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Endocrine array

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Endocrine array BIOCHIP ARRAY TECHNOLOGY 4x45 (180 biochips) EV3711 POA
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Evidence Endocrine Array is to be used for the in-vitro simultaneous quantitative detection of multiple related Endocrine Array immunoassays from a single sample.

The Endocrine Array is for research purposes only and should not be used for diagnostic procedures.


Endocrinology is hormone science that has grown into a diverse and complex field of biological research and clinical practice. The inexorable rise of this field has been based on the integration of knowledge from multiple scientific disciplines. It cuts across the life sciences and impacts heavily on global health and well being. Continuing research into the biomedical processes involved is shedding new light on causes and consequences of normal and abnormal cell-to-cell signalling and therefore providing ever more effective molecular tools to improve health and tackle disease(1). The Endocrine array can be used as a tool to further this field of hormone research.


Evidence Biochip Array Technology is used to perform simultaneous quantitative detection of multiple analytes from a single sample. The core technology is the Randox Biochip, a 9 mm(2) solid substrate containing an array of discrete test regions of immobilized antibodies specific to different endocrine hormones. A combination of sandwich and competitive chemiluminescent immunoassays is employed. Increased levels of Leptin in a specimen will lead to increased binding of antibody labeled with horseradish peroxidase (HRP) and thus an increase in the chemiluminescent signal emitted. Increased levels of Cortisol, DHEAS or 17αHydroxyprogesterone in a specimen will lead to decreased binding of antigen labeled with horse radish peroxidase (HRP) and thus a decrease in the chemiluminescent signal emitted.

The light signal generated from each of the test regions on the biochip is detected using digital imaging technology and compared to that from a stored calibration curve. From this the concentration is calculated.

Several different immunoassay based multi-analyte panels have been developed for use on Evidence. The Endocrine Array will successfully quantitatively test for Cortisol, Dehydroepiandrosterone-sulphate (DHEAs), 17αHydroxyprogesterone and Leptin simultaneously.


1. Hillier S.G. (2005) 100 years of hormones: pathway biology as the fifth force in endocrinology. J Endocrinol. 184(1): 3-4.


Cortisol (CORT) Assay


The Evidence Cortisol (CORT) assay has been designed for the quantitative measurement of Cortisol in human serum and plasma samples. This assay is for research and development use only.


Cortisol is the most important glucocorticoid and is produced by the adrenal gland at approximately 20 mg per 24 hours(1). It is derived from cholesterol following a cascade of enzymatic reactions. 90-95% of cortisol is bound to albumin and cortisol binding globulin and free cortisol only accounts for 5-10% of the total cortisol. Under normal conditions glucocorticoid production has a circadian rhythm and is influenced by several factors. The zenith is between 6 and 8 am and the nadir at midnight(2). ACTH stimulates the adrenal synthesis and secretion of cortisol with plasma cortisol following a parallel pattern to that of ACTH(1).

Stress induced activation of the hypothalamic-pituitary-adrenal axis causes release of corticotrophin releasing hormone and vasopressin from the hypothalamus via the hypophyseal portal system to the pituitary, stimulating systemic ACTH secretion(3). ACTH then applies a trophic action on the adrenal gland, increasing the production and release of cortisol. Many factors such as anti-diuretic hormone, amines, angiotensin II, serotonin and vasoactive intestinal peptide can enhance ACTH production. Cortisol exerts a negative feedback on the hypothalamic-pituitary axis reducing CRH and ACTH production(2).

Only free cortisol can enter the cell and in tissues cortisol is converted into cortisone, an inactivated form of glucocorticoid. Cortisone presents an affinity for the mineralocorticoid receptor and confers the weak mineralocorticoid activity of the glucocorticoids(2). Glucocorticoids exert their effects in all parts of the body and are involved in a number of physiological processes(4). Glucocorticoids function in metabolism as counter-regulatory hormones increasing blood glucose concentration, liver gluconeogenesis and glycogenolysis. They also enhance lipolysis and proteolysis, thus providing amino acids for gluconeogenesis. They are also involved in the immune response and in the cardiovascular system(2) .

