Home
HelpTest Code DHTS Dihydrotestosterone, Serum
Reporting Name
Dihydrotestosterone, SUseful For
Monitoring patients receiving 5-alpha reductase inhibitor therapy or chemotherapy
Evaluating patients with possible 5-alpha reductase deficiency
Testing Algorithm
For more information see Steroid Pathways.
Method Name
Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS)
Portions of this test are covered by patents held by Quest Diagnostics
Performing Laboratory
Mayo Clinic Laboratories in Rochester
Specimen Type
SerumSpecimen Required
Supplies: Sarstedt Aliquot Tube, 5 mL (T914)
Collection Container/Tube:
Preferred: Red top
Acceptable: Serum gel
Submission Container/Tube: Plastic vial
Specimen Volume: 1 mL
Collection Instructions: Centrifuge and aliquot serum into a plastic vial.
Specimen Minimum Volume
0.6 mL
Specimen Stability Information
| Specimen Type | Temperature | Time | Special Container |
|---|---|---|---|
| Serum | Refrigerated (preferred) | 28 days | |
| Frozen | 90 days | ||
| Ambient | 28 days |
Reject Due To
| Gross hemolysis | OK |
| Gross lipemia | OK |
| Gross icterus | OK |
Special Instructions
Reference Values
Males
Cord blood: ≤100 pg/mL
≤6 months: ≤1,200 pg/mL
Tanner Stages
|
Mean |
Age |
Reference range (pg/mL) |
|
Stage I (>6 months and prepubertal) |
7.1 years |
≤50 |
|
Stage II |
12.1 years |
≤200 |
|
Stage III |
13.6 years |
80-330 |
|
Stage IV |
15.1 years |
220-520 |
|
Stage V |
18 years |
240-650 |
>19 years: 112-955 pg/mL
Females
Cord blood: ≤50 pg/mL
≤6 months: ≤1,200 pg/mL
Tanner Stages
|
Mean |
Age |
Reference range (pg/mL) |
|
Stage I (>6 months and prepubertal) |
7.1 years |
≤50 |
|
Stage II |
10.5 years |
≤300 |
|
Stage III |
11.6 years |
≤300 |
|
Stage IV |
12.3 years |
≤300 |
|
Stage V |
14.5 years |
≤300 |
20-55 years: ≤300 pg/mL
>55 years: ≤128 pg/mL
1. Pang S, Levine LS, Chow D, Sagiani F, Saenger P, New MI. Dihydrotestosterone and its relationship to testosterone in infancy and childhood. J Clin Endocrinol Metab. 1979;48(5):821-826
2. Stanczyk FZ. Diagnosis of hyperandrogenism: biochemical criteria. Best Pract Res Clin Endocrinol Metab. 2006;20(2):177-191
Day(s) Performed
Monday, Wednesday, Friday
CPT Code Information
82642
LOINC Code Information
| Test ID | Test Order Name | Order LOINC Value |
|---|---|---|
| DHTS | Dihydrotestosterone, S | 1848-1 |
| Result ID | Test Result Name | Result LOINC Value |
|---|---|---|
| 81479 | Dihydrotestosterone, S | 1848-1 |
Clinical Information
The principal prostatic androgen is dihydrotestosterone (DHT). Levels of DHT remain normal with aging, despite a decrease in the plasma testosterone, and are not elevated in benign prostatic hyperplasia.(1)
DHT is generated by reduction of testosterone by 5-alpha reductase. Two isoenzymes of 5-alpha reductase have been discovered. Type 1 is present in most tissues in the body where 5-alpha reductase is expressed and is the dominant form in sebaceous glands. Type 2 is the dominant isoenzyme in genital tissues, including the prostate.
Androgenetic alopecia (AGA; male-pattern baldness) is a hereditary and androgen-dependent progressive thinning of the scalp hair that follows a defined pattern.(2) While the genetic involvement is pronounced, but poorly understood, major advances have been achieved in understanding the principal elements of androgen metabolism that are involved. DHT may be related to baldness. High concentrations of 5-alpha reductase have been found in frontal scalp and genital skin and androgen-dependent processes are predominantly due to the binding of DHT to the androgen receptor. Since the clinical success of treatment of AGA with modulators of androgen metabolism or hair growth promoters is limited, sustained microscopic follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is considered a possible cofactor in the complex etiology of AGA.
Currently available AGA treatment modalities with proven efficacy are oral finasteride, a competitive inhibitor of 5-alpha reductase type 2, and topical minoxidil, an adenosine triphosphate-sensitive potassium channel opener that has been reported to stimulate the production of vascular endothelial growth factor in cultured dermal papilla cells.
Currently, many patients with prostate disease receive treatment with a 5-alpha reductase inhibitor such as finasteride (Proscar) to diminish conversion of DHT from testosterone.
For more information see Steroid Pathways.
Interpretation
Patients taking 5-alpha reductase inhibitor have decreased dihydrotestosterone (DHT) serum levels.
Patients with genetic 5-alpha reductase deficiency (a rare disease) also have reduced DHT serum levels.
DHT should serve as the primary marker of peripheral androgen production. However, because it is metabolized rapidly and has a very high affinity for sex hormone-binding globulin, DHT does not reflect peripheral androgen action. Instead, its distal metabolite, 3-alpha, 17-beta-androstanediol glucuronide, serves as a better marker of peripheral androgen action.
For more information see Steroid Pathways.
Cautions
Patients with benign prostatic hyperplasia or prostatic cancer may not have elevated dihydrotestosterone (DHT) levels even though growth of the prostate gland may be stimulated by DHT.
Method Description
High Performance Liquid Chromatography with Triple Quad Tandem Mass Spectrometer Deuterated stable isotope of dihydrotestosterone (13C3-DHT) is added to a 0.5 mL serum sample as internal standard. The DHT and internal standard are extracted from the sample by liquid/liquid extraction. This is followed by high performance liquid chromatography on a Cohesive LX4 System and analysis on a tandem mass spectrometer equipped with an electrospray ion source.(Unpublished Mayo Method)