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			{{About|DHEA sulfate as a hormone|its use as a medication|Prasterone sulfate}}
	{{chembox
			{{Chembox
	| verifiedrevid = 424662531
			| Verifiedfields = changed
	|ImageFile=DHEA sulfate.png
			| Watchedfields = changed
	|ImageSize=200px
			| verifiedrevid = 449062634
	|ImageFile2=Sulfato de dehidroepiandrosterona3D.png
			| ImageFile=DHEA sulfate.png
	|ImageSize2=200px
			| ImageSize=250
	|IUPACName=phenanthren-3-yl] hydrogen sulfate
			| ImageFile2=Sulfato de dehidroepiandrosterona3D.png
	|OtherNames=Prasterone sulfate
			| ImageSize2=250
	|Section1= {{Chembox Identifiers
			| IUPACName=17-Oxoandrost-5-en-3β-yl hydrogen sulfate
	| Abbreviations = DHEAS
			| SystematicName=(3a''S'',3b''R'',7''S'',9a''R'',9b''S'',11a''S'')-9a,11a-Dimethyl-1-oxo-2,3,3a,3b,4,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1''H''-cyclopentaphenanthren-7-yl hydrogen sulfate
	| CASNo=651-48-9
			| OtherNames=Androstenolone sulfate; Prasterone sulfate; Androst-5-en-3β-ol-17-one 3β-sulfate
	| PubChem=12594
			|Section1={{Chembox Identifiers
	| SMILES=C12CC3(1CCC2=O) CC=C43(CC(C4)OS(=O)(=O)O)C
			| Abbreviations = DHEA sulfate; DHEA-S; DHEAS
			| CASNo_Ref = {{cascite|correct|??}}
			| CASNo=651-48-9
			| UNII_Ref = {{fdacite|correct|FDA}}
			| UNII = 57B09Q7FJR
			| PubChem=12594
			| SMILES=C12CC3(1CCC2=O)CC=C43(CC(C4)OS(=O)(=O)O)C
			| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}}
			| ChemSpiderID = 12074
			| InChI = 1/C19H28O5S/c1-18-9-7-13(24-25(21,22)23)11-12(18)3-4-14-15-5-6-17(20)19(15,2)10-8-16(14)18/h3,13-16H,4-11H2,1-2H3,(H,21,22,23)/t13-,14-,15-,16-,18-,19-/m0/s1
			| InChIKey = CZWCKYRVOZZJNM-USOAJAOKBK
			| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
			| StdInChI = 1S/C19H28O5S/c1-18-9-7-13(24-25(21,22)23)11-12(18)3-4-14-15-5-6-17(20)19(15,2)10-8-16(14)18/h3,13-16H,4-11H2,1-2H3,(H,21,22,23)/t13-,14-,15-,16-,18-,19-/m0/s1
			| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
			| StdInChIKey = CZWCKYRVOZZJNM-USOAJAOKSA-N
	}}		}}
	|Section2= {{Chembox Properties		|Section2={{Chembox Properties
	| Formula=C<sub>19</sub>H<sub>28</sub>O<sub>5</sub>S		| Formula=C<sub>19</sub>H<sub>28</sub>O<sub>5</sub>S
	| MolarMass=368.49 g/mol		| MolarMass=368.49 g/mol
	| Appearance=		| Appearance=
	| Density=		| Density=
	| MeltingPt=		| MeltingPt=
	| BoilingPt=		| BoilingPt=
	| Solubility=		| Solubility=
	}}		}}
	|Section3= {{Chembox Hazards		|Section3={{Chembox Hazards
	| MainHazards=		| MainHazards=
	| FlashPt=		| FlashPt=
			| AutoignitionPt =
	| Autoignition=
	}}		}}
	}}		}}
	'''Dehydroepiandrosterone sulfate''' or '''DHEA sulfate''' is a ] of ] (DHEA) produced by the addition of a sulfate group, ] by the ] ]s ] and ], which also produce ] from ]. DHEA sulfate can also be back-converted to DHEA through the action of ].		'''Dehydroepiandrosterone sulfate''', abbreviated as '''DHEA sulfate''' or '''DHEA-S''', also known as '''androstenolone sulfate''', is an ] ] ] that is produced by the ].<ref name="Erkkola2006" /> It is the 3β-] ] and a ] of ] (DHEA) and circulates in far greater relative concentrations than DHEA.<ref name="pmid26908835" /> The steroid is ]ly inert and is instead an important ] and ].<ref name="pmid26908835" />
			{{TOC limit|3}}
			==Biological activity==
	In the ] layer of the ], DHEA-sulfate is generated by ].<ref name="pmid17945481">{{cite journal | author = Rainey WE, Nakamura Y | title = Regulation of the adrenal androgen biosynthesis | journal = J. Steroid Biochem. Mol. Biol. | volume = 108 | issue = 3-5 | pages = 281–6 | year = 2008 | month = February | pmid = 17945481 | doi = 10.1016/j.jsbmb.2007.09.015 | pmc = 2699571}}</ref> This layer of the adrenal cortex is thought to be the primary source of serum DHEA-sulfate. DHEA sulfate levels decline as a person ages as the reticularis layer diminishes in size.
