making it important to provide enough drinking water. If the owner knows about an upcoming stressful situation (shows, traveling, etc.), patients generally need an increased dose of prednisone to help deal with the added stress.


  • ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab “Adrenal Insufficiency and Addison’s Disease”. NIDDK. May 2014. Archived from the original on 13 March 2016. Retrieved 13 March 2016. 
  • ^ a b Napier, C; Pearce, SH (June 2014). “Current and emerging therapies for Addison’s disease”. Current Opinion in Endocrinology, Diabetes and Obesity. 21 (3): 147–53. doi:10.1097/med.0000000000000067. PMID 24755997. 
  • ^ a b c Brandão Neto, RA; de Carvalho, JF (2014). “Diagnosis and classification of Addison’s disease (autoimmune adrenalitis)”. Autoimmunity reviews. 13 (4–5): 408–11. doi:10.1016/j.autrev.2014.01.025. PMID 24424183. 
  • ^ a b Adam, Andy (2014). Grainger & Allison’s Diagnostic Radiology (6 ed.). Elsevier Health Sciences. p. 1031. ISBN 9780702061288. Archived from the original on 2016-03-14. 
  • ^ Napier, C; Pearce, SH (December 2012). “Autoimmune Addison’s disease”. Presse Médicale. 41 (12 P 2): e626–35. doi:10.1016/j.lpm.2012.09.010. PMID 23177474. 
  • ^ Rajagopalan, Murray Longmore, Ian B. Wilkinson, Supraj R. (2006). Mini Oxford handbook of clinical medicine (6 ed.). Oxford: Oxford University Press. p. 312. ISBN 9780198570714. Archived from the original on 2016-03-14. 
  • ^ Rose, Noel R.; Mackay, Ian R. (2014). The autoimmune diseases (5 ed.). San Diego, CA: Elsevier Science. p. 605. ISBN 9780123849304. Archived from the original on 2016-03-14. 
  • ^ a b c d e f g h Ten S, New M, Maclaren N (2001). “Clinical review 130: Addison’s disease 2001”. The Journal of Clinical Endocrinology and Metabolism. 86 (7): 2909–2922. doi:10.1210/jc.86.7.2909. PMID 11443143. 
  • ^ Nieman LK, Chanco Turner ML (2006). “Addison’s disease”. Clinics in Dermatology. 24 (4): 276–280. doi:10.1016/j.clindermatol.2006.04.006. PMID 16828409. 
  • ^ de Herder WW, van der Lely AJ (May 2003). “Addisonian crisis and relative adrenal failure”. Reviews in Endocrine and Metabolic Disorders. 4 (2): 143–7. doi:10.1023/A:1022938019091. PMID 12766542. 
  • ^ a b Freeman HJ (2016). “Endocrine manifestations in celiac disease”. World J Gastroenterol (Review). 22 (38): 8472–8479. doi:10.3748/wjg.v22.i38.8472. PMC 5064028 . PMID 27784959. 
  • ^ Zhernakova A, Withoff S, Wijmenga C (2013). “Clinical implications of shared genetics and pathogenesis in autoimmune diseases”. Nat Rev Endocrinol (Review). 9 (11): 646–59. doi:10.1038/nrendo.2013.161. PMID 23959365. 
  • ^ Denham JM, Hill ID (2013). “Celiac disease and autoimmunity: review and controversies”. Curr Allergy Asthma Rep (Review). 13 (4): 347–53. doi:10.1007/s11882-013-0352-1. PMC 3725235 . PMID 23681421. 
  • ^ “Autoimmune polyglandular syndrome type 1 | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program”. Archived from the original on 12 April 2017. Retrieved 26 June 2017. 
  • ^ “Autoimmune polyglandular syndrome type 2 | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program”. Archived from the original on 13 April 2017. Retrieved 26 June 2017. 
  • ^ “Addison’s Disease”. National Endocrine and Metabolic Diseases Information Service. Archived from the original on 28 October 2007. Retrieved 26 October 2007. 
