Clinical Significance:
Pancreastatin is a 49 amino acid peptide produced by degradation of Chromo-granin A. It inhibits Chromogranin A and Parathyroid Hormone release. Pancreastatin also inhibits release of Somatostatin upon glucose stimulation. It may also control carbohydrate metabolism and hyperglycemia. Although there are no compounds with significant structural homology with Pancreastatin, there are minor similarities to Gastrin and Anti-Diuretic Hormone. Pancreastatin reduces the the early phase of Glucose induced Insulin release. Suppression of Insulin release upon Glucose stimulation is a characteristic feature of Type II Diabetes. Pancreastatin could play an important therapeutic role in the treatment of diabetes. Pancreastatin also inhibits release of Somatostatin. It may also control carbohydrate metabolism and hyperglycemia.
Reference Range:
Up to 135 pg/ml
Procedure:
Pancreastatin is measured by direct radioimmunoassay.
Patient Preparation:
Patient shoud be fasting for 10 - 12 hours prior to collection of specimen. Patient should not be on any medications that may influence Insulin levels, if possible, for at least 48 hours prior to collection.
Specimen Collection:
Collect 10 mL EDTA plasma in special tube containing the Z-tube (G.I. Preservative) and separate as soon as possible. Freeze plasma immediately after separation. Special Z-tube (G.I. Preservative tube) is available from Inter Science Institute (ISI). Minimum specimen size is 1 ml.
Important Precaution:
Specimens for this assay must be collected using the Z-tube (G.I. Preservative). Specimens must be shipped frozen; specimens are not stable at refrigerated or room temperatures. No other specimens are acceptable.
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. E Piero, P Mirelles, RA Silvestre, ML Villanueva and J Marco. Pancreastatin Inhibits Insulin Secretion as Induced by Glucagon, Vasoactive Intestinal Polypeptide, Gastric Inhibiting Peptide, and 8-Cholecystokinin in the Perfused Rat Pancreas. Metabolism 38: 679-682, 1989.
2. K Tatemoto, S Efendic, V Mutt, G Makk, GJ Feistner and JD Barchas. Pancreastatin, A Novel Pancreatic Peptide that Inhibits Insulin Secretion. Nature 324: 476-478, 1986.
Clinical Significance:
Pancreatic Polypeptide (HPP) is a 36 amino acid peptide produced primarily in the PP-cells of the pancreas. It is secreted as ProPancreatic Polypeptide which is metabolized to Pancreatic Polypeptide and Icosapeptide. HPP exerts a prolonged stimulation in response to ingestion of food. HPP can be stimulated by several peptides including Secretin, Bombesin, and Caerulin. It is also stimulated by vagal activity. Hypoglycemia results in an increase in HPP levels. Somatostatin causes a decrease in HPP levels. Elevated levels have been detected in endocrine pancreatic tumors, the watery-diarrhea (Verner-Morrison) syndrome, and in Diabetes (especially juvenile-onset patients), and in duodenal ulcers. Gastric ulcers patients show a reduced response to protein compared to normal and duodenal ulcer patients. Patients with pancreatic exocrine failure have reduced levels of HPP.
Reference Range:
Age: Range:
20 - 29 10 - 140 pg/ml
30 - 39 20 - 500 pg/ml
40 - 49 25 - 880 pg/ml
50 - 59 25 - 925 pg/ml
60 - 69 40 - 600 pg/ml
Procedure:
Pancreatic Polypeptide is measured by direct radioimmunoassay.
Patient Preparation:
Patient should be fasting 10 - 12 hours prior to collection of specimen. Antacid medication or medications that affect Insulin levels should be discontinued, if possible, for at least 48 hours prior to collection.
Specimen Collection:
Collect 10 mL EDTA plasma in special tube containing the Z-tube (G.I. Preservative) and separate as soon as possible. Freeze plasma immediately after separation. Special Z-tube (G.I. Preservative tube) is available from Inter Science Institute (ISI). Minimum specimen size is 1 ml.
Important Precaution:
Specimens for this assay must be collected using the Z-tube (G.I. Preservative). Specimens must be shipped frozen; specimens are not stable at refrigerated or room temperatures. No other specimens are acceptable.
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. FP Kennedy, VLW Go, PE Cryer. Subnormal Pancreatic Polypeptide and Epinephrine Response to Insulin-Induced Hypoglycemia Identify Patients with Insulin-Dependent Diabetes Mellitis Predisposal to Develop Overt Autonomic Neuropathy. Annals of Internal Medicine 108: 54, 1988.
2. AI Stern and J Hansky. Pancreatic Polypeptide Release in Gastric Ulcer. Digestive Diseases and Sciences 26: 289, 1981.
