Androstenediol (Δ-5 Androstenediol)
Contact ISI for details.
Clinical Significance
Angiotensinogen is a peptide of about 60,000 molecular weight. It is an alpha2 globulin produced by the liver. It is metabolized by the enzyme Renin to form the biologically inactive decapeptide Angiotensin I. Active forms of Angiotensin are formed by further metabolism. Levels of Angiotensinogen are affected by Estrogens, ACTH, and glucocorticoids. The level of Angiotensinogen is the rate determining factor in renin activity.
Reference Range
800 - 1500 pg/ml
Procedure
Angiotensinogen is measured by direct radioimmunoassay.
Patient Preparation
Patient should be on a normal sodium diet, 110 mEq. sodium. Patient should be in a recumbent posture for at least 30 minutes prior to collection of specimen. Diuretics, mineralocorticoids, glucocorticoids, estrogens, oral contraceptives, and ACTH medications and sodium, potassium, and posture all affect Angiotensinogen levels.
Specimen Collection
3 ml EDTA plasma should be collected and separated as soon as possible. Freeze plasma immediately after separation. Minimum specimen size is 1 ml.
Special Specimens
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions
Ship specimens frozen in dry ice.
References
1. van Hooft IMS, Grobbee DE, Derkx FHM, et al. Renal Hemodynamics and the Renin-Angiotensin-Aldosterone System in Normotensive Subjects with Hypertensive and Normotensive Patients. N Engl J Med 324:1305-1311, 1991.
2. Genain C, Aldigier JC, Guyenne TT et al. Direct Radioimmunoassays of Renin and Renin Substrate During Converting-Enzyme Inhibition. Clin Experimen Hypertens - Theory and Practice A4: 2193-2202, 1982.
CPT Code:
Unspecified
Quantitative
Immunoassay 83519
Clinical Significance
Bradykinin is a nonapeptide formed when Kallikrein acts upon kininogens. Bradykinin is involved in several physiological functions including Prostaglandin synthesis, vasodilation, changes in blood pressure and vascular permeability, shock and pain production. It is also involved in the pharmacology of converting enzyme inhibitors. Elevated levels are also found in patients with myocardial infarction. Bradykinin levels are inhibited by glucocorticoids. Bradykinin can cause pulmonary vasodilation or contraction, bronchoconstriction through pulmonary release of Prostaglandins and Thromboxanes, and increase permeability of pulmonary endothelium.
Reference Range
50 - 500 pg/ml
Procedure
Bradykinin is measured by radioimmunoassay after immediate extraction of the specimen. See special instructions for collection and shipping of specimen.
Patient Preparation
Patient should not be on any diuretics, glucocorticosteroids, hypertension or blood pressure medication, if possible, for at least 48 hours prior to collection of specimen. The patient should be fasting for 10-12 hours and be recumbent for at least 30 minutes prior to collection of specimen.
Specimen Collection
Contact the Institute for complete specimen collection instructions. Special preservative tube is required for collection. No other specimen is acceptable for Bradykinin specimens.
Special Specimens
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions
Ship specimens frozen in dry ice. Note! Because of the essential Acetone extraction procedure, the specimen may not freeze even at dry ice temperature. Specimens must be shipped in a tightly sealed vial.
References
1. Vavrek RJ and Stewart JM. Competitive Antagonists of Bradykinin. Pept 6: 161, 1985.
2. Jauch KW, Hartl WH, Georgieff M. Low-Dose Bradykinin Infusion Reduces Endogenous Glucose Production in Surgical Patients. Metab 37: 185, 1988.
CPT Code:
Bradykinin 82286
Cortisol Binding Globulin Index (CBG-I)
Clinical Significance
Cortisol Binding Globulin (Transcortin) is an a1-Glycoprotein of approximately 50,000 MW. CBG has a strong affinity for several steroids including Cortisol, 11-Deoxycortisol, Corticosterone, and Progesterone. Cortisol Binding Globulin is the specific transport protein for Cortisol. Specific binding sites for Cortisol Binding Globulin have been located on some Cortisol target cells and may be able to transfer the Cortisol intracellularly. Cortisol Binding Globulin binding capacity is increased by Thyroid supplements, Estrogens, and pregnancy. Levels are substantially decreased by septic shock. Decreased binding capacity seen in pregnancy may be due to displacement of Cortisol by Progesterone and other compounds rather than a substantial decrease in the quantity and affinity of binding sites.
Reference Range
19 - 30 ug Cortisol/dl
Procedure
Cortisol Binding Globulin Index is measured by a radiodisplacement assay.
Patient Preparation
Patient should not be on any Corticosteroid, ACTH, Estrogen or Thyroid medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Special Specimens
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions
Ship specimens at room temperature or frozen in dry ice.
References
1. Pugeat M, Bonnetson A, Perrot D, et al. Decreased Immunoreactivity and Binding Activity of Corticosteroid-Binding Globulin in Serum in Septic Shock. Clin Chem 35:1675-1679, 1989.
2. Hryb DJ, Khan MS, Romas NA, and Rosner W. Specific Binding of Human Corticosteroid Binding Globulin to Cell Membranes. Proc Nat Acad Sci 83: 3253-3256, 1986.
