ACTH
產(chǎn)品名稱：ACTH ELISA
產(chǎn) 地：Demeditec
產(chǎn)品貨號：DE3647
產(chǎn)品規(guī)格：96 Tests
產(chǎn)品說明：
Special remarks:
1 INTENDED USE
The DEMEDITEC ACTH ELISA is intended for the quantitative determination of ACTH (Adrenocorticotropic Hormone) in human plasma. This assay is intended for in vitro diagnostic use.
2 SUMMARY AND EXPLANATION
ACTH (Adrenocorticotropic hormone) or corticotropin is a 39-amino acid peptide hormone (MW=4500) secreted by the pituitary to regulate the production of steroid hormones by the adrenal cortex. ACTH secretion from the anterior pituitary is controlled by both a classical negative feedback control mecha-
nism and CNS-stress mediated control system. Various types of stress or pain perceived in higher levels of the brain modulate secretion of the hypothalamic neurosecretory hormone, corticotropin releasing hormone (CRH), a 41-amino acid peptide. CRH stimulates pituitary ACTH secretion. The second peptide that modulates ACTH secretion is vasopressin (AVP). AVP secretion is also stimulated by stress and acts synergistically with CRH to increase ACTH secretion in the pituitary portal circulation. ACTH increases the synthesis and release of all adrenal sterioids, aldosterone, cortisol and adrenal androgens. It is the principal modulator of cortisol, the most important glucocorticoid in man. As the cortisol level in blood increases, release of ACTH is inhibited directly at the pituitary level. Through this same mechanism, decreasing cortisol levels lead to elevated ACTH levels.
Biologically active ACTH results from enzymatic cleavage of a large precursor molecule, proopiomelanocortin (POMC). This molecule contains within its structure the amino acid sequences of ACTH, Pro-ACTH, ß-melanocyte stimulating hormone, lipotropin, as well as endorphin and the enkephalins. Because the reaction in immunoassays is determined by antigenic structure, not biological function, the usual ACTH RIA reacts with POMC, Pro-ACTH, ACTH and some fragments of the ACTH.
Like other pituitary hormones, ACTH is secreted in a pulsatile manner. These small pulses are superimposed on a characteristic diurnal fluctuation of greater amplitude. In healthy individuals, ACTH reaches a peak in the early morning (6:00 - 8:00 hour) and levels become lowest late in the day and near the beginning of the sleep period. Because of this diurnal rhythm it is customary to draw plasma ACTH samples between 8:00 and 10:00 hour. However, differentiation of patients with Cushing’s disease from normal individuals may be best achieved on samples obtained in the evening (16:00 - 18:00 hour). In Cushing’s disease and in ectopic ACTH syndromes, the diurnal pattern of ACTH secretion is generally absent. Stress may also override the diurnal variation.
3 CLINICAL SIGNIFICANCE
Plasma ACTH assays are useful in the differential diagnosis of pituitary Cushing’s disease, Addison’s disease, autonomous ACTH producing pituitary tumors (e.g. Nelson’s syndrome), hypopituitarism with ACTH deficiency and ectopic ACTH syndrome.
Cushing’s syndrome is caused by the effects of excess glucocorticoid actions. All causes of Cushing’s syndrome, with the exception of glucocorticoid medication, are associated with increased 24-hour urinary cortisol. The most common cause of Cushing’s syndrome is bilateral adrenal hyperplasia, due to pituitary ACTH hypersecretion (Cushing’s disease) from a pituitary adenoma or corticotroph hyperplasia. Laboratory diagnosis of Cushing’s disease is supported by the following:
suppression of plasma ACTH and cortisol concentrations, by high-dose (2.0 mg q 6h x 8) dexamethasone administration,
absence of ACTH and cortisol suppression with low-dose (0.5 mg q 6h x 8 or 1 mg
given at 23:30 hour) dexamethasone,
larger than normal response to metyrapone (Metopirone) stimulation and normal or elevated plasma ACTH levels.
When Cushing’s syndrome is caused by primary adrenal abnormality (adenoma or carcinoma), the adrenal gland acts independently of ACTH and pituitary ACTH secretion is suppressed. Hence, there is no response to dexamethasone suppression or metyrapone stimulation. This type of Cushing’s syndrome is characterized by very low, or undetectable levels of ACTH. Therefore, measurement of plasma ACTH is helpful in differential diagnosis of pituitary Cushing’s syndrome. In patients with adrenal tumors, ACTH levels are low. High levels of ACTH are seen in patients with ectopic ACTH syndrome. Patients with bilateral adrenal hyperplasia will have ACTH levels inappropriately elevated for their degree of hypercortisolism, which should suppress ACTH. However, in most cases the ACTH concentration will be within the normal range.
Adrenocortical insufficiency or inadequate cortisol production can be due to destruction of the adrenal cortex or to abnormalities of the pituitary or hypothalamus, which result in inadequate ACTH production of release. Primary adrenocortical insufficiency, Addison’s disease, is characterized by markedly elevated plasma ACTH levels and adrenal unresponsiveness to stimulation with exogenous ACTH. Hypopituitarism with ACTH deficiency, which is secondary adrenocortical insufficiency, is characterized by low plasma ACTH and cortisol concentrations, and a subnormal, but usually distinct adrenal response to stimulation with synthetic ACTH (Cortrosyn ® ). If hypoglycemic stress or metyrapone stimulation is required for diagnosis, ACTH and cortisol responses are less than normal.
Aggressive and invasive ACTH producing pituitary tumors occurring before or following bilateral adrenalectomy for Cushing’s disease (Nelson’s syndrome) are characterized by the development of Addisonian pigmentation, often in an adrenalectomized patient who is taking adequate glucocorticoid replacement therapy. In these patients, plasma ACTH levels are markedly elevated and do not respond well to dexamethasone suppression.
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