Addison Disease


Article Author:
William Gossman
Sadaf Munir


Article Editor:
Muhammad Waseem


Editors In Chief:
Laurie Graham
Andrew Wilt
Mary Cataletto


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
7/11/2019 11:50:02 PM

Introduction

Addison disease is an acquired primary adrenal insufficiency, which is a rare but potentially life-threatening endocrine disorder that results from bilateral adrenal cortex destruction leading to decreased production of adrenocortical hormones including cortisol, aldosterone, and/or adrenal. Addison disease's insidious course of action usually presents with glucocorticoid deficiency followed by mineralocorticoid; however, it can present acutely, especially with inter-current illness, with adrenal crisis.

The most common cause of primary adrenal insufficiency is autoimmune adrenalitis (Addison disease) which is associated with increased levels of 21-hydroxylase antibodies.[1][2]

Etiology

Any disease process which causes direct injury to the adrenal cortex can result in primary adrenal insufficiency (Addison disease). In the developing world, autoimmune destruction of the adrenal glands is the most common cause of Addison disease; while, worldwide, other possible causes include infection such as sepsis, tuberculosis, and HIV, bilateral adrenal hemorrhages (secondary to sepsis, coagulopathy, or trauma), and neoplastic processes affect adrenal glands. Rare causes include sarcoidosis, amyloidosis, fungal infection, and certain genetic conditions (e.g., adrenal leukodystrophy, Wolman disease). Autoimmune destruction can be an isolated finding or part of autoimmune polyglandular endocrinopathies (type 1 and 2). Patients with autoimmune adrenal disease are more likely to have polyglandular autoimmune syndromes. [3][4]

Epidemiology

The incidence is 0.6/100,000 of population per year. The total number of people affected with this condition at a given time 4 to 11/100,000 of the population.

Pathophysiology

Addison disease is initially due to adrenal failure resulting in decreased production of cortisol, and subsequently, aldosterone which leads to loss of negative feedback on adrenocorticotropic hormone (ACTH) and plasma renin activity, respectively, both of which are elevated with complete adrenal failure.[5]

History and Physical

Addison disease usually has an insidious course with gradual onset of symptoms which are non-specific and attributed to other conditions often resulting in delayed diagnosis. In many cases the diagnosis is made only after the patient is presented with an acute adrenal crisis (hypotension, hyponatremia, hyperkalemia, and hypoglycemia) precipitated by a stressful illness or factors such as infection, trauma, surgery, vomiting, and diarrhea.

Addison disease can occur at any age but most often presents during the second to third decade of life. As mentioned above, the presentation is usually insidious in onset, and symptoms may be non-specific and include fatigue, generalized weakness, weight loss, nausea, vomiting or abdominal pain, dizziness, tachycardia and/or postural hypotension. Hyperpigmentation of skin and mucous membranes can be seen later in the course of disease resulting from elevated ACTH (as both ACTH and melanocyte-stimulating hormone (MSH) derived from the same precursor POMC). The presentation can be variable therefore a high index of suspicion is necessary for the presence of multiple non-specific symptoms including unexplained fatigue, poor appetite, chronic abdominal pain, weight loss, hyponatremia with or without hyperkalemia and/or hypotension. The manifestations of Addisonian crisis may include dehydration, refractory hypotension, and shock.

It should be suspected in

  • Patients receiving steroids
  • Hemodynamically unstable patients despite aggressive fluid therapy
  • Septic shock.

Evaluation

Hyponatremia is the most common initial laboratory finding which is not unexpected because cortisol has weak mineralocorticoid activity and it is also needed for free water excretion. Loss of aldosterone activity leads to natriuresis and potassium retention, thus further confounding electrolyte abnormalities (including life-threatening hyperkalemia).[6]

Hypoglycemia is multifactorial including decreased oral intake and lack of glucocorticoids, which is needed for gluconeogenesis.

Low random and stimulated cortisol and aldosterone level. A cortisol level less than 18 µg/dL to 20 µg/dL is considered diagnostic.

High ACTH level is diagnostic of primary adrenal destruction in the absence of ACTH resistance.