Measurement of serum or plasma cortisol level is indicated in the diagnosis of hyper- and hypocortisolism and in the differential diagnosis of hyper- and hypocortisolism as part of numerous functional tests. An elevated basal cortisol level suggests the presence of Cushing's syndrome but the diagnosis can only be confirmed with further functional tests. Plasma cortisol levels can also be elevated with exposure to major stresses (severe systemic diseases, surgical procedures) as well as in conjunction with acute psychosis, obesity, anorexia nervosa, alcoholism and elevated estrogen concentrations during pregnancy, estrogen therapy or with oral contraceptives. Reduced basal plasma cortisol levels indicate primary or secondary adrenocortical insufficiency(1).


The Evidence Cortisol assay is a competitive chemiluminescent assay for the detection of Cortisol in human serum and plasma.


1. Thomas, L., Clinical Laboratory Diagnosis: Use and Assessment of Clinical Laboratory Results. 1st Ed. Frankfurt/Main: TH-Books-Verl.-Ges., 1998.

2. Allary, J. and Annane, D. (2005) Glucocorticoids and sepsis. Minerva Anestesiol. 71(12): 759-68.

3. Bornstein, S.R. and Chrousos, G.P. (1999) Clinical review 104: Adrenocorticotropin (ACTH)- and non-ACTH-mediated regulation of the adrenal cortex: neural and immune inputs. J Clin Endocrinol Metab. 84(5): 1729-36.

4. Andersen, C.Y. (2002) Possible new mechanism of cortisol action in female reproductive organs: physiological implications of the free hormone hypothesis. J Endocrinol. 173(2): 211-7.

Dehydroepiandrosterone-sulphate (DHEAs) Assay


The Evidence DHEAs assay has been designed for the quantitative measurement of DHEAs in human serum and plasma samples. This assay is for research and development use only.


Dehydroepiandrosterone-sulphate (DHEAs) is a very important prohormone that is secreted in large amounts by the adrenals(1). DHEAs along with DHEA are the main secretory products of the adrenal zona reticularis and are known as 'adrenal androgens'. DHEAs can be converted to DHEA by the activity of the enzyme sulphatase in peripheral tissues and converted to DHEA by the enzyme sulphotransferase in the liver and adrenal glands. DHEA is lipophilic whereas DHEAs is the hydrophilic form that circulates in the blood bound to albumin(2).

DHEA and DHEAs are converted into active sex steroids in peripheral target tissues, e.g. hair follicles, prostate, external genitalia, adipose tissue and the brain. The conversion of DHEA and DHEAs to active androgens (androstenedione, testosterone) and oestrogens (estradiol and oestrone) is dependent on the tissue activity of the metabolizing enzymes. In men, about 50% of androgens are derived from adrenal precursor steroids. In pre-menopausal women, about 75% of oestrogen synthesis occurs in peripheral target cells and this is almost 100% in post-menopausal women(2). Plasma DHEAs levels in adult men and women are 100 to 500 times higher than those of testosterone and 1000 to 10000 times higher than those of estradiol thus providing a large reservoir of substrate for conversion into androgens and/or estrogens in peripheral intracrine tissues(3).

The production of DHEAs is strongly associated with age(2) in that secretion by the adrenals increases during adrenarche in children at the age of 6-8 years(1) reaching a peak in early adulthood followed by a decline throughout adult life so that levels in the 7(th) decade are only 10-20% of the earlier individual peak concentrations(2).

Measurement of DHEAs is an indicator of adrenal androgen secretion(4) and elevated levels can be measured in adrenocortical tumors, adrenal cancer and congenital adrenal hyperplasia. It is indicated for differential diagnosis of hirsutism and virilism(5), polycystic ovary syndrome, infertility and amenorrhea(6).

Although the physiological and pathophysiological functions of DHEAs have not been fully identified(7) its contribution to the continuous formation of sex steroids in peripheral tissues is likely to play a major role in the maintenance of adequate functioning of most tissues(3). DHEAs has been reported to have anti-diabetic effects, to be related to chronic heart failure and that lower levels correlate with the incidence of depressive symptoms and poor results in the MMSE test in an elderly population. It also has links to obesity(7) and in post-menopausal women plasma levels of DHEAs are positively associated with breast cancer risk(8).


The Evidence DHEAs assay is a competitive chemiluminescent assay for the detection of DHEAS in human serum and plasma.


1. Labrie, F., Luu-The, V., Bélanger, A., Lin, S.X., Simard, J., Pelletier, G. and Labrie, C. (2005) Is dehydroepiandrosterone a hormone? J Endocrinol. 187(2): 169-96.

