Dihydrotestosterone, Serum

CPT CODE:

USEFUL FOR:

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

SPECIMEN REQUIRED:

Draw blood in a plain, red-top tube(s) or a serum gel tube(s). Spin down and send 1 mL of serum refrigerated.

TRANSPORT TEMPERATURE:

Refrig\Frozen OK\Ambient NO

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 andandrogen-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.

CLINICAL INTERPRETATION:

Patients taking 5 alpha-reductase inhibitor have decreased 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

REFERENCE VALUES:

                                       Males

Cord blood:  < or =100 pg/mL

< or =6 months:  < or =1,200 pg/mL

Tanner Stages              Mean Age         Reference Range

Stage I:                                 7.1                          < or =50 pg/mL

      (>6 months and prepubertal)                 

Stage II:                                12.1                        < or =200 pg/mL

Stage III:                               13.6                        80-330 pg/mL

Stage IV:                              15.1                        220-520 pg/mL

Stage V:              &