CPT Code:
Unspecified
Quantitative
Immunoassay 83519
Dehydroepiandrosterone Sulfate (DHEA-S)
Clinical Significance
Dehydroepiandrosterone is a 17-Ketosteroid produced primarily by the adrenal gland by side chain cleavage of 17-HydroxyPregnenolone. It is reversibly converted to Dehydroepiandrosterone-Sulfate and Androstenediol. It is also converted to Androstenedione. DHEA-Sulfate is strongly bound to Albumin which decreases its metabolic clearance rate and provides a high concentration storage system for production of the sex steroids. It is excreted in the urine directly as DHEA-Sulfate. DHEA-Sulfate is one of the first androgens to increase significantly at the onset of adrenarche. Levels increase throughout puberty until adulthood. In females, levels drop off sharply after menopause. Although DHEA-Sulfate has only weak androgenic properties, it is one of the most abundant steroids present and may be readily converted to the more potent sex steroids. DHEA-Sulfate may distinguish adrenal causes of overandrogenization from gonadal causes. In pregnancy, DHEA-Sulfate is an immediate precursor to Estriol production.
Reference Ranges
Male: 200 - 350 ug/dl
Female: Premenopausal: 40 - 300 ug/dl
Postmenopausal: 10 - 60 ug/dl
Procedure
Dehydroepiandrosterone-Sulfate is measured by direct radioimmunoassay on unextracted specimens.
Patient Preparation
Patient should not be on any Steroid, ACTH, Estrogen, or Gonadotropin medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection
3 ml serum or EDTA plasma should be collected and separated. Minimum specimen size is 0.5 ml.
Special Specimens
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions
Ship specimens at room temperature or frozen in dry ice.
References
1. Braithwaite SS, Collins S, Prinz RA, et al. Decreased Dehydroepiandrosterone Sulfate in Pigmented Nodular Adrenal Dysplasia. Clin Chem 35: 2216-2219, 1989.
2. Carmina E, Levin JH, Malizia G, and Lobo RA. Ovine Corticotropin-Releasing Factor and Dexamethasone Responses in Hyperandrogenic Women. Fertil Steril 54: 245-250, 1990.
CPT Code:
DHEA-S 82627
Dehydroepiandrosterone-Sulfate (DHEA-S), urine
Clinical Significance:
Dehydroepiandrosterone is a 17-Ketosteroid produced primarily by the adrenal gland by side chain cleavage of 17-HydroxyPregnenolone. It is reversibly converted to Dehydroepiandrosterone-Sulfate and Androstenediol. It is also converted to Androstenedione. It is excreted in the urine directly as DHEA-Sulfate. Up to 90% of the DHEA excreted into the urine is in the Sulfate form. This assay measures only the Sulfate form present in the urine. DHEA-Sulfate is one of the first androgens to increase significantly at the onset of adrenarche. Levels increase throughout puberty until adulthood. In females, levels drop off sharply after menopause. DHEA-Sulfate may distinguish adrenal causes of overandrogenization from gonadal causes. Elevated levels of urine DHEA-Sulfate are found in third trimester pregnancies as DHEA-Sulfate becomes a direct precursor to Estriol formation.
Reference Ranges:
Male: 0.5 - 6.5 mg/24 hours
Female: Up to 4.0 mg/24 hours
Procedure:
Urine Dehydroepiandrosterone-Sulfate is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on any Steroid, ACTH, Estrogen, or Gonadotropin medications, if possible for at least 48 hours prior to collection of specimen.
Specimen Collection:
5 ml of a 24 hour urine collection should be submitted. Do not acidify urine! No special preservatives are required. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. LH Parker and W O'Dell. Decline of Adrenal Androgen Production as Measured by Radioimmunoassay of Urinary Unconjugated Dehydro-epiandrosterone. Journal of Clinical Endocrinology and Metabolism 47: 600, 1978.
2. E Carmina, JH Levin, G Malizia, and RA Lobo. Ovine Corticotropin-Releasing Factor and Dexamethasone Responses in Hyperandrogenic Women. Fertility and Sterility 54: 245-250, 1990.
Clinical Significance
11-Deoxycortisol is a glucocorticoid produced primarily from hydroxylation of 17-HydroxyProgesterone. It is further hydroxylated to Cortisol, the major glucocorticoid. 11-Deoxycortisol is excreted into the urine as conjugated and unconjugated forms of 11-Deoxycortisol and Tetrahydrocortisol. 11-Deoxycortisol secretion is controlled by ACTH. It is increased by metapyrone and inhibited by Dexamethasone. 11-Deoxycortisol levels are very elevated in the 11b-Hydroxylase deficient form of congenital adrenal hyperplasia. Inhibition of 11-Deoxycortisol conversion to Cortisol decreases the negative feedback control system and can lead to hyperandrogenization.
Reference Range
Up to 500 ng/dl
Procedure
11-Deoxycortisol is measured by radioimmunoassay following extraction and chromatographic purification of specimens.
Patient Preparation
Patient should not be on any Corticosteroid, ACTH, Dexamethasone or Metapyrone treatment or medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Special Specimens
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions
Ship specimens at room temperature or frozen in dry ice.