  • ^ Winqvist O, Karlsson FA, Kämpe O (June 1992). “21-Hydroxylase, a major autoantigen in idiopathic Addison’s disease”. The Lancet. 339 (8809): 1559–62. doi:10.1016/0140-6736(92)91829-W. PMID 1351548. 
  • ^ Husebye ES, Perheentupa J, Rautemaa R, Kämpe O (May 2009). “Clinical manifestations and management of patients with autoimmune polyendocrine syndrome type I”. Journal of Internal Medicine. 265 (5): 514–29. doi:10.1111/j.1365-2796.2009.02090.x. PMID 19382991. 
  • ^ Kennedy, Ron. “Addison’s Disease”. The Doctors’ Medical Library. Archived from the original on 2013-04-12. 
  • ^ Laureti S, Casucci G, Santeusanio F, Angeletti G, Aubourg P, Brunetti P (1996). “X-linked adrenoleukodystrophy is a frequent cause of idiopathic Addison’s disease in young adult male patient”. The Journal of Clinical Endocrinology and Metabolism. 81 (2): 470–474. doi:10.1210/jc.81.2.470. PMID 8636252. 
  • ^ Quinkler M, Dahlqvist P, Husebye ES, Kämpe O (Jan 2015). “A European Emergency Card for adrenal insufficiency can save lives”. Eur J Intern Med. 26 (1): 75–6. doi:10.1016/j.ejim.2014.11.006. PMID 25498511. 
  • ^ a b c Michels A, Michels N (1 Apr 2014). “Addison disease: early detection and treatment principles”. Am Fam Physician. 89 (7): 563–8. PMID 24695602. Archived from the original on 2015-09-05. 
  • ^ White, Katherine (28 July 2004). “What to do in an emergency -Addisonian crisis”. Addison’s Disease Self Help Group. 
  • ^ “Adrenal Insufficiency and Addison’s Disease”. National Endocrine and Metabolic Diseases Information Service. Archived from the original on 26 April 2011. Retrieved 26 November 2010. 
  • ^ “Addison Disease”. MedicineNet. Archived from the original on 24 June 2007. Retrieved 2007-07-25. 
  • ^ a b Odeke, Sylvester. “Addison Disease”. eMedicine. Archived from the original on 7 July 2007. Retrieved 2007-07-25. 
  • ^ Volpé, Robert (1990). Autoimmune Diseases of the Endocrine System. CRC Press. p. 299. ISBN 0-8493-6849-9. 
  • ^ “Addison’s disease – Treatment”. NHS Choices. Archived from the original on 2016-10-09. Retrieved 2016-10-08. 
  • ^ Bergthorsdottir, Ragnhildur; Leonsson-Zachrisson, Maria; Odén, Anders; Johannsson, Gudmundur (2006-12-01). “Premature Mortality in Patients with Addison’s Disease: A Population-Based Study”. The Journal of Clinical Endocrinology & Metabolism. 91 (12): 4849–4853. doi:10.1210/jc.2006-0076. ISSN 0021-972X. 
  • ^ Dimitrios Chantzichristos; Anders Persson; Björn Eliasson; Mervete Miftaraj; Stefan Franzén; Ragnhildur Bergthorsdottir; Soffia Gudbjörnsdottir; Ann-Marie Svensson; Gudmundur Johannsson (2016-04-01). Cushing Syndrome and Primary Adrenal Disorders. Meeting Abstracts. Endocrine Society. pp. OR25–4–OR25–4. doi:10.1210/endo-meetings.2016.ahpaa.9.or25-4. 
  • ^ Addison, Thomas (1855). On The Constitutional And Local Effects Of Disease Of The Supra-Renal Capsules. London: Samuel Highley. Archived from the original on 2005-04-14. 
  • ^ Patnaik MM, Deshpande AK (May 2008). “Diagnosis–Addison’s Disease Secondary to Tuberculosis of the Adrenal Glands”. Clinical Medicine & Research. 6 (1): 29. doi:10.3121/cmr.2007.754a. PMC 2442022 . PMID 18591375. Archived from the original on 2010-06-09. 
  • ^ Bishop PM (1950). “The history of the discovery of Addison’s disease”. Proceedings of the Royal Society of Medicine. 43 (1): 35–42. PMC 2081266 . PMID 15409948. 
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  • External links[edit]

