Is lipid lowering treatment aiming for very low LDL levels safe in terms of the synthesis of steroid hormones?

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dc.contributor.authorKanat, Mustafa
dc.contributor.authorSipahioğlu, Murat
dc.contributor.authorArınç, Hüseyin
dc.contributor.authorSerin, Erdinç
dc.contributor.authorYıldız, Özcan
dc.contributor.authorTunçkale, Aydın
dc.contributor.authorÇelebi, Harika
dc.date.accessioned2020-04-30T23:18:45Z
dc.date.available2020-04-30T23:18:45Z
dc.date.issued2007
dc.departmentDÜ, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümüen_US
dc.descriptionWOS: 000247232900022en_US
dc.descriptionPubMed: 17234355en_US
dc.description.abstractToday atherosclerotic diseases are among the most important causes of death in the world. Epidemiological, clinical, genetic, experimental and pathological studies have clearly shown the role of lipoproteins in atherosclerosis. LDL is the major atherogenic lipoprotein and has been defined as the primary target of lipid lowering treatment by NCEP. Although the level of LDL, the primary target in the treatment of dyslipidemia, has been set as below 100 mg/dl in coronary heart diseases (CHD) and CHD risk equivalents, this level has been putted down to below 70 mg/dl for the group defined as very high risk group by the ATP (Adult Treatment Panel) guide that has been updated following the new clinical studies. As we already know, cholesterol is the precursor of glucocorticoids, mineralocorticoids and sex steroids, besides being a structural component of the cell membrane. Both adrenal and non-adrenal (ovarian + testicular) all steroid hormones are primarily synthesized using the LDL-cholesterol in the circulation. In addition to this, there is 'de novo' cholesterol synthesis in both the adrenals and gonads controlled by the HMG-CoA reductase enzyme. A third pathway, which under normal circumstances has little contribution as compared to the first two, is the use of circulatory HDL-cholesterol by the adrenal and gonadal tissues for the synthesis of steroids. Our knowledge on extremely towered LDL levels is quite limited. However, since statins both decrease circulatory LDL and inhibit de novo cholesterol synthesis, they are likely to affect the synthesis of steroid hormones. (c) 2006 Elsevier Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.mehy.2006.10.058en_US
dc.identifier.endpage112en_US
dc.identifier.issn0306-9877
dc.identifier.issn1532-2777
dc.identifier.issue1en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage104en_US
dc.identifier.urihttps://doi.org/10.1016/j.mehy.2006.10.058
dc.identifier.urihttps://hdl.handle.net/20.500.12684/3506
dc.identifier.volume69en_US
dc.identifier.wosWOS:000247232900022en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherChurchill Livingstoneen_US
dc.relation.ispartofMedical Hypothesesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.titleIs lipid lowering treatment aiming for very low LDL levels safe in terms of the synthesis of steroid hormones?en_US
dc.typeArticleen_US

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