References
1. Pescovitz OH, Cutler GB Jr, and Loriaux DL. Synthesis and Secretion of Corticosteroids. In Prin Prac Endocrinol Metab. Ed. KL Becker. JB Lippincott, Philadelphia 579-590, 1990.
2. Nieman LK, Chrousos GP and Oldfield CH. The Corticotropin-Releasing Hormone Stimulation Test and the Dexamethasone Suppression Test in the Differential Diagnosis of Cushing's Syndrome. Ann Intern Medic 105: 862, 1986.
class="style6"CPT Code:
11-Deoxycortisol 82634
11-Deoxycortisol, urine (Compound S) (As Metabolite of 11-Deoxycortisol)
Clinical Significance:
11-Deoxycortisol is a glucocorticoid produced primarily from hydroxylation of 17-HydroxyProgesterone. It is further hydroxylated to Cortisol, the major glucocorticoid. 11-Deoxycortisol is excreted into the urine as conjugated and unconjugated forms of 11-Deoxycortisol and Tetrahydrocortisol. This assay measures the conjugated and unconjugated forms of 11-Deoxycortisol but not the Tetrahydro-11-Deoxycortisol. 11-Deoxycortisol secretion is controlled by ACTH. It is increased by metapyrone and inhibited by Dexamethasone. Urine 11-Deoxycortisol levels are very elevated in the 11b-Hydroxylase deficient form or congenital adrenal hyperplasia. Inhibition of 11-Deoxycortisol conversion to Cortisol decreases the negative feedback control system and can lead to hyperandrogenization.
Procedure:
Tetrahydro Cortisol is measured by GC/MS following hydrolysis, derivatizations and chromatographic purification of specimens.
Patient Preparation:
Patient should not be on any Corticosteroid, ACTH, Dexamethasone or Metapyrone treatment or medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
5 ml of a 24 hour urine should be submitted. No special preservatives are required. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. OH Pescovitz, GB Cutler Jr, and DL Loriaux. Synthesis and Secretion of Corticosteroids. In Principles and Practice of Endocrinology and Metabolism Ed. KL Becker. JB Lippincott, Philadelphia 579-590, 1990.
2. BM Luttrell and AW Steinbeck. The Urinary Excretion of Glucosiduronates of Cortisol and Cortisone. Journal of Clinical Endocrinology and Metabolism 42: 567, 1976.
Clinical Significance
Dexamethasone is a synthetic Glucocorticoid inhibitor. It is a Methylated, Fluorinated derivative of Prednisolone. Dexamethasone mimics the negative feedback properties of Cortisol and is able to decrease or prevent the release of ACTH from the Pituitary gland. Dexamethasone has potent, long-acting Glucocorticoid activty but little or no Mineralocorticoid activity. Dexamethasone causes a major reduction in Adrenal produced Androgens and Steroids. Dexamethasone can enhance the effectiveness of Clomiphene Citrate in treating women with Poly Cystic Ovarian Disease by suppressing excessive adrenal Androgen production. Dexamethasone has also been noted to suppress secretion of Melatonin. Measurement of Dexamethasone levels provides a quantitative determination of the dose-related effectiveness of adrenal suppression.
Reference Range
Non-Detectable. Limit of sensitivity is 1 ug/dl.
Procedure
Dexamethasone is measured by radioimmunoassay following extraction of specimens.
Patient Preparation
Patient should not be on any other Corticosteroid or ACTH therapy, if possible, for at least 48 hours prior to collection of specimen. Because Dexamethasone is not a naturally occurring steroid, no other patient preparation is required.
Specimen Collection
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Shipping Instructions
Ship specimens at room temperature or frozen in dry ice.
References
1. Carmina E, Levin JH, Malizia G, and Lobo RA. Ovine Corticotropin-Releasing Factor and Dexamethasone Responses in Hyperandrogenic Women. Steril Fertil 54: 245-250, 1990.
2. Abraham GE, Maroulis GB, Boyers SP, et al. Predictive Value of Dexamethasone (DEX) Suppression Test in the Clinical Response of Hyperandrogenized Patients to Endocrine Therapy. Obstet Gynenecol 57: 2, 1981.
CPT Code:
Unspecified
Quantitative
Immunoassay 83519
Clinical Significance:
b-Endorphin is a 31 amino acid peptide produced by cleavage of proopiomelanocortin. Proopioimelanocortin is first cleaved into b-Lipotropin (also the precursor of a and g Endorphins) and ACTH. b-Endorphin contains potent morphine-like activity. b-Endorphin is in the same family of hormones as the Enkephalins and the Dynorphins. b-Endorphin has a slight biphasic variation throughout the menstrual cycle. Levels of b-Endorphin increase during the luteal phase leading to the increase of Luteinizing Hormone at midcycle. b-Endorphin levels are elevated in luteal phase dect patients. Some studies have shown b-Endorphin levels are suppressed in patients with the symptoms of Pre Menstrual Syndrome. b-Endorphin secretion runs parallel with ACTH secretion and is controlled by the same factors as ACTH.
Reference Range:
Up to 40 pg/ml
Procedure:
b-Endorphin is measured by direct radioimmunoassay .
Patient Preparation:
Patient should not be on any ACTH, Corticosteroid, Gonadotropin or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen. Patient should be fasting 10 - 12 hours prior to collection. Morning specimens are preferred.
