Datasets:

---

Recag

/

Rp_CommonC_93

like 0

ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjA4OTE1OC1vdmVydmlldw==\nDrugs & Diseases > Laboratory Medicine\nHuman Chorionic Gonadotropin (hCG)\nAuthor: Abimbola Farinde, PharmD, PhD; Chief Editor: Eric B Staros, MD more...\nSections Human Chorionic Gonadotropin (hCG)\nReference Range\nCollection and Panels\nHuman chorionic gonadotropin (hCG) is produced during pregnancy. It can support pregnancy by allowing for the production of progesterone, which can help to prepare the lining of the uterus for implantation. It consists of cells that ultimately form the placenta, which provides nutrition to the egg after it has been fertilized and connects to the uterine wall. [1, 2]\nhCG is a dimer consisting of a 145 amino acid beta-subunit that is unique to hCG and a 92 amino acid alpha-subunit. The alpha-subunit is identical to that for luteinizing hormone (LH), follicle-stimulating hormone (FSH), and thyroid-stimulating hormone (TSH). The alpha and beta-subunits have separate genes on separate chromosomes (chromosomes 6 and 19, respectively). After synthesis, the alpha and beta-subunits are bonded with a noncovalent bond before being released into the circulation.\nChildren reference range\nThe reference ranges for pediatric males are as follows:\nBirth-3 months - 50 IU/L or less*\n3 months-18 years - 0.8 IU/L or less\nThe reference ranges for pediatric females are as follows:\nBirth-3 months - 50.0 IU/L* or less\n*hCG, produced in the placenta, partially passes the placental barrier. Newborn serum beta hCG concentrations are approximately 1/400th of the corresponding maternal serum concentrations, resulting in neonate beta hCG levels of 10-50 IU/L at birth. Clearance half-life is approximately 2-3 days. Therefore, by 3 months of age, levels comparable to adults should be reached.\nAdult reference range (97.5 percentile)\nMales - 0.8 IU/L or less\nFemales - Premenopausal, nonpregnant: 2.3 IU/L or less. Postmenopausal: 7.3 IU/L or less.\nElevated levels are seen with pregnancy and with HCG-secreting tumors.\nA rise in hCG levels above the reference range in patients with a history of an hCG-producing condition is suggestive of recurrent disease.\nSpecimen type is as follows:\nSpecimen required is as follows:\nContainer/tube: Red top (preferred)\nAcceptable: Serum gel\nSpecimen volume: 1.5 mL\nSpecimen minimum volume: 1 mL\nReject due to the following:\nHemolysis (mild okay; gross reject)\nLipemia (mild okay; gross okay)\nIcterus (not applicable)\nSpecimen Stability Information\nTable. (Open Table in a new window)\nRefrigerated (preferred)\nHuman chorionic gonadotropin (hCG) is a dimer consisting of a 145 amino acid beta-subunit that is unique to hCG and a 92 amino acid alpha-subunit. The alpha-subunit is identical to that for luteinizing hormone (LH), follicle-stimulating hormone (FSH), and thyroid-stimulating hormone (TSH). The alpha and beta-subunits have separate genes on separate chromosomes (chromosomes 6 and 19, respectively). After synthesis, the alpha and beta-subunits are bonded with a noncovalent bond before being released into the circulation.\nCarbohydrate side chains comprise 25-40% of the molecular weight of hCG. The alpha-subunit contains 2 N-linked oligosaccharides; the beta-subunit contains 2 N-linked oligosaccharides, as well as 4 O-linked oligosaccharides on the C-terminal extension. The 2 most common forms of hCG synthesized by cells are regular hCG and hyperglycosylated hCG (hCG-H). HCG-H contains more sugar residues than regular hCG: 1.5-fold more sugar residues on the N-linked oligosaccharides (16 versus 11 sugar residues for regular hCG) and 2-fold more sugar residues on O-linked oligosaccharides.\nIndications/Applications\nGestational and nongestational trophoblasts are by far the most common sources of hCG, but a small amount of the hormone may also be produced by the pituitary gland and nontrophoblastic malignancies.