Clinical Significance:
The Pepsinogens are gastric acid protease zymogens. They are divided into two distinct immunochemical groups: Pepsinogen I and II. Pepsinogen I is produced primarily in the Oxyntic gland mucosa of the stomach. It is secreted mainly into the gastric lumen and into circulation. Pepsinogen I has little or no biological activity but in acid is converted to the active enzyme Pepsin which exhibits proteolytic actions. Pepsinogen I is cleared by the kidney and secreted into the urine. Patients with pernicious anemia and gastrectomized patients have low to non-detectable levels of Pepsinogen I. Pepsinogen I levels are slightly elevated in gastric ulcer, higher in gastroduodenal ulcer and significantly elevated in duodenal ulcer. Patients with Zollinger-Ellison's syndrome exhibit greatly elevated levels. Pepsinogen I has been shown to correlate with presence of genetic duodenal ulcer, and has been used as a subclinical marker of increased risk for stomach cancer.
Reference Range:
28 - 100 ng/ml
Procedure:
Pepsinogen I is measured by direct radioimmunoassay.
Patient Preparation:
Patient should be fasting 10 - 12 hours prior to collection of specimen. Antacids or other medications affecting stomach acidity or gastrointestinal motility should be discontinued, if possible, for at least 48 hours prior to collection.
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. M Plebani, F DiMauro, PL Dal Santo. D Faggian, B Germana, and F Vianello. Measurement of Pepsinogen Group I in Endoscopic Gastroduodenal Biopsies. Clinical Chemistry 36: 682-684, 1990.
2. IM Samloff and WM Liebmann. Radioimmunoassay of Group I Pepsinogens in Serum. Gastroenterology 66: 494, 1974.
Clinical Significance:
The Pepsinogens are gastric acid protease zymogens. They are divided into two distinct immunochemical groups: Pepsinogen I and II. Pepsinogen is produced primarily in the Oxyntic gland mucosa of the stomach. It is secreted mainly into the gastrin lumen and into circulation. Pepsinogen II is not detected in the urine under normal conditions. Pepsinogen I is cleared by the kidney and secreted into the urine. Patients with pernicious anemia and gastrectomized patients have low to nondetectable levels of urine Pepsinogen I. Urine Pepsinogen I levels are slightly elevated in gastric ulcer, higher in gastroduodenal ulcer and significantly elevated in duodenal ulcer. Patients with Zollinger-Ellison syndrome exhibit greatly elevated levels. Pepsinogen I has been shown to correlate with presence of genetic juodenal ulcer, and has been used as a subclinical marker of increased risk of stomach cancer. Urine Pepsinogen I levels give an integrated picture of Pepsinogen I production over a 24 hour period.
Reference Range:
150 - 400 ng/24 hours
Procedure:
Urine Pepsinogen I is measured by direct radioimmunoassay on unextracted specimens.
Patient Preparation:
Patient should be fasting 10 - 12 hours prior to collection of specimen. Antacids or other medications affecting stomach acidity or gastrointestinal motility should be discontinued, if possible, for at least 48 hours prior to collection.
Specimen Collection:
5 ml of a 24 hour urine collection should be submitted. No special preservatives are required. Do not acidify urine! Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
1. M Plebani, F DiMauro, PL Dal Santo. D Faggian, B Germana, and F Vianello. Measurement of Pepsinogen Group I in Endoscopic Gastroduodenal Biopsies. Clinical Chemistry 36: 682-684, 1990.
2. IM Samloff and WM Liebmann.Radioimmunoassay of Group I Pepsinogens in Serum. Gastroenterology 66: 494, 1974.
Clinical Significance:
The Pepsinogens are gastric acid protease zymogens. They are divided into two distinct immunochemical groups: Pepsinogen I and II. Pepsinogen II is one of four aspartic proteinases: PG I, PG II, Cathepsin E and D. Pepsinogen II is produced primarily in the Oxyntic gland mucosa of the stomach, the gastric antrum and the duodenum. It is secreted mainly into the gastric lumen and into circulation. Pepsinogen II has little or no biological activity but in acid is converted to the active enzyme Pepsin which exhibits proteolytic actions. Unlike Pepsinogen I, Pepsinogen II is not normally found in the urine. Patients with pernicious anemia have low to non-detectable levels of Pepsinogen I but normal levels of Pepsinogen II. Pepsinogen II levels are slightly elevated in gastric ulcer. Patients with Zollinger-Ellison's syndrome exhibit greatly elevated levels.
Reference Range:
Up to 22 ng/ml
Procedure:
Pepsinogen II is measured by direct radioimmunoassay.
Patient Preparation:
Patient should be fasting 10 - 12 hours prior to collection of specimen. Antacids or other medications affecting stomach acidity or gastrointestinal motility should be discontinued, if possible, for at least 48 hours prior to collection.
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. M Plebani, M Masiero, F DiMauro, A Boniolo, and A Burlina. Radioimmunoassay for Pepsinogen C. Clinical Chemistry 36: 1690, 1990.
2. S Matzkum, M Zoller, and W Rapp. Radioimmunological Quantification of Human Group-II Pepsinogens. Digestion 18: 16, 1978.
Clinical Significance:
Peptide YY is a 36 amino acid peptide that shares sequential homology with Human Pancreatic Polypeptide (HPP) and Neuropeptide Y. Peptide YY is found throughout the small intestine. High concentrations are found in the terminal ileum and colon, being maximal in the rectum. Smaller amounts have been found in the duodenum and jejunum. Peptide YY causes intestinal constriction inhibiting jejunal and colonic motility. It also inhibits pancreatic bicarbonate and protein secretion. Peptide YY rises in response to food and remains elevated for several hours, with the peak response occurring at about one hour.