			===Neurosteroid activity===
	==See also==
			Similarly to other ] steroids, DHEA-S is devoid of ] activity, lacking ] for the ]s.<ref name="Krause2008" /><ref name="pmid16524719">{{cite journal | vauthors = Mo Q, Lu SF, Simon NG | title = Dehydroepiandrosterone and its metabolites: differential effects on androgen receptor trafficking and transcriptional activity | journal = J. Steroid Biochem. Mol. Biol. | volume = 99 | issue = 1 | pages = 50–8 | year = 2006 | pmid = 16524719 | doi = 10.1016/j.jsbmb.2005.11.011 | s2cid = 30489004 }}</ref> However, DHEA-S retains activity as a ] and ].<ref name="pmid26908835">{{cite journal | vauthors = Prough RA, Clark BJ, Klinge CM | title = Novel mechanisms for DHEA action | journal = J. Mol. Endocrinol. | volume = 56 | issue = 3 | pages = R139–55 | year = 2016 | pmid = 26908835 | doi = 10.1530/JME-16-0013 | doi-access = free }}</ref> It has been found to act as a ] of the ] (50&nbsp;nM–1&nbsp;μM), ] of the ] and ]s, and weak ] of the ] (K<sub>d</sub> > 50&nbsp;μM).<ref name="pmid26908835" /><ref name="King2012">{{cite book|author=Steven R. King|title=Neurosteroids and the Nervous System|url=https://books.google.com/books?id=D1fOTC6CP3kC&pg=PA1|date=9 November 2012|publisher=Springer Science & Business Media|isbn=978-1-4614-5559-2|pages=1, 12}}</ref> In addition, DHEA-S has been found to directly bind to and activate the ] and ] – receptors of neurotrophins like ] (NGF) and ] (BDNF) – with high affinity (around 5&nbsp;nM).<ref name="pmid26908835" /><ref name="pmid21541365">{{cite journal | vauthors = Lazaridis I, Charalampopoulos I, Alexaki VI, Avlonitis N, Pediaditakis I, Efstathopoulos P, Calogeropoulou T, Castanas E, Gravanis A | title = Neurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosis | journal = PLOS Biol. | volume = 9 | issue = 4 | pages = e1001051 | year = 2011 | pmid = 21541365 | pmc = 3082517 | doi = 10.1371/journal.pbio.1001051 | doi-access = free }}</ref><ref name="pmid25330101">{{cite journal | vauthors = Pediaditakis I, Iliopoulos I, Theologidis I, Delivanoglou N, Margioris AN, Charalampopoulos I, Gravanis A | title = Dehydroepiandrosterone: an ancestral ligand of neurotrophin receptors | journal = Endocrinology | volume = 156 | issue = 1 | pages = 16–23 | year = 2015 | pmid = 25330101 | doi = 10.1210/en.2014-1596 | doi-access = free }}</ref><ref name="pmid23074265">{{cite journal | vauthors = Gravanis A, Calogeropoulou T, Panoutsakopoulou V, Thermos K, Neophytou C, Charalampopoulos I | title = Neurosteroids and microneurotrophins signal through NGF receptors to induce prosurvival signaling in neuronal cells | journal = Sci Signal | volume = 5 | issue = 246 | pages = pt8 | year = 2012 | pmid = 23074265 | doi = 10.1126/scisignal.2003387 | s2cid = 26914550 }}</ref>
	*]
			===Hormonal activity===
	==References==
			Although DHEA-S itself is hormonally inert, it has been thought that it can be converted back into DHEA,<ref name="Morfin2003">{{cite book|author=Robert Morfin|title=DHEA and the Brain|url=https://books.google.com/books?id=uZp62ctguF0C&pg=PA28|date=2 September 2003|publisher=CRC Press|isbn=978-0-203-30121-0|pages=28–}}</ref> which is weakly ]ic and ]ic, and that DHEA in turn can be transformed into more potent androgens like ] and ] (DHT) as well as estrogens like ].