2. Bovenberg, S.A., van Uum, S.H. and Hermus, A.R. (2005) Dehydroepiandrosterone administration in humans: evidence based? Neth J Med. 63(8): 300-4.

3. Labrie, F., Luu-The, V., Lin, S.X., Simard, J., Labrie, C., El-Alfy, M., Pelletier, G. and Bélanger, A. (2000) Intracrinology: role of the family of 17 beta-hydroxysteroid dehydrogenases in human physiology and disease. J Mol Endocrinol. 25(1): 1-16.

4. Lobo, R.A., Paul, W.L. and Goebelsmann, U. (1981) Dehydroepiandrosterone sulfate as an indicator of adrenal androgen function. Obstet Gynecol. 57(1): 69-73.

5. Thomas, L., Clinical Laboratory Diagnostics: Use and Assessment of Clinical Laboratory Results. 1st Ed. Frankfurt/Main: TH-Books-Verl.-Ges., 1998.

6. Jacobs, D.S., Kasten Jr., B.L., Demott, W.R. and Wolfson, W.L., Laboratory Test Handbook 2nd Ed. Lexi-Comp Inc., Ohio, USA 1990.

7. Celec, P. and Stárka, L. (2003) Dehydroepiandrosterone - is the fountain of youth drying out? Physiol Res. 52(4): 397-407.

8. Page, J.H., Colditz, G.A., Rifai, N., Barbieri, R.L., Willett, W.C. and Hankinson, S.E. (2004) Plasma adrenal androgens and risk of breast cancer in premenopausal women. Cancer Epidemiol Biomarkers Prev. 13(6): 1032-6.

17α Hydroxy progesterone (17αOHP) Assay


The Evidence 17αOHP assay has been designed for the quantitative measurement of 17αOHP in human serum and plasma samples. This assay is for research and development use only.


17-OH Progesterone [17α Hydroxy progesterone (17αOHP)] is a steroid with relatively little progestational activity that is produced by both the adrenal cortex and gonads. It is the immediate precursor to 11-desoxycortisol, which is the precursor of cortisol. As 11-desoxycortisol is produced from 17αOHP by 21-hydroxylase measurement of 17αOHP is an indirect measurement of 21-hydroxylase activity.

17αOHP has a marked circadian variation in secretion with the highest levels in the morning and also menstrual-cycle dependent fluctuations. The luteal phase levels are higher than the follicular phase levels and indicate corpus luteum activity. There is a significant rise one day prior to the luteinizing hormone peak followed by a peak that coincides with that of the luteinizing hormone peak. This is followed by a short decrease and rise which correlate with those of estradiol and progesterone(1,2). Levels of 17αOHP also rise during pregnancy with a peak at week 38 (3,4).

In 95% of cases of congenital adrenal hyperplasia 21-hydroxylase deficiency is the underlying cause. 21-hydroxylase deficiency results in accumulation of 17αOHP, which is normally metabolized into 11-deoxycortisol. The increase in 17αOHP leads to enhanced synthesis of androgens such as DHEA and DHEAS. The incidence of homozygous deficiency is approximately 1 in 10000 whereas in the heterozygous form it is approximately 2%. In more than half of the children with congenital adrenal hyperplasia the disorder becomes clinically apparent during the 1(st) to 3(rd) week of life in the form of the so-called salt-losing syndrome. In premature newborns and sick newborns 17αOHP concentrations may be elevated due to stress(1).

Late on-set and mild heterozygous forms of adrenal hyperplasia can also occur and may manifest themselves during the peripubertal period in the form of menstrual disturbances and hirsutism or not until adulthood in the form of hirsutism. Late-onset 21-hydroxylase deficiency is present in 6-12% of all adult women with hirsutism and usually results in basal 17αOHP levels being mildly elevated(1). 17αOHP can be elevated in some cases of adrenal or ovarian neoplasms. 11β-hydroxylase deficiency is associated with modest elevations of 17αOHP( 2).


The Evidence assay is a competitive chemiluminescent assay for the detection of 17αOHP in human serum and plasma.


1. Thomas, L., Clinical Laboratory Diagnostics: Use and Assessment of Clinical Laboratory Results. 1st Ed. Frankfurt/Main: TH-Books-Verl.-Ges., 1998.

