The IDS-iSYS ACTH assay:

  • is fully automated, with excellent precision and a functional sensitivity of 6.0pg/mL, allowing you to provide accurate results for ACTH concentrations in plasma samples
  • has a wide assay range up to 1800pg/mL, allowing maximum number of samples to be run directly without the need for dilution
  • has proven accuracy demonstrated by high recovery of the NIBSC WHO 74/586 standard in human plasma samples
  • has excellent correlation to other commercially available methods
  • has low levels of cross-reactivity to an extensive list of potentially interfering substances
  • is an effective tool in the assessment of pituitary and adrenal function, Cushing’s syndrome and Addison’s disease

The IDS-iSYS ACTH assay is an in vitro diagnostic device intended for the quantitative determination of adrenocorticotropic hormone (ACTH) in human plasma on the IDS‑iSYS Multi-Discipline Automated System.

Results are to be used in conjunction with other clinical and laboratory data for the assessment of pituitary and adrenal gland function, the differential diagnosis of hyper- and hypo-cortisolism, as well as the evaluation of causes of endocrine hypertension.

ACTH, also known as corticotropin, is a 39 amino acid peptide hormone synthesized in the anterior pituitary gland which signals the adrenal cortex and other parts of the human body1. The synthesis of ACTH is typically regulated by corticotropin releasing hormone from the hypothalamus and arginine vasopressin2. ACTH increases steroid production such as cortisol, so that high levels of steroids in turn control the levels of ACTH by way of a negative feedback loop3. Clinical studies in Cushing’s disease, small cell lung carcinoma, and subjects with pituitary adenomas have shown that the ACTH-related peptides and precursors can also have relevant biological activity4-6.

ACTH measurements are frequently used in the assessment of adrenocortical function and other disturbances of the hypothalamic-pituitary-adrenal (HPA) axis. These include the differential diagnosis of Cushing’s syndrome (CS), a group of signs and symptoms due to high levels of glucocorticoids7, particularly in diagnosing ectopic ACTH production as a cause of CS, and in patients undergoing petrosal sinus catheter sampling3. Endogenous CS may be caused by excess ACTH production (80-85% of cases) or be ACTH-independent due to excess secretion of cortisol by the adrenal8. Normal or high ACTH concentrations indicate pituitary or ectopic sources of ACTH, while low concentrations indicate an adrenal tumour secreting glucocorticoids. Ectopic sources of ACTH production are most commonly small cell lung carcinoma, thymus or pancreatic carcinoma, phaeochromocytoma, thyroid and bronchial carcinomas. Accurate diagnosis of pituitary-derived ACTH is important for the correct tumour removal. ACTH measurements are also used in the follow-up after surgery for Cushing’s due to a pituitary adenoma.

ACTH levels are additionally used in the diagnosis of Addison’s disease, a failure of the adrenal gland to produce cortisol. Patients with primary adrenal insufficiency, most frequently caused by autoimmune adrenalitis, can be diagnosed based on a combined measurement of early morning serum cortisol and plasma ACTH levels. Secondary adrenal insufficiency, due to an impaired regulation of the adrenal gland by the HPA axis, most commonly requires dynamic testing such as the insulin tolerance test or the overnight metyrapone test9-11. Raised ACTH levels indicate a primary or adrenal cause whereas normal or low concentrations point to a pituitary cause.

Finally, ACTH measurements may have diagnostic value in follow-up of patients on steroid therapy for Addison’s or Congenital Adrenal Hyperplasia, subjects with large invasive pituitary tumours with no clinical evidence of Cushing’s, and rare disorders such as congenital ACTH deficiency 3,12.

    1. Schwyzer, R. ACTH: a short introductory review. Annals of the New York Academy of Sciences 297, 3-26 (1977).
    2. Raff, H. & Findling, J. W. A physiologic approach to diagnosis of the Cushing syndrome. Annals of Internal Medicine 138, 980-991 (2003).
    3. Talbot, J. A., Kane, J. W. & White, A. Analytical and clinical aspects of adrenocorticotrophin determination. Annals of Clinical Biochemistry 40, 453-471, (2003).
    4. White, A. & Gibson, S. ACTH precursors: biological significance and clinical relevance. Clinical Endocrinology 48, 251-255 (1998).
    5. Ray, D. W. et al. Elevated levels of adrenocorticotropin (ACTH) precursors in post-adrenalectomy Cushing’s disease and their regulation by glucocorticoids. The Journal of Clinical Endocrinology and Metabolism 80, 2430-2436, (1995).
    6. Stewart, P. M. et al. ACTH precursors characterize the ectopic ACTH syndrome. Clinical Endocrinology 40, 199-204 (1994).
    7. Lacroix, A., Feelders, R. A., Stratakis, C. A. & Nieman, L. K. Cushing’s syndrome. Lancet 386, 913-927, (2015).
    8. Arnaldi, G. et al. Diagnosis and complications of Cushing’s syndrome: a consensus statement. The Journal of Clinical Endocrinology and Metabolism 88, 5593-5602, (2003).
    9. Charmandari, E., Nicolaides, N. C. & Chrousos, G. P. Adrenal insufficiency. Lancet 383, 2152-2167, (2014).
    10. Bancos, I., Hahner, S., Tomlinson, J. & Arlt, W. Diagnosis and management of adrenal insufficiency. The Lancet. Diabetes & Endocrinology 3, 216-226, (2015).
    11. Arlt, W. & Allolio, B. Adrenal insufficiency. Lancet 361, 1881-1893, (2003).
    12. Nussey, S. S. et al. Isolated congenital ACTH deficiency: a cleavage enzyme defect? Clinical Endocrinology 39, 381-385 (1993).

IDS-iSYS Aldosterone

IDS-iSYS Direct Renin

IDS-iSYS Salivary Cortisol