eMedicine Specialties > Dermatology > Internal Medicine

Addison Disease: Follow-up

Author: Elizabeth A Liotta, MD, Assistant Professor, Department of Dermatology, Uniformed Services University of the Health Sciences
Coauthor(s): Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center; Alexander Brough, MD, Consulting Surgeon, Department of Dermatology, Sewell's Point Clinic
Contributor Information and Disclosures

Updated: Jan 21, 2009

Follow-up

Further Inpatient Care

  • Admit patients with any of the systemic manifestations of Addison disease to the hospital.
    • Immediately treat patients with acute adrenal insufficiency with glucocorticoid replacement. Hydrocortisone can be administered both as a bolus and as an infusion.
    • Treat hypovolemia and hyponatremia with intravenous fluid and sodium replacement until the patient's condition is stable and he or she can tolerate oral fluids.
    • Consider treating the patient on an outpatient basis once the symptoms of adrenal insufficiency improve enough to enable oral replacement therapy.

Further Outpatient Care

  • Monitoring glucocorticoid and mineralocorticoid replacement therapy is perhaps more of an art than a science.
    • The ideal dose of glucocorticoids in replacement therapy adequately supplements the adrenal insufficiency while minimizing any adverse effects.
    • If the dose of the replacement glucocorticoids is too low, adrenal insufficiency continues.
    • In children, nocturnal hypoglycemia may result in seizures.
    • Overdoses of replacement glucocorticoids result in many undesired adverse effects, including weight gain and osteoporosis.
    • Correct dosing may be guided by monitoring urine cortisol levels.
  • Monitor mineralocorticoid replacement by observing the patient's blood pressure levels, which are low when doses of the mineralocorticoid are too low.
    • Monitor serum potassium levels to ensure resolution of the initial hyperkalemia.
    • Plasma renin concentrations may be monitored as well.
    • An overdose of fludrocortisone is difficult to assess, but overdoses may result in hypokalemia and increased atrial natriuretic peptide levels.
  • Exact dosing of both glucocorticoid and mineralocorticoid replacement is elusive.

Deterrence/Prevention

  • Avoid the use of diuretics to prevent excessive sodium loss.

Complications

  • Pay attention to potential drug interactions. Concomitant use of rifampin, phenytoin, or barbiturates increases the metabolism of replaced hormones; therefore, the patient's hormone levels may decrease to subtherapeutic levels.
  • Excessive sodium loss may result from the use of diuretics.

Prognosis

  • With proper control, the long-term prognosis is good.

Patient Education

  • Advise patients to wear medical alert tags at all times to reduce the time to the treatment and diagnosis of an addisonian crisis.
  • Inform patients about salt loss during vigorous exercise.

Miscellaneous

Medicolegal Pitfalls

  • Failure to diagnose and treat acute adrenal insufficiency immediately when the condition is suspected is a pitfall.
  • Failure to perform diagnostic laboratory tests when acute adrenal insufficiency is suspected is a pitfall.

Special Concerns

  • Pregnancy increases the physiologic stress on the patient.
    • The diagnosis of Addison disease may be delayed in pregnant women because the presenting symptoms of nausea, vomiting, and skin hyperpigmentation may be confused with symptoms of pregnancy.
    • Glucocorticoid and mineralocorticoid doses may need to be adjusted in patients who are pregnant. For example, the fludrocortisone dose may need to be decreased if preeclampsia develops.
    • Glucocorticoid and mineralocorticoid doses may need to be increased, especially during labor. Commonly, 1-3 doses of hydrocortisone 100 mg are intramuscularly or intravenously administered during labor.
  • Pediatric patients receiving adequate hormone replacement maintain a normal growth pattern, although their growth is rarely above the 50th percentile. Pubertal development is also normal.
  • The presenting symptoms of Addison disease in children are similar to those in adults, with the exception of weight loss, which is not a common finding in the pediatric population.
 
Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Dr. Quenby Erickson, to the development and writing of this article. The authors and editors of eMedicine also gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.



More on Addison Disease

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References
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Further Reading

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Keywords

Addison disease, Addison's disease, primary adrenal insufficiency, chronic adrenal insufficiency, hypoadrenalism, polyglandular autoimmune diseases, polyglandular autoimmune disease I, PGAD I, polyglandular autoimmune disease II, PGAD II, Schmidt syndrome, addisonian crisis, adrenocorticotropic hormone, ACTH, corticotropin, melanocyte-stimulating hormone, MSH

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Contributor Information and Disclosures

Author

Elizabeth A Liotta, MD, Assistant Professor, Department of Dermatology, Uniformed Services University of the Health Sciences
Elizabeth A Liotta, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Alexander Brough, MD, Consulting Surgeon, Department of Dermatology, Sewell's Point Clinic
Alexander Brough, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Robin Travers, MD, Assistant Professor of Medicine (Dermatology), Dartmouth University School of Medicine; Staff Dermatologist, New England Baptist Hospital; Private Practice, SkinCare Physicians
Robin Travers, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Informatics Association, Massachusetts Medical Society, Medical Dermatology Society, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting; Genetech Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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