Specimen Collection:
3 ml EDTA plasma should be collected and separated as soon as possible. Freeze plasma immediately after separation. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. H Hohtari, K Salminen-Lappalainen, and T Laatkkainen. Response of Plasma Endorphins, Corticotropin, Cortisol, and Luteinizing Hormone in the Corticotropin-Releasing Hormone Stimulation Test in Eumenorrheic and Amenorrheic Athletes. Fertility and Sterility 55: 276-280, 1991.
2. M Shaarawy, HA Shaaban, MM Eid, and O Abdel-Aziz. Plasma b-Endorphin Level in Cases of Luteal Phase Defect. Fertility and Sterility 56: 248-253, 1991.
Clinical Significance:
b-Endorphin is a 31 amino acid peptide produced by cleavage of proopiomelanocortin. Proopioimelanocortin is first cleaved into b-Lipotropin (also the precursor of a and g Endorphins) and ACTH. b-Endorphin contains potent morphine-like activity. b-Endorphin is in the same family of hormones as the Enkephalins and the Dynorphins. b-Endorphin has a slight biphasic variation throughout the menstrual cycle. Levels of b-Endorphin increase during the luteal phase leading to the increase of Luteinizing Hormone at midcycle. b-Endorphin levels are elevated in luteal phase dect patients. Some studies have shown b-Endorphin levels are suppressed in patients with the symptoms of Pre Menstrual Syndrome. b-Endorphin secretion runs parallel with ACTH secretion and is controlled by the same factors as ACTH.
Reference Range:
Up to 40 pg/ml
Procedure:
b-Endorphin is measured by direct radioimmunoassay .
Patient Preparation:
Patient should not be on any ACTH, Corticosteroid, Gonadotropin or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen. Patient should be fasting 10 - 12 hours prior to collection. Morning specimens are preferred.
Specimen Collection:
3 ml EDTA plasma should be collected and separated as soon as possible. Freeze plasma immediately after separation. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. H Hohtari, K Salminen-Lappalainen, and T Laatkkainen. Response of Plasma Endorphins, Corticotropin, Cortisol, and Luteinizing Hormone in the Corticotropin-Releasing Hormone Stimulation Test in Eumenorrheic and Amenorrheic Athletes. Fertility and Sterility 55: 276-280, 1991.
2. M Shaarawy, HA Shaaban, MM Eid, and O Abdel-Aziz. Plasma b-Endorphin Level in Cases of Luteal Phase Defect. Fertility and Sterility 56: 248-253, 1991.
Clinical Significance:
Epiandrosterone is an androgen derived primarily from metabolism of Epitestosterone. It is excreted into the urine as conjugated and unconjugated derivatives. Epiandrosterone is a weak androgen, produced in an inverse relationship with Androsterone, a potent androgen. Elevated Epiandrosterone levels occur in patients with elevated androgen precursors but without androgenization of target organs. Hypogonadic males also often have elevated levels of Epiandrostrone demonstrating the Androsterone/Epiandrostrone balance.
Reference Range:
24 - 60 ng/dl
Procedure:
Epiandrosterone is measured by radioimmunoassay following extraction and chromatographic purification of the specimens.
Patient Preparation:
Patient should not be on any ACTH, Steroid, Gonadotropin, or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. RS Rosenfield, J Kream, I Paul, and L Hellman. Preparation and Antigenic Properties of Androsterone-7-BSA Conjugate. Steroids 5: 153-162, 1975.
2. E Carmina, FZ Stanczyk, RK Matteir, and RA Lobo. Serum Androstrone Conjugates Differentiate Between Acne and Hirsutism in Hyperandrogenic Women. Fertility and Sterility 55: 872-876, 1991.
Clinical Significance:
Epitestosterone is an androgen derived primarily from metabolism of Androstenedione. It is converted primarily to Epiandrosterone. It is excreted into the urine as conjugated and unconjugated derivatives. Epitestosterone is a weak androgen, produced in an inverse relationship with Testosterone, a potent androgen. Epitestosterone and Testosterone are produced in static ratio which can vary from equimolar production to a 1 : 6 ratio. Ratios lower than 1 : 6 have been taken to be indicative of exogenous Testosterone or Testosterone derivative use. Hirsute females with normal or slightly elevated levels of Testosterone frequently have elevated levels of Epitestosterone.
Reference Range:
Male: 200 - 600 ng/dl
Female: Up to 30 ng/dl
Procedure:
Epitestosterone is measured by radioimmunoassay following extraction of the specimens.
Patient Preparation:
Patient should not be on any ACTH, Steroid, Gonadotropin, or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. M Okamoto, C Setaishi, Y Horiuchi, K Mashimo, K Moriya and S Itoh. Urinary Excretion of Testosterone and Epitestosterone and Plasma Levels of LH and Testosterone in the Japanese and Ainu. Journal of Clinical Endocrinology and Metabolism 32: 673, 1971.
2. E Carmina, FZ Stanczyk, RK Matteir and RA Lobo. Serum Androsterone Conjugates Differentiate between Acne and Hirsutism in Hyperandrogenic Women. Fertility and Sterility 55: 872-876, 1991.