Reference Range:
30 - 120 pg/ml
Procedure:
Peptide YY is measured by direct radioimmunoassay.
Patient Preparation:
Patient should be fasting 10 - 12 hours prior to collection. Antacid medication or medications that affect intestinal motility should be discontinued, if possible, for at least 48 hours prior to collection.
Specimen Collection:
10 ml EDTA plasma containing the G.I. Preservative should be collected and separated as soon as possible. Freeze plasma immediately after separation. Special G.I. Preservative tubes are available from Inter Science. Minimum specimen size is 1 ml.
Important Precaution:
Peptide YY specimens must be collected using the G.I. Preservative. No other specimens are acceptable.
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. TE Adrian, G-L Ferri, AJ Bacarese-Hamilton, HS Fuessi, JM Polak, and SR Bloom. Human Distribution and Release of a Putative New Gut Hormone, Peptide YY. Gastroenterology 89: 1070, 1985.
2. TE Adrian, AJ Bacarese-Hamilton, AP Savage, K Wolfe, HS Besterman, and SR Bloom. Plasma PYY Concentrations in Gastrointestinal Diseases. Digestive Diseases Science 29: 35, 1984.
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:
1. I Juhan-Vague, MC Alessi, and P Vague. Increased Plasma Plasminogen Activator Inhibitor I Levels. A Possible Link between Insulin Resistance and Atherothrombosis. Diabetologia 34: 457-462, 1991.
2. K Landin, L Tengborn, and U Smith. Elevated Fibrinogen and Plasminogen Activator Inhibitor (PAI-I) in Hypertension are Related to Metabolic Risk Factors for Cardiovascular Disease. Journal of Internal Medicine 227: 273-278, 1990.
*Research Basis only.
Clinical Significance:
Prednisolone is a synthetic Corticosteroid with potent anti-inflammatory properties. It is also the most widely used Glucosteroid along with Prednisone in immunosupressive therapy. It is closely related to Cortisone. Prednisolone can be reversibly converted to Prednisone. Prednisolone is also excreted into the urine in conjugated and unconjugated forms. Administration is often in the form of MethylPrednisolone, which is also detected in this assay. Its measurement can be used to determine noncompliance - the leading cause of allograft rejection. Prednisolone administration will greatly decrease the concentrations of Cortisol and Cortisone. Prednisolone is separated from other natural and synthetic Glucocorticoids prior to measurement.
Reference Range:
Non-Detectable. Limit of sensitivity is 1 ug/dl.
Procedure:
Prednisolone is measured by radioimmunoassay following extraction and chromatographic purification 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 Prednisolone 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. JH McBride, DO Rodgerson, SS Park, and AF Reyes. Rapid Liquid-Chromatographic Method for Simultaneous Determination of Plasma Prednisolone, Prednisone, and Cortisol in Pediatric Renal-Transplant Recipients. Clinical Chemistry 37: 643-646, 1991.
2. WA Colburn and RH Butler. Radioimmunoassay for Prednisolone. Steroids 21: 833, 1973.
Clinical Significance:
Prednisolone is a synthetic Corticosteroid with potent anti-inflammatory properties. It is also the most widely used Glucosteroid along with Prednisone in immunosupressive therapy. It is closely related to Cortisone. Prednisolone can be reversibly converted to Prednisone. Prednisolone is also excreted into the urine in conjugated and unconjugated forms. This assay measures both the conjugated and unconjugated forms of Prednisolone. Administration is often in the form of MethylPrednisolone, levels of which are also detected in this assay. Its measurement can be used to determine noncompliance - the leading cause of allograft rejection. Prednisolone administration will greatly decrease the concentrations of Cortisol and Cortisone. Prednisolone is separated from other natural and synthetic Glucocorticoids prior to measurement. Urine Prednisolone measures excretion over a 24 hour period.
Reference Range:
Non-Detectable. Limit of sensitivity is 10 ug/liter.
Procedure:
Urine Prednisolone is measured by radioimmunoassay following extraction and chromatographic purification 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 Prednisolone is not a naturally occurring steroid, no other patient preparation is required.
Specimen Collection:
10 ml of a 24 hour urine collection 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. JH McBride, DO Rodgerson, SS Park, and AF Reyes. Rapid Liquid-Chromatographic Method for Simultaneous Determination of Plasma Prednisolone, Prednisone, and Cortisol in Pediatric Renal-Transplant Recipients. Clinical Chemistry 37: 643-646, 1991.