\nThe syncytiotrophoblast covers the villous tree and has several functions, such as transport of gases, nutrients, and waste products and synthesis of peptide and steroid hormones that regulate placental, fetal, and maternal systems. The syncytiotrophoblast produces regular hCG, which promotes progesterone production by the corpus luteum until placental progesterone production becomes established (after 6 weeks of gestation). Regular hCG also appears to play a role in myometrial spiral artery angiogenesis.\nThe level of free beta-subunit of hCG is often determined in pregnant women as part of maternal serum screening for Down syndrome. The free beta-subunit variants measured depend on the assay. Increased total hCG levels in the first and second trimester are associated with Down syndrome, while decreased levels may occur in trisomy 18. Elevations of hCG can also occur in multiple pregnancies, singleton pregnancies in which the gestational age has been overestimated, triploidy, fetal loss, and hydrops fetalis. [3, 4]\nSerum total hCG concentration peaks at about 93,000 mIU/mL (range 27,300-233,000 mIU/mL) at 8- 11 weeks of gestation.\nHCG promotes trophoblast growth and invasion. The invasion may be controlled, as in implantation of pregnancy and complete/partial mole, or malignant, as in the invasive gestational trophoblastic diseases, choriocarcinoma and invasive mole.\nComplete and partial mole\nRegular hCG is the principal form of hCG associated with complete and partial hydatidiform mole.\nA total hCG result greater than 100,000 mIU/mL strongly suggests complete hydatidiform mole, although the peak hCG in many normal pregnancies can reach this level.\nPartial moles produce less regular hCG than complete moles. In the USA hCG Reference Service experience, the median hCG concentration in 21 partial moles was about 49,000 mIU/mL (range 11,600-220,114 mIU/mL), and only 14% of cases exceeded 100,000 mIU/mL.\nInvasive mole and choriocarcinoma\nIn gestational trophoblastic neoplasias, such as invasive mole and choriocarcinoma, a high level of hCG can help to distinguish invasive from noninvasive mole, although some overlap occurs in their normal ranges.\nSerial measurement of hCG levels is standard follow-up of women diagnosed with complete or partial mole. An increasing or plateauing level of total hCG is diagnostic of invasive disease (invasive mole or choriocarcinoma).\nChoriocarcinoma consists of sheets of anaplastic cytotrophoblasts and syncytiotrophoblasts without chorionic villi. Some intermediate trophoblasts may also be seen. HCG levels approaching 600,000 mIU/mL are seen. The level of hCG correlates with tumor mass.\nPituitary gland\nThe normal pituitary gland produces a small amount of hCG. The level of hCG attributable to pituitary production ranges from 1-32 mIU/mL.\nPituitary production of hCG is most notable around the time of menopause (natural or surgical) and prior to ovulation, which are times when LH levels peak. One possible explanation is that a small amount of hCG is produced along LH because the single LH beta-subunit gene is buried among the 7 back-to-back hCG beta-subunit genes.\nReturn of the serum hCG concentration to undetectable following pregnancy termination varies widely from 7-60 days. The period of time depends primarily upon the hCG concentration at the time of termination. The hCG concentration peaks at 8-11 weeks at approximately 90,000 mIU. This is in contrast with term pregnancy, for which the hCG concentration is lower. The decline in serum hCG is rapid for the first several days (half-life 9-31 hours) and then proceeds more slowly (half-life 55-64 hours).