    • Addison’s disease at Curlie (based on DMOZ)

    pituitary axes





    • ovarian: Polycystic ovary syndrome
    • Premature ovarian failure
    • testicular: enzymatic
      • 5α-reductase deficiency
      • 17β-hydroxysteroid dehydrogenase deficiency
      • aromatase excess syndrome
    • Androgen receptor (Androgen insensitivity syndrome)
    • general: Hypogonadism (Delayed puberty)
    • Hypergonadism
      • Precocious puberty
    • Hypoandrogenism
    • Hypoestrogenism
    • Hyperandrogenism
    • Hyperestrogenism
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      • IgG

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    Cold weather poses risks for everything from medications to pets

    <h1>Cold weather poses risks for everything from medications to pets</h1>

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    The cold temperatures are enough to make most people cringe but there are medical warnings that go along with them for everything from medications to pets. 10TV spoke with experts to find out what people need to know. When it comes to medications, some, like …

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    Up in Arms About Prednisone For Dogs?

    Prednisone For Dogs

    Prednisone shouldn’t be stopped suddenly. It has been around for a long time (so there are several generic options) and it isn’t terribly expensive. It is not a chemotherapy drug, but is used in conjunction with chemotherapy protocols to treat dog cancers such as mast cell cancer, lymphosarcoma and lymphoma. It is a helpful substance for aiding dogs with a number of different illnesses, however, you should be aware of the possible drug interactions and contraindications of its use. Sometimes it is a necessary medication, but in many cases, the need for prednisone can be avoided with some extra care in nutrition. Prednisone, also sometimes thought of as prednisolone, is in a category of drugs called glucocorticords and is a synthetic type of the hormone cortisol. Prednisone and prednisolone may also mask signals of infection, including an elevated temperature.

    How to Find Prednisone For Dogs

    Unfortunately, prednisone may lead to many side results. It is also used alone or with other drugs to treat many other diseases and conditions. It can also interact with other steroids. It can be taken in a high dosage for short amount of time, perhaps just a few days, which is called a steroid burst. Unfortunately, it is not available over the counter, and you’ll need a veterinarian’s prescription to purchase it. Prednisone for dogs is used for lots of medical autoimmune conditions it’s really a corticosteroid that’s manufactured synthetically.

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    A 100 mg Rimadyl pill approximately 19 mm (0.75 in) wide and 8.6 mm (0.34 in) thick, sold in the United States

    Carprofen, marketed under many brand names worldwide,[1] is a nonsteroidal anti-inflammatory drug (NSAID) that veterinarians prescribe as a supportive treatment for various conditions in animals.[2] It provides day-to-day treatment for pain and inflammation from various kinds of joint pain as well as post-operative pain.[2] Carprofen reduces inflammation by inhibition of COX-1 and COX-2; its specificity for COX-2 varies from species to species.[2]


    • 1 Use in dogs
    • 2 Adverse effects
    • 3 Human use
    • 4 Equine use
    • 5 Brands and dosage forms for veterinary use
    • 6 References

    Use in dogs[edit]

    Adverse effects[edit]

    Most dogs respond well to carprofen use, but like all NSAIDs, it may cause gastrointestinal, liver and kidney problems in some patients.

    After introduction, significant anecdotal reports of sudden animal deaths from its use arose. To date[when?], the FDA has received more than 6,000 adverse reaction reports about the drug (manufactured by Pfizer). As a result, the FDA requested that Pfizer advise consumers in their advertising that death is a possible side effect.[3] Pfizer refused and pulled their advertising; however, they now include death as a possible side effect on the drug label. Plans call for a “Dear Doctor” letter to advise veterinarians, and a safety sheet attached to pill packages.

    Adverse effects include:

    • Loss of appetite
    • Vomiting
    • Diarrhea
    • Increase in thirst
    • Increase in urination
    • Fatigue and/or lethargy (drowsiness)
    • Loss of coordination
    • Seizures
    • Liver dysfunction: jaundice (yellowing of eyes)
    • Blood or dark tar-like material in urine or stools
    • Lethargy.
    • Staggering, stumbling, weakness or partial paralysis, full paralysis.[4]
    • Change in skin (redness, scabs, or scratching)
    • Change in behavior (such as decreased or increased activity level, seizure or aggression).[5]

    Effects of overdose include gastritis and ulcer formation.[6]

    In healthy dogs given carprofen, no perioperative adverse effects on the cardiovascular system have been reported at recommended dosages.[7] [8] Perioperative administration of carprofen to cats did not effect postoperative respiratory rate nor heart rate.[9]

    Carprofen should not be administered concurrently with steroids, as this can cause ulcers in the stomach. Dogs should be taken off carprofen for three full days before ingesting a steroid (such as prednisolone). Carprofen should not be given at the same time with other types of medications such as other NSAIDs (aspirin, etodolac, deracoxib, meloxicam, tepoxalin) or steroids such as dexamethasone, triamcinolone, cortisone or prednisone.

    Carprofen must be used with caution within the supervision of a veterinarian in dogs with liver or kidney disease, dehydration, bleeding deficits, or other health problems. It is not recommended for use in dogs with bleeding disorders (such as Von Willebrand’s disease), as safety has not been established in dogs with these disorders.[10] It has not been established whether carprofen can be safely used in pregnant dogs, dogs used for breeding purposes, or in lactating female dogs.

