Adrenocorticotropic hormone (ACTH) is produced by the pituitary gland and its key function is to stimulate the production and release of cortisol from the cortex. ACTH also plays a role in circadian rhythm in many organisms.

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Name Type Format Host/Source Isotype Tested Apps Unit Catalog Buffer Immunogen Recombinant Description Notes SDS COA New Product Recommended Product Order a Sample
MAb to ACTH N-terminal Monoclonal Purified Mouse IgG1 EIA,IHC MG E54057M No View SDS View COA 0 Order a Sample

Adrenocorticotropic Hormone (ACTH)

Deficiency of ACTH leads to a reduction in the secretion of adrenal hormones (e.g. adrenaline, aldosterone, and cortisol), resulting in secondary adrenal insufficiency (hypoadrenalism), the manifestations of which are clinically indistinguishable from those of glucocorticoid deficiency. Symptoms include weight loss, lack of appetite, muscle weakness, nausea and vomiting, and low blood pressure (hypotension). ACTH deficiency can either be congenital or acquired, and several genetic mutations have been linked to this disease. In contrast, chronically elevated ACTH levels occur in primary adrenal insufficiency in which damage to the adrenal glands prevents them from producing the hormones in adequate amounts. An example is Addison’s disease which can be caused by autoimmune disorders or infections, such as TB or HIV, and tumors. Another disorder, Cushing’s disease, can be caused by medication or by a pituitary tumor and leads to an excess of cortisol (hypercortisolism). Quantitative 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. Hypopituitarism with ACTH deficiency, which is secondary adrenocortical insufficiency, is characterized by low plasma ACTH and cortisol concentrations, and a subnormal, but usual distinct adrenal response to stimulation with synthetic ACTH (Cortrosyn).


Laboratory diagnosis of parainfluenza viruses can be performed by isolation and detection of the virus in cell culture, or detection of viral antigens directly within respiratory tract secretions using immunofluorescence (IFA), enzyme immunoassays (EIA), fluroimmunoassays or polymerase chain reaction (PCR). Also, analysis of specific IgG antibodies showing a subsequent rise in titer following infection (using paired serum specimens) can demonstrate an acute infection. However, individual parainfluenza virus types are known to cross-react making subtyping difficult. Hemagglutination inhibition tests (HIT), complement fixation (CF), and neutralization tests (NT) can be performed to differentiate the HPIV types by evaluating the specific IgM, IgG, and IgA antibody titers.

During the acute phase of infection, two-thirds of patients show a high serum titer of specific HPIV IgM antibodies which persist 2-11 weeks. In 70 – 80% of patients, an increase in specific IgG antibodies (at least fourfold within 10 days) is found during primary infection with HPIV-1, 2, or 3. New EIA assays rely on purified viral envelope glycoprotein and nucleocapsid preparations. In a differential diagnosis, tests for other paramyxoviruses like mumps, pneumonia, or simian virus type 5 should be performed to identify possible cross-reactions.

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