Hirsutism laboratory findings: Difference between revisions
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==Laboratory Findings== | ==Laboratory Findings== | ||
* Testosterone: The most important assay is the level of serum testosterone, | * [[Testosterone]]: The most important assay is the level of serum [[testosterone]],. If the total serum testosterone level is normal, measure the free serum level because [[hyperandrogenism]] (and [[insulin resistance]], if present) decreases sex steroid-binding globulin, such that the unbound, biologically active [[testosterone]] moiety may be elevated even if the total level is unremarkable. Extremely high testosterone levels are likely to be associated with [[Adrenal gland|adrenal]] or [[Ovarian tumor|ovarian tumors]], whereas [[idiopathic]] and [[benign]] etiologies result in very mild elevations. Indeed, in idiopathic hirsutism, the results from testing androgen levels are often normal. In some of these women, hirsutism is thought to be caused by increased skin sensitivity to androgen or by increased skin [[5-alpha-reductase]] activity. | ||
* Dehydroepiandrosterone sulfate (DHEAS): An elevated testosterone level does not indicate the gland of origin. Accordingly, measurement of elevated plasma levels of DHEAS, an androgen synthesized almost exclusively by the adrenal cortex, can indicate excess adrenal function. Elevations in both testosterone and DHEAS suggest an adrenal origin, whereas an isolated testosterone elevation indicates an ovarian source. | * [[Dehydroepiandrosterone sulfate]] (DHEAS): An elevated testosterone level does not indicate the gland of origin. Accordingly, measurement of elevated plasma levels of [[DHEAS]], an androgen synthesized almost exclusively by the [[adrenal cortex]], can indicate excess adrenal function. Elevations in both testosterone and DHEAS suggest an adrenal origin, whereas an isolated testosterone elevation indicates an [[ovarian]] source. | ||
* Dexamethasone suppression: Dexamethasone-mediated suppression of androgens is observed in healthy women who do not have hirsutism and in those with congenital adrenal hyperplasia (CAH) and idiopathic hirsutism. | * [[Dexamethasone suppression test|Dexamethasone suppression]]: [[Dexamethasone]]-mediated suppression of androgens is observed in healthy women who do not have hirsutism and in those with [[Congenital adrenal hyperplasia|congenital adrenal hyperplasia (CAH)]] and idiopathic hirsutism. | ||
* Adrenocorticotropin stimulation: An ACTH-stimulation test (250 mcg for 30 min) can help differentiate between CAH and idiopathic hirsutism because CAH produces abnormal findings (elevations in metabolic precursors of cortisol). | * [[Adrenocorticotropic hormone|Adrenocorticotropin]] stimulation: An [[Adrenocorticotropic hormone|ACTH]]-stimulation test (250 mcg for 30 min) can help differentiate between [[Congenital adrenal hyperplasia|CAH]] and idiopathic hirsutism because CAH produces abnormal findings (elevations in metabolic [[precursors]] of [[cortisol]]). | ||
** Hirsutism caused by CAH is due to 1 of 3 cortisol biosynthetic defects, ie, 21-hydroxylase deficiency, 3 3 β -hydroxysteroid dehydrogenase, or 11-β -hydroxylase deficiency. | ** Hirsutism caused by [[CAH]] is due to 1 of 3 cortisol biosynthetic defects, ie, [[21-hydroxylase deficiency]], 3 3 β -hydroxysteroid dehydrogenase, or 11-β -hydroxylase deficiency. | ||
** 17-hydroxyprogesterone levels should be also obtained because 21-hydroxylase deficiency is responsible for the majority of cases of CAH (approximately 90%) and 17-hydroxyprogesterone values of less than 7 nmol/L exclude the diagnosis, and values of greater than 45 nmol/L (in women who are nongestational) confirm 21-hydroxylase deficiency. When basal values of 17-hydroxyprogesterone are between 7 and 45 nmol/L, an ACTH-stimulated concentration of greater than 45 nmol/L is also diagnostic. | ** [[17-Hydroxyprogesterone|17-hydroxyprogesterone]] levels should be also obtained because [[21-hydroxylase deficiency]] is responsible for the majority of cases of [[CAH]] (approximately 90%) and [[17-Hydroxyprogesterone|17-hydroxyprogesterone]] values of less than 7 nmol/L exclude the diagnosis, and values of greater than 45 nmol/L (in women who are nongestational) confirm [[21-hydroxylase deficiency]]. When basal values of [[17-Hydroxyprogesterone|17-hydroxyprogesterone]] are between 7 and 45 nmol/L, an [[ACTH]]-stimulated concentration of greater than 45 nmol/L is also diagnostic. | ||
* Cortisol suppression: PCOS and adrenal and ovarian tumors are associated with normal suppression of cortisol by dexamethasone, whereas cortisol levels in patients with Cushing syndrome are not suppressed. | * [[Cortisol]] suppression: PCOS and adrenal and ovarian tumors are associated with normal suppression of cortisol by [[dexamethasone]], whereas cortisol levels in patients with [[Cushing's syndrome|Cushing syndrome]] are not suppressed. | ||