Clinical Significance:
Etiocholanolone is one of the three major 17-ketosteroids. It is derived primarily from Androstenedione although it can also be produced from other androgens. It is excreted into the urine as conjugated (Sulfate and Glucuronide forms) and unconjugated (free) derivatives. Etiocholanolone is a potent pyrogen and has been found in elevated concentrations in patients with Meditterranean fever (Etiocholanolone fever). Etiocholanolone has been found to be elevated in hirsute females. Patients suffering from long term diseases usually have decreased levels of Etiocholanolone.
Reference Range:
Male: 10 - 75 ng/dl
Female: 10 - 60 ng/dl
Procedure:
Etiocholoanolone is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on any Steroid, ACTH, Gonadotropin or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. H Stolecke, W Muller, and HA Heinz. The Endocrine and Histological Pattern of a Gonadoblastoma with Teratoid Elements and Normal Female Karotype. Z Kinderjeilkd 117: 213, 1974.
2. CW Weykamp, TJ Penders, N A Schmidt, AJ Borburgh, F van de Calseyde, and BJ Wolthers. Steroid Profile for Urine: Reference Values. Clinical Chemistry 35: 2181-2184, 1989.
Follicle Stimulating Hormone (FSH)
Clinical Significance:
Follicle Stimulating Hormone is a pituitary hormone consisting of two subunits, a and b. The release of FSH is controlled by the hypothalamic hormone Luteinizing Hormone Releasing Hormone and Inhibin. FSH has a negative feedback control system mediated by androgen and estrogen activity on the hypothalamus and directly on the receptor sites of the pituitary. FSH levels are greatly increased in menopausal females and castrated males due to the lack of estrogen and androgen shut-off systems. In females, FSH levels vary throughout the menstrual cycle peaking at mid-cycle. Hypopituitary hypogonadism patients are characterized by low FSH, LH and sex steroid levels. Hypogonadic patients with normal or elevated FSH levels indicate a gonadal site of disorder.
Reference Ranges:
Male: 4 - 19 mIU/ml
Female:
Follicular: 2 - 20 mIU/ml
Mid-cycle: 3 - 30 mIU/ml
Luteal: 2 - 11 mIU/ml
Postmenopausal: 40 - 200 mIU/ml
Procedure:
Follicle Stimulating Hormone is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on any Steroid, ACTH, Gonadotropin, or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. Z Shoham, A Patel, and HS Jacobs. Polycystic Ovarian Syndrome: Safety and Effectiveness of Stepwise and Low-Dose Administration of Purified Follicle-Stimulating Hormone. Fertility and Sterility 55: 1051-1056, 1991.
2. L Anttila, Y-Q Ding, K Ruutiainen, R Erkkola, K Irjala, and I Huhtaniemi. Clinical Features and Circulating Gonadotropin, Insulin and Androgen Interactions in Women with Polycystic Ovarian Disease. Fertility and Sterility 55: 1057-1061, 1991.
Test performed on a research basis only.
Follicle Stimulating Hormone (FSH), urine
Reference Ranges:
Male: 5 - 25 IU/24 hours
Female:
Follicular: 5 - 20 IU/24 hours
Mid-cycle: 15 - 60 IU/24 hours
Luteal: 5 - 15 IU/24 hours
Postmenopausal: 50 - 100 IU/24 hours
Procedure:
Follicle Stimulating Hormone is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on any Steroid, ACTH, Gonadotropin, or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
5 ml of a 24 hour urine collection should be submitted. No special preservatives are required. Minimum specimin size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. Z Shoham, A Patel, and HS Jacobs. Polycystic Ovarian Syndrome: Safety and Effectiveness of Stepwise and Low-Dose Administration of Purified Follicle-Stimulating Hormone. Fertility and Sterility 55: 1051-1056, 1991.
2. L Anttila, Y-Q Ding, K Ruutiainen, R Erkkola, K Irjala, and I Huhtaniemi. Clinical Features and Circulating Gonadotropin, Insulin and Androgen Interactions in Women with Polycystic Ovarian Disease. Fertility and Sterility 55: 1057-1061, 1991.
18-Hydroxy Corticosterone (18-OH B)
Clinical Significance:
18-Hydroxy 11-Deoxycorticosterone is a mineralocorticoid derived from adrenal hydroxylation of 11-Deoxycorticosterone. It is metabolized to 18-Hydroxy-Corticosterone and eventually to Aldosterone. 18-Hydroxy 11-Deoxy-corticosterone is excreted into the urine as 18-Hydroxy 11-Deoxycorticosterone conjugates and Tetrahydro 18-Hydroxy 11-Deoxycorticosterone. 18-Hydroxy 11-Deoxycorticosterone acts on the kidney, gut, salivary glands, sweat glands, vascular endothelium and the brain. Elevated levels of 18-Hydroxy 11-Deoxycorticosterone are associated in patients with adrenal tumors, congenital adrenal hyperplasia, Cushing's syndrome, hypertension (especially in patients with 17a-Hydroxylase and 11b-hydroxylase deficiencies), low renin hypertension, edema, hypokalemia and metabolic alkalosis. Low levels of 18-Hydroxy 11-Deoxycorticosterone are associated with weight loss, hypotension and hyperkalemia.
