Testosterone is the male sex hormone, which in men is produced approximately 95% in the Leydig cells of the testis and 5% in the adrenal cortex.In women, production occurs predominantly in the adrenal cortex.Testosterone is synthesized from cholesterol. It is one of the fat-soluble hormones. More than 40 percent of it is bound to sex hormone-binding globulin (SHBG) and more than 50 percent to albumin. Only about two percent is present as free testosterone. Metabolization: In the androgen target tissue, conversion to the more potent androgen dihydrotestosterone (DHT) usually takes place with the help of the enzyme 5α-reductase. Testosterone is subject to circadian rhythms, which in this case means that it is predominantly secreted in the morning (8:00-10:00 am).
The procedure
Material needed
- Blood serum
Preparation of the patient
- Blood collection is done in the morning (8:00-10:00 am).
- If necessary, perform three blood collections to be able to perform a determination from “pooled” serum
Interfering factors
- See preparation of the patient
Normal values total testosterone
| Gender | Age | Normal values in µg/l | Standard values in nmol/l |
| Female | Infants | 0,04-0,2 | 0,1-0,6 |
| 1st-8th year of life (LY) | 0,03-0,12 | 0,1-0,4 | |
| 9-12 LY | 0,03-0,4 | 0,1-1,4 | |
| 13-18 LY | 0,06-0,5 | 0,2-1,8 | |
| Adults | 0,15-0,55 | 0,5-2,0 | |
| Male | Infants | 0,05-3,5 | 0,1- 12,1 |
| 1ST-8TH LY | 0,05-0,15 | 0,1-0,5 | |
| 9-12 LY | 0,1-3,0 | 0,3-10,4 | |
| 13-18 LY | 0,1-9,0 | 0,3-31,2 | |
| Adults | 3,5-9,0 | 12,1-31,2 |
Conversion factor
- Μg/l x 3.467 = nmol/l
Indications
- Suspected hormonal disorders (hypogonadism; AGS; virilization (masculinization) of women).
- Erectile dysfunction (erectile dysfunction).
- Cryptorchidism
- Therapy monitoring due totestosterone substitution therapy.
- Suspicion of hormonally active tumors (eg, testicular tumors; ovarian tumors).
Interpretation
Interpretation of elevated values
Ms.
- Adrenogenital syndrome (AGS) – autosomal recessive inherited metabolic disorder characterized by disorders of hormone synthesis in the adrenal cortex. These disorders lead to a deficiency of aldosterone and cortisol.
- Androgen-producing adrenal carcinoma.
- Hyperthyroidism (hyperthyroidism) – leads to increased SHBG.
- Liver cirrhosis (connective tissue remodeling of the liver with functional impairment) – leads to increased SHBG.
- Menopause (menopause) – leads to increased SHBG.
- Cushing’s disease – disease caused by an excess of cortisol.
- Adrenal hypertrophy – excessive growth of the adrenal glands.
- Ovarian tumors (ovarian tumors)
- Pubertas praecox – premature puberty
- Pregnancy – leads to increased SHBG
- Testosterone-producing tumor (testosterone levels > 1.2 ng/ml).
- Polycystic ovary syndrome (PCO) – gynecological disorder associated with excessive cyst formation on the ovaries (ovaries) and associated hormone disruption.
Man
- Hormone regulatory disorders due to genetic defects (androgen resistance; androgen receptor defects).
- Hormonally active tumors such as testicular tumors or androgen-producing adrenal carcinoma.
- Hyperthyroidism (hyperthyroidism) – leads to increased SHBG.
- Liver cirrhosis (connective tissue remodeling of the liver with functional impairment) – leads to increased SHBG.
- Testosterone supply
Interpretation of lowered valuesWoman
- Primary gonadal insufficiency (prepubertal; postmenopausal).
- Drug abuse (anabolic steroids)
- Liver cirrhosis – connective tissue remodeling of the liver with functional impairment.
- Drug therapy with antiandrogens, estrogens or anabolic steroids.
- Addison’s disease – adrenal insufficiency
- Malnutrition (including anorexia nervosa).
Man
- Primary (hypergonadotropic) hypogonadism: e.g. Klinefelter syndrome (47, XXY or other variants)Note: The testosterone serum level is often still in the middle to lower normal range for many years. The decrease in testosterone serum level occurs only with decreasing testicular secretory capacity or increasing fibrosis. Serum gonadotropins are elevated.
- Secondary (hypogonadotropic) hypogonadism – gonadotropins decreased (LH↓, FSH↓).
- Drug abuse (anabolic steroids)
- Liver cirrhosis – connective tissue remodeling of the liver with functional impairment.
- Drug therapy with synthetic androgens, glucocorticoids, opioids.
- Malnutrition (including anorexia nervosa).
Other notes
- Man: Testosterone replacement therapy should not be initiated based on a single decreased testosterone level without clinic and cause clarification (see below andropause).
- In symptomatic hypogonadism (total testosterone serum level < 12 nmol/l (3.5 ng/ml), there is a good chance of achieving an improvement in symptoms through testosterone substitution.
- At total testosterone serum levels < 8 nmol/l (231 ng/dl), a need for therapy is given and probable; at total testosterone serum levels between these values (< 12 nmol/l and < 8 nmol/l), an indication for probationary therapy for 6-12 months with re-evaluation is given.
- Diseases that lead to increased SHBG synthesis condition, since testosterone is mostly present in serum bound to SHBG (sex hormone-binding hormone), that the free testosterone (biologically active fraction) decreases.
- Laboratory calculator: determination of free testosterone from total testosterone, albumin and SHGB.