  •  Primary adrenal insufficiency: Elevated ACTH
  •  Central adrenal insufficiency: Abnormally normal or low ACTH

Increased Plasma Renin Activity (PRA) often late in the course of the disease (due to mineralocorticoid deficiency).

Anti-adrenal antibodies (such as 21-hydroxylase antibodies) serves as the markers of autoimmune destruction of the adrenal gland.

In suspected cases of adrenal hemorrhages, abdominal CT scan may provide useful information.

A chest x-ray may reveal a small heart.

PPD should be performed to evaluate for tuberculosis.

Plasma very long-chain fatty acid profile in cases where adrenal leukodystrophy is suspected (based on family history or etiology is unclear after evaluation).

Treatment / Management

Treatment should be immediately initiated if the diagnosis of acute adrenal crisis is suspected as it is a potentially life-threatening condition. However, blood samples should be saved for subsequent measurement of ACTH and cortisol levels. It is important to remember that a random measurement of plasma cortisol cannot confirm or exclude the diagnosis unless cortisol is unequivocally elevated. Elevation of ACTH with low cortisol is diagnostic of a primary adrenal problem. Measurement of cortisol in the ACTH stimulation test may be performed in equivocal cases where baseline lab evaluation cannot confirm the diagnosis. PRA is often elevated and is indicative of mineralocorticoid deficiency along with low aldosterone level.[7][8][9]

Patients with adrenal crisis require the following

  • Fluid resuscitation with intravenous (IV) normal saline (to correct volume depletion)
  • Dextrose (to correct hypoglycemia)
  • Hormone replacement to correct a lack of circulating glucocorticoid.

The first-line hormonal treatment is hydrocortisone. As stress dose hydrocortisone has significant mineralocorticoid activity, fludrocortisone (synthetic mineralocorticoid) is usually not required in the acute phase. Stress dose hydrocortisone for acute adrenal crisis is 50 mg/m2 to -100 mg/m2, which can be given as a continuous infusion. Typical replacement fluid after normal saline bolus is D5 Normal saline. Beware that if left untreated, adrenal crisis can be fatal.

 In adults, the typical replacement oral dose of hydrocortisone is 10-15 mg/m2/day divided into two to three doses. If compliance with frequent dosing is an issue, more potent glucocorticoids can be given less frequently, for example, prednisone qd-bid and dexamethasone qd; however, prednisone and dexamethasone do not have mineralocorticoid activity.

Also, mineralocorticoids should be replaced in the form of fludrocortisone at 50 µg/day to 200 µg/day (0.05-0.2 mg/day). In the presence of fever, infection, or other illnesses, the dose of hydrocortisone should be doubled to account for stress response. This should be tailored according to the degree to stress. Identification and treatment of underlying cause such as sepsis are critical for an optimal outcome.

During replacement treatment, the following should be monitored to assess the adequacy of replacement therapy:

  • Signs and symptoms suggestive of adrenal insufficiency
  • Measurement of serum electrolytes, cortisol, and ACTH
  • Measurement of plasma renin activity.

Patients who are non-stressed can be treated with either hydrocortisone or prednisone with or without fludrocortisone.

Differential Diagnosis

  • Septic shock
  • Hemorrhage
  • Eosinophilia
  • Miliary tuberculosis

Pearls and Other Issues

Symptoms of Addison disease can be nonspecific and therefore may be difficult to recognize. A high index of suspicion is required to make this diagnosis.

In Addison crisis, treatment is a priority and should not be delayed for diagnostic confirmation.

Glucocorticoid doses should be doubled in the presence of fever, infection, or other stresses.

Enhancing Healthcare Team Outcomes

Addison disease is a serious life-threatening disorder that affects many organs. If the diagnosis is delayed, it carries a very high morbidity and mortality. Thus, the condition is best managed by a multidisciplinary team of healthcare workers that includes an endocrinologist, intensivist, an infectious disease expert, gastroenterologist, and a pharmacist. Once the diagnosis is made, the outcomes depend on the primary cause. Any delay in starting corticosteroid treatment can lead to mortality rates in excess of 50%. All patients diagnosed with Addison disease must be urged to wear a medical alert bracelet. Patients should be educated on the signs and symptoms and contact their primary care provider at the slightest change in their vital signs. Finally, in times of stressful situations even a common cold, the patient should be told to double on the dose of steroids and see the primary care provider.  [10][7](Level V)

 


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Addison Disease - Questions

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What is the major cause of primary adrenocortical deficiency in patients over the age of 2 years?