\nNongestational malignancies\nOutside of pregnancy, hCG may be secreted by abnormal germ cell, placental, or embryonal tissues, in particular seminomatous and nonseminomatous testicular tumors; ovarian germ cell tumors; gestational trophoblastic disease (GTD, hydatidiform mole, and choriocarcinoma); and benign or malignant nontesticular teratomas. Rarely, other tumors including hepatic, neuroendocrine, breast, ovarian, pancreatic, cervical, and gastric cancers may secrete hCG, usually in relatively modest quantities\nDuring pathologic hCG production, the highly coordinated secretion of alpha and beta subunits of hCG may be disturbed. In addition to secreting intact hCG, tumors may produce disproportionate quantities of free alpha subunits or, more commonly, free beta subunits. Assays that detect both intact hCG and free beta hCG, including this assay, therefore, tend to be more sensitive in detecting hCG-producing tumors.\nWith successful treatment of hCG-producing tumors, hCG levels should fall, with a half-life of 24-36 hours, and eventually return to within normal limits.\nAn elevated HCG level may be physiologic, pathophysiologic from a tumor or artifactual from a false-positive hCG test. Unless a tumor is evident, excluding these possibilities before initiating chemotherapy for assumed persistence of disease is essential.\nA false-positive HCG test may be caused by naturally occurring cross-reacting antibodies that interfere with the test. The capture and tracer antibodies used for hCG testing may be goat, sheep, or rabbit polyclonal antibodies or mouse, goat, or sheep monoclonal antibodies. Humans extensively exposed to animals or certain animal byproducts can develop human antibodies against these animal antibodies (HAAA). In addition, humans naturally generate human anti-human immunoglobulin antibodies that can cross-react with and bind animal antibodies; these are called heterophilic antibodies.\nAlso, recent infections or exposure to mononucleosis can produce these HAAAs; those with IgA deficiency syndrome also often have heterophilic antibodies. Each human antibody is bivalent, so if an HAAA or heterophilic antibody is present in a person's serum, it can bind and link together the immobilized and tracer antibodies of the hCG test, making an immobilized capture antibody-heterophilic antibody/HAAA-tracer antibody sandwich, which results in a false positive hCG result. The false positive HCG test can lead to the misdiagnosis of cancer and sometimes lead to needless surgery and chemotherapy.\nTo prevent false testing, animal serum and nonspecific animal antibodies are added to HCG assays with capture antibody, tracer antibody, and other components. This excess of nonspecific antibodies overwhelming saturates heterophilic antibodies and HAAA in human serum samples and usually eliminates their interference with the assay. This method does not always work, however, and false positive cases still occur. This understandably creates confusion, as some false positive cases are incorrectly interpreted as recurrence of gestational trophoblastic disease.\nTwo main methods for identifying false-positive hCG tests exist are as follows:\nThe most readily available approach is to show the absence of hCG in the patient's urine. A true hCG elevation should be present in both serum and urine. Urine HCG is usually never detected in patients with false-positive serum hCG tests. A sensitive urine hCG test should be used to avoid missing low-level true-positive tests. Alternatively, to detect low concentrations of hCG, urine samples can be tested on the same instrument used to quantitate hCG in serum samples; these tests are typically sensitive. Avoid using a point-of-care urine test, as these tests tend to be insensitive to low levels of hCG.\nA second useful way of identifying a false-positive serum hCG result is to send the serum to 2 laboratories using different commercial assays. If the assay results vary greatly or are negative in one or both alternative tests, then a false-positive hCG can be presumed.\nPatients who have false-positive hCG test results are also at risk for other false positives, such as CA-125 and thyroid antibodies. They should make their future health care providers aware of this problem and it should be noted in their medical records.\nFertility Authority. What is Human Chorionic Gonadotropin (hCG)?. FertilityAuthority.com. Available at http://www.fertilityauthority.com/daily-shot-archive/what-human-chorionic-gonadotropin-hcg. Accessed: June 17, 2014.