Secondary adrenal insufficiency

Secondary adrenal insufficiency is an adrenal hypofunction caused by a deficiency of ACTH. Symptoms are the same as the symptoms of Addison's disease. Diagnosis is based on clinical and laboratory data, including low levels of ACTH and plasma cortisol. Treatment depends on the cause, but mainly consists of the appointment of hydrocortisone.

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Causes of the secondary adrenal insufficiency

Secondary adrenal insufficiency can be observed with panhypopituitarism, isolated insufficiency of ACTH production, in patients taking glucocorticoids, or after stopping the intake of glucocorticoids. Insufficient production of ACTH can also be caused by the absence of hypothalamic stimulation of ACTH production, which is sometimes called a tertiary adrenal insufficiency.

Pangipopituitarism may be secondary due to tumors of the pituitary gland, craniopharyngioma in young people, various tumors, granulomas, less often infections or traumas that destroy the pituitary gland tissue. In patients taking glucocorticoids for more than 4 weeks, inadequate production of ACTH can develop which, during metabolic stress, does not provide sufficient stimulation of the adrenal glands and production of sufficient amounts of glucocorticoids, or these patients may develop adrenal atrophy with no response to stimulation of ACTH. These problems can last more than 1 year after the end of glucocorticoid therapy.

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Symptoms of the secondary adrenal insufficiency

Symptoms and signs are similar to those in  Addison's disease. The distinctive clinical and general laboratory features include absence of hyperpigmentation, a relatively normal level of electrolytes and urea blood; Hyponatremia in case of occurrence is a consequence of breeding.

In patients with panhypopituitarism, suppression of thyroid and sexual functions is observed, hypoglycemia, with secondary adrenal insufficiency accompanied by severe symptoms, coma may develop. The adrenal crisis is most likely in patients receiving treatment for the replacement of the function of one endocrine gland, especially when treated with thyroxine without hydrocortisone replacement.

Tests for differential diagnosis of primary and secondary adrenal insufficiency are discussed in the description of Addison's disease. Patients with confirmed secondary adrenal insufficiency should undergo CT or MRI of the brain to detect a tumor or pituitary atrophy. The adequacy of the hypothalamic-pituitary-adrenal connection during long-term treatment with glucocorticoids can be determined by intravenous injection of 250 μg of the synthetic analog of ACTH. After 30 minutes, the plasma cortisol level should be greater than 20 μg / dL (> 552 nmol / L). The "gold standard" for testing communication in the hypothalamic-pituitary-adrenal axis is an insulin stress test that causes hypoglycemia and increases the level of cortisol.

The corticobiliary test (CRH) can be used to differentiate the hypothalamic and pituitary variants, but is rarely used in clinical practice. After the administration of corticoliberin at a dose of 100 μg (or 1 μg / kg), an intravenously normal reaction is an increase in the plasma ACTH level by 30-40 pg / ml; in patients with hypothalamic insufficiency, the response usually develops, and in hypophysial insufficiency - no.

Treatment of the secondary adrenal insufficiency

Glucocorticoid replacement therapy is similar to that of Addison's disease. In each case, there are differences depending on the type and extent of deficiency of a specific hormone. Fludrocortisone is not required, since intact adrenals produce aldosterone.

During an acute illness or after an injury, patients receiving glucocorticoids for non-endocrine diseases may need additional doses to increase the endogenous production of hydrocortisone. With panhypopituitarism, adequate treatment of other types of pituitary insufficiency is necessary.