Causes of Adrenal adenoma, familial
Adrenal adenoma, familial Causes: Book Excerpts
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Adrenal hypofunction:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Adrenal hypofunction occurs when more than 90% of both adrenal glands are destroyed, an occurrence that typically results from an autoimmune process in which circulating antibodies react specifically against the adrenal tissue. Other causes include tuberculosis (once the chief cause; now responsible for less than 10% of adult cases), bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, and infections (acquired immunodeficiency syndrome, histoplasmosis, and cytomegalovirus). Rarely, a familial tendency to autoimmune disease predisposes the patient to adrenal hypofunction and other endocrinopathies.
Secondary adrenal hypofunction that results in glucocorticoid deficiency can stem from hypopituitarism (causing decreased corticotropin secretion), abrupt withdrawal of long-term corticosteroid therapy (long-term exogenous corticosteroid stimulation suppresses pituitary corticotropin secretion and results in adrenal gland atrophy), or removal of a nonendocrine, corticotropin-secreting tumor. Adrenal crisis follows when trauma, surgery, or other physiologic stress exhausts the body’s stores of glucocorticoids in a person with adrenal hypofunction.
Adrenal hypofunction affects 1 in 16,000 neonates congenitally. In adults, it affects 8 in 100,000 people, and males and females are affected equally. There’s no racial predilection.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Hyperaldosteronism:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Hyperaldosteronism may be primary (uncommon) or secondary. In 70% of patients, hyperaldosteronism results from a benign aldosterone-producing adrenal adenoma. In 15% to 30% of patients, the cause is unknown; rarely, the cause is bilateral adrenocortical hyperplasia (in children) or carcinoma. Incidence is three times higher in females than in males and is highest between ages 30 and 50.
In primary hyperaldosteronism, chronic aldosterone excess is independent of the renin-angiotensin system and, in fact, suppresses plasma renin activity. This aldosterone excess enhances sodium reabsorption by the kidneys, which leads to mild hypernatremia and, simultaneously, hypokalemia and increased extracellular fluid (ECF) volume. Expansion of intravascular fluid volume also occurs and results in volume-dependent hypertension and increased cardiac output. Excessive ingestion of English black licorice or licorice-like substances can produce a syndrome similar to primary hyperaldosteronism due to the mineralocorticoid action of glycyrrhizic acid.
Secondary hyperaldosteronism results from an extra-adrenal abnormality that stimulates the adrenal gland to increase production of aldosterone. For example, conditions that reduce renal blood flow (renal artery stenosis) and ECF volume or produce a sodium deficit activate the renin-angiotensin system and, subsequently, increase aldosterone secretion. Thus, secondary hyperaldosteronism may result from conditions that induce hypertension through increased renin production (such as Wilms’tumor), ingestion of hormonal contraceptives, and pregnancy.
However, secondary hyperaldosteronism may also result from disorders unrelated to hypertension, which may or may not cause edema. For example, nephrotic syndrome, hepatic cirrhosis with ascites, and heart failure commonly induce edema, whereas Bartter’s syndrome and salt-losing nephritis don’t.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Adrenal hypofunction:
Causes
(Handbook of Diseases)
The following are causes of primary and secondary adrenal hypofunction and adrenal crisis.
Primary hypofunction
Addison’s disease occurs when more than 90% of both adrenal glands are destroyed. Such destruction usually results from an autoimmune process (autoimmune adrenalitis) in which circulating antibodies react specifically against the adrenal tissue.
CLINICAL TIP: Suspect adrenal insufficiency in patients with acquired immunodeficiency syndrome. Although symptoms may not be present, testing frequently reveals abnormal results.
Other causes include tuberculosis (once the chief cause; now responsible for less than 10% of adult cases), bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, and infections (histoplasmosis, cytomegalovirus). Rarely, a family history of autoimmune disease predisposes the patient to Addison’s disease and other endocrinopathies.
Secondary hypofunction
Secondary hypofunction, which results in glucocorticoid deficiency, can stem from hypopituitarism (causing decreased corticotropin secretion), abrupt withdrawal of long-term corticosteroid therapy (long-term exogenous corticosteroid stimulation suppresses pituitary corticotropin secretion and results in adrenal gland atrophy), or the removal of a corticotropin-secreting tumor.
Adrenal crisis
After trauma, surgery, or other physiologic stress, adrenal crisis exhausts the body’s stores of glucocorticoids in a person with adrenal hypofunction.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
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