<ref name="pmid26908835" /><ref name="Erkkola2006" /><ref name="FritzSperoff2012">{{cite book|author1=Marc A. Fritz|author2=Leon Speroff|title=Clinical Gynecologic Endocrinology and Infertility|url=https://books.google.com/books?id=KZLubBxJEwEC&pg=PA545|date=28 March 2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-4511-4847-3|pages=545–}}</ref> As such, it has been thought that DHEA-S is a ] with the potential for androgenic and estrogenic effects.<ref name="pmid26908835" /><ref name="Erkkola2006" /><ref name="FritzSperoff2012" /> However, a 2005 study found that DHEA could be converted into DHEA-S but found no evidence of conversion of DHEA-S into DHEA.<ref name="pmid15755854">{{cite journal | vauthors = Hammer F, Subtil S, Lux P, Maser-Gluth C, Stewart PM, Allolio B, Arlt W | title = No evidence for hepatic conversion of dehydroepiandrosterone (DHEA) sulfate to DHEA: in vivo and in vitro studies | journal = J. Clin. Endocrinol. Metab. | volume = 90 | issue = 6 | pages = 3600–5 | year = 2005 | pmid = 15755854 | doi = 10.1210/jc.2004-2386 | doi-access = }}</ref>
	<references/>
			===Other activity===
	]
			DHEA-S has also been found to inhibit the ] and ] ]s and to inhibit the ].<ref name="King2012" />
	]
	]
			==Biochemistry==
			], showing DHEA, the precursor of DHEA-S, at left among the androgens.<ref name="HäggströmRichfield2014">{{cite journal|last1=Häggström|first1=Mikael|last2=Richfield|first2=David|title=Diagram of the pathways of human steroidogenesis|journal=WikiJournal of Medicine|volume=1|issue=1|year=2014|issn=2002-4436|doi=10.15347/wjm/2014.005|doi-access=free}}</ref>]]
			===Biosynthesis===
	{{biochem-stub}}
			DHEA and DHEA-S are produced in the ] of the ] under the control of ] (ACTH).<ref name="Erkkola2006">{{cite book|author=Risto Erkkola|title=The Menopause|url=https://books.google.com/books?id=1AU_NI__fpUC&pg=PA5|year=2006|publisher=Elsevier|isbn=978-0-444-51830-9|pages=5–}}</ref> DHEA is synthesized from ] via the ]s ] (CYP11A1; P450scc) and ] (CYP17A1), with ] and ] as ]s.<ref name="pmid17945481">{{cite journal |vauthors=Rainey WE, Nakamura Y | title = Regulation of the adrenal androgen biosynthesis | journal = J. Steroid Biochem. Mol. Biol. | volume = 108 | issue = 3–5 | pages = 281–86 |date=February 2008 | pmid = 17945481 | doi = 10.1016/j.jsbmb.2007.09.015 | pmc = 2699571}}</ref> Then, DHEA-S is formed by ] of DHEA at the C3β position via the ] ]s ] and to a lesser extent ].<ref name="pmid17945481" /><ref name="pmid26213785">{{cite journal | vauthors = Mueller JW, Gilligan LC, Idkowiak J, Arlt W, Foster PA | title = The Regulation of Steroid Action by Sulfation and Desulfation | journal = Endocr. Rev. | volume = 36 | issue = 5 | pages = 526–63 | year = 2015 | pmid = 26213785 | pmc = 4591525 | doi = 10.1210/er.2015-1036 }}</ref><ref name="Lash2005">{{cite book|author=Lawrence H Lash|title=Drug Metabolism and Transport: Molecular Methods and Mechanisms|url=https://books.google.com/books?id=-sK8NM_9UVsC&pg=PA353|year=2005|publisher=Springer Science & Business Media|isbn=978-1-59259-832-8|pages=353–}}</ref> Whereas DHEA is derived mostly from the adrenal cortex but is also secreted to a lesser extent by the ]s (10%),<ref name="SchillComhaire2006">{{cite book|author1=Wolf-Bernhard Schill|author2=Frank H. Comhaire|author3=Timothy B. Hargreave|title=Andrology for the Clinician|url=https://books.google.com/books?id=5Ts_AAAAQBAJ&pg=PA243|date=26 August 2006|publisher=Springer Science & Business Media|isbn=978-3-540-33713-3|pages=243–}}</ref> DHEA-S is almost exclusively produced and secreted by the adrenal cortex, with 95 to 100% originating from the adrenal cortex in women.