Addison’s disease, or hypoproduction of cortisol, is usually the result of atrophy of the adrenal cortex by unknown causes (idiopathic). This can be the result of failure at other levels of the cascade from the limbic system downward. There is a requirement for life-long treatment with daily steroid replacement. The results of Addison’s disease are sodium loss (since aldosterone usually is also deficient), excess potassium in the blood, low blood pressure, hypoglycemia, high levels of ACTH and MSH (loss of negative feedback), and pigmentation of the skin due to the high levels of MSH and/ or ACTH (Figure 1). The acute onset of Addison’s disease, referred to as Addisonian shock, is shock associated with adrenal insufficiency and most commonly occurs when an individual with long-standing adrenal insufficiency is exposed to a stressful stimulus. It is treated with large intravenous doses of cortisol, fluid replacement, and antibiotics. With the correct daily replacement of medication, the Addisonians are mostly able to continue life as they had before diagnosis of their illness.

Fig1. Example of pigmentation disorders associated with idiopathic Addison’s disease. The hand on the left highlights the skin pigmentation problems experienced by a patient with Addison’s disease. The hand on the right side is from a healthy person. Reproduced from Ezrin, C., Godden, J. O., Volpe, R. and Wilson, R. (Eds) (1973). Systematic Endocrinology, p. 178. Harper & Row, New York.

Tuberculosis is the most common cause of Addison’s disease worldwide. TB is a bacterial infection that mostly affects the lungs but can also spread to other parts of the body such as the adrenal gland. There is not a high death rate explicitly attributable to Addison’s disease. The death rate of the entire population as a whole varies from 1:25,000 persons to 1:100,000 persons from country to country. With respect to the death rate of persons with Addison’s dis ease, it displays on a country-by-country basis the same proportion of deaths around the world.

Mineralocorticoid excess can be a feature of Cushing’s syndrome, as mentioned earlier. It can be the cause of reduced potassium levels in blood, resulting in weakness, sodium retention, and hypertension.

An inborn error of metabolism can result in a deficiency of the adrenal cortical enzyme, C-21 hydroxy lase, whose function is required for the synthesis of cortisol. This deficiency results in lowered cortisol levels and enlarged output of ACTH by the anterior pituitary due to reduced negative feedback. High ACTH results in adrenal hyperplasia and hypersecretion, especially in the products of the zona reticularis (DHEA), which, together with adrenal testosterone, can lead to masculinization of female babies. Precocious puberty in males can also result from this condition. Treatment is centered on cortisol replacement therapy, which restores the negative feedback mechanism.

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