| Test Name | Sex Hormone Binding Globulin |
|---|---|
| Used For | Diagnosis and follow-up of women with symptoms or signs of androgen excess (eg, polycystic ovarian syndrome and idiopathic hirsutism). An adjunct in monitoring sex-steroid and anti-androgen therapy. An adjunct in the diagnosis of disorders of puberty. An adjunct in the diagnosis and follow-up of anorexia nervosa. An adjunct in the diagnosis of thyrotoxicosis (tissue marker of thyroid hormone excess). A possible adjunct in diagnosis and follow-up of insulin resistance and cardiovascular and type 2 diabetes risk assessment, particularly in women |
| Method | |
| Aliases | SHBG, Sex Steroid Binding Protein (SBP), Testosterone-Oestradiol Binding Globulin |
| Specimen Type | Serum (Yellow) |
| Volume of sample | >0.25ml |
| Refrigerated stability | 7 days |
| Interfering substances | Haemolysis |
| Clinical Information | Sex hormone-binding globulin (SHBG) is synthesised in the liver. Metabolic clearance of SHBG is biphasic, with a fast initial distribution from vascular compartment into extracellular space (half-life of a few hours), followed by a slower degradation phase (half-life of several days). The main function of SHBG is sex-steroid transport within the blood stream and to extravascular target tissues. SHBG also plays a key role in regulating bioavailable sex-steroid concentrations through competition of sex steroids for available binding sites and fluctuations in SHBG concentrations. Because of the higher affinity of SHBG for dihydrotestosterone and testosterone, compared to oestradiol / oestrone, SHBG also has profound effects on the balance between bioavailable androgens and oestrogens. Increased SHBG levels may be associated with symptoms and signs of hypogonadism in men, while decreased levels can result in androgenisation in women. |
| Interpretation | Many conditions of mild-to-moderate androgen excess in women, particularly polycystic ovarian syndrome, are associated with low sex hormone-binding globulin (SHBG) levels. Most of these women are also insulin resistant and many are obese. A defect in SHBG production could lead to bioavailable androgen excess, in turn causing insulin resistance that depresses SHBG levels further. There are rare cases of SHBG mutations that clearly follow this pattern. SHBG levels are typically very low in these individuals. However, in most patients, SHBG levels are mildly depressed or even within the lower part of the normal range. In these patients, the primary problem may be androgen overproduction, insulin resistance, or both. A definitive cause cannot be usually established. Any therapy that either increases SHBG levels (eg, oestrogens or weight loss), reduces bioactivity of androgens (eg, androgen receptor antagonists, alpha-reductase inhibitors), or reduces insulin resistance (eg, weight loss, metformin, peroxisome proliferator-activated receptor [PPAR] gamma agonists), can be effective. Improvement is usually associated with a rise in SHBG levels, but bioavailable or free testosterone levels should also be monitored. |
| Turnaround | 1h |
| Retention Time | 7 days |
| References | Mayo Clinic Laboratories |
| Lab Tests On Line |
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