Addison's disease overview: Difference between revisions
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==Overview== | ==Overview== | ||
Addison disease develops as a result of bilateral adrenal cortex destruction. Both cortisol and aldosterone production are | Addison disease develops as a result of bilateral adrenal cortex destruction. Both cortisol and aldosterone production are reduced. Autoimmune destruction of the adrenal glands is the most common cause in the western world, but infections such as tuberculosis, hemorrhage, adrenal vein thrombosis, and carcinoma are also known to significant causes. Tuberculosis remains the most common cause worldwide of Addison disease. The onset of Addison disease is often gradual, and symptoms of the disease can be difficult to recognize. It may go undetected until an illness or other stress precipitates adrenal crisis. Treatment should not be withheld to confirm diagnosis. Treatment should be the priority, as the disease is fatal if it remains untreated. Diagnosis is made with rapid, high-dose adrenocorticotropic hormone (ACTH) stimulation testing. If the patient is hypovolemic, dexamethasone and intravenous normal saline should be given before stimulation testing is performed. Drug therapy is with a combination of glucocorticoids and mineralocorticoids. Glucocorticoid doses needs to be doubled when patients have an episode of minor fever, infection, minor trauma, or minor physical (not emotional) stress. Intravenous stress-dose corticosteroids are needed for surgery requiring general anesthesia and for major trauma. | ||
==Historical Perspective== | ==Historical Perspective== | ||
The condition is named after Dr. [[Thomas Addison]], the British [[physician]] who first described the condition in his 1855 ''On the Constitutional and Local Effects of Disease of the Suprarenal Capsules''.<ref>{{cite book | author = Thomas Addison | authorlink = Thomas Addison | title = On The Constitutional And Local Effects Of Disease Of The Supra-Renal Capsules | origyear = 1855 | url = http://www.wehner.org/addison/x1.htm | format = HTML reprint | publisher = Samuel Highley | location = London}}</ref> The adjective "Addisonian" is used for features of the condition, as well as for patients with Addison's disease.<ref name=Ten>{{cite journal |author=Ten S, New M, Maclaren N |title=Clinical review 130: Addison's disease 2001 |journal=J. Clin. Endocrinol. Metab. |volume=86 |issue=7 |pages=2909-22 |year=2001 |pmid=11443143 |url=http://jcem.endojournals.org/cgi/content/full/86/7/2909}}</ref> | The condition is named after Dr. [[Thomas Addison]], the British [[physician]] who first described the condition in his 1855 ''On the Constitutional and Local Effects of Disease of the Suprarenal Capsules''.<ref>{{cite book | author = Thomas Addison | authorlink = Thomas Addison | title = On The Constitutional And Local Effects Of Disease Of The Supra-Renal Capsules | origyear = 1855 | url = http://www.wehner.org/addison/x1.htm | format = HTML reprint | publisher = Samuel Highley | location = London}}</ref> The adjective "Addisonian" is used for features of the condition, as well as for patients with Addison's disease.<ref name="Ten">{{cite journal |author=Ten S, New M, Maclaren N |title=Clinical review 130: Addison's disease 2001 |journal=J. Clin. Endocrinol. Metab. |volume=86 |issue=7 |pages=2909-22 |year=2001 |pmid=11443143 |url=http://jcem.endojournals.org/cgi/content/full/86/7/2909}}</ref> | ||
==Diagnosis== | ==Diagnosis== |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Addison disease develops as a result of bilateral adrenal cortex destruction. Both cortisol and aldosterone production are reduced. Autoimmune destruction of the adrenal glands is the most common cause in the western world, but infections such as tuberculosis, hemorrhage, adrenal vein thrombosis, and carcinoma are also known to significant causes. Tuberculosis remains the most common cause worldwide of Addison disease. The onset of Addison disease is often gradual, and symptoms of the disease can be difficult to recognize. It may go undetected until an illness or other stress precipitates adrenal crisis. Treatment should not be withheld to confirm diagnosis. Treatment should be the priority, as the disease is fatal if it remains untreated. Diagnosis is made with rapid, high-dose adrenocorticotropic hormone (ACTH) stimulation testing. If the patient is hypovolemic, dexamethasone and intravenous normal saline should be given before stimulation testing is performed. Drug therapy is with a combination of glucocorticoids and mineralocorticoids. Glucocorticoid doses needs to be doubled when patients have an episode of minor fever, infection, minor trauma, or minor physical (not emotional) stress. Intravenous stress-dose corticosteroids are needed for surgery requiring general anesthesia and for major trauma.
Historical Perspective
The condition is named after Dr. Thomas Addison, the British physician who first described the condition in his 1855 On the Constitutional and Local Effects of Disease of the Suprarenal Capsules.[1] The adjective "Addisonian" is used for features of the condition, as well as for patients with Addison's disease.[2]
Diagnosis
Ultrasound
Abdominal ultrasound is typically normal in Addison's disease except for the small size of adrenal glands.
Treatment
Surgery
Surgeries may require significant adjustments to medication regimens prior to, during, and following any surgical procedure. The best preparation for any surgery, regardless of how minor or routine it may be, is to speak to one's primary care physician about the procedure and medication implications well in advance of the surgery.
References
- ↑ Thomas Addison. On The Constitutional And Local Effects Of Disease Of The Supra-Renal Capsules (HTML reprint). London: Samuel Highley.
- ↑ Ten S, New M, Maclaren N (2001). "Clinical review 130: Addison's disease 2001". J. Clin. Endocrinol. Metab. 86 (7): 2909–22. PMID 11443143.