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Epic Test Code LAB977 Dihydrotestosterone, Serum

Additional Codes

MML Code: DHTS

 

NY State Approved

Yes

Performing Laboratory

Mayo Clinic Laboratories in Rochester

Reporting Name

Dihydrotestosterone, S

Method Name

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

Specimen Stability Information

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


Specimen Required


Container/Tube:

Preferred: Red top

Acceptable: Serum gel

Specimen Volume: 1 mL


Bassett Healthcare Network Clinical Laboratories Note:

Blood Tube Draw Volume
Min 50% draw volume  

Specimen Type

Serum

Specimen Minimum Volume

0.6 mL

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, 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

Analytic Time

2 days

Day(s) and Time(s) Performed

Monday, Wednesday, Thursday, Friday; 9 a.m.

CPT Code Information

82642

G0480 (if appropriate)

Reject Due To

Hemolysis

Mild OK; Gross OK

Lipemia

Mild OK; Gross OK

Icterus

Mild OK; Gross OK

Other

NA

Special Instructions

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.

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.

Specimen Retention Time

2 weeks

Testing Algorithm

See Steroid Pathways in Special Instructions.

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.