    Several laboratory studies and clinical trials have been conducted to establish the safety of using Carprofen. Clinical studies were conducted in nearly 300 dogs, coming from different breeds. The dogs were treated with Rimadyl at the recommended dose for 2 weeks. According to these studies, the drug was clinically well tolerated and the treated dogs did not have a greater incidence of adverse reactions when compared to the control group.[11]

    A number of factors that may contribute to the high incidence of adverse reports received for carprofen by the Center for Veterinary Medicine in the late 1990s. These include:

    • The type of drug;
    • Wide use;
    • Duration of use. While the side effects from carprofen are known to occur within a short period of time after administration, it is believed that long-term use may actually result in a higher risk for adverse reactions[citation needed];
    • Senior dog use. Older dogs are generally more prone to side effects caused by carprofen.

    Human use[edit]

    Carprofen was used in humans for almost 10 years, starting in 1988. It was used for the same conditions as in dogs, viz., joint pain and inflammation. Side effects tended to be mild, usually consisting of nausea or gastro-intestinal pain and diarrhea. Carprofen was available only by prescription in 150 to 600 mg doses.[12] Dosage over 250 mg was only for relieving pain after severe trauma, such as post-surgery inflammation. 150 mg doses were commonly used to relieve the pain of arthritis, while 200 mg doses were commonly prescribed in cases of severe arthritis or severe inflammation pain. The drug was taken orally. Pfizer voluntarily removed it from the market for human use on commercial grounds.[12]

    Equine use[edit]

    Carprofen may be administered intravenously to horses.[13] A single dose has been shown to reduce prostaglandin E2 production and inflammatory exudate for up to 15 hours,[14] although there was less effect on eicosanoid production when compared to the effects produced by NSAIDs such as phenylbutazone or flunixin.[15] Prostaglandin E2 and inflammatory exudate are also reduced and leukotriene B4 is inhibited. Carprofen can also be given orally, but intramuscular use may produce muscle damage.[16]

    Brands and dosage forms for veterinary use[edit]

    It is marketed under many brand names including: Acticarp, Austiofen, Bomazeal, Canidryl, Carporal, Carprieve , Carprocow, Carprodolor, Carprodyl, Carprofelican, Carprofen, Carprofène, Carprofeno, Carprofenum, Carprogesic, Carprosol, Carprotab, Carprox, Comforion, Dolagis, Dolocarp, Dolox, Eurofen, Kelaprofen, Librevia, Norocarp, Norodyl, Novocox, Prolet, Reproval, Rimadyl, Rimifin, Rofeniflex, Rycarfa, Scanodyl, Tergive, Vetprofen, and Xelcor.[1]

    Veterinary dosage forms include 25 mg, 75 mg, and 100 mg tablets, and 50 mg per mL injectable form.[17]


  • ^ a b International brand names for Carprofen Page accessed October 4, 2017
  • ^ a b c Carprofen/Rimadyl (Carprofen) prescribing instructions
  • ^ “Update On Rimadyl, FDA’s Center for Veterinary Medicine, December 1, 1999”. 
  • ^ “A Review of Signs of a Potentially Life-threatening Reaction to Rimadyl”. Retrieved 2010-05-20. 
  • ^ “Dog Owner Information About Rimadyl (carprofen)”. Retrieved 2010-05-20. 
  • ^ “Generic Dog Rimadyl Online”. Retrieved 2010-05-20. 
  • ^ Boström, IM; Nyman, GC; Lord, PE; Häggström, J; Jones, BE; Bohlin, HP (May 2002). “Effects of carprofen on renal function and results of serum biochemical and hematologic analyses in anesthetized dogs that had low blood pressure during anesthesia”. American journal of veterinary research. 63 (5): 712–21. doi:10.2460/ajvr.2002.63.712. PMID 12013473. 
  • ^ Frendin, JH; Boström, IM; Kampa, N; Eksell, P; Häggström, JU; Nyman, GC (December 2006). “Effects of carprofen on renal function during medetomidine-propofol-isoflurane anesthesia in dogs”. American journal of veterinary research. 67 (12): 1967–73. doi:10.2460/ajvr.67.12.1967. PMID 17144795. 
  • ^ Höglund, Odd V; Dyall, Barbara; Gräsman, Victoria; Edner, Anna; Olsson, Ulf; Höglund, Katja (22 November 2017). “Effect of non-steroidal anti-inflammatory drugs on postoperative respiratory and heart rate in cats subjected to ovariohysterectomy”. Journal of Feline Medicine and Surgery: 1098612X1774229. doi:10.1177/1098612X17742290. 
  • ^ “Rimadyl (Carprofen)”. Retrieved 2010-05-20. 
  • ^ “Rimadyl [package insert]. New York, NY: Pfizer Animal Health, 2007” (PDF). Retrieved 2014-08-13. 
  • ^ a b Committee for Veterinary Medicinal Products: Carprofen, European Agency for the Evaluation of Medicinal Products
  • ^ McIlwraith CW, Frisbie DD, Kawcak CE. Nonsteroidal Anti-Inflammatory Drugs. Proc. AAEP 2001 (47): 182-187.
  • ^ Lees, P; McKellar, Q; May, SA; Ludwig, B (May 1994). “Pharmacodynamics and pharmacokinetics of carprofen in the horse”. Equine veterinary journal. 26 (3): 203–8. doi:10.1111/j.2042-3306.1994.tb04370.x. PMID 8542839. 
  • ^ Lees, P; Ewins, CP; Taylor, JB; Sedgwick, AD (1987). “Serum thromboxane in the horse and its inhibition by aspirin, phenylbutazone and flunixin”. The British veterinary journal. 143 (5): 462–76. doi:10.1016/0007-1935(87)90024-8. PMID 3119142. 
  • ^ McKellar, QA; Bogan, JA; von Fellenberg, RL; Ludwig, B; Cawley, GD (July 1991). “Pharmacokinetic, biochemical and tolerance studies on carprofen in the horse”. Equine veterinary journal. 23 (4): 280–4. doi:10.1111/j.2042-3306.1991.tb03718.x. PMID 1915228. 
  • ^ Carprofen (Veterinary—Systemic) The United States Pharmacopeial Convention, 2007
  • EP (E2)

