Addison's disease should be diagnosed biochemically

Editor—The reports on Addison's disease in the BMJ emphasised the problems of diagnosing the condition at an early stage.¹,² Addison's disease needs to be diagnosed as early as possible. Current protocols make the biochemical confirmation of the diagnosis comparatively straightforward for most patients. Considering this diagnosis in patients whose symptoms are vague and non-specific can be life saving.

Although we understand and sympathise with the statement that “Getting diagnosed is the hardest part of the disease,”² many patients can be diagnosed as having Addison's disease and be given corticosteroid “replacement” without a proper biochemical diagnosis. This is increasingly seen in the treatment of patients diagnosed as having the chronic fatigue syndrome, the postviral fatigue syndrome, or myalgic encephalomyelitis. Some of these patients have been shown to have mildly impaired pituitary-adrenal function but not in all studies³; it is generally believed that this is a consequence rather than a cause of the disorder.

Corticosteroid “replacement” has been used empirically in these situations, but it has not generally been found to produce dramatic changes. Certainly any use of this treatment should be closely monitored. The therapeutic benefits should be carefully considered in the light of the possible long term, deleterious consequences of inappropriate corticosteroid treatment, including the additive effects of pharmacological corticosteroids to endogenous production; this could cause not only long term suppression of the pituitary-adrenal axis but also adverse effects, such as hypertension and osteoporosis.

Without a formal diagnosis a young patient could face a lifetime of inappropriate corticosteroid use. Although the diagnosis of Addison's disease should be seriously considered against a background of malaise and fatigue, confirmation should be rooted on firm biochemical footing.