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Article: Alterations in hepatic lipase and lipoprotein subfractions with transdermal testosterone replacement therapy

TitleAlterations in hepatic lipase and lipoprotein subfractions with transdermal testosterone replacement therapy
Authors
Issue Date1999
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0300-0664
Citation
Clinical Endocrinology, 1999, v. 51 n. 6, p. 765-769 How to Cite?
AbstractOBJECTIVES. The effect of sex hormone replacement therapy on lipoprotein metabolism is thought to be less marked with the transdermal route because of the lack of hepatic first-pass effect. The aim of this study was to evaluate the effects of testosterone replacement therapy given transdermally via a permeation-enhanced system on plasma lipolytic enzymes (hepatic and lipoprotein lipase), LDL and HDL subfraction concentrations. MEASUREMENTS. Ten patients with primary testicular failure were started on transdermal testosterone (Testoderm®). Plasma lipids, lipoproteins and post-heparin plasma lipolytic enzymes were evaluated before and after 3 months of treatment. LDL and HDL subfractions were measured by density gradient ultracentrifugation and hepatic and lipoprotein lipase activities by radio- enzymatic method. RESULTS. Serum testosterone level increased to within the normal range in all subjects whereas serum dihydrotestosterone (DHT) increased to supra-normal values. Plasma hepatic lipase (HL) activity increased after testosterone replacement (24.7 ± 7.5 vs. 29.2 ± 8.3 μmol free fatty acid released per hour, P < 0.05) and the increase in HL correlated with the increase in DHT (r = 0.64, P < 0.05). Small changes were observed in LDL subfraction pattern with an increase in the concentration of small dense LDL-III (80.1 ± 30.3 vs. 93.0 ± 27.8 mg/l, P < 0.05). No significant change was seen in the HDL2 subfraction but HDL3 decreased after treatment (0.93 ± 0.17 vs. 0.79 ± 0.14 mmol/l, P < 0.01). CONCLUSIONS. Testosterone replacement, given via a permeation-enhanced transdermal system, is associated with changes in hepatic lipase activity and in LDL and HDL subfractions. Whether these changes adversely influence the cardiovascular risk in the longterm remains to be determined.
Persistent Identifierhttp://hdl.handle.net/10722/78238
ISSN
2015 Impact Factor: 3.487
2015 SCImago Journal Rankings: 1.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_HK
dc.contributor.authorShiu, SWMen_HK
dc.contributor.authorKung, AWCen_HK
dc.date.accessioned2010-09-06T07:40:40Z-
dc.date.available2010-09-06T07:40:40Z-
dc.date.issued1999en_HK
dc.identifier.citationClinical Endocrinology, 1999, v. 51 n. 6, p. 765-769en_HK
dc.identifier.issn0300-0664en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78238-
dc.description.abstractOBJECTIVES. The effect of sex hormone replacement therapy on lipoprotein metabolism is thought to be less marked with the transdermal route because of the lack of hepatic first-pass effect. The aim of this study was to evaluate the effects of testosterone replacement therapy given transdermally via a permeation-enhanced system on plasma lipolytic enzymes (hepatic and lipoprotein lipase), LDL and HDL subfraction concentrations. MEASUREMENTS. Ten patients with primary testicular failure were started on transdermal testosterone (Testoderm®). Plasma lipids, lipoproteins and post-heparin plasma lipolytic enzymes were evaluated before and after 3 months of treatment. LDL and HDL subfractions were measured by density gradient ultracentrifugation and hepatic and lipoprotein lipase activities by radio- enzymatic method. RESULTS. Serum testosterone level increased to within the normal range in all subjects whereas serum dihydrotestosterone (DHT) increased to supra-normal values. Plasma hepatic lipase (HL) activity increased after testosterone replacement (24.7 ± 7.5 vs. 29.2 ± 8.3 μmol free fatty acid released per hour, P < 0.05) and the increase in HL correlated with the increase in DHT (r = 0.64, P < 0.05). Small changes were observed in LDL subfraction pattern with an increase in the concentration of small dense LDL-III (80.1 ± 30.3 vs. 93.0 ± 27.8 mg/l, P < 0.05). No significant change was seen in the HDL2 subfraction but HDL3 decreased after treatment (0.93 ± 0.17 vs. 0.79 ± 0.14 mmol/l, P < 0.01). CONCLUSIONS. Testosterone replacement, given via a permeation-enhanced transdermal system, is associated with changes in hepatic lipase activity and in LDL and HDL subfractions. Whether these changes adversely influence the cardiovascular risk in the longterm remains to be determined.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0300-0664en_HK
dc.relation.ispartofClinical Endocrinologyen_HK
dc.rightsClinical Endocrinology. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAdministration, Cutaneousen_HK
dc.subject.meshAdulten_HK
dc.subject.meshDihydrotestosterone - blooden_HK
dc.subject.meshHormone Replacement Therapyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypogonadism - drug therapy - metabolismen_HK
dc.subject.meshLipase - metabolismen_HK
dc.subject.meshLipoproteins - metabolismen_HK
dc.subject.meshLipoproteins, HDL - blooden_HK
dc.subject.meshLipoproteins, LDL - blooden_HK
dc.subject.meshLiver - enzymology - metabolismen_HK
dc.subject.meshLongitudinal Studiesen_HK
dc.subject.meshMaleen_HK
dc.subject.meshTestosterone - administration & dosage - metabolismen_HK
dc.titleAlterations in hepatic lipase and lipoprotein subfractions with transdermal testosterone replacement therapyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0300-0664&volume=51&spage=765&epage=769&date=1999&atitle=Alterations+in+hepatic+lipase+and+lipoprotein+subfractions+with+transdermal+testosterone+replacement+therapy.en_HK
dc.identifier.emailTan, KCB:kcbtan@hku.hken_HK
dc.identifier.emailKung, AWC:awckung@hku.hken_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.identifier.authorityKung, AWC=rp00368en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2265.1999.00882.xen_HK
dc.identifier.pmid10619982-
dc.identifier.scopuseid_2-s2.0-0033379825en_HK
dc.identifier.hkuros51189en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033379825&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume51en_HK
dc.identifier.issue6en_HK
dc.identifier.spage765en_HK
dc.identifier.epage769en_HK
dc.identifier.isiWOS:000084991800013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.scopusauthoridShiu, SWM=7005550652en_HK
dc.identifier.scopusauthoridKung, AWC=7102322339en_HK

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