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Mayo Test Catalog, (Sorted By Test Name) - Mayo Medical ...

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anti-androgen therapy An adjunct in the diagnosis of disorders of puberty An adjunct in the diagnosis and<br />

follow-up of anorexia nervosa An adjunct in the diagnosis of thyrotoxicosis (tissue marker of thyroid<br />

hormone excess) A possible adjunct in diagnosis and follow-up of insulin resistance and cardiovascular<br />

and type 2 diabetes risk assessment, particularly in women In laboratories without access to bioavailable<br />

testosterone or equilibrium dialysis-based "true" free testosterone assays, sex hormone-binding globulin<br />

measurement is crucial in cases when assessment of the free testosterone fraction (aka free androgen<br />

index or calculated free testosterone) is required. At <strong>Mayo</strong> <strong>Medical</strong> Laboratories, both bioavailable<br />

testosterone (TTBS/80065 <strong>Test</strong>osterone, Total and Bioavailable, Serum) and free testosterone<br />

(TGRP/8508 <strong>Test</strong>osterone, Total and Free, Serum) measurements are available. Free testosterone<br />

(TGRP/8508) is measured by equilibrium dialysis, obviating the need for sex hormone-binding globulin<br />

measurements to calculate free androgen fractions.<br />

Interpretation: Many conditions of mild-to-moderate androgen excess in women, particularly<br />

polycystic ovarian syndrome, are associated with low sex hormone-binding globulin (SHBG) levels.<br />

Most of these women are also insulin resistant and many are obese. A defect in SHBG production could<br />

lead to bioavailable androgen excess, in turn causing insulin resistance that depresses SHBG levels<br />

further. There are rare cases of SHBG mutations that clearly follow this pattern. SHBG levels are<br />

typically very low in these individuals. However, in most patients, SHBG levels are mildly depressed or<br />

even within the lower part of the normal range. In these patients, the primary problem may be androgen<br />

overproduction, insulin resistance, or both. A definitive cause cannot be usually established. Any<br />

therapy that either increases SHBG levels (eg, estrogens or weight loss), reduces bioactivity of<br />

androgens (eg, androgen receptor antagonists, alpha-reductase inhibitors), or reduces insulin resistance<br />

(eg, weight loss, metformin, peroxisome proliferator-activated receptor [PPAR] gamma agonists), can<br />

be effective. Improvement is usually associated with a rise in SHBG levels, but bioavailable or free<br />

testosterone levels should also be monitored. The primary method of monitoring sex-steroid or<br />

antiandrogen therapy is direct measurement of the relevant sex-steroids and gonadotropins. However,<br />

for many synthetic androgens and estrogens (eg, ethinyl-estradiol) clinical assays are not available. In<br />

those instances, rises in SHBG levels indicate successful anti-androgen or estrogen therapy, while falls<br />

indicate successful androgen treatment. Adult SHBG levels in boys with signs of precocious puberty<br />

support that the condition is testosterone driven, rather than representing premature adrenarche. Patients<br />

with anorexia nervosa have high SHBG levels. With successful treatment, levels start to fall as<br />

nutritional status improves. Normalization of SHBG precedes, and may be predictive of, future<br />

normalization of reproductive function. Thyrotoxicosis increases SHBG levels. In situations when<br />

assessment of true functional thyroid status may be difficult (eg, patients receiving amiodarone<br />

treatment, individuals with thyroid hormone transport-protein abnormalities, patients with suspected<br />

thyroid hormone resistance or suspected inappropriate thyroid-stimulating hormone (TSH) secretion<br />

such as a TSH-secreting pituitary adenoma), an elevated SHBG level suggests tissue thyrotoxicosis,<br />

while a normal level indicates euthyroidism or near-euthyroidism. In patients with gradual worsening of<br />

thyrotoxicosis (eg, toxic nodular goiter), serial SHBG measurement, in addition to clinical assessment,<br />

thyroid hormone, and TSH measurement, may assist in the timing of treatment decisions. Similarly,<br />

SHBG measurement may be of value in fine-tuning suppressive TSH therapy for patients with nodular<br />

thyroid disease or treated thyroid cancer. Results are not definitive in the short-term in patients<br />

receiving drugs that displace total thyroxine (T4) from albumin. SHBG is also produced by placental<br />

tissue and therefore values will be elevated during pregnancy. Reference ranges for pregnant females<br />

have not been established in our institution. In patients with known insulin resistance, "metabolic<br />

syndrome," or high risk of type 2 diabetes (eg, women with a history of gestational diabetes), low<br />

SHBG levels may predict progressive insulin resistance, cardiovascular complications, and progression<br />

to type 2 diabetes. An increase in SHBG levels may indicate successful therapeutic intervention. A<br />

genetic variant of SHBG (Asp327->Asn) introduces an additional glycosylation site in 10% to 20% of<br />

the population, resulting in significantly slower degradation. These individuals tend to have higher<br />

SHBG levels for any given level of other factors influencing SHBG.<br />

Reference Values:<br />

Tanner Stages* Mean Age Reference Range (nmol/L)<br />

Stage I 7.1 31-167<br />

Stage II 11.5 49-179<br />

Current as of January 3, 2013 2:22 pm CST 800-533-1710 or 507-266-5700 or <strong>Mayo</strong><strong>Medical</strong>Laboratories.com Page 1595

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