2. Tietz, N.W., Clinical Guide to Laboratory Tests. 2nd Ed. W.B. Saunders Company, Philadelphia, USA, 1990.

3. Buster, J.E. (1983) Gestational changes in steroid hormone biosynthesis, secretion, metabolism, and action. Clin Perinatol. 10(3): 527-52.

4. Dorr, H.G., Heller, A., Versmold, H.T., Sippell, W.G., Herrmann, M., Bidlingmaier, F. and Knorr, D. (1989) Longitudinal study of progestins, mineralocorticoids, and glucocorticoids throughout human pregnancy. J Clin Endocrinol Metab. 68(5): 863-8.


Leptin (LEPT) Assay


The Evidence Leptin assay has been designed for the quantitative measurement of Leptin in human serum and plasma samples. This assay is for research and development use only.


Leptin is a 16 kDa polypeptide containing 167 amino acids(1) that is encoded by the obese (ob) gene(2), and is structurally and functionally related to the IL-6 cytokine family(3). Leptin (derived from the Greek word leptos, which means thin)(1) functions as a signal in a feedback loop regulating food intake and body weight(3). Adipocytes secrete leptin in direct proportion to adipose tissue mass as well as nutritional status and this secretion is greater from sub cutaneous relative to visceral adipose tissue(1). Although leptin is produced predominantly by adipocytes low levels have been detected in the hypothalamus, pituitary, stomach, skeletal muscle, mammary epithelia, chrondocytes and a variety of other tissues(3).

Leptin expression and secretion are regulated by a variety of factors as levels are increased by insulin, glucocorticoids, TNFα, estrogens and CCAAT/enhancer-binding protein-α. Leptin is decreased by β3-adrenergic activity, androgens, free fatty acids, GH, and peroxisome proliferators-activated receptor-γ agonists(1).

Although initially viewed as an antiobesity hormone, leptin's primary role is to serve as a metabolic signal of energy sufficiency rather than excess. In addition to its effects on energy homeostatis, leptin regulates neuroendocrine function and traditional endocrine systems. Important endocrine effects of leptin include regulation of immune function, hematopoiesis, angiogenesis, and bone development. It normalises the suppressed immune function associated with malnutrition and leptin deficiency. It also promotes proliferation and differentiation of hematopoietic cells, alters cytokine production by immune cells, stimulates endothelial cell growth and angiogenesis and accelerates wound healing(1). Enhanced levels of leptin are associated with the advent of reproductive maturity and fertility(4) with leptin having direct effects via peripheral leptin receptors in the ovary, testis, prostate and placenta(1).

As plasma leptin concentrations correlate with the amount of fat tissue, obese individuals produce higher levels of leptin than lean individuals (3) with the only known cause of leptin hypersecretion being diet-induced obesity. This infers that hyperleptinemia plays an important physiological role in diet-induced obesity(5). It also suggests that most obese people are insensitive to endogenously produced leptin (3) and that the consequences of obesity result in a failure of hyperleptinemia to prevent surplus lipids from causing lipotoxicity. Leptin deficiency states are extremely rare, the most common form being congenital generalised lipodystrophy which is caused by a lack of leptin secreting adipocytes. Patients with this condition develop a severe facsimile of metabolic syndrome, or with insulin resistance, hyperleptinemia, severe diabetes, cardiomyopathy and fatty liver(5). Also associated with this condition are hypogonadotropic hypogonadism, morbid obesity and frequent deaths due to infections(3). Leptin treatment can dramatically improve this condition. A rare mutation of the leptin gene can also cause leptin deficiency and severe obesity(5).


The Evidence Leptin assay is a sandwich chemiluminescent assay for the detection of Leptin in human serum and plasma.


1. Kershaw, E.E. and Flier, J.S. (2004) Adipose tissue as an endocrine organ. J Clin Endocrinol Metab. 89(6): 2548-56.

2. Harvey, J. (2007) Leptin: a diverse regulator of neuronal function. J Neurochem. 100(2): 307-13.

3. Bernotiene, E., Palmer, G. and Gabay, C. (2006) The role of leptin in innate and adaptive immune responses. Arthritis Res Ther. 8(5): 217.

4. Henson, M.C. and Castracane, V.D. (2006) Leptin in pregnancy: an update. Biol Reprod. 74(2):218-29.

5. Unger, R.H. (2005) Hyperleptinemia: protecting the heart from lipid overload. Hypertension. 45(6):1031-4.