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# 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 (DHTS)
Test Code: DIHYDSO
Synonyms/Keywords
​Ref Lab Code: 81479, 5-a-dihydrotestosterone, 5-Alpha-Dihydrotestosterone, Allodihydrotestosterone,
Androstanolone, DHT, Serum Dihydrotestosterone, Stanolone
Useful For
Monitoring patients receiving 5 alpha-reductase inhibitor therapy or chemotherapy
 
Evaluating patients with possible 5 alpha-reductase deficiency
Specimen Requirements
Specimen Type Preferred Container/Tube Acceptable Container/Tube Specimen Volume Specimen Minimum Volume
(allows for 1 repeat)
Pediatric Minimum Volume
(no repeat)
Serum​ ​Red Top Tube (RTT) ​Serum Separator Tube (SST) ​1 mL ​0.6 mL
Specimen Stability Information
Specimen Type Temperature Time
​Serum ​Refrigerated (preferred) ​7 days
​Frozen ​90 days
Rejection Criteria
Hemolysis Mild OK; Gross OK 
Lipemia​ ​Mild OK; Gross OK
​Icterus ​Mild OK; Gross OK
Performing Laboratory Information
Performing Location Day(s) Test Performed Analytical Time Methodology/Instrumentation
​Mayo Medical Laboratories Monday, Wednesday, Friday ​2 days
Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS)​
Reference Lab
Test 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.​
Reference Range Information
Interpretive report
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
Outreach CPTs
CPT Modifier
(if needed)
Quantity Description Comments
82648 ​1
Synonyms/Keywords
​Ref Lab Code: 81479, 5-a-dihydrotestosterone, 5-Alpha-Dihydrotestosterone, Allodihydrotestosterone,
Androstanolone, DHT, Serum Dihydrotestosterone, Stanolone
Ordering Applications
Ordering Application Description
​Centricity ​Dihydrotestosterone
​Cerner ​Dihydrotestosterone (81479)
If the ordering application you are looking for is not listed, contact your local laboratory for assistance.
Specimen Requirements
Specimen Type Preferred Container/Tube Acceptable Container/Tube Specimen Volume Specimen Minimum Volume
(allows for 1 repeat)
Pediatric Minimum Volume
(no repeat)
Serum​ ​Red Top Tube (RTT) ​Serum Separator Tube (SST) ​1 mL ​0.6 mL
Specimen Stability Information
Specimen Type Temperature Time
​Serum ​Refrigerated (preferred) ​7 days
​Frozen ​90 days
Rejection Criteria
Hemolysis Mild OK; Gross OK 
Lipemia​ ​Mild OK; Gross OK
​Icterus ​Mild OK; Gross OK
Useful For
Monitoring patients receiving 5 alpha-reductase inhibitor therapy or chemotherapy
 
Evaluating patients with possible 5 alpha-reductase deficiency
Test 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.​
Reference Range Information
Interpretive report
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
For more information visit:
Performing Laboratory Information
Performing Location Day(s) Test Performed Analytical Time Methodology/Instrumentation
​Mayo Medical Laboratories Monday, Wednesday, Friday ​2 days
Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS)​
Reference Lab
For billing questions, see Contacts
Outreach CPTs
CPT Modifier
(if needed)
Quantity Description Comments
82648 ​1
For most current information refer to the Marshfield Laboratory online reference manual.