\nAmerican Pregnancy Association. Human Chorionic Gonadotropin (hCG); The Pregnancy Hormone. AmericanPregnancy.com. Available at http://americanpregnancy.org/duringpregnancy/hcglevels.html. Accessed: June 17, 2014.\nValbuena H, Ramis J, Sagalá J, Sánchez MA, Aulesa C. First-trimester screening biochemical markers (free beta-subunit human chorionic gonadotropin, pregnancy-associated plasma protein-A) and risk of early fetal loss. J Obstet Gynaecol Res. 2014 Aug 27. [Medline].\nHaavaldsen C, Fedorcsak P, Tanbo T, Eskild A. Maternal age and serum concentration of human chorionic gonadotropin in early pregnancy. Acta Obstet Gynecol Scand. 2014 Aug 19. [Medline].\nBarlow LJ, Badalato GM, McKiernan JM. Serum tumor markers in the evaluation of male germ cell tumors. Nat Rev Urol. 2010 Nov. 7(11):610-7. [Medline].\nBatzer FR. Hormonal evaluation of early pregnancy. Fertil Steril. 1980 Jul. 34(1):1-13. [Medline].\nBillieux MH, Petignat P, Anguenot JL, Campana A, Bischof P. Early and late half-life of human chorionic gonadotropin as a predictor of persistent trophoblast after laparoscopic conservative surgery for tubal pregnancy. Acta Obstet Gynecol Scand. 2003 Jun. 82(6):550-5. [Medline].\nBirken S, Maydelman Y, Gawinowicz MA, Pound A, Liu Y, Hartree AS. Isolation and characterization of human pituitary chorionic gonadotropin. Endocrinology. 1996 Apr. 137(4):1402-11. [Medline].\nChakraborty C, Gleeson LM, McKinnon T, Lala PK. Regulation of human trophoblast migration and invasiveness. Can J Physiol Pharmacol. 2002 Feb. 80(2):116-24. [Medline].\nCole LA. Immunoassay of human chorionic gonadotropin, its free subunits, and metabolites. Clin Chem. 1997 Dec. 43(12):2233-43. [Medline].\nCole LA, Butler SA. Hyperglycosylated human chorionic gonadotropin and human chorionic gonadotropin free beta-subunit: tumor markers and tumor promoters. J Reprod Med. 2008 Jul. 53(7):499-512. [Medline].\nCole LA, Dai D, Butler SA, Leslie KK, Kohorn EI. Gestational trophoblastic diseases: 1. Pathophysiology of hyperglycosylated hCG. Gynecol Oncol. 2006 Aug. 102(2):145-50. [Medline].\nCole LA, Gutierrez JM. Production of human chorionic gonadotropin during the normal menstrual cycle. J Reprod Med. 2009 Apr. 54(4):245-50. [Medline].\nCole LA, Khanlian SA, Muller CY. Detection of perimenopause or postmenopause human chorionic gonadotropin: an unnecessary source of alarm. Am J Obstet Gynecol. 2008. 198:275.e1-275.e7.\nCole LA, Khanlian SA, Riley JM, Butler SA. Hyperglycosylated hCG in gestational implantation and in choriocarcinoma and testicular germ cell malignancy tumorigenesis. J Reprod Med. 2006 Nov. 51(11):919-29. [Medline].\nFlam F, Hambraeus-Jonzon K, Hansson LO, Kjaeldgaard A. Hydatidiform mole with non-metastatic pulmonary complications and a false low level of hCG. Eur J Obstet Gynecol Reprod Biol. 1998 Apr. 77(2):235-7. [Medline].\nGenest DR, Laborde O, Berkowitz RS, Goldstein DP, Bernstein MR, Lage J. A clinicopathologic study of 153 cases of complete hydatidiform mole (1980-1990): histologic grade lacks prognostic significance. Obstet Gynecol. 1991 Sep. 78(3 Pt 1):402-9. [Medline].\nKhanlian SA, Cole LA. Management of gestational trophoblastic disease and other cases with low serum levels of human chorionic gonadotropin. J Reprod Med. 2006 Oct. 51(10):812-8. [Medline].\nKhanlian SA, Smith HO, Cole LA. Persistent low levels of human chorionic gonadotropin: A premalignant gestational trophoblastic disease. Am J Obstet Gynecol. 2003 May. 188(5):1254-9. [Medline].\nKovalevskaya G, Birken S, Kakuma T, Ozaki N, Sauer M, Lindheim S. Differential expression of human chorionic gonadotropin (hCG) glycosylation isoforms in failing and continuing pregnancies: preliminary characterization of the hyperglycosylated hCG epitope. J Endocrinol. 2002 Mar. 172(3):497-506. [Medline].\nKovalevskaya G, Genbacev O, Fisher SJ, Caceres E, O'Connor JF. Trophoblast origin of hCG isoforms: cytotrophoblasts are the primary source of choriocarcinoma-like hCG. Mol Cell Endocrinol. 