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Which type of anemia is frequently present in patients with autoimmune Addison disease?



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A 50-year-old man presents with fatigue. He denies nausea, vomiting, diarrhea, or fever. His mucous membranes are dry, blood pressure is 90/60 mmHg, sodium is 127 mg/dL, and potassium is 5.4 mEq/L. What is the most likely cause of the patient's hyponatremia?



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What is the most common symptom on initial presentation of an adult with chronic Addison disease?



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What is the most common cause of Addison disease?



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What is the dosing frequency of fludrocortisone for adults with Addison disease?



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In a Caucasian patient with Addison disease, what skin finding may be present?



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Addison disease does not present with which of the following?



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Which is not a feature of Addison disease?



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Which of the following is not a laboratory feature of Addison disease?



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Addison disease is not associated with which of the following?



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Which of the following is least likely to be found in a patient with Addison disease?



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In a patient with Addison disease, which of the following is the best way to monitor fluid status?



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Which strategy is most appropriate in managing a patient with Addison disease during a stressful event?



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A 45-year-old female is diagnosed with Addison disease. What is the most likely color of her skin?



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Which is least likely to be found in a patient with Addison disease?



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Which of the following hormones is implicated in skin darkening of patient's with Addison disease?



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Addison disease results from destruction or dysfunction of what organ?



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What is the risk associated with prescribing levothyroxine 0.125 mg a day to a patient with untreated or unrecognized Addison disease?



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Which of the following tests would not be useful in the diagnosis of Addison disease?



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A 44 year old female complains of dizziness and weakness when stressed. Exam shows mild hypotension and diffuse skin hyperpigmentation. Laboratories are remarkable for hyperkalemia, hyponatremia, normal TSH, elevated ACTH, low aldosterone, low fasting cortisol, and low glucose. What is the most probable cause of these findings?



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What type of hypersensitivity reaction causes Addison disease?



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A patient with Addison disease is started on hydrocortisone 25 mg by mouth daily. What dosage adjustments may be necessary?



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A patient with Addison disease is started on hydrocortisone 30 mg PO daily. Select the correct statement about dose adjustment.



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A 7-year-old girl presents with Addisonian crisis. What lab values would be expected?



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Which disease process is commonly associated with hyperpigmentation?



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What is the most appropriate oral fluid for a patient with Addison disease?



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Which electrolyte disturbance is most likely in a patient with Addison disease?



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Which statement is most accurate regarding mineralocorticoid therapy for Addison disease?



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Which statement is most accurate regarding oral glucocorticoid therapy for Addison disease?



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Which is the most appropriate way to monitor whether a patient with Addison disease is receiving the correct amount of mineralocorticoid?



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Which finding suggests that a patient with Addison disease is receiving inadequate treatment?



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Patient education regarding Addison disease should include all except which of the following?



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Which advice is least appropriate for a patient with Addison disease?



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Hyperpigmentation in Addison disease is most likely due to which of the following?



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Which of the following symptoms are not associated with Addison disease?



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Which of the following signs is not present in Addison disease?



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What percent of patients with Addison disease also presented with hypercalcemia?



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Which is suggested by hyperpigmentation is scars and creases?



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Which is true of patients with Addison disease?



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Which of the following patients is suspected to have Addison disease?



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Which of the following patients would be suspected to have Addison disease?



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What is caused by Addison disease?



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A 30-year-old female presents with chest pain. She also complains of fatigue and recent weight loss. Upon examination, the patient has darkened oral mucosa. The blood pressure is 100/70 mmHg, heart rate 86 bpm, temperature 98.7 F, and respiratory rate 14/minute. Which of the following is most likely to also be found in this patient?



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Addison Disease - References

References

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