About Pregnancy

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about pregnancyPregnancy tests are based on the detection of elevated levels of human Chorionic Gonadotrophin (hCG) in serum or urine, which is produced by the developing placenta following implantation1,2. Urine and serum of samples non-pregnant females usually contain less than 5 mIU/ml hCG3. After conception levels of hCG in a normal pregnancy will increase rapidly with levels reaching between 100,000 – 200,000 mIU/ml at the end of the first trimester1,2,4,5,6. The appearance and rapid rise in the level of hCG makes it an excellent marker for pregnancy.

HCG is a dimeric glycoprotein hormone consisting of an alpha and beta subunit. The alpha subunit is common to Follicle Stimulating Hormone (FSH), Luteinising Hormone (LH), Thyroid Stimulating Hormone (TSH) and hCG. The beta subunit is specific to each hormone and is responsible for its biological activity7,8,9 The development of antibodies to the beta subunit of hCG allows reliable measurement of this hormone with no cross reactivity with the other glycoprotein hormones.

The Function of hCG During Pregnancy

Pregnancy begins with fertilisation of the egg and implantation of the fertilised egg in the lining of the uterus. Implantation will normally occur during the week following ovulation. hCG begins to be produced around the time of implantation8.

A pregnancy will usually only continue after implantation if menstruation is prevented. Estrogen and Progesterone are produced by the corpus luteum and prevent menstruation by maintaining the lining of the uterus. The corpus luteum itself is maintained by hCG that is produced by the trophoblast cells of the fertilised ovum.

Levels of hCG are considered to be identical in both serum and urine10,11. HCG levels increase rapidly in the first stages of pregnancy and will normally begin to appear in the blood and subsequently in the urine of the pregnant woman a week after conception. By the day the period is due hCG levels of approximately 50 - 250 mIU/ml are expected1,2,4,5,6. During the first trimester, levels of hCG should double every 48- 72 hours peaking between 100,000 – 200,000 mIU/ml at the end of the trimester, thereafter levels of hCG drop dramatically with levels remaining well above the basal level throughout the pregnancy.

TestPack hCG Urine is sensitive to 25 mIU/ml hCG in urine samples.

Why Test Early?

During the early stages of pregnancy, the foetus is extremely susceptible to influences from its external environment. Medical professionals believe that certain measures should be taken to ensure the best possible chance of the baby being healthy at birth.

In a hospital environment testing early for pregnancy allows the mother to avoid exposure to other hazards such as x-rays, chemicals and medication.

Some infections are more serious in pregnant than non-pregnant women because of the risk they may pass across the placental or amniotic barriers. Some examples of these are Rubella, Toxoplasmosis, Syphilis, Listeriosis and Cytomegalovirus. Testing early for pregnancy may allow for the mother to test for immunity to rubella which can cause severe congenital defects or to avoid foods that might harbour Listeria monocytogenes that could cause spontaneous abortion16,17.

Smoking can reduce the level of oxygen and nutrients reaching the foetus and increase the levels of nicotine in the blood. This increases the risk of spontaneous abortion, developing placental complications and giving birth to low weight babies. Alcohol intake during pregnancy can cause growth defects, central nervous system impairment and facial deformities in the foetus as well as increasing the risk of spontaneous abortion11. Early detection of pregnancy is therefore useful to avoid putting the foetus at risk by smoking and drinking alcohol.

Research has shown that the incidence of neural tube defects such as spina bifida and hydrocephalous can be greatly reduced by taking folic acid supplements both before and during pregnancy12. Many countries recommend an intake of 0.4mg of folic acid per day prior to and during the first stages of pregnancy18. In addition there are certain foods that should be avoided during pregnancy. Foods which contain high levels of vitamin A should be avoided as it has been shown to be teratogenic14. Excessive intake of vitamin D and caffeine should also be avoided15. Testing early for pregnancy can therefore help to plan a healthy balanced diet during pregnancy.

Environmental causes of foetal malformations account for approximately 10% of malformations, with less than 1% related to prescription drug exposure, chemicals or radiation18.

Elevated hCG levels in non-pregnant individuals

There are a number of medical conditions other than pregnancy that cause elevated levels of hCG and these may cause false positive results with TestPack hCG Urine.