Reference Range:
Up to 12 ng/dl
Procedure:
18-Hydroxy 11-Deoxycorticosterone is measured by radiommunoassay following extraction and chromatographic purification of the specimens.
Patient Preparation:
Patient should be on a normal sodium diet, and not be on any ACTH, corticosteroid, diuretic, and hypertension medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Freeze specimen immediately after separation. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. K Yamigabashi, M Mania and JE Shively. The Synthesis of Aldosterone by the Adrenal Cortex: Two Zones (Fasciculata and Glomerulosa) Possess One Enzyme for 11b-, 18-Hydroxylation, and Aldosterone Synthesis. Journal of Biological Chemistry 261: 3556, 1986.
2. OB Holland and C Gomez-Sanchez. Mineralocorticoids and Hypertension. American Journal of Nephrology 3: 156, 1983.
18-Hydroxy 11-Deoxy Corticosterone (18-OH DOC)
Clinical Significance:
18-Hydroxy 11-Deoxycorticosterone is a mineralocorticoid derived from adrenal hydroxylation of 11-Deoxycorticosterone. It is metabolized to 18-Hydroxy-Corticosterone and eventually to Aldosterone. 18-Hydroxy 11-Deoxy-corticosterone is excreted into the urine as 18-Hydroxy 11-Deoxycorticosterone conjugates and Tetrahydro 18-Hydroxy 11-Deoxycorticosterone. 18-Hydroxy 11-Deoxycorticosterone acts on the kidney, gut, salivary glands, sweat glands, vascular endothelium and the brain. Elevated levels of 18-Hydroxy 11-Deoxycorticosterone are associated in patients with adrenal tumors, congenital adrenal hyperplasia, Cushing's syndrome, hypertension (especially in patients with 17a-Hydroxylase and 11b-hydroxylase deficiencies), low renin hypertension, edema, hypokalemia and metabolic alkalosis. Low levels of 18-Hydroxy 11-Deoxycorticosterone are associated with weight loss, hypotension and hyperkalemia.
Reference Range:
Up to 12 ng/dl
Procedure:
18-Hydroxy 11-Deoxycorticosterone is measured by radiommunoassay following extraction and chromatographic purification of the specimens.
Patient Preparation:
Patient should be on a normal sodium diet, and not be on any ACTH, corticosteroid, diuretic, and hypertension medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Freeze specimen immediately after separation. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.), contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. K Yamigabashi, M Mania and JE Shively. The Synthesis of Aldosterone by the Adrenal Cortex: Two Zones (Fasciculata and Glomerulosa) Possess One Enzyme for 11b-, 18-Hydroxylation, and Aldosterone Synthesis. Journal of Biological Chemistry 261: 3556, 1986.
2. OB Holland and C Gomez-Sanchez. Mineralocorticoids and Hypertension. American Journal of Nephrology 3: 156, 1983.
Clinical Significance:
Insulin is a 51 amino acid peptide comprised of two subchains joined by disulfide bridges. Insulin is derived from Proinsulin by metabolism releasing an inactive peptide, Insulin and C-Peptide (Connecting Peptide). Insulin is excreted directly into the urine in equimolar concentration to C-Peptide, but it has a much shorter half-life. The ingestion of carbohydrates provides the necessary stimulus to release Insulin from the beta cells of the pancreas. The primary action of Insulin is the suppression of elevated blood glucose levels achieved by stimulating the uptake of glucose by Insulin-sensitive target tissues including the liver, muscle and adipose tissues. A deficiency in Insulin secretion is one of the signs of diabetes mellitus. Urine Insulin levels are greatly increased in patients with Insulinoma which can lead to hypoglycemia. Hyperinsulinemia has been found in patients with cirrhosis, Acanthosis Nigricans, and Insulin resistant syndromes. Insulin release is strongly suppressed by Somatostatin. Urine Insulin levels are often elevated in cases of acromegaly.
Reference Range:
Up to 20 uIU/24 hours
Procedure:
Insulin is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on any medications, if possible, that influence Insulin production or secretion.
Specimen Collection:
10 ml of a 24 hour urine collection should be submitted. Store specimen refrigerated during collection. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. RA Wild, D Applebaum-Bowden, LM Demers, M Bartholomew, JR Landis, WR Hazzard, and RJ Santen. Lipoprotein Lipids in Women with Androgen Excess: Independent Associations with Increased Insulin and Androgen. Clinical Chemistry 36: 283-289, 1990.
2. GM Argoud, DS Schade and RP Eaton. Insulin Suppresses Its Own Secretion in vivo. Diabetes 36: 959-962, 1987.
Clinical Significance:
Kallikrein is a 95,000 - 114,000 molecular weight peptide originating from the liver, exocrine glands, and the kidney. It exists as PreKallikreins which are activated in the blood by various chemical and physical factors including the Hageman factor (Kallikrein activator), Trypsin, Plasmin and Factor XI. Kallikrein has a functional link in the Renin-Aldosterone system promoting the conversion of ProRenin to Renin. Kallikrein regulates renal blood flow and modulation of water-electrolyte metabolism. The Kallikrein inhibitors, Aprotinin and Gabexate Mesilate, suppress activity of Kallikrein but not its concentration. In low or normal renin essential hypertension patients, Kallikrein levels are significantly lower than normal.
