Secondary adrenal insufficiency

Substitution therapy for deficiency states acute or chronic adrenal insufficiency, congenital adrenal hyperplasia, and adrenal insufficiency secondary to pituitary insufficiency, nonendocrine disorders arthritis rheumatic carditis allergic, collagen, intestinal tract, liver, ocular, renal, shin diseases bronchial asthma cerebral edema malignancies PO 5-60 mg/day in divided doses. Intra-articular, Intralesional (acetate) 4-100 mg, repeated as needed. Intra-articular, Intralesional (sodium phosphate) 2-30 mg, repeated at 3-day to 3-week intervals, as needed. IM (acetate, sodium phosphate) 4-60 mg a day. 

Substitution therapy in deficiency states acute or chronic adrenai insufficiency, congenital adrenal hyperplasia, and adrenal insufficiency secondary to pituitary insufficiency nonendocrine disorders arthritis rheumatic carditis aiiergic, coiiagen, intestinai tract, liver, ocular, renal, shin diseases bronchiai asthma cerebrai edema maiignancies PO... 

An acute episode of adrenal insufficiency secondary to adrenal hemorrhage occurred in one patient receiving aldesleukin (5). 

Secondary adrenal insufficiency most commonly results from exogenous corticosteroid use, leading to suppression of the hypothalamic-pituitary-adrenal axis and decreased release of ACTH, resulting in impaired androgen and cortisol production. Mirtazapine and progestins (e.g., medroxyprogesterone acetate, megestrol acetate) have also been reported to induce secondary adrenal insufficiency. Secondary disease typically presents with normal mineralocorticoid concentrations. 

Congenital adrenal hyperplasia Primary adrenal insufficiency Secondary adrenal insufficiency Selective aldosterone deficiency Musculoskeletal Diseases Mixed connective tissue syndromes Polymyalgia rheumatica Polymyositis Rheumatoid arthritis... 

A 46-year-old man with chronic hepatitis C developed antiphospholipid syndrome after taking peginterferon alfa -I- ribavirin for 12 weeks the presentation was primary adrenal insufficiency secondary to bilateral adrenal hematoma and subclavian vein thrombosis [55 ]. 

Drug-induced (most common cause of secondary adrenal insufficiency)... 

Secondary adrenal insufficiency occurs as a result of a pituitary gland dysfunction whereby decreased production and secretion of ACTH leads to a decrease in cortisol synthesis. Tertiary adrenal insufficiency is a disorder of the hypothalamus that results in decreased production and release of CRH, which, in turn, decreases pituitary ACTH production and release. In contrast to Addison s disease (i.e., primary adrenal insufficiency), aldosterone production is unaffected in the secondary and tertiary forms of the disease. Chronic adrenal insufficiency often has a good prognosis if diagnosed early and treated appropriately. 

Tests to Determine Diagnosis of Primary, Secondary, and Tertiary Adrenal Insufficiency ... 

Secondary or tertiary adrenal insufficiency plasma ACTH low or ... 

Once diagnosis is confirmed, perform further testing to differentiate between primary, secondary, and tertiary adrenal insufficiency. 

Determine the duration of treatment for patients with secondary and tertiary adrenal insufficiency. 

Damage and destruction of the pituitary gland may result in secondary hypothyroidism, hypogonadism, adrenal insufficiency, growth hormone deficiency, hypoprolactinemia, or... 

Adrenal gland hypofimction is associated with primary (Addison s disease) or secondary adrenal insufficiency. Adrenal insufficiency occurs when the adrenal glands do not produce enough cortisol and, in some cases, aldosterone. 

Hyperpigmentation is common in Addison s disease and may involve exposed and nonexposed parts of the body. Hyperpigmentation is usually not seen in secondary adrenal insufficiency because of low amounts of melanocyte-stimulating hormone. 

Patients with Addison s disease have an abnormal response to the short cosyntropin-stimulation test. Plasma ACTH levels are usually 400 to 2,000 pg/mL in primary insufficiency versus normal to low (0 to 50 pg/mL) in secondary insufficiency. A normal cosyntropin-stimulation test does not rule out secondary adrenal insufficiency. 

Treatment of secondary adrenal insufficiency is identical to primary disease treatment with the exception that mineralocorticoid replacement is usually not necessary. 

Adrenal insufficiency may result from hypofunction of the adrenal cortex (primary adrenal insufficiency, Addison s disease) or from a malfunctioning of the hypothalamic-pituitary system (secondary adrenal insufficiency). In treating primary adrenal insufficiency, one should administer sufficient cortisol to diminish hyperpigmentation and abolish postural hypotension these are the cardinal signs of Addison s disease. 

Cortisone acetate and hydrocortisone are usually the corticoids of choice for replacement therapy in patients with primary adrenocortical insufficiency (such as Addison s disease), or after adrenalectomy where both glucocorticoid and mineralo-corticoid replacement is needed. In secondary adrenal insufficiency, associated with inadequate corticotrophin (ACTH) secretion, glucocorticoid replacement alone is usually adequate [62]. 

Four boys 4—8 years old with symptomatic adrenal insufficiency had all used consistent high doses of fluticasone propionate 1000-1500 micrograms/day over extended periods (16 months to 5 years) (58). They presented with acute hypoglycemia secondary to iatrogenic adrenal suppression, with abnormal corticotropin tests, although none had Cushingoid features. 

ACTH stimulation of the adrenals will fail to elicit an appropriate response in states of adrenal insufficiency. A rapid test for ruling out adrenal insufficiency employs cosyntropin (see below). Plasma cortisol levels are measured before and either 30 minutes or 60 minutes following an intramuscular or intravenous injection of 0.25 mg of cosyntropin. A normal plasma cortisol response is a stimulated peak level exceeding 20 g/dL. A subnormal response indicates primary or secondary adrenocortical insufficiency that can be differentiated using endogenous plasma ACTH levels (which are increased in primary adrenal insufficiency and decreased in the secondary form). 

An incremental rise in plasma aldosterone generally occurs in secondary but not primary adrenal insufficiency after cosyntropin stimulation. 

Because most adrenal crises occur because of glucocorticoid dose reductions or lack of stress-related dose adjustments, patients receiving corticosteroid-replacement therapy should add 5 to 10 mg hydrocortisone (or equivalent) to their normal daily regimen shortly before strenuous activities such as exercise. During times of severe physical stress (e.g., febrile illnesses, after accidents), patients should be instructed to double their daily dose until recovery. Treatment of secondary adrenal insufficiency is identical to primary disease treatment with the exception that mineralocorticoid replacement is usually not necessary. 

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