<ref name="Erkkola2006" /><ref name="LentzLobo2012">{{cite book|author1=Gretchen M. Lentz |author2= Rogerio A. Lobo |author3= David M. Gershenson |author4= Vern L. Katz |title= Comprehensive Gynecology|url=https://books.google.com/books?id=OmpULog7A_QC&pg=PA850|year=2012|publisher=Elsevier Health Sciences|isbn=978-0-323-06986-1|pages=850–}}</ref><ref name="LinosHeerden2005">{{cite book|author1=Dimitrios A. Linos|author2=Jon A. van Heerden|title=Adrenal Glands: Diagnostic Aspects and Surgical Therapy|url=https://books.google.com/books?id=r8OLj1LLw3IC&pg=PA161|date=5 December 2005|publisher=Springer Science & Business Media|isbn=978-3-540-26861-1|pages=161–}}</ref> Approximately 10 to 15&nbsp;mg of DHEA-S is secreted by the adrenal cortex per day in young adults.<ref name="RookLightman2012">{{cite book|author1=G.A.W. Rook|author2=S. Lightman|title=Steroid Hormones and the T-Cell Cytokine Profile|url=https://books.google.com/books?id=JG_rBwAAQBAJ&pg=PA205|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-1-4471-0931-0|pages=205–}}</ref>
	{{Cholesterol and steroid intermediates}}
			===Distribution===
			Unlike DHEA, which is weakly bound to ], DHEA-S is strongly bound to albumin (i.e., with very high affinity), and this is the reason for its much longer comparative ].<ref name="Becker2001">{{cite book|author=Kenneth L. Becker|title=Principles and Practice of Endocrinology and Metabolism|url=https://books.google.com/books?id=FVfzRvaucq8C&pg=PA712|year=2001|publisher=Lippincott Williams & Wilkins|isbn=978-0-7817-1750-2|pages=712–}}</ref><ref name="WhitePorterfield2013">{{cite book|author1=Bruce Alan White|author2=Susan P. Porterfield|title=Endocrine and Reproductive Physiology, Mosby Physiology Monograph Series (with Student Consult Online Access),4: Endocrine and Reproductive Physiology|url=https://books.google.com/books?id=zMb4uoiXzzcC&pg=PA164|year=2013|publisher=Elsevier Health Sciences|isbn=978-0-323-08704-9|pages=164–}}</ref> In contrast to DHEA, DHEA-S is not bound to any extent to ] (SHBG).<ref name="CoatesPaul2004">{{cite book|author1=Paul M. Coates|author2=M. Coates Paul|author3=Marc Blackman |author4= Marc R. Blackman, Gordon M. Cragg, Mark Levine, Jeffrey D. White, Joel Moss, Mark A. Levine|title=Encyclopedia of Dietary Supplements (Print)|url=https://books.google.com/books?id=Sfmc-fRCj10C&pg=PA170|date=29 December 2004|publisher=CRC Press|isbn=978-0-8247-5504-1|pages=170–}}</ref>
			Whereas DHEA easily crosses the ] into the ],<ref name="Pizzorno2013">{{cite book|author=Joseph E. Pizzorno|title=Textbook of Natural Medicine|url=https://books.google.com/books?id=6cjgo1IixvEC&pg=PA711|year=2013|publisher=Elsevier Health Sciences|isbn=978-1-4377-2333-5|pages=711–}}</ref> DHEA-S poorly crosses the blood–brain barrier.<ref name="YenJaffe1999">{{cite book|author1=Samuel S. C. Yen|author2=Robert B. Jaffe|author3=Robert L. Barbieri|title=Reproductive Endocrinology: Physiology, Pathophysiology, and Clinical Management|url=https://archive.org/details/reproductiveendo00yens|url-access=registration|date=January 1999|publisher=Saunders|isbn=978-0-7216-6897-0|page=|quote=Thus, the formation of DHEA-S occurs directly in the brain, particularly because DHEA-S does not cross the blood-brain barrier }}</ref>
