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Any of the complications of the underlying disease (eg, tuberculosis) are more likely to occur, and the patient is susceptible to intercurrent infections that may precipitate crisis Associated autoimmune diseases are common (see above)
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Treatment
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A Specific Therapy
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Replacement therapy should include a combination of corticosteroids and mineralocorticoids In mild cases, hydrocortisone alone may be adequate Hydrocortisone is the drug of choice Most addisonian patients are well maintained on 15 25 mg of hydrocortisone orally daily in two divided doses, two-thirds in the morning and one-third in the late afternoon or early evening Some patients respond better to prednisone in a dosage of about 2 3 mg in the morning and 1 2 mg in the evening Adjustments in dosage are made according to the clinical response A proper dose usually results in a normal differential WBC count Many patients, however, do not obtain sufficient salt-
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Endocrine Disorders
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retaining effect and require fludrocortisone supplementation or extra dietary salt Fludrocortisone acetate has a potent sodium-retaining effect The dosage is 005 03 mg orally daily or every other day In the presence of postural hypotension, hyponatremia, or hyperkalemia, the dosage is increased Similarly, in patients with fatigue, elevated plasma renin activity indicates the need for a higher replacement dose of fludrocortisone If edema, hypokalemia, or hypertension ensues, the dose is decreased DHEA is given to some women with adrenal insufficiency Women taking DHEA 50 mg orally each morning have experienced an improvement in their overall sense of wellbeing, mood, and sexuality Because over-the-counter preparations of DHEA have variable potencies, it is best to have the pharmacy formulate this with pharmaceutical-grade DHEA
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Betterle C et al Autoimmune polyglandular syndrome Type 2: the tip of an iceberg Clin Exp Immunol 2004 Aug;137 (2):225 33 [PMID: 15270837] Libe R et al Effects of dehydroepiandrosterone (DHEA) supplementation on hormonal, metabolic and behavioral status in patients with hypoadrenalism J Endocrinol Invest 2004 Sep;27(8):736 41 [PMID: 15636426]
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CUSHING S SYNDROME (HYPERCORTISOLISM)
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ESSENTIALS OF DIAGNOSIS
Central obesity, muscle wasting, thin skin, hirsutism, purple striae Psychological changes Osteoporosis, hypertension, poor wound healing Hyperglycemia, glycosuria, leukocytosis, lymphocytopenia, hypokalemia Elevated serum cortisol and urinary free cortisol Lack of normal suppression by dexamethasone
B General Measures
All infections should be treated immediately and vigorously, and the dose of hydrocortisone should be raised appropriately The dose of corticosteroid should also be raised in case of trauma, surgery, stressful diagnostic procedures, or other forms of stress The maximum hydrocortisone dose for severe stress is 50 mg intravenously or intramuscularly every 6 hours Lower doses, oral or parenteral, are used for less severe stress The dose is reduced back to normal as the stress subsides Patients are advised to wear a medical alert bracelet or medal reading, Adrenal insufficiency takes hydrocortisone For patients with adrenoleukodystrophy, therapy with Lorenzo s oil normalizes serum very long-chain fatty acid concentrations but is ineffective clinically Neurologic manifestations may improve following hematopoietic stem cell transplantation from normal donors
General Considerations
The term Cushing s syndrome refers to the manifestations of excessive corticosteroids, commonly due to supraphysiologic doses of corticosteroid drugs and rarely due to spontaneous production of excessive corticosteroids by the adrenal cortex Cases of spontaneous Cushing s syndrome are rare (26 new cases yearly per million population) and have several possible causes About 40% of cases are due to Cushing s disease, by which is meant the manifestations of hypercortisolism due to ACTH hypersecretion by the pituitary Cushing s disease is caused by a benign pituitary adenoma that is typically very small (< 5 mm) It is at least three times more frequent in women than men About 10% of cases are due to nonpituitary neoplasms (eg, small cell lung carcinoma), which produce excessive amounts of ectopic ACTH Hypokalemia and hyperpigmentation are commonly found in this group About 15% of cases are due to ACTH from a source that cannot be initially located About 30% of cases are due to excessive autonomous secretion of cortisol by the adrenals independently of ACTH, serum levels of which are usually low Most such cases are due to a unilateral adrenal tumor: Benign adrenal adenomas are generally small and produce mostly cortisol; adrenal carcinomas are usually large when discovered and can produce excessive cortisol as well as androgens, with resultant hirsutism and virilization ACTH-independent macronodular adrenal hyperplasia can also produce hypercortisolism due to the adrenal cortex cells abnormal stimulation by hormones such as catecholamines, arginine vasopressin, serotonin, hCG/LH, or gastric inhibitory polypeptide; in the latter case, hypercortisolism may be intermittent and food dependent and serum ACTH may not be completely suppressed
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