* Serum prolactin or FSH: Women with hirsutism and amenorrhea of unknown cause should have a serum prolactin or FSH test to evaluate for either a prolactinoma or ovarian failure. | * Serum [[prolactin]] or [[FSH]]: Women with hirsutism and [[amenorrhea]] of unknown cause should have a serum [[prolactin]] or [[FSH]] test to evaluate for either a [[prolactinoma]] or [[ovarian failure]]. | ||
* Diabetes screening: Women with hirsutism, PCOS, obesity, or acanthosis nigricans may have insulin resistance, and screening for diabetes and hyperlipidemia is recommended. | * [[Diabetes]] screening: Women with hirsutism, [[PCOS]], [[obesity]], or [[acanthosis nigricans]] may have [[insulin resistance]], and screening for diabetes and [[hyperlipidemia]] is recommended. | ||
* Prostate-specific antigen (PSA): Ultrasensitive assays can detect PSA in women and is a potential marker for androgen excess. Studies thus far, however, have not shown a good correlation with the change in androgen levels after treatment | * [[Prostate specific antigen|Prostate-specific antigen]] ([[Prostate specific antigen|PSA]]): Ultrasensitive assays can detect PSA in women and is a potential marker for androgen excess. Studies thus far, however, have not shown a good correlation with the change in androgen levels after treatment. <sup>[[null 11]]</sup><ref name="urlHirsutism Workup: Laboratory Studies, Imaging Studies">{{cite web |url=http://emedicine.medscape.com/article/121038-workup |title=Hirsutism Workup: Laboratory Studies, Imaging Studies |format= |work= |accessdate=}}</ref> | ||
==References== | ==References== | ||
Revision as of 20:57, 14 September 2017
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Overview
Laboratory Findings
- Testosterone: The most important assay is the level of serum testosterone,. If the total serum testosterone level is normal, measure the free serum level because hyperandrogenism (and insulin resistance, if present) decreases sex steroid-binding globulin, such that the unbound, biologically active testosterone moiety may be elevated even if the total level is unremarkable. Extremely high testosterone levels are likely to be associated with adrenal or ovarian tumors, whereas idiopathic and benign etiologies result in very mild elevations. Indeed, in idiopathic hirsutism, the results from testing androgen levels are often normal. In some of these women, hirsutism is thought to be caused by increased skin sensitivity to androgen or by increased skin 5-alpha-reductase activity.
- Dehydroepiandrosterone sulfate (DHEAS): An elevated testosterone level does not indicate the gland of origin. Accordingly, measurement of elevated plasma levels of DHEAS, an androgen synthesized almost exclusively by the adrenal cortex, can indicate excess adrenal function. Elevations in both testosterone and DHEAS suggest an adrenal origin, whereas an isolated testosterone elevation indicates an ovarian source.
- Dexamethasone suppression: Dexamethasone-mediated suppression of androgens is observed in healthy women who do not have hirsutism and in those with congenital adrenal hyperplasia (CAH) and idiopathic hirsutism.
- Adrenocorticotropin stimulation: An ACTH-stimulation test (250 mcg for 30 min) can help differentiate between CAH and idiopathic hirsutism because CAH produces abnormal findings (elevations in metabolic precursors of cortisol).
- Hirsutism caused by CAH is due to 1 of 3 cortisol biosynthetic defects, ie, 21-hydroxylase deficiency, 3 3 β -hydroxysteroid dehydrogenase, or 11-β -hydroxylase deficiency.
- 17-hydroxyprogesterone levels should be also obtained because 21-hydroxylase deficiency is responsible for the majority of cases of CAH (approximately 90%) and 17-hydroxyprogesterone values of less than 7 nmol/L exclude the diagnosis, and values of greater than 45 nmol/L (in women who are nongestational) confirm 21-hydroxylase deficiency. When basal values of 17-hydroxyprogesterone are between 7 and 45 nmol/L, an ACTH-stimulated concentration of greater than 45 nmol/L is also diagnostic.
- Cortisol suppression: PCOS and adrenal and ovarian tumors are associated with normal suppression of cortisol by dexamethasone, whereas cortisol levels in patients with Cushing syndrome are not suppressed.
- Serum prolactin or FSH: Women with hirsutism and amenorrhea of unknown cause should have a serum prolactin or FSH test to evaluate for either a prolactinoma or ovarian failure.
- Diabetes screening: Women with hirsutism, PCOS, obesity, or acanthosis nigricans may have insulin resistance, and screening for diabetes and hyperlipidemia is recommended.
- Prostate-specific antigen (PSA): Ultrasensitive assays can detect PSA in women and is a potential marker for androgen excess. Studies thus far, however, have not shown a good correlation with the change in androgen levels after treatment. null 11[1]