			===Metabolism===
			DHEA-S can be converted back into DHEA via ] (STS).<ref name="Morfin2003" /> In ] women, 40 to 75% of circulating testosterone is derived from peripheral ] of DHEA-S, and in ] women, over 90% of estrogens, mainly ], are derived from peripheral metabolism of DHEA-S.<ref name="pmid26908835" /> A study found that administration of exogenous DHEA-S in women who were pregnant increased circulating levels of estrone and ].<ref name="pmid18493132">{{cite journal | vauthors = Nguyen AD, Conley AJ | title = Adrenal androgens in humans and nonhuman primates: production, zonation and regulation | journal = Endocr Dev | volume = 13 | pages = 33–54 | date = 2008 | pmid = 18493132 | doi = 10.1159/000134765 | series = Endocrine Development | isbn = 978-3-8055-8580-4 }}</ref> DHEA-S serves as a ] for potent androgens like testosterone and dihydrotestosterone in ], which fuel the growth of this cancer.<ref name="pmid30029732">{{cite journal | vauthors = Penning TM | title = Dehydroepiandrosterone (DHEA)-SO4 Depot and Castration-Resistant Prostate Cancer | journal = Vitam. Horm. | volume = 108 | pages = 309–331 | date = 2018 | pmid = 30029732 | pmc = 6226251 | doi = 10.1016/bs.vh.2018.01.007 | series = Vitamins and Hormones | isbn = 9780128143612 }}</ref>
			The elimination half-life of DHEA-S is 7 to 10&nbsp;hours, which is far longer than that of DHEA, which has an elimination half-life of only 15 to 30&nbsp;minutes.<ref name="WhitePorterfield2013" />
			===Elimination===
			DHEA-S is ] in the ] via the ]s.<ref name="NusseyWhitehead2013">{{cite book|author1=S.S. Nussey|author2=S.A. Whitehead|title=Endocrinology: An Integrated Approach|url=https://books.google.com/books?id=pjZvmnZpKXsC&pg=PA158|date=8 April 2013|publisher=CRC Press|isbn=978-0-203-45043-7|pages=158–}}</ref>
			===Levels===
			]
			DHEA and DHEA-S are the most abundant circulating steroids in the body.<ref name="HarrisBouloux2014">{{cite book|author1=Philip E. Harris|author2=Pierre-Marc G. Bouloux|title=Endocrinology in Clinical Practice, Second Edition|url=https://books.google.com/books?id=jaPSBQAAQBAJ&pg=PA521|date=24 March 2014|publisher=CRC Press|isbn=978-1-84184-952-2|pages=521–}}</ref> Plasma levels of DHEA-S are 100 or more times higher than those of DHEA, 5 to 10&nbsp;times higher than those of ], 100 to 500&nbsp;times those of testosterone, and 1,000 to 10,000&nbsp;times higher than those of estradiol.<ref name="Weizman2008">{{cite book|author=Abraham Weizman|title=Neuroactive Steroids in Brain Function, Behavior and Neuropsychiatric Disorders: Novel Strategies for Research and Treatment|url=https://books.google.com/books?id=uABKkFdPjhkC&pg=PA261|date=1 February 2008|publisher=Springer Science & Business Media|isbn=978-1-4020-6854-6|pages=261–}}</ref><ref name="Krause2008">{{cite book|author=Walter K.H. Krause|title=Cutaneous Manifestations of Endocrine Diseases|url=https://books.google.com/books?id=QymSmuV-fvUC&pg=PA79|date=30 November 2008|publisher=Springer Science & Business Media|isbn=978-3-540-88367-8|pages=79–|quote=Plasma DHEA-S levels in adult men and women are 100-500 times higher than those of testosterone and 1000-10000 times higher than those of estradiol.}}</ref>