Gestational trophoblastic diseases can result in partial or complete hydatiform moles (cystic trophoblast tissue from a non-viable pregnancy) or choriocarcinomas (proliferation of trophoblastic tissue in the maternal tissues). Hypersecretion of hCG is common to all conditions19,20. It is also known that non-trophoblastic neoplasms can hypersecrete hCG. Braunstein (1980) reported that immunoreactive hCG is found in the sera of approximately 20% of cancer patients21. It is important to remember that trophoblastic disease and non-trophoblastic neoplasms may produce altered forms of hCG and different proportions of alpha and beta forms8TestPack hCG Urine is a qualitative test for the detection of intact hCG and is not intended for the diagnosis of these conditions, although these conditions may give positive results.


1. Braunstein G.D., Rasor J., Adler D., Danzer H. & Wade M.E. (1976) Serum human Chorionic Gonadotrophin levels throughout normal pregnancy. Am. J. Obstet. Gynecol. 126(6), 678-681.

2. Chard T. (1992) Pregnancy test – a review. Human Reproduction. 7(5), 701-710.

3. Alfthan H., Hagland C., Dabek J. & Stenman U.H. (1992)Concentrations of human Chorionogonadotropin, its b -subunit, and the core fragment of the b -subunit in serum and urine of men and non-pregnant women. Clin. Chem. 38(10), 1981-1987.

4. Lenton E.A., Neal L.M. & Sulaiman R. (1982) Plasma concentrations of human Chorionic Gonadptrophin from the time of implantation until the second week of pregnancy.Fertil. Steril. 37(6), 773-778.

5. Lau H.L., Lawrence K.W., Linkins S.E. & Jones G.S. (1978) Early detection of human Chorionic Gonadotrophin in urine by simple immunoassays. Am. J. Obstet. Gynecol. 132(6), 691-693.

6. Hsu M.I., Kolm P., Leete J., Dong K.W., Mausher S. & Oehninger S. (1998) Analysis of implantation in Assisted Reproduction through Use of Serial hCG Measurements. J. Assisted Reprod Genetics. 15(8) 496-505.

7. Bahl O.P., Carlsen R.B., Bellisario R. & Swaminathan N. (1972) Human Chorionic Gonadotropin Amino Acid Sequence of the Alpha and Beta Subunits. Biochem. Biophys. Res. Commun. 48, 416-422.

8. Hussa R.O. (1987) The Clinical Marker hCG. Praeger, New York.

9. Strickland T.W. & Puett D. (1981) Contribution of Subunits to the Function of Luteinising Hormone/Human Chorionic Gonadotrophin Recombinants. Endocrinology. 109, 1933-1942.

10. Kent A., Kitau M.J. & Chard T. (1991) Absence of Diurnal Variation in Urinary Chorionic Gonadotrophin Excretion At 8-13 Weeks Gestation. B J Obstet. Gynaecol. 98. 1180-1181.

11. Cogswell M.E., Weisberg P. & Spong C. (2003) Cigarette Smoking, Alcohol use and Adverse Pregnancy Outcomes: Implications for Micronutrient Supplementation. J. Nutr. 133, 1722S-1731S.

12. Czeizel A.E. (2000) Primary prevention of neural-tube defects and some other major congenital abnormalities: recommendations for the appropriate use of folic acid during pregnancy. Paediatric Drugs. 2(6), 437-49.

13. Egen V. & Hasford J. (2003) Prevention of neural tube defects: effect of an intervention aimed at implementing the official recommendations. Soz Praventivmed. 48(1), 24-32.

14. Bendich A. & Langseth L. (1989) Safety of Vitamin A. Am J Clin Nutr. 49(2), 358-371.

15. Ross M.P. & Brundage S. (2002) Preconception counselling about nutrition and exercise. J S C Med Assoc.98(6), 260-3.

16. Grangeot-Keros L. (1992) Rubella and Pregnancy.Pathol Biol. 40(7), 706-710.

17. Gilbert G.L. (2002) Infections in Pregnant Women.175(5), 229-236.

18. Brent R.L. & Beckman D.A. (1994) The contribution of environmental teratogens to embryonic and fetal loss. Clin Obstet. Gynecol. 37(3), 646-670.

19. Dreyfus M., Tissier I. & Phillippe E. (2000) Gestational Trophoblastic Diseases. Classification, Epidemiology and Genetic Data. J. Gynecol. Obstet. Biol. Reprod. 29(7), 687-689.

20. Quinonez Zarza C. (1995) Hydatiform Mole. Clinical aspects, incidence and risk factors. Ginecol. Obstet. Mex. 63, 391-394.

21. Braunstein G.D., Rasor J. & Wade M.E. (1980) Presence of an hCG-like substance in non-pregnant humans. In: Chorionic gonadotropin. Segal S.J. (ed) Plenum Press, New York, 383-409.


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