2. WA Colburn and RH Butler. Radioimmunoassay for Prednisolone. Steroids 21: 833, 1973.
Clinical Significance:
Prednisone is a synthetic Corticosteroid with potent anti-inflammatory properties. It is also the most widely used Glucosteroid along with Prednisolone in immunosupressive therapy. It is closely related to Cortisol. Prednisone can be reversibly converted to Prednisolone. Prednisone is also excreted into the urine in conjugated and unconjugated forms. Administration is often in the form of MethylPrednisone, which is also detected in this assay. Its measurement can be used to determine noncompliance - the leading cause of allograft rejection. Prednisone administration will greatly decrease the concentrations of Cortisol and Cortisone. Prednisone is separated from other natural and synthetic Glucocorticoids prior to measurement.
Reference Range:
Non-Detectable. Quantitative if present: limit of sensitivity is 1 ug/dl.
Procedure:
Prednisone is measured by radioimmunoassay following extraction and chromatographic purification 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 Prednisone 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. JH McBride, DO Rodgerson, SS Park, and AF Reyes. Rapid Liquid-Chromatographic Method for Simultaneous Determination of Plasma Prednisolone, Prednisone, and Cortisol in Pediatric Renal-Transplant Recipients. Clinical Chemistry 37: 643-646, 1991.
2. WA Colburn. Radioimmunoassay for Prednisone. Steroids 24: 95, 1974.
Clinical Significance:
Prednisone is a synthetic Corticosteroid with potent anti-inflammatory properties. It is also the most widely used Glucosteroid along with Prednisolone in immunosupressive therapy. It is closely related to Cortisol. Prednisone can be reversibly converted to Prednisolone. Prednisone is also excreted into the urine in conjugated and unconjugated forms. This assay measures both the conjugated and unconjugated forms of Prednisone. Administration is often in the form of MethylPrednisone, levels of which are also detected in this assay. Its measurement can be used to determine noncompliance - the leading cause of allograft rejection. Prednisone administration will greatly decrease the concentrations of Cortisol and Cortisone. Prednisone is separated from other natural and synthetic Glucocorticoids prior to measurement. Urine Prednisone measures Prednisone excretion over a 24 hour period.
Reference Range:
Non-Detectable. Limit of sensitivity is 10 ug/liter.
Procedure:
Urine Prednisone is measured by radioimmunoassay following extraction and chromatographic purification 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 Prednisone is not a naturally occurring steroid, no other patient preparation is required.
Specimen Collection:
10 ml of a 24 hour urine collection 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. JH McBride, DO Rodgerson, SS Park, and AF Reyes. Rapid Liquid-Chromatographic Method for Simultaneous Determination of Plasma Prednisolone, Prednisone, and Cortisol in Pediatric Renal-Transplant Recipients. Clinical Chemistry 37: 643-646, 1991.
2. WA Colburn. Radioimmunoassay for Prednisone. Steroids 24: 95, 1974.
* Test available on a research basis only. Contact ISI for details.
Clinical Significance:
Pregnenolone is the first steroid formed from the metabolism of Cholesterol. It is enzymatically metabolized to Progesterone and 17-Hydroxy Pregnenolone. It is excreted into the urine as conjugated and unconjugated forms of Pregnenolone. Pregnenolone is secreted by both the gonads and adrenal glands and is the original precursor for all of the other steroids. It is stimulated by ACTH and is suppressed by Dexamethasone and gonadal suppressants. Pregnenolone is the marker steroid for determining the Congenital Adrenal Hyperplasia syndromes caused by 17-Hydroxylase Deficiency and 20, 22-Desmolase Deficiency. Levels are elevated in Cushing's syndrome and adrenal adenoma, but adrenal adenoma patients have non-suppressible levels of Pregnenolone. Many patients with idiopathic hirsutism also have elevated levels of Pregnenolone.
Reference Ranges:
Male: 30 - 100 ng/dl
Female: 30 - 200 ng/dl
Postmenopausal: 10 - 70 ng/dl
Procedure:
Pregnenolone is measured by radioimmunoassay following extraction and purification of specimens
Patient Preparation:
Patient should not be on any Corticosteroid, ACTH, Estrogen or Gonadotropin 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. 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. TJ McKenna and RD Brown. Pregnenolone in Man: Plasma Levels in States of Normal and Abnormal Steroidogenesis. Journal of Clinical Endocrinology and Metabolism 38: 480, 1974.
2. GA Abraham, JE Buster, FW Kyle, PC Corrales, and RC Teller. Radioimmunoassay of Plasma Pregnenolone. Journal of Clinical Endocrinology and Metabolism 37: 40, 1973.
Clinical Significance:
Pregnenolone is the first steroid formed from the metabolism of Cholesterol. It is enzymatically metabolized to Progesterone and 17-Hydroxy Pregnenolone. It is excreted into the urine as conjugated and unconjugated forms of Pregnenolone. This assay measures the total of the conjugated and unconjugated froms of Pregnenolone. Pregnenolone is secreted by both the gonads and adrenal glands and is the original precursor for all of the other steroids. It is stimulated by ACTH and is suppressed by Dexamethasone and gonadal suppressants. Pregnenolone is the marker steroid for determining the Congenital Adrenal Hyperplasia syndromes caused by 17-Hydroxylase Deficiency and 20, 22-Desmolase Deficiency. Urine levels are elevated in Cushing's syndrome and adrenal adenoma. Many patients with idiopathic hirsutism also have elevated levels of urine Pregnenolone.
