Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 28 N2.3

Department of Diabetes & Endocrinology, Leicester Royal Infirmary, Leicester, United Kingdom.


Addison's disease was first described by Thomas Addison in 1855 and at that time was mostly caused by destruction of the adrenal glands by tuberculosis. In current endocrine practice the most common cause of Addison's is an autoimmune attack on the adrenals, and TB is a rare cause. Other adrenal diseases and infiltrations can also rarely cause the condition. Prevalence is approximately 40–60 cases per million population with incidence of 3–4 new cases/million per year. Addison's involves deficiency of both cortisol and aldosterone (in contrast to ACTH deficiency where the mineralocorticoid axis is mostly normal). The clinical presentation is therefore typically with tiredness and malaise and usually pigmentation of the skin (caused by high ACTH levels) progressing ultimately to presentation with adrenal or Addisonian crisis. In crisis, the typical biochemical findings include hyponatraemia, hyperkalaemia and dehydration - but these findings may be normal in symptomatic patients who are not in crisis. Investigation will typically include basal cortisol, synacthen test and other investigations to confirm the diagnosis of primary rather than secondary adrenal failure (e.g. ACTH, Renin, Adrenal antibodies, tests of other pituitary function). Treatment includes replacement with glucocorticoid (usually as hydrocortisone in thrice daily dosage), mineralocorticoid (as fludrocortisone) and appropriate education of self-adjustment of steroid replacement dosage during acute intercurrent illness. Monitoring and adjustment of these medications will be discussed. Modified release forms of hydrocortisone are currently awaiting regulatory approval, but their role has not yet been clearly established. Common problems and pitfalls in diagnosis, differential diagnosis and treatment will be discussed.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

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