2002 Aug 30. 194(1-2):147-55. [Medline].\nMenczer J, Modan M, Serr DM. Prospective follow-up of patients with hydatidiform mole. Obstet Gynecol. 1980 Mar. 55(3):346-9. [Medline].\nMidgley AR Jr, Jaffe RB. Regulation of human gonadotropins. II. Disappearance of human chorionic gonadotropin following delivery. J Clin Endocrinol Metab. 1968 Dec. 28(12):1712-8. [Medline].\nMock P, Chardonnens D, Stamm P, Campana A, Bischof P. The apparent late half-life of human chorionic gonadotropin (hCG) after surgical treatment for ectopic pregnancy. A new approach to diagnose persistent trophoblastic activity. Eur J Obstet Gynecol Reprod Biol. 1998 May. 78(1):99-102. [Medline].\nMuller CY, Cole LA. The quagmire of hCG and hCG testing in gynecologic oncology. Gynecol Oncol. 2009 Mar. 112(3):663-72. [Medline].\nNaylor SL, Chin WW, Goodman HM, Lalley PA, Grzeschik KH, Sakaguchi AY. Chromosome assignment of genes encoding the alpha and beta subunits of glycoprotein hormones in man and mouse. Somatic Cell Genet. 1983 Nov. 9(6):757-70. [Medline].\nO'Connor JF, Ellish N, Kakuma T, Schlatterer J, Kovalevskaya G. Differential urinary gonadotrophin profiles in early pregnancy and early pregnancy loss. Prenat Diagn. 1998 Dec. 18(12):1232-40. [Medline].\nPolicastro PF, Daniels-McQueen S, Carle G, Boime I. A map of the hCG beta-LH beta gene cluster. J Biol Chem. 1986 May 5. 261(13):5907-16. [Medline].\nPratap D, Kumar P, Adiga SK. Advancing or postponing the day of human chorionic gonadotropin does not matter for the outcome in assisted reproductive technology. J Hum Reprod Sci. 2014 Apr. 7(2):107-10. [Medline]. [Full Text].\nSeckl MJ, Sebire NJ, Berkowitz RS. Gestational trophoblastic disease. Lancet. 2010 Aug 28. 376(9742):717-29. [Medline].\nSteier JA, Bergsjø P, Myking OL. Human chorionic gonadotropin in maternal plasma after induced abortion, spontaneous abortion, and removed ectopic pregnancy. Obstet Gynecol. 1984. 64:391.\nSturgeon CM, Duffy MJ, Stenman UH et al. National Academy of Clinical Biochemistry laboratory medicine practice guidelines for use of tumor markers in testicular, prostate, colorectal, breast, and ovarian cancers. Clin Chem. 2008 Dec. 54(12):e11-79.\nSutton-Riley JM, Khanlian SA, Byrn FW, Cole LA. A single serum test for measuring early pregnancy outcome with high predictive value. Clin Biochem. 2006 Jul. 39(7):682-7. [Medline].\nAbimbola Farinde, PharmD, PhD Faculty, Columbia Southern University\nAbimbola Farinde, PharmD, PhD is a member of the following medical societies: American College of Clinical Pharmacy, American Academy of HIV Medicine, American Pharmacists Association, Academy of Managed Care Pharmacy\nEric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital\nEric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology\nencoded search term (Human Chorionic Gonadotropin (hCG)) and Human Chorionic Gonadotropin (hCG)\nPulmonary Disease and Pregnancy\nHIV in Pregnancy\nPregnancy Special Considerations\nRenal Disease and Pregnancy\nShock and Pregnancy\nTransplantation and Pregnancy\nPostterm Pregnancy\nPregnancy Intention and Health Behaviors: Results from the Central Pennsylvania Women's Health Study Cohort\nDoes Bariatric Surgery Affect the Risk of Adverse Outcomes in Pregnancy?\nTreating Infertility in Polycystic Ovary Syndrome\nDon't Bump the Bump: Trauma in Pregnancy\nAccording to Pathologists\nUS Pathologist Supply Down Relative to Diagnostic Demands\nThe FDA-Approved Breast Cancer HER2 Evaluation Kit (HercepTest; Dako) May Miss Some HER2-Positive Breast Cancers\nDoping-Drug Testing Methods Stuck in the 1970s, Says Former WADA\nStratification of Follicular Lymphoma\nFrozen-Section Checklist Implementation Improves Quality and Patient Safety\nJournal Article Pregnancy and Neonatal Outcomes Following Prenatal Exposure to Dolutegravir\nNews Exposing the 'Great Masquerader' in Maternal Mortality\nNews Pregnancy Outcomes Improved in Lupus\nDiseases & Conditions Anemia and Thrombocytopenia in Pregnancy"