Reference Range:
10 - 100 ng/ml
Procedure:
Kallikrein is measured by direct radioimmunoassay.
Patient Requirements:
Patient should be on a normal sodium diet for 48 hours prior to collection of specimen. Patient should not be on Steroid, ACTH, diuretic, or hypertension medication, if possible, for at least 48 hours prior to collection.
Specimen Collection:
3 ml EDTA plasma should be collected and separated as soon as possible. Freeze specimens immediately after separation. Avoid glass contact. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. AD Cumming, S Jeffrey, AT Lambic, and JS Robson. The Kallikrein-Kinin and Renin-Angiotensin Systems in Nephrotic Syndrome. Nephron 51: 185, 1989.
2. MA Bothwell, WH Wilson, and EM Shooter. The Relationship between Glandular Kallikrein and Growth-Factor Processing Proteases of Mouse Submaxillary Gland. Journal of Biological Chemistry 254: 7287, 1979.
Clinical Significance:
Luteinizing Hormome is a pituitary hormone comprised of two subunits, a and b. Luteinizing Hormone causes release of Testosterone from the gonads. Luteinizing Hormone release is controlled by the hypothalamic hormone Luteinizing Hormone-Releasing Hormone. Testosterone and Estradiol suppress Luteinizing Hormone release by exerting a negative feedback control on the hypothalamus and by inhibiting Luteinizing Hormone Receptor activity in the pituitary. In males, Luteinizing Hormone is involved in the development and maturation of spermatozoa. In females, Luteinizing Hormone affects development and maturation of follicle and thecal tissue. Luteinizing Hormone peaks prior to ovulation. Levels increase dramatically after menopause due to decreased Estradiol production. Elevated levels of Luteinizing Hormone are seen in ovarian failure patients, low levels are seen in pituitary failure.
Reference Ranges:
Male: 5 - 20 mIU/ml
Female:
Follicular: 2 - 25 mIU/ml
Mid-cycle: 30 - 110 mIU/ml
Luteal: 0 - 30 mIU/ml
Postmenopausal: 40 - 120 mIU/ml
Procedure:
Luteinizing Hormone is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on any steroid, ACTH, estrogen, or gonadotropin medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. G Banfi, M Marinelli, M Murone, and P Bonini. Discordant Results for Lutotropin amoung Immunoassays in Two Cases of Male Hypogonadism. Clinical Chemistry 36: 1689-1690, 1990.
2. L Dunkel, H Alfthan, U-H Stenman, and A Perheentupa. Gonadal Control of Pulsatile Secretion of Luteinizing Hormone and Follicle-Stimulating Hormone in Prepubertal Boys Evaluated by Ultrasensitive Time-Resolved Immunofluorimetric Assays. Journal of Clinical Endocrinology and Metabolism 70: 107-114, 1990.
Clinical Significance:
Oxytocin is one of the two major posterior pituitary hormones. The nine amino acid peptide has potent uterus contracting and milk ejecting properties, achieved by stimulating contraction of myoepithelial cells in the mammary gland. Oxytocin given to pregnant women increases the frequency and intensity of uterine contraction. Oxytocin is synthesized and secreted together with one of the Neurophysins, which acts as a carrier protein for Oxytocin. Oxytocin is structurally very similar to Vasopressin. It possesses luteolytic action. It increases to a peak at ovulation and is lowest in the late luteal phase. Women on Estrogens and oral contraceptives have increased levels of both Oxytocin and Estrogen-stimulated Neurophysin. Levels of Oxytocin are suppressed by stress.
Reference Range:
25 – 150 pg/ml
Procedure:
Oxytocin is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on Steroid, ACTH, Gonadotropin, or Estrogen medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Freeze specimens immediately after separation. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. SEF Guldenaar, DC Wathes, and BT Pickering. Immunocytochemical Evidence for the Prescence of Oxytocin and Neurophysin in the Large cells of the Bovine Corpus Luteum. Cell Tissue Research 237: 349, 1984.
2. RD Leake, RE Weitzman, TH Glatz, and DA Fisher. Plasma Oxytocin Concentration in Men, Nonpregnant Women, and Pregnant Women before and during Spontaneous Labor. Journal of Clinical Endocrinology and Metabolism 53: 730, 1981.
Plasminogen Activator Inhibitor I* (PAI-I)
Clinical Significance:
Plasminogen Activator Inhibitor I (PAI-I) is a plasma protein that rapidly and specifically inhibits tissue Plasminogen Activator. It plays a role in the development of arterial and venous thromboembolism. Elevated levels are found in patients with Systemic Lupus Erythematosis and in patients with Hypofibrolysis. Levels are correlated with Insulin release. It shows a independent risk factor for myocardial infarction and hyperinsulinemia - Insulin resistance. Attempts to reduce Insulin resistance also reduce levels of PAI-I. Levels of PAI-I are elevated in coronary artery disease. In patients with Glucose resistance, PAI-I may be the best predictor of disease progression or coronary atherosclerosis.
Reference Range:
Up to 1.0 IU/ml
Procedure:
Plasminogen Activator Inhibitor I is measured by direct radioimmunoassay.
