Hypoadrenia or “a bit of Addison's disease”

In the fully developed form of Addison's disease, first described in 1855 and now usually called acute adrenocortical failure or adrenal insufficiency, the signs and symptoms are unmistakable. They are weakness, tiredness, low blood pressure and pigmentation which is especially prominent in scars, flexures and inside the mouth. By the end of the nineteenth century it was generally agreed that the adrenal glands were essential to life and that they consisted of two glands, the medulla and cortex, in a single capsule. The discovery of the pressor effects of adrenal extracts in 1895, and isolation and synthesis of adrenaline in the subsequent decade diverted the attention of clinicians and physiologists away from the adrenal cortex.1 Adrenaline raised the blood pressure and increased muscular strength and, since these were the antithesis of the symptoms of Addison's disease, many concluded that Addison's disease was adrenaline deficiency. Final proof that Addison's disease was due to failure of the adrenal cortex did not come until the early 1930s,2 and even then there were major difficulties in diagnosis in patients with "doubtful pigmentation, loss of weight, fatigability, weakness and hypotension".3 These, with the exception of pigmentation, are common and non-specific and in the context of neurasthenia form part of what Sicherman has described as "the staggering variety of symptoms that had long taxed the ingenuity and patience of physicians".4 They were seized on by some pioneer endocrinologists in the period 1902-1925 to construct a disease, "hypoadrenia", or aformefruste of Addison's disease.