			Levels of DHEA and DHEA-S vary throughout life.<ref name="pmid26908835" /><ref name="Erkkola2006" /> They remain low during childhood until ] around 6 to 8&nbsp;years of age, at which point they markedly increase,<ref name="CarrellPeterson2010">{{cite book|author1=Douglas T. Carrell|author2=C. Matthew Peterson|title=Reproductive Endocrinology and Infertility: Integrating Modern Clinical and Laboratory Practice|url=https://books.google.com/books?id=lcBEheiufVcC&pg=PA158|date=23 March 2010|publisher=Springer Science & Business Media|isbn=978-1-4419-1436-1|pages=158–}}</ref> eventually peaking at around 20 to 30&nbsp;years of age.<ref name="pmid26908835" /><ref name="Erkkola2006" /> From the third decade of life on, DHEA and DHEA-S levels gradually decrease.<ref name="HarrisBouloux2014" /> By the age of 70, levels of DHEA and DHEA-S are 80 to 85% lower than those of young adults, and in people more than 80&nbsp;years of age, DHEA and DHEA-S levels can reach 80 to 90% lower than those of younger individuals.<ref name="HarrisBouloux2014" />
			DHEA-S levels are higher in men than in women.<ref name="pmid26908835" /><ref name="HarrisBouloux2014" />
			====Reference ranges====
			{|class="wikitable"
			|+]s for DHEA-S in females<ref name=mayo> {{Webarchive|url=https://web.archive.org/web/20180314080932/https://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/8493 |date=2018-03-14 }} at Mayo Foundation For Medical Education And Research. Retrieved July 2012</ref>
			|-
			!colspan=2| ] and average age !! Lower limit !! Upper limit !! Unit
			|-
			! Tanner stage I
			| >14 days || 16 || 96 ||rowspan=10| ]/dL
			|-
			! Tanner stage II
			| 10.5 years || 22 || 184
			|-
			! Tanner stage III
			| 11.6 years || <15 || 296
			|-
			! Tanner stage IV
			| 12.3 years || 17 || 343
			|-
			! Tanner stage V
			| 14.5 years || 44 || 332
			|-
			!colspan=2| 18–29 years
			| 44 || 332
			|-
			!colspan=2| 30–39 years
			| 31 ||228
			|-
			!colspan=2| 40–49 years
			| 18 || 244
			|-
			!colspan=2| 50–59 years
			| <15 || 200
			|-
			!colspan=2| > or =60 years
			| <15 || 157
			|}
			{|class="wikitable"
			|+]s for DHEA-S in males<ref name=mayo/>
			|-
			!colspan=2| ] and average age !! Lower limit !! Upper limit !! Unit
			|-
			! Tanner stage I
			| >14 days || <15 || 120 ||rowspan=10| ]/dL
			|-
			! Tanner stage II
			| 11.5 years || <15 || 333
			|-
			! Tanner stage III
			| 13.6 years || <15 || 312
			|-
			! Tanner stage IV
			| 15.1 years || 29 || 412
			|-
			! Tanner stage V
			| 18.0 years || 89 || 457
			|-
			!colspan=2| 18–29 years
			| 89 || 457
			|-
			!colspan=2| 30–39 years
			| 65 || 334
			|-
			!colspan=2| 40–49 years
			| 48 || 244
			|-
			!colspan=2| 50–59 years
			| 35 || 179
			|-
			!colspan=2| > or =60 years
			| 25 || 131
			|}
			==Medical use==
			===Deficiency===
