What is a common cause of secondary adrenal insufficiency?

What is a common cause of secondary adrenal insufficiency?

• A. Autoimmune destruction of the adrenal cortex
• B. Long-term exogenous glucocorticoid therapy
• C. 21-hydroxylase deficiency
• D. Pheochromocytoma

Answer: (B)

Chronic suppression of the hypothalamic-pituitary-adrenal axis by long-term glucocorticoid therapy is a common cause of secondary adrenal insufficiency. When you take glucocorticoids for a long period, the body's CRH and ACTH production drops due to negative feedback. The adrenal cortex then atrophies from under-stimulation, so endogenous cortisol production is blunted, especially if steroids are withdrawn or during stress. Aldosterone regulation—primarily driven by the renin–angiotensin system—remains largely intact, so mineralocorticoid deficiency is not typical. Hyponatremia can occur, but hyperkalemia is not a hallmark. In contrast, autoimmune destruction of the adrenal cortex directly damages the gland and reduces both cortisol and aldosterone, leading to hyperkalemia and often hyperpigmentation from high ACTH. A congenital enzyme deficiency like 21-hydroxylase deficiency is a primary, often early-onset condition affecting the adrenal gland itself. A pheochromocytoma is a tumor of the adrenal medulla that causes catecholamine excess and hypertension, not adrenal insufficiency. So the evidence points to exogenous glucocorticoid use as the common cause of secondary adrenal insufficiency.

Chronic suppression of the hypothalamic-pituitary-adrenal axis by long-term glucocorticoid therapy is a common cause of secondary adrenal insufficiency. When you take glucocorticoids for a long period, the body's CRH and ACTH production drops due to negative feedback. The adrenal cortex then atrophies from under-stimulation, so endogenous cortisol production is blunted, especially if steroids are withdrawn or during stress. Aldosterone regulation—primarily driven by the renin–angiotensin system—remains largely intact, so mineralocorticoid deficiency is not typical. Hyponatremia can occur, but hyperkalemia is not a hallmark.

In contrast, autoimmune destruction of the adrenal cortex directly damages the gland and reduces both cortisol and aldosterone, leading to hyperkalemia and often hyperpigmentation from high ACTH. A congenital enzyme deficiency like 21-hydroxylase deficiency is a primary, often early-onset condition affecting the adrenal gland itself. A pheochromocytoma is a tumor of the adrenal medulla that causes catecholamine excess and hypertension, not adrenal insufficiency.

So the evidence points to exogenous glucocorticoid use as the common cause of secondary adrenal insufficiency.