Progesterone

Establish the presence of a functioning corpus luteum or luteal cell function; confirm basal body temperature measurements for the occurrence of ovulation; obtain an indication of the day of ovulation; evaluate the functional state of the corpus luteum in infertility patients; assess placental function during pregnancy; ovarian function test

As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from samples taken from patients who have been treated with monoclonal mouse antibodies or who have received them for diagnostic purposes.1 In rare cases, interference due to extremely high titers of antibodies to streptavidin and ruthenium can occur.1 The test contains additives that minimize these effects.

Progesterone is a steroid hormone with a molecular weight of 314.5 daltons.2 Progesterone is mainly formed in the cells of the corpus luteum and during pregnancy in the placenta. Progesterone is increased in congenital adrenal hyperplasia due to 21-hydroxylase, 17-hydroxylase, and 11-β-hydroxylase deficiency. Progesterone is decreased in primary or secondary hypogonadism and short luteal phase syndrome.

The progesterone concentration correlates with the development and regression of the corpus luteum. Whereas progesterone is barely detectable in the follicular phase of the female cycle, a rise in the progesterone level is observed one day prior to ovulation. Increased progesterone synthesis occurs during the luteal phase. In the second half of the cycle pregnanediol is excreted in urine as the main degradation product of progesterone.

Progesterone brings about the conversion of the uterine mucosa into a tissue rich in glands (secretion phase), in order to prepare for the intrauterine implantation of the fertilized ovum. During pregnancy, progesterone inhibits the contraction of the myometrium. In the mammary gland, progesterone (together with estrogens) promotes the proliferation and secretion disposition of the alveoli.2,3

The determination of progesterone is utilized in fertility diagnosis for the detection of ovulation and assessment of the luteal phase.3,4

1. Progesterone on Elecsys 1010/2010 and Modular Analytics E170, 2007-09, V 11 [package insert] Indianapolis, Ind: Roche Diagnostics; 2007.

2. Johnson MR, Carter G, Grint C, Lightman SL. Relationship between ovarian steroids, gonadotrophins and relaxin during the menstrual cycle. Acta Endocrinol. 1993 Aug; 129(2):121-125. PubMed 8372595

3. Runnebaum B, Rabe T. Gynäkologische Endokrinologie und Fortpflanzungsmedizin. Berlin, Germany: Springer Verlag 1994, Band 1: 36-38, 70, 116; Band 2: 137, 360, 398-399, 408-409, 422-423.

4. Guillaume J, Benjamin F, Sicuranza B, Wang CF, Garcia A, Friberg J. Maternal serum levels of estradiol, progesterone and human chorionic gonadotropin in ectopic pregnancy and their correlation with endometrial histologic findings. Surg Gynecol Obstet. 1987 Jul; 165(1):9-12. PubMed 3589936

Hilborn S, Krahn J. Effect of time of exposure of serum to gel-barrier tubes on results for progesterone and some other endocrine tests. Clin Chem. 1987 Jan; 33(1):203-204. PubMed 3802491

Nippoldt TB, Reame NE, Kelch RP, Marshall JC. The roles of estradiol and progesterone in decreasing luteinizing hormone pulse frequency in the luteal phase of the menstrual cycle. J Clin Endocrinol Metab. 1989 Jul; 69(1):67-76. PubMed 2499593

Rebar RW. The ovaries. In: Wyngaarden JB, Smith LH Jr, eds.Cecil Textbook of Medicine. 18th ed. vol 2. Philadelphia, Pa: WB Saunders Co;1988:1425-1446.

Romero R, Scoccia B, Mazor M, Wu YK, Benveniste R. Evidence for a local change in the progesterone/estrogen ratio in human parturition at term. Am J Obstet Gynecol. 1988 Sep; 159(3):657-660. PubMed 2971319

Stewart MO1, Whittaker PG, Persson B, Hanson U, Lind T. A longitudinal study of circulating progesterone, oestradiol, hCG and hPL during pregnancy in type 1 diabetic mothers. Br J Obstet Gynaecol. 1989 Apr; 96(4):415-423. PubMed 2751954