			The ] recommends against the therapeutic use of DHEA-S in both healthy women and those with ], as its role is not clear from studies performed so far.<ref name=Wierman>{{cite journal|last1=Wierman|first1=Margaret E.|last2=Arlt|first2=Wiebke|last3=Basson|first3=Rosemary|last4=Davis|first4=Susan R.|last5=Miller|first5=Karen K.|last6=Murad|first6=Mohammad H.|last7=Rosner|first7=William|last8=Santoro|first8=Nanette|title=Androgen Therapy in Women: A Reappraisal: An Endocrine Society Clinical Practice Guideline|journal=The Journal of Clinical Endocrinology & Metabolism|volume=99|issue=10|pages=3489–510|doi=10.1210/jc.2014-2260|pmid=25279570|year=2014|doi-access=free}}</ref> The routine use of DHEA-S and other androgens is discouraged in the treatment of women with low androgen levels due to ], ], menopause due to ovarian surgery, ] use, or other conditions associated with low androgen levels; this is because there are limited data supporting improvement in signs and symptoms with therapy and no long-term studies of risk.<ref name=Wierman/>
			In otherwise elderly women, in whom an age-related fall of DHEA-S may be associated with menopausal symptoms and reduced libido, DHEA-S supplementation cannot currently be said to improve outcomes.<ref>{{cite journal|last1=Elraiyah|first1=Tarig|last2=Sonbol|first2=Mohamad Bassam|last3=Wang|first3=Zhen|last4=Khairalseed|first4=Tagwa|last5=Asi|first5=Noor|last6=Undavalli|first6=Chaitanya|last7=Nabhan|first7=Mohammad|last8=Altayar|first8=Osama|last9=Prokop|first9=Larry|last10=Montori|first10=Victor M.|last11=Murad|first11=Mohammad Hassan|title=The Benefits and Harms of Systemic Dehydroepiandrosterone (DHEA) in Postmenopausal Women With Normal Adrenal Function: A Systematic Review and Meta-analysis|journal=The Journal of Clinical Endocrinology & Metabolism|volume=99|issue=10|pages=3536–42|doi=10.1210/jc.2014-2261|pmid=25279571|year=2014|pmc=5393492}}</ref>
			===Childbirth===
			{{Main|Prasterone sulfate}}
			As the ], ], DHEA-S is used as a ] in ] in the treatment of insufficient ] and ] during ].<ref name="Elks2014">{{cite book|author=J. Elks|title=The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies|url=https://books.google.com/books?id=0vXTBwAAQBAJ&pg=PA641|date=14 November 2014|publisher=Springer|isbn=978-1-4757-2085-3|pages=641–}}</ref><ref name="BluntMunro2007">{{cite book|author1=John W. Blunt|author2=Murray H. G. Munro|title=Dictionary of Marine Natural Products with CD-ROM|url=https://books.google.com/books?id=w1bLBQAAQBAJ&pg=PA1075|date=19 September 2007|publisher=CRC Press|isbn=978-0-8493-8217-8|pages=1075–}}</ref><ref name="KleemannEngel2014">{{cite book|author1=A. Kleemann|author2=J. Engel|author3=B. Kutscher |author4=D. Reichert|title=Pharmaceutical Substances, 5th Edition, 2009: Syntheses, Patents and Applications of the most relevant APIs|url=https://books.google.com/books?id=fO2IAwAAQBAJ&pg=PT2441|date=14 May 2014|publisher=Thieme|isbn=978-3-13-179525-0|pages=2441–2442}}</ref><ref name="NegwerScharnow2001">{{cite book|author1=Martin Negwer|author2=Hans-Georg Scharnow|title=Organic-chemical drugs and their synonyms: (an international survey)|url=https://books.google.com/books?id=zmpqAAAAMAAJ|year=2001|publisher=Wiley-VCH|isbn=978-3-527-30247-5|page=1831|quote=3β-Hydroxyandrost-5-en-17-one hydrogen sulfate = (3β)-3-(Sulfooxy)androst-5-en-17-one. R: Sodium salt (1099-87-2). S: Astenile, Dehydroepiandrosterone sulfate sodium, DHA-S, DHEAS, KYH 3102, Mylis, PB 005, Prasterone sodium sulfate, Teloin}}</ref><ref name="Jianqiu1992">{{cite journal | author = Jianqiu Y | year = 1992 | title = Clinical Application of Prasterone Sodium Sulfate | journal = Chinese Journal of New Drugs | volume = 5 | page = 015 }}</ref><ref name="pmid1403604">{{cite journal | vauthors = Sakaguchi M, Sakai T, Adachi Y, Kawashima