Primary adrenocortical insufficiency: Symptoms & Causes
Causes
The causes of primary adrenocortical insufficiency can be divided into the following five categories; Gland destruction (chronic & acute), impaired hormone production, ACTH-blocking antibodies, mutation of ACTH receptor gene, adrenal hypoplasia congenital.
More than 90% of both glands must be destroyed before adrenal insufficiency develops. The most common cause of gland destruction is tuberculosis infection in Korea, and the most common cause of gland destruction is caused by autoimmune among idiopathic atrophy. This autoimmune destruction is due to cytotoxic T lymphocyte. Other causes of gland destruction include surgical removal, tuberculosis, infection with fungi and viruses, hemorrhagic infarction due to anticoagulation, and invasion of the tumor.
Secondary adrenocortical insufficiency is a disease that lacks ACTH in the pituitary. Therefore, hypothyroid-pituitary disease-induced hypopituitarism, exogenous steroids, or endogenous steroids produced by tumors may cause hypothalamic-pituitary axis suppression. The most common cause of this is iatrogenic cushing by exogenous steroids. In Iatrogenic Cushing, the hypothalamus-pituitary is inhibited, the adrenal gland is atrophied, the adrenal response to ACTH is reduced, and the secretion of ACTH from the pituitary gland is also reduced. Other examples of secondary adrenocortical insufficiency include pituitary adenoma, Sheehan's syndrome, surgery for pituitary tumors or radiation therapy, and craniopharyngiomas.
Symptoms
In the case of primary adrenal insufficiency, cortisol and aldosterone secretion decline due to decreased adrenal function. In the case of secondary adrenal insufficiency, cortisol function is reduced by ACTH because RAAS is maintained normally. These hormone reductions are reflected in clinical features.
First, weakness, fatigue, and weight loss are the main symptoms, which are similar to primary and secondary. This is due to a decrease in overall metabolic function and a decrease in gluconeogenesis. Primary adrenal insufficiency causes hyperpigmentation of the pigment in the whole skin and mucous membranes. This is because the melanin content of the skin is increased because the MSH is also increased when the ACTH is increased to stimulate the adrenal gland without reaction. However, since secondary adrenal insufficiency is a disease with reduced ACTH, hyperpigmentation is not seen. In addition, unlike secondary, primary adrenal insufficiency may show arterial hypotension (≤80 / 50) because of lack of aldosterone. In addition, anorexia, nausea / vomiting, such as digestive system dysfunction, personality changes, hypoglycemia, such as fasting can occur.
Primary adrenal insufficiency is characterized by low serum cortisol levels and high ACTH levels, and cortisol levels may be normal at high stress levels. In addition, hyponatremia (80%) and hyperkalemia (40%) are seen as a cause of deficiency of aldosterone. Anti-adrenal antibodies are found in approximately one-half of autoimmune Addison's disease, and calcification occurs in the adrenal glands at half the tuberculous Addison's disease.
Secondary adrenal insufficiency has low levels of cortisol and ACTH in the blood, and aldosterone secretion is almost normal. It has the same hyponatremia as Primary, because of the reduced cortisol-induced ADH suppression. However, severe mineralocorticoid deficiency findings such as severe dehydration, hyponatremia, and hyperkalemia suggest primary adrenal insufficiency.
Adrenal insufficiency may be seen in patients who have received long-term steroid treatment despite physical findings of Cushing's syndrome. This is due to a decrease in ACTH secretion due to prolonged steroid administration, resulting in atrophy of the adrenal cortex.
The causes of primary adrenocortical insufficiency can be divided into the following five categories; Gland destruction (chronic & acute), impaired hormone production, ACTH-blocking antibodies, mutation of ACTH receptor gene, adrenal hypoplasia congenital.
More than 90% of both glands must be destroyed before adrenal insufficiency develops. The most common cause of gland destruction is tuberculosis infection in Korea, and the most common cause of gland destruction is caused by autoimmune among idiopathic atrophy. This autoimmune destruction is due to cytotoxic T lymphocyte. Other causes of gland destruction include surgical removal, tuberculosis, infection with fungi and viruses, hemorrhagic infarction due to anticoagulation, and invasion of the tumor.
Secondary adrenocortical insufficiency is a disease that lacks ACTH in the pituitary. Therefore, hypothyroid-pituitary disease-induced hypopituitarism, exogenous steroids, or endogenous steroids produced by tumors may cause hypothalamic-pituitary axis suppression. The most common cause of this is iatrogenic cushing by exogenous steroids. In Iatrogenic Cushing, the hypothalamus-pituitary is inhibited, the adrenal gland is atrophied, the adrenal response to ACTH is reduced, and the secretion of ACTH from the pituitary gland is also reduced. Other examples of secondary adrenocortical insufficiency include pituitary adenoma, Sheehan's syndrome, surgery for pituitary tumors or radiation therapy, and craniopharyngiomas.
Symptoms
In the case of primary adrenal insufficiency, cortisol and aldosterone secretion decline due to decreased adrenal function. In the case of secondary adrenal insufficiency, cortisol function is reduced by ACTH because RAAS is maintained normally. These hormone reductions are reflected in clinical features.
First, weakness, fatigue, and weight loss are the main symptoms, which are similar to primary and secondary. This is due to a decrease in overall metabolic function and a decrease in gluconeogenesis. Primary adrenal insufficiency causes hyperpigmentation of the pigment in the whole skin and mucous membranes. This is because the melanin content of the skin is increased because the MSH is also increased when the ACTH is increased to stimulate the adrenal gland without reaction. However, since secondary adrenal insufficiency is a disease with reduced ACTH, hyperpigmentation is not seen. In addition, unlike secondary, primary adrenal insufficiency may show arterial hypotension (≤80 / 50) because of lack of aldosterone. In addition, anorexia, nausea / vomiting, such as digestive system dysfunction, personality changes, hypoglycemia, such as fasting can occur.
Primary adrenal insufficiency is characterized by low serum cortisol levels and high ACTH levels, and cortisol levels may be normal at high stress levels. In addition, hyponatremia (80%) and hyperkalemia (40%) are seen as a cause of deficiency of aldosterone. Anti-adrenal antibodies are found in approximately one-half of autoimmune Addison's disease, and calcification occurs in the adrenal glands at half the tuberculous Addison's disease.
Secondary adrenal insufficiency has low levels of cortisol and ACTH in the blood, and aldosterone secretion is almost normal. It has the same hyponatremia as Primary, because of the reduced cortisol-induced ADH suppression. However, severe mineralocorticoid deficiency findings such as severe dehydration, hyponatremia, and hyperkalemia suggest primary adrenal insufficiency.
Adrenal insufficiency may be seen in patients who have received long-term steroid treatment despite physical findings of Cushing's syndrome. This is due to a decrease in ACTH secretion due to prolonged steroid administration, resulting in atrophy of the adrenal cortex.
