Luteinizing Hormone (LH), Serum
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Luteinizing hormone (LH) is a glycoprotein hormone consisting of 2 noncovalently bound subunits (alpha and beta). The alpha subunit of LH, follicle-stimulating hormone (FSH), thyroid stimulating hormone (TSH), and human chorionic gonadotropin (hCG) are identical and contain 92 amino acids. The beta subunits of these hormones vary and confer the hormones' specificity. LH has a beta subunit of 121 amino acids and is responsible for interaction with the LH receptor. This beta subunit contains the same amino acids in sequence as the beta subunit of hCG and both stimulate the same receptor, however, the hCG beta subunit contains an additional 24 amino acids, and the hormones differ in the composition of their sugar moieties. Gonadotropin-releasing hormone from the hypothalamus controls the secretion of the gonadotropins, FSH and LH, from the anterior pituitary.
In both males and females, LH is essential for reproduction. In females, the menstrual cycle is divided by a midcycle surge of both LH and FSH into a follicular phase and a luteal phase. This "LH surge" triggers ovulation thereby not only releasing the egg, but also initiating the conversion of the residual follicle into a corpus luteum that, in turn, produces progesterone to prepare the endometrium for a possible implantation. LH is necessary to maintain luteal function for the first 2 weeks. In case of pregnancy, luteal function will be further maintained by the action of hCG (a hormone very similar to LH) from the newly established pregnancy. LH supports thecal cells in the ovary that provide androgens and hormonal precursors for estradiol production. LH in males acts on testicular interstitial cells of Leydig to cause increased synthesis of testosterone.
An adjunct in the evaluation of menstrual irregularities
Evaluating patients with suspected hypogonadism
Diagnosing pituitary disorders
In both males and females, primary hypogonadism results in an elevation of basal follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels.
Postmenopausal LH levels are generally >40 IU/L. (Note: FSH is the preferred test to confirm menopausal status.)
FSH and LH are generally elevated in:
- Primary gonadal failure
- Complete testicular feminization syndrome
- Precocious puberty (either idiopathic or secondary to a central nervous system lesion)
- Primary ovarian hypodysfunction in females
- Polycystic ovary disease in females
- Primary hypogonadism in males
LH is decreased in:
- Primary ovarian hyperfunction in females
- Primary hypergonadism in males
FSH and LH are both decreased in failure of the pituitary or hypothalamus.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Twelve hours before this blood test, do not take multivitamins or dietary supplements containing biotin or vitamin B7 that are commonly found in hair, skin and nail supplements and multivitamins.
No clinically significant cross-reactivity has been demonstrated with follicle-stimulating hormone, thyroid stimulating hormone, or human chorionic gonadotropin.
Some patients who have been exposed to animal antigens, either in the environment or as part of treatment or imaging procedures, may have circulating antianimal antibodies present. These antibodies may interfere with the assay reagents to produce unreliable results.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
0-14 days: not established
15 days-10 years: 0.3-2.8 IU/L
11 years: 0.3-1.8 IU/L
12 years: 0.3-4.0 IU/L
13 years: 0.3-6.0 IU/L
14 years: 0.5-7.9 IU/L
15-16 years: 0.5-10.8 IU/L
17 years: 0.9-5.9 IU/L
> or =18 years: 1.8-8.6 IU/L
Stage l: 0.3-2.7 IU/L
Stage ll: 0.3-5.1 IU/L
Stage lll: 0.3-6.9 IU/L
Stage lV: 0.5-5.3 IU/L
Stage V: 0.8-11.8 IU/L
*Puberty onset occurs for boys at a median age of 11.5 (+/- 2) years. For boys there is no proven relationship between puberty onset and body weight or ethnic origin. Progression through Tanner stages is variable. Tanner stage V (adult) should be reached by age 18.
0-14 days: not established
15 days-3 years: 0.3-2.5 IU/L
4-6 years: < or =1.9 IU/L
7-8 years: < or =3.0 IU/L
9-10 years: < or =4.0 IU/L
11 years: < or =6.5 IU/L
12 years: 0.4-9.9 IU/L
13 years: 0.3-5.4 IU/L
14 years: 0.5-31.2 IU/L
15 years: 0.5-20.7 IU/L
16 years: 0.4-29.4 IU/L
17 years: 1.6-12.4 IU/L
> or =18 years
Follicular: 2.1-10.9 IU/L
Midcycle: 20.0-100.0 IU/L
Luteal: 1.2-12.9 IU/L
Postmenopausal: 10.0-60.0 IU/L
Stage I: < or =2.0 IU/L
Stage II: < or =6.5 IU/L
Stage III: 0.3-17.2 IU/L
Stage IV: 0.5-26.3 IU/L
Stage V: 0.6-13.7 IU/L
*Puberty onset (transition from Tanner stage I to Tanner stage II) occurs for girls at a median age of 10.5 (+/- 2) years. There is evidence that it may occur up to 1 year earlier in obese girls and in African American girls. Progression through Tanner stages is variable. Tanner stage V (adult) should be reached by age 18.
Pediatric ranges derived for DXI method from analytic comparison to reference method in: Elmlinger MW, Kuhnel W, Ranke MB: Reference ranges for serum concentrations of lutropin (LH), follitropin (FSH), estradiol (E2), prolactin, progesterone, sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), cortisol and ferritin in neonates, children and young adults. Clin Chem Lab Med 2002;40(11):1151-1160
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Kaplan LA, Pesce AJ: The gonads. In Clinical Chemistry: Theory, Analysis, and Correlation. Third edition. Edited by SC Kazmierczak. St. Louis, MO, Mosby-Year Book, Inc, 1996, p 894
2. Dumesic DA: Hyperandrogenic anovulation: a new view of polycystic ovary syndrome. Postgrad Ob Gyn 1995;15:1-5