A secondary adrenal insufficiency is a sub-function of the adrenal glands, which is caused by a lack of adrenocorticotropic hormone (ACTH). The symptoms are the same as in Addison’s disease, but it is a lower hypovolemia, as a rule. The diagnosis is made clinically and by laboratory tests. Typical are low plasma ACTH levels and low cortisol levels. The treatment consists of hydrocortisone substitution.

(See illustration of the adrenal function.)

A secondary adrenal insufficiency is a sub-function of the adrenal glands, which is caused by a lack of adrenocorticotropic hormone (ACTH). The symptoms are the same as in Addison’s disease, but it is a lower hypovolemia, as a rule. The diagnosis is made clinically and by laboratory tests. Typical are low plasma ACTH levels and low cortisol levels. The treatment consists of hydrocortisone substitution. (See illustration of adrenal function.) A secondary adrenal insufficiency can be a result of a panhypopituitarism, disorder isolated occurring of ACTH production, in patients receiving corticosteroid therapy (by any route, including high-dose inhaled intraarticular or topical corticosteroids), or after settling of corticosteroids arise. Inadequate secretion of ACTH may also result from the inability of the hypothalamus to the pituitary ACTH production stimulation, which is also called tertiary adrenal insufficiency. A Panhypopituitarism can in tumors of the pituitary gland, by Craniopharyngiomas in younger patients, by various other tumors, granulomas and rarely by infections or traumas that destroy the tissue of the pituitary gland, occur. In younger people, a Panhypopituitarism can occur secondary to a craniopharyngioma. Patients receiving corticosteroids for> 4 weeks, can under metabolic stress have a insufficient for adequate adrenal cortisol ACTH secretion or have atrophied adrenal glands, which no longer respond to ACTH. These problems may occur up to 1 year after discontinuation of corticosteroid therapy. Symptoms and signs The symptoms and findings are similar to those in an Addison’s disease, and include fatigue, weakness, weight loss, nausea, vomiting and diarrhea. Hyponatremia occurs on, it is usually a dilution effect. To distinguish but the absence of hyperpigmentation and relatively normal electrolyte and blood urea nitrogen values ??are used. Patients with Panhypopituitarism have limited function of the thyroid gland and the gonads and hypoglycemia. If a symptomatic secondary adrenal insufficiency, coma may be added. Adrenergic crisis is especially likely if a patient is treated for a single glandular insufficiency, particularly using thyroxine without hydrocortisone is substituted. Serum cortisol diagnostic serum ACTH ACTH stimulation test CNS imaging studies, by means of which one can distinguish a primary of a secondary adrenal insufficiency, are discussed below Addison’s disease. Patients with a secured secondary adrenal insufficiency (see table: Confirmatory Serumuntersuchngen for Secondary adrenal insufficiency) should get better MRI of the brain to rule out a pituitary tumor or atrophy CT or. Confirmatory Serumuntersuchngen for secondary adrenal insufficiency process result ACTH low (<5 pg / ml) cortisol low (<5 ug / dL [138 nmol / l]) ACTH stimulation test normal or subnormal Extended (24-h) ACTH stimulation test cortisol should continue rise for 24 h ACTH = adrenocorticotropic hormone The integrity of the hypothalamic-pituitary axis adrenal during Ausschleichens or exiting a long-term corticosteroid therapy, by the i v. Injection of 250 micrograms Cosyntropin / Synacthen be checked. After 30 min the Plasmakortisolspiegel should be> 20 g / dL (> 552 nmol / l); the specific levels vary slightly depending of the used laboratory assays. An insulin tolerance test, which helps hypoglycaemia induced with subsequent cortisol levels, is the standard for checking the axis hypothalamus-pituitary-adrenal. A corticotropin-releasing hormone (CRH) test can be used to distinguish between hypothalamic and pituitary causes, but is rarely performed in clinical practice. Patients with a pituitary disorder show, unlike patients with hypothalamic disorder, no reaction. After i.v. Administration of 100 micrograms (or 1 ug / kg) CRH is the normal reaction, an increase in serum ACTH 30-40 pg / ml. Therapy hydrocortisone or prednisone fludrocortisone is not given dose increase during prolonged illness The Glukokorticoidsubstitution is similar to the Addison’s disease. Each case is different in kind and degree of hormone deficiency. Fludrocortisone is not needed because the intact adrenal aldosterone secrete ACTH-independent. While acute febrile diseases or after trauma, it may be that patients receiving corticosteroids due nichtendokriner diseases require additional doses, since their endogenous hydrocortisone production can not adequately respond to the load. When Panhypopituitarism the other pituitary deficiencies should be adequately treated. Conclusion A secondary adrenal insufficiency includes an ACTH deficiency due to a malfunction of the pituitary gland or – often – due to hypothalamic disorder with a (including suppression by long-term use of corticosteroids). Other endocrine disorders (eg. As hypothyroidism, growth hormone deficiency) can coexist. In contrast to the Addison’s no hyperpigmentation occurs and the values ??of serum sodium and -potassium are relatively normal. ACTH and cortisol levels are both low. It is a glucocorticoid replacement required but not mineralocorticoids (z. B. fludrocortisone).

Health Life Media Team

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