T, Awata N | title = The biological fate of sodium prasterone sulfate after vaginal administration. I. Absorption and excretion in rats | journal = J. Pharmacobio-Dyn. | volume = 15 | issue = 2 | pages = 67–73 | year = 1992 | pmid = 1403604 | doi = 10.1248/bpb1978.15.67| doi-access = free }}</ref><ref name="SakaiSakaguchi1992">{{cite journal | year = 1992 | title = The Biological Fate of Sodium Prasterone Sulfate after Vaginal Administration II: Distribution after Single and Multiple Administration to Pregnant Rats | journal = 薬物動態 | volume = 7 | issue = 1| pages = 87–101 | doi=10.2133/dmpk.7.87| last1 = Sakai | first1 = Takanori | last2 = Sakaguchi | first2 = Minoru | last3 = Adachi | first3 = Yoshiko | last4 = Kawashima | first4 = Tsuneo | last5 = Awata | first5 = Norio }}</ref>
			==Diagnostic use==
			DHEA-S levels above 1890&nbsp;μM or 700 to 800&nbsp;μg/dL are highly suggestive of ] because DHEA-S is made by the adrenal glands<ref name="pmid18844715">{{cite journal |vauthors=Somani N, Harrison S, Bergfeld WF |title=The clinical evaluation of hirsutism |journal=Dermatologic Therapy |volume=21 |issue=5 |pages=376–91 |year=2008 |pmid=18844715 |doi=10.1111/j.1529-8019.2008.00219.x|s2cid=34029116 }}</ref><ref name=emedicine_workup>{{cite web|url=http://emedicine.medscape.com/article/256806-workup#showall|title=Polycystic Ovarian Syndrome Workup|publisher=]|date=25 October 2011|access-date=19 November 2011}}</ref> and also synthesized in the brain.<ref>{{cite journal | year = 2011 | title = Neurosteroid Biosynthesis in the Brain of Amphibians | journal = Frontiers in Endocrinology | volume = 2 | page = 79 | doi = 10.3389/fendo.2011.00079 | pmid = 22649387 | pmc = 3355965 | last1 = Vaudry | first1 = H. | last2 = Do Rego | first2 = J. L. | last3 = Burel | first3 = D. | last4 = Luu-The | first4 = V. | last5 = Pelletier | first5 = G. | last6 = Vaudry | first6 = D. | last7 = Tsutsui | first7 = K. | doi-access = free }}</ref> The presence of DHEA-S is therefore used to rule out ovarian or testicular origin of excess androgen.
			Women with ] commonly present with mildly elevated DHEA-S levels.<ref name="pmid20418968">{{Cite journal|last=Sachdeva|first=Silonie|date=2010|title=Hirsutism: Evaluation and Treatment|journal=Indian Journal of Dermatology|series=55|volume=1|issue=1|pages=3–7|doi=10.4103/0019-5154.60342|pmc=2856356|pmid=20418968 |doi-access=free }}</ref> Common ] for hirsutism include ] dysfunction (]) and ] dysfunction (], ], ] secreting tumors); 90% of these cases are caused by ] or are ] in nature.<ref name="pmid20418968" /> However, severely increased DHEA-S levels (>700&nbsp;μg/dL) necessitate further workup and are almost stem from benign or malignant adrenal alterations.<ref name="pmid20418968" />
			==Chemistry==
			{{See also|List of neurosteroids}}
			DHEA-S, also known as androst-5-en-3β-ol-17-one 3β-sulfate, is a ] ] ] and the C3β ] ] of DHEA.
			==References==
			{{Reflist}}
			{{Endogenous steroids}}
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			{{GABA receptor modulators}}
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			{{Growth factor receptor modulators}}
			{{Ionotropic glutamate receptor modulators}}
			{{Transient receptor potential channel modulators}}
			{{Xenobiotic-sensing receptor modulators}}
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