Reference Ranges:
Male: Up to 0.5 ug/24 hours
Female: Up to 4.0 ug/24 hours
Procedure:
Urine Pregnenolone is measured by radioimmunoassay following hydrolysis, extraction, and purification of specimens
Patient Preparation:
Patient should not be on any Corticosteroid, ACTH, Estrogen or Gonadotropin medication, 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. TJ McKenna and RD Brown. Pregnenolone in Man: Plasma Levels in States of Normal and Abnormal Steroidogenesis. Journal of Clinical Endocrinology and Metabolism 38: 480, 1974.
2. GA Abraham, JE Buster, FW Kyle, PC Corrales, and RC Teller. Radioimmunoassay of Plasma Pregnenolone. Journal of Clinical Endocrinology and Metabolism 37: 40, 1973.
Clinical Significance:
Progesterone is a Progestin produced primarily from enzymatic metabolism of Pregnenolone. It is enzymatically converted to 17-Hydroxy Progestrone and 11-Deoxycorticosterone. It is secreted by both the gonads and the adrenal glands. It is bound to Cortisol Binding Globulin and Albumin, but a small percentage is present in the "Free" bioactive form. It is excreted into the urine as its conjugated and unconjugated forms and as Pregnanediol (conjugated and unconjugated). Progesterone is responsible for cellular changes in the cervix, vagina, and uterus. Levels are lowest in the follicular phase and increase rapidly following the luteal surge. Increased Progesterone inhibits ovulation. Progesterone increases greatly during pregnancy. Measurement of Progesterone can be useful to monitor fertility, corpus luteum function, endometrial development, and be helpful in in-vitro fertilization patients.
Reference Ranges:
Male: 5 - 50 ng/dl
Female:
Follicular: 10 - 100 ng/dl
Luteal: 200 - 1800 ng/dl
Procedure:
Progesterone is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on any Corticosteroid, ACTH, Estrogen, or Gonadotropin 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. 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. MS Gelder, LR Boots,and JB Younger. Use of a Single Random Progesterone Value as a Diagnostic Aid for Ectopic Pregnancy. Fertility and Sterility 55: 497-500, 1991.
2. CJ Munro, GH Stabenfeldt, JR Cragun, LA Addiego, JW Overstreet, and BL Lasley. Relationship of Serum Estradiol and Progesterone Concentrations to the Excretion Profiles of Their Major Urinary Metabolites as Measured by Enzyme Immunoassay and Radioimmunoassay. Clinical Chemistry 37: 38-44, 1991.
Clinical Significance:
Progesterone is a Progestin produced primarily from enzymatic metabolism of Pregnenolone. It is enzymatically converted to 17-Hydroxy Progestrone and 11-Deoxycorticosterone. It is secreted by both the gonads and the adrenal glands. It is bound to Cortisol Binding Globulin and Albumin, but a small percentage is present in the "Free" bioactive form. It is excreted into the urine as its conjugated and unconjugated forms and as Pregnanediol (conjugated and unconjugated). This assay measures the conjugated and unconjugated forms of Progesterone. Progesterone is responsible for cellular changes in the cervix, vagina, and uterus. Levels are lowest in the follicular phase and increase rapidly following the luteal surge. Progesterone increases greatly during pregnancy. Measurement of Urine Progesterone can be useful to monitor fertility, corpus luteum function, endometrial development, and be helpful in in-vitro fertilization patients yielding an integrated look of Progesterone activity over a 24 hour period.
Reference Ranges:
Male: Up to 0.5 ug/24 hours
Female: Up to 2.8 ug/24 hours
Procedure:
Urine Progesterone is measured by radioimmunoassay following hydrolysis, extraction, of specimens.
Patient Preparation:
Patient should not be on any Corticosteroid, ACTH, Estrogen, or Gonadotropin medication, 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 specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. SC Chattoraj, JS Rankin, AK Turner, and EW Lowe. Urinary Progesterone as an Index of Ovulation and Corpus Luteal Function. Journal of Clinical Endocrinology and Metabolsim 43: 1402, 1976.
2. CJ Munro, GH Stabenfeldt, JR Cragun, LA Addiego, JW Overstreet, and BL Lasley. Relationship of Serum Estradiol and Progesterone Concentrations to the Excretion Profiles of Their Major Urinary Metabolites as Measured by Enzyme Immunoassay and Radioimmunoassay. Clinical Chemistry 37: 38-44, 1991.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin D2 is derived mainly from Prostaglandin H2, and is metabolized to Dihydroketo Prostaglandin D2. Prostaglandin D2 is excreted directly into the urine. The sites of highest Prostaglandin D2 activity are the brain, spinal cord, intestines, and stomach. Prostaglandin D2 is the major Prostaglandin produced by uterine tissue. Prostaglandin D2 is a potent bronchoconstrictor, neuromodulator, and anti-antithrombin agent. It also stimulates the secretion of Pancreatic Glucagon. Prostaglandin D2 has been found to have an anti-metastatic effect on many malignant tumor cells. Prostaglandin D2 production and circulating levels are drastically suppressed by aspirin and indomethacin.
