A B C D E F G H I J K L M N O P Q R S T U V W X Y Z #

Dihydrotestosterone, Serum

Test Code
DHTES


Alias/See Also
Epic: LAB977
Mayo: DHTS


CPT Codes
82642, G0480 (if appropriate)

Includes


TESTING ALGORITHM

See Steroid Pathways in Special Instructions.




Preferred Specimen
Specimen Type: Serum Red
Collection Container: Red top
Specimen Volume: 1 mL



Other Acceptable Specimens

Collection Container: Serum gel




Instructions
Centrifuge and aliquot serum into a plastic vial.


Transport Container
Plastic vial


Specimen Stability
Specimen Type Temperature Time Special Container
Serum Refrigerated (preferred) 7 days  
  Frozen 90 days
 


Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Gross hemolysis OK
Gross lipemia OK
Gross icterus OK


Methodology
Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS)

Portions of this test are covered by patents held by Quest Diagnostics

Setup Schedule
Monday, Wednesday, Friday


Report Available
2 to 8 days


Limitations


CAUTIONS 

Patients with benign prostatic hyperplasia (BPH) or prostatic cancer may not have elevated dihydrotestosterone (DHT) levels even though growth of the prostate gland may be stimulated by DHT.




Reference Range


REFERENCE VALUES

Males

Cord blood: < or =100 pg/mL
< or =6 months: < or =1,200 pg/mL
Tanner Stages 
Mean Age Reference range (pg/mL)
Stage I (>6 months and prepubertal) 7.1 years < or =50
Stage II 12.1 years < or =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: < or =50 pg/mL
< or =6 months: < or =1,200 pg/mL
Tanner Stages 
Mean Age Reference range (pg/mL)
Stage I (>6 months and prepubertal) 7.1 years < or =50
Stage II 10.5 years < or =300
Stage III 11.6 years < or =300
Stage IV 12.3 years < or =300
Stage V 14.5 years < or =300
20-55 years: < or =300 pg/mL
>55 years: < or =128 pg/mL
 
1. Pang S, Levine LS, Chow D, et al: Dihydrotestosterone and its relationship to testosterone in infancy and childhood. J Clin Endocrinol Metab 1979;48:821-826
2. Stanczyk FZ: Diagnosis of hyperandrogenism: biochemical criteria. Best Pract Res Clin Endocrinol Metab 2006;20(2):177-191

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 (SHBG), 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.
 
See Steroid Pathways in Special Instructions.


Clinical Significance


USEFUL FOR 

Monitoring patients receiving 5-alpha reductase inhibitor therapy or chemotherapy
 
Evaluating patients with possible 5-alpha reductase deficiency




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 (BPH).(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 (AR). 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.
 
See Steroid Pathways in Special Instructions.




Performing Laboratory
Mayo Clinic Laboratories - Rochester
3050 Superior Drive NW
Rochester, MN 55901

Additional Information
Dihydrotestosterone, Serum

Last Updated: December 27, 2023
Last Review: N. Wolford, December 27, 2023


The CPT Codes provided in this document are based on AMA guidelines and are for informational purposes only. CPT coding is the sole responsibility of the billing party. Please direct any questions regarding coding to the payor being billed. Any Profile/panel component may be ordered separately. Reflex tests are performed at an additional charge.