Patient Preparation:
Patient should be fasting for 10 - 12 hours prior to collecton of specimen. Patient should not be on any medications, if possible, that influence Insulin secretion.
Specimen Collection:
3 ml EDTA plasma should be collected and separated as soon as possible. Freeze plasma immediately after separation. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
Clinical Significance:
Pregnanediol-3-Glucuronide is excreted into the urine primarily from metabolism of Progesterone. Measurement offers a non-invasive method of determing luteal phase adequacy. Patients with luteal phase defect have significantly lower levels during the first few days of the luteal phase even though levels are not suppressed though the later days of the luteal phase or during the follicular phase. Levels of Pregnanediol-3-Glucuronide increase steadily throughout the term of pregnancy although it is not a good indicator of fetal stress. Pregnanediol-3-Glucuronide may indicate the onset of endometrial cancer.
Reference Ranges:
Male: Up to 1.0 mg/24 hours
Female:
Follicular: 1.6 - 3.0 mg/24 hours
Luteal: 3.5 - 15 mg/24 hours
Pregnancy: Levels increase throughout pregnancy
Procedure:
Pregnanediol-3-Gucuronide is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on any Steroid, ACTH, Estrogen, oral contraceptive or Gonadotropin medications, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
10 ml of a 24 hour urine collection should be submitted. Do not acidify urine! No special preservatives are required. Store urine refrigerated during collection. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. MM Miller, DI Hoffman, M Creinen, JH Levin, RT Chatterton Jr, T Murad, and RE Rebar. Comparison of Endometrial Biopsy and Urinary Pregnanediol Glucuronide Concentration in the Diagnosis of Luteal Phase Defects. Fertility and Sterility 54: 1008-1011, 1990.
2. RJ Chatterton Jr, JN Haan, JM Jenco, and KL Cheesman. Radioimmunoassay of Pregnanediol Concentrations in Early Morning Urine Specimens for Assessment of Luteal Function in Women. Fertility and Sterility 37: 361-366, 1982.
Clinical Significance:
Retinol-Binding Protein is a 21,000 molecular weight a-globulin synthesized in the liver. It is used as a carrier protein for Retinol (Vitamin A). Approximately 90% of Retinol-Binding Protein is bound to Transthyretin The free fraction (not bound to Transthyretin) is filtered through the glomerules and resorbed in the proximal tubules. The excretion of Retinol-Binding Protein in the urine is a sensitive index of tubular proteinuria. Retinol-Binding Proteins levels are usually low in Vitamin A deficiency and other nutritional disorders. Elevated levels have been found in renal dysfunction disorders and Insulin-Dependent Diabetics. Low levels have been found in many liver and gastrointestinal disorders.
Reference Range:
2.0 - 7.0 mg/dl
Procedure:
Retinol-Binding Protein is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on Vitamin supplements, Corticosteroids, Estrogens, or Thyroid medication, if possible, for at least 48 hours prior to collection of specimen.
Specimen Collection:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Freeze specimen immediately after separation. Minimum specimen size is 0.5 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. R Beethan, A Dawnay, J Landon, and WR Cattell. A Radioimmunoassay for Retinol-Binding Protein in Serum and Urine. Clinical Chemistry 31: 1364, 1985.
2. BJ Burri, DD Dankson, and TR Neidlinger. Use of Free Transthyretin-Bound Retinol-Binding Protein in Serum as Tests of Vitamin A Status in Humans: Effect of High Creatinine Concentrations in Serum. Clinical Chemistry 36: 674-676, 1990.
Tetrahydrodeoxycorticosterone (TH-DOC), urine
Clinical Significance:
11-Deoxycorticosterone is a mineralocorticoid derived primarily from adrenal metabolism of Progesterone. It is metabolized to Corticosterone. 11-Deoxycorticosterone is excreted into the urine as Tetrahydro Deoxycorticosterone and conjugated and unconjugated Deoxycorticosterone. Tetrahydro Deoxycorticosterone levels are increased following ACTH administration and decreased following Dexamethasone administration. Measurements of urine Tetrahydro Deoxycorticosterone give an accurate assessment of Deoxycorticosterone production and clearance integrated over a 24 hour period. Urine Tetrahydro Deoxycorticosterone eliminates much of the fluctuations seen in blood levels due to a variety of factors including diurnal variation, posture and episodic secretion.
Reference Range:
By report.
Procedure:
Tetrahydro Deoxycorticosterone is measured by GC/MS following hydrolysis and chromatographic purification of specimens.
Patient Preparation:
Patient should not be on any Corticosteroid or ACTH medications, if possible, for at least 48 hours prior to collection.
Specimen Collection:
5 ml of a 24 hour urine collection should be submitted. Store specimen refrigerated during collection. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. CW Weykamp, TJ Penders, NA Schmidt, AJ Borburgh, JF van de Calseyde. amd BJ Worthers. Steroid Profile for Urine: Reference Values. Clinical Chemistry 35: 2281-2284, 1989.
2. B Zumoff, C Monder, and HL Bradlow. Studies in the Biotransformation of Cortisol to the Cortoic Acids in Man. II: The Central Role Of Tetrahydrocortisol and Tetrahydrocortisone as Intermediates. Journal of Clinical Endocrinology and Metabolism 44: 647, 1977.
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