Reference Range:
35 - 115 pg/ml
Procedure:
Prostaglandin D2 is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. B Bennegard, M Halin, and L Hamberger. Luteotropic Effects of Prostaglandins I2 and D2 on Isolated Human Corpora Luteum. Fertility and Sterility 54: 459-464, 1990.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin D2 is derived mainly from Prostaglandin H2, and is metabolized to Dihydroketo Prostaglandin D2. Prostaglandin D2 is excreted directly into the urine.The sites of highest Prostaglandin D2 activity are the brain, spinal cord, intestines, and stomach. Prostaglandin D2 is the major Prostaglandin produced by uterine tissue. Prostaglandin D2 is a potent bronchoconstrictor, neuromodulator, and anti-antithrombin agent. It also stimulates the secretion of Pancreatic Glucagon. Prostaglandin D2 has been found to have an anti-metastatic effect on many malignant tumor cells. Prostaglandin D2 production and circulating levels are drastically suppressed by aspirin and indomethacin. Urine Prostaglandin D2 levels give an integrated picture of Prostaglandin D2 production over a 24 hour period minimizing the effect of diurnal variation and episodic secretion.
Reference Range:
100 - 280 ng/24 hours
Procedure:
Urine Prostaglandin D2 is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. No special preservatives are required. The following however, are acceptable: indomehacin, boric acid and hydrochloric acid are acceptable. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prosta-glandins. Gastroenterology 96: 596, 1989.
2. B Bennegard, M Halin, and L Hamberger. Luteotropic Effects of Prostaglandins I2 and D2 on Isolated Human Corpora Luteum. Fertility and Sterility 54: 459-464, 1990.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin E1 is derived mainly from Prostaglandin H1, and is metabolized to Prostaglandin F1a. Prostaglandin E1 is excreted directly into the urine. Prostaglandin E1 relaxes the circular muscle of the gut in opposition to Prostaglandin F2a, and also relaxes the lower esophageal sphincter. Prostaglandin E1 reduces gastric secretion preventing the formation of ulcers. Prostaglandin E1 is also a potent inhibitor of platelet aggregation. Prostaglandin E1 stimulates accumulation of cyclic AMP and can stimulate thyroid activity in a manner similar to that of TSH. Elevated levels have been found in patients with tuberculosis, lung cancer, Medullary Carcinoma of the Thyroid, Carcinoid Syndrome, neuroblastomas, and the Watery Diarrhea Syndrome. Prostaglandin E1 production and circulating levels are drastically suppressed by aspirin and indomethacin.
Reference Range:
250 - 500 pg/ml
Procedure:
Prostaglandin E1 is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. MJ Dunn and EJ Zambraski. Renal Effects of Drugs that Inhibit Prostaglandin Synthesis. Kidney International 18: 609, 1980.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin E1 is derived mainly from Prostaglandin H1, and is metabolized to Prostaglandin F1a. Prostaglandin E1 is excreted directly into the urine. Prostaglandin E1 relaxes the circular muscle of the gut in opposition to Prostaglandin F2a, and also relaxes the lower esophageal sphincter. Prostaglandin E1 reduces gastric secretion preventing the formation of ulcers. Prostaglandin E1 is also a potent inhibitor of platelet aggregation. Prostaglandin E1 stimulates accumulation of cyclic AMP and can stimulate thyroid activity in a manner similar to that of TSH. Elevated leves have been found in patients with tuberculosis, lung cancer, medullary carcinoma of the thyroid, carcinoid syndrome, neuroblastomas, and the Watery Diarrhea Syndrome. Prostaglandin E1 production and circulating levels are drastically suppressed by aspirin and indomethacin. Urine Prostaglandin E1 levels give an integrated picture of Prostaglandin E1 production over a 24 hour minimizing the effect of diurnal variation and episodic secretion.
Reference Range:
350 - 820 ng/24 hours
Procedure:
Urine Prostaglandin E1 is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. No special preservative is required. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prosta-glandins. Gastroenterology 96: 596, 1989.
2. MJ Dunn and EJ Zambraski. Renal Effects of Drugs that Inhibit Prostaglandin Synthesis. Kidney International 18: 609, 1980.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin E2 is derived mainly from Prostaglandin H2, and is metabolized to Prostaglandin F2a, A2, and Dihydroketo Prostaglandin E2. Prostaglandin E2 is excreted directly into the urine. Prostaglandin E2 is a potent vasodilator and also a stimulus for Renin release. Prostaglandin E2 release is stimulated by cholinergic and alpha adrenergic agents. Prostaglandin E2 potentiates the actions of Histamine and Bradykinin causing pain and accumulation of edema fluid. It relaxes the circular muscle of the gut in opposition to Prostaglandin F2a, and also relaxes the lower esophageal sphincter. Prostaglandin E2 also causes accumulation of water and electrolytes in the lumen of the gut by stimulating their secretion. Elevated levels of Prostaglandin E2 have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Prostaglandin E2 production and circulating levels are drastically suppressed by aspirin and indomethacin.