    FP (F2α)

    • Agonists: Alfaprostol
    • Bimatoprost
    • Carboprost
    • Cloprostenol
    • Enprostil
    • Fluprostenol
    • Latanoprost
    • Prostaglandin D2
    • Prostaglandin F2α (dinoprost)
    • Sulotroban
    • Tafluprost
    • Travoprost
    • Unoprostone

    IP (I2)

    • Agonists: ACT-333679
    • AFP-07
    • Beraprost
    • BMY-45778
    • Carbacyclin
    • Cicaprost
    • Iloprost (ciloprost)
    • Isocarbacyclin
    • MRE-269
    • NS-304
    • Prostacyclin (prostaglandin I2, epoprostenol)
    • Prostaglandin E1 (alprostadil)
    • Ralinepag
    • Selexipag
    • Taprostene
    • TRA-418
    • Treprostinil
    • Antagonists: RO1138452

    TP (TXA2)

    • Agonists: Carbocyclic thromboxane A2
    • I-BOP
    • Thromboxane A2
    • U-46619
    • Vapiprost
    • Antagonists: 12-HETE
    • 13-APA
    • AA-2414
    • Argatroban
    • Bay U3405
    • BMS-180,291
    • Daltroban
    • Domitroban
    • EP-045
    • GR-32191
    • ICI-185282
    • ICI-192605
    • Ifetroban
    • Imitrodast
    • L-655240
    • L-670596
    • Linotroban
    • Mipitroban
    • ONO-3708
    • ONO-11120
    • Picotamide
    • Pinane thromboxane A2
    • Ramatroban
    • Ridogrel
    • S-145
    • Samixogrel
    • Seratrodast
    • SQ-28,668
    • SQ-29,548
    • Sulotroban
    • Terbogrel
    • Terutroban
    • TRA-418


    • Arbaprostil
    • Ataprost
    • Ciprostene
    • Clinprost
    • Cobiprostone
    • Delprostenate
    • Deprostil
    • Dimoxaprost
    • Doxaprost
    • Ecraprost
    • Eganoprost
    • Enisoprost
    • Eptaloprost
    • Esuberaprost
    • Etiproston
    • Fenprostalene
    • Flunoprost
    • Froxiprost
    • Lanproston
    • Limaprost
    • Luprostiol
    • Meteneprost
    • Mexiprostil
    • Naxaprostene
    • Nileprost
    • Nocloprost
    • Ornoprostil
    • Oxoprostol
    • Penprostene
    • Pimilprost
    • Piriprost
    • Posaraprost
    • Prostalene
    • Rioprostil
    • Rivenprost
    • Rosaprostol
    • Spiriprostil
    • Tiaprost
    • Tilsuprost
    • Tiprostanide
    • Trimoprostil
    • Viprostol



    • Precursors: Linoleic acid
    • γ-Linolenic acid (gamolenic acid)
    • Dihomo-γ-linolenic acid
    • Diacylglycerol
    • Arachidonic acid
    • Prostaglandin G2
    • Prostaglandin H2

    See also
    Receptor/signaling modulators
    Leukotriene signaling modulators
    Nuclear receptor modulators


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