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Pancreastatin

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 should not be on any medications that may influence Insulin levels, if possible, for at least 48 hours prior to collection.

Specimen Collection:
Collect 10mL blood directly into ISI's Z-tubeTM Preservative and separate as soon as possible. Freeze plasma immediately after separation. Special Z-tubeTM Preservatives are available from ISI. Minimum specimen size is 1mL. Note: one Z-tubeTM may be shared for up to three tests. After centrifuging tube, aliqout 1mL per test in separate vials, mark with name of test and freeze.

Important Precaution:
Specimens for this assay must be collected using the Z-tube. 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. Raines D, Chester M, Diebold AE, et al. A prospective evaluation of the effect of chronic proton pump inhibitor use on plasma biomarker levels in humans. Pancreas. 2012;41(4):508-511.
2. O'Dorisio TM, Krutzik SR, Woltering EA, et al. Development of a highly sensitive and specific carboxy-terminal human Pancreastatin assay to monitor neuroendocrine tumor behavior. Pancreas. 2010;39(5):611-616.
3. Piero E, Mirelles P, Silvestre RA, et al. Pancreastatin inhibits insulin secretion as induced by glucagon, vasoactive intestinal polypeptide, gastric inhibiting peptide, and 8-cholecystokinin in the perfused rat pancreas. Metabolism. 1989;38:679-82.
4. Tatemoto K, Efendi S, Mutt S, et al. Pancreastatin, a novel pancreatic peptide that inhibits insulin secretion. Nature. 1986;324:476-8.
5. Calhoun K, Toth-Fejel S, Chee J, et al. Serum peptide profiles in patients with carcinoid tumors. Am J Surg. 2003;186(1):28-31
6. Syversen U, Jacobsen MB, O'Connor DT, et al. Immunoassays for measurement of chromogranin A and pancreastatin-like immunoreactivity in humans: correspondence in patients with neuroendocrine neoplasia. Neuropeptides. 1994;26(3):201-6
7. Kogner P, Bjellerup P, Svensson T, et al. Pancreastatin immunoreactivity in favourable childhood neuroblastoma and ganglioneuroma. Eur J Cancer 1995;31A(4):557-60.
8. Desai DC, O'Dorisio TM, Schirmer WJ, et al. Serum pancreastatin levels predict response to hepatic artery chemoembolization and somatostatin analog therapy in metastatic neuroendocrine tumors. Regul Pept. 2001;96(3):113-17.

 

Pancreatic Polypeptide   (PP)*

* Test available on a research basis only. Contact ISI for details.

 

Pepsinogen I
(PG I)

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.

 

Pepsinogen I
(PG I), urine*

* Test available on a research basis only. Contact ISI for details.

 

Pepsinogen II
(PG II)

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.

 

Peptide YY
(PYY)

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.

 

Plasminogen Activator Inhibitor I* (PAI-I)

* Test available on a research basis only. Contact ISI for details.

 

Prednisolone

* Test available on a research basis only. Contact ISI for details.

 

Prednisolone, urine*

* Test available on a research basis only. Contact ISI for details.

 

Prednisone

* Test available on a research basis only. Contact ISI for details.

 

Prednisone, urine

* Test available on a research basis only. Contact ISI for details.

 

Pregnanediol-3-Glucuronide*

* Test available on a research basis only. Contact ISI for details.

 

Pregnenolone

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 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.

 

Pregnenolone, urine

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 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.

 

Progesterone

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.

 

Progesterone, Saliva*

* Test available on a research basis only. Contact ISI for details.

 

Progesterone, urine

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:
10 ml of a 24 hour urine collection should be submitted for analysis. No special preservatives are required. Store specimen refrigerated during collection. Specimens should be frozen prior to shipping. Minimum specimen size is 5 ml.

Shipping Instructions:
Ship specimens frozen in dry ice. Provide the total volume per 24 hours.

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.

 

Prostaglandin D2
(PG D2)

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.

 

Prostaglandin D2
(PG D2), urine

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 for analysis. No special preservatives are required. Store specimen refrigerated during collection and freeze after adding the final voiding the next morning. Specimens should be frozen once the 24 hour sample has been collected, and prior to and during shipping. Minimum specimen size is 5 ml.

Shipping Instructions:
Ship specimens frozen in dry ice. Provide the 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 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.

 

Prostaglandin E1
(PG E1)

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.

 

Prostaglandin E1
(PG E1), urine

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 for analysis. No special preservatives are required. Store specimen refrigerated during collection. Specimens should be frozen prior to shipping. Minimum specimen size is 5 ml.

Shipping Instructions:
Ship specimens frozen in dry ice. Provide the 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 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.

 

Prostaglandin E2
(PG E2)

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.

 

Prostaglandin E2
(PG E2), urine

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 for analysis. No special preservatives are required. Store specimen refrigerated during collection. Specimens should be frozen prior to shipping. Minimum specimen size is 5 ml.

Shipping Instructions:
Ship specimens frozen in dry ice. Provide the 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. 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.

 

Prostaglandin F1a
(PG F1a)*

* Test available on a research basis only. Contact ISI for details.

 

Prostaglandin F1a
(PG F1a), urine*

* Test available on a research basis only. Contact ISI for details.

 

Prostaglandin F1a, 6-Keto
(6Keto-PG F1a, PGI2 Metabolite)*

* Test available on a research basis only. Contact ISI for details.

 

Prostaglandin F1a, 6-Keto (6-Keto PG F1a), urine*
(Prostaglandin I2 Metabolite)*

* Test available on a research basis only. Contact ISI for details.

 

Prostaglandin F2a
(PG F2a)

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.

 

Prostaglandin F2a
PG F2a), urine

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:
10 ml of a 24 hour urine collection should be submitted for analysis. No special preservatives are required. Store specimen refrigerated during collection and freeze after adding the final voiding the next morning. Specimens should be frozen once the 24 hour sample has been collected, and prior to and during shipping. Minimum specimen size is 5 ml.

Shipping Instructions:
Ship specimens frozen in dry ice. Provide the 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.

 

Prostaglandin F2a, Dihydroketo*
(DHK-PG F2a), urine

* Test available on a research basis only. Contact ISI for details.

 

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