Reference Range:
250 - 400 pg/ml
Procedure:
Prostaglandin E2 is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. J Balasch, V Arroyo, F Carmona, J Llach, W Jimenez, JC Pare, and JA Vanrell. Severe Ovarian Hyperstimulation Syndrome: Role of Peripheral Vasodilation. Fertility and Sterility 56: 1077-1083, 1991.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin E2 is derived mainly from Prostaglandin H2, and is metabolized to Prostaglandin F2a, A2, and Dihydroketo Prostaglandin E2. Prostaglandin E2 is excreted directly into the urine. Prostaglandin E2 is a potent vasodilator and also a stimulus for Renin release. Prostaglandin E2 release is stimulated by cholinergic and alpha adrenergic agents. Prostaglandin E2 potentiates the actions of Histamine and Bradykinin causing pain and accumulation of edema fluid. It relaxes the circular muscle of the gut in opposition to Prostaglandin F2a, and also relaxes the lower esophageal sphincter. Prostaglandin E2 also causes accumulation of water and electrolytes in the lumen of the gut by stimulating their secretion. Elevated levels of Prostaglandin E2 have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Prostaglandin E2 production and circulating levels are drastically suppressed by aspirin and indomethacin. Urine Prostaglandin E2 levels give an integrated picture of Prostaglandin E2 production over a 24 hour minimizing the effect of diurnal variation and episodic secretion.
Reference Range:
400 - 620 ng/24 hours
Procedure:
Urine Prostaglandin E2 is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. No special preservative is required. Minimum specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. J Balasch, V Arroyo, F Carmona, J Llach, W Jimenez, JC Pare, and JA Vanrell. Severe Ovarian Hyperstimulation Syndrome: Role of Peripheral Vasodilation. Fertility and Sterility 56: 1077-1083, 1991.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin F1a is derived mainly from Prostaglandin E1, and is metabolized to 6-Keto Prostaglandin F1a. Prostaglandin F1a is excreted directly into the urine. Prostaglandin F1a contracts the circular muscle of the gut in opposition to the Prostaglandins of the E series. Prostaglandin F1a is a cytoprotector, protecting mucosal tissue from damage produced by ulcerogenic stimuli. Elevated levels of Prostaglandin F1a are often accompanied by migraine-like headaches and flushing. Elevated levels of Prostaglandin F1a have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Prostaglandin F1a production and circulating levels are drastically suppressed by aspirin and indomethacin.
Reference Range:
30 - 100 pg/ml
Procedure:
Prostaglandin F1a is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. F Dray, B Charbonnel, and J Maclouf. Radioimmunoassay of Prostaglandins F alpha, E1, and E2 in Human Plasma. European Journal of Clinical Investigation 5: 311, 1975.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin F1a is derived mainly from Prostaglandin E1, and is metabolized to 6-Keto Prostaglandin F1a. Prostaglandin F1a is excreted directly into the urine. Prostaglandin F1a contracts the circular muscle of the gut in opposition to the Prostaglandins of the E series. Prostaglandin F1a is a cytoprotector, protecting mucosal tissue from damage produced by ulcerogenic stimuli. Elevated levels of Prostaglandin F1a are often accompanied by migraine-like headaches and flushing. Elevated levels of Prostaglandin F1a have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Prostaglandin F1a production and circulating levels are drastically suppressed by aspirin and indomethacin. Urine Prostaglandin F1a levels give an integrated picture of Prostalgandin F1a production over a 24 hour period minimizing the effect of diurnal variation and episodic secretion.
Reference Range:
50 - 400 ng/24 hours
Procedure:
Urine Prostaglandin F1a is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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 specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. F Dray, B Charbonnel, and J Maclouf. Radioimmunoassay of Prostaglandins F alpha, E1, and E2 in Human Plasma. European Journal of Clinical Investigations 5: 311, 1975.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. 6-Keto Prostaglandin F1a is derived mainly from Prostaglandin I2 , and is metabolized to 2,3-dinor 6-Keto Prostaglandin F1a in the liver and to 6-Keto Prostaglandin E1. It is produced in the renal blood vessels. 6-Keto Prostaglandin F1a is excreted directly into the urine. 6-Keto Prostaglandin F1a is a very stable compound and its measurement can give an accurate assessment of Prostaglandin I2 activity. 6-Keto Prostaglandin F1a is a strong vasoconstrictor but is less potent than Prostaglandin I2. Elevated levels of 6-Keto Prostaglandin F1a have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. 6-Keto Prostaglandin F1a production and circulating levels are drastically suppressed by aspirin and indomethacin.
Reference Range:
Up to 15 pg/ml
Procedure:
6-Keto Prostaglandin F1a is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. W Schramm, RH Smith, TM Jackson, PA Craig, HE Grates, and LL Minton. Rapid Solid-Phase Immunoassay for 6-Keto Prostaglandin F1a on Microplates. Clinical Chemistry 36: 509-514, 1990.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. 6-Keto Prostaglandin F1a is derived mainly from Prostaglandin I2 , and is metabolized to 2,3 dinor 6-Keto Prostaglandin F1a in the liver. 6-Keto Prostaglandin F1a is produced in the renal blood vessels. 6-Keto Prostaglandin F1a is excreted directly into the urine. It is a very stable metabolite and its measurement can give an accurate assessment of Prostaglandin I2 activity. 6-Keto Prostaglandin F1a is a strong vasoconstrictor but is less potent than Prostaglandin I2. Elevated levels of 6-Keto Prostaglandin F1a have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Urine 6-Keto Prostaglandin F1a production and circulating levels are drastically suppressed by aspirin and indomethacin. Urine 6-Keto Prostaglandin F1a levels give an integrated picture of 6-Keto Prostalgandin F1a production over a 24 hour period minimizing the effect of diurnal variation and episodic secretion.
Reference Ranges:
Male: 200 - 450 ng/24 hours
Female: 85 - 300 ng/24 hours
Procedure:
Urine 6-Keto Prostaglandin F1a is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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 specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. S Zureick, J Nadler, J Yamamoto, and R Horton. Simultaneous Measurement of Two Major Prostacyclin Metabolites in Urine. Clinical Chemistry 36: 1978-1980, 1990.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin F2a is derived mainly from Prostaglandins E2 and H2, and is metabolized to Dihydroketo Prostaglandin F2a. Prostaglandin F2a is excreted directly into the urine. Prostaglandin F2a contracts the circular muscle of the gut in opposition to the Prostaglandins of the E series. Prostaglandin F2a causes accumulation of water and electrolytes in the lumen of the gut by stimulating their secretion. It also inhibits glucose absorption. Prostaglandin F2a has luteolytic actions in the corpus luteum. Elevated levels of Prostaglandin F2a have been found in the spinal fluid of children with febrile convulsions and menningitis. Elevated levels of Prostaglandin F2a have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Prostaglandin F2a production and circulating levels are drastically suppressed by aspirin and indomethacin.
Reference Range:
80 - 240 pg/ml
Procedure:
Prostaglandin F2a is measured by radioimmunoassay following extraction of specimens.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. B Bennegard, M Hahlin, E Wennberg, and H Noren. Local Luteolytic Effect of Prostaglandin F2a in the Human Corpus Luteum. Fertility and Sterility 56: 1070-1076, 1991.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin F2a is derived mainly from Prostaglandins E2 and H2, and is metabolized to Dihydroketo Prostaglandin F2a. Prostaglandin F2a is excreted directly into the urine. Prostaglandin F2a contracts the circular muscle of the gut in opposition to the Prostaglandins of the E series. Prostaglandin F2a causes accumulation of water and electrolytes in the lumen of the gut by stimulating their secretion. It also inhibits glucose absorption. Prostaglandin F2a has luteolytic actions in the corpus luteum. Elevated levels of Prostaglandin F2a have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Prostaglandin F2a production and circulating levels are drastically suppressed by aspirin and indomethacin. Urine Prostaglandin F2a levels give an integrated picture of Prostaglandin F2a production over a 24 hour period minimizing the effect of diurnal variation and episodic secretion.
Reference Range:
375 - 800 ng/24 hours
Procedure:
Urine Prostaglandin F2a is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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 specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice. Please provide total volume per 24 hours.
References:
1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. B Bennegard, M Hahlin, E Wennberg, and H Noren. Local Luteolytic Effect of Prostaglandin F2a in the Human Corpus Luteum. Fertility and Sterility 56: 1070-1076, 1991.
Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Dihydroketo Prostaglandin F2a is derived mainly from metabolism of Prostaglandin F2a and it is a stable end product. Dihydroketo Prostaglandin F2a is excreted directly into the urine. Dihydroketo Prostaglandin F2a has only minor biological activity but measurement gives an accurate assessment of Prostaglandin F2a activity. Levels increase significantly during early labor and continue to increase as labor progresses. Elevated levels of Dihydroketo Prostaglandin F2a have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Dihydroketo Prostaglandin F2a production and circulating levels are drastically suppressed by aspirin and indomethacin. Urine Dihydroketo Prostaglandin F2a levels give an integrated picture of Prostaglandin F2a production over a 24 hour period minimizing the effect of diurnal variation and episodic secretion.
Reference Range:
100 - 500 ng/24 hours
Procedure:
Urine Dihydroketo Prostaglandin F2a is measured by direct radioimmunoassay.
Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory 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 specimen size is 1 ml.
Shipping Instructions:
Ship specimens at room temperature or frozen in dry ice.
References:
1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration: Induction of Ulcers by Antibodies to Prostaglandins. Gastroenterology 96: 596, 1989.
2. DM Strickland, SP Brennecke, and MD Mitchell. Measurement of 13, 14-Dihydro-15-Keto-Prostaglandin F2a and 6-Keto-Prostaglandin F1a in Plasma by Radioimmunoassay without Prior Extraction or Chromatography. Prostaglandins, Leukotrienes, and Medicine 9: 491, 1982.
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