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العنوان
Impact of high doses of Statins on testosterone level in males with atherosclerotic coronary artery disease \
المؤلف
Ibrahim, Walid Said.
هيئة الاعداد
باحث / وليد سعيد إبراهيم عواد سيف الدين
مشرف / شريف سمير الزهوي
مشرف / مازن توفيق
مشرف / محمد مصطفي فاروق
تاريخ النشر
2019.
عدد الصفحات
91 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
أمراض القلب والطب القلب والأوعية الدموية
تاريخ الإجازة
1/1/2019
مكان الإجازة
جامعة عين شمس - كلية الطب - القلب و الاوعية الدموية
الفهرس
Only 14 pages are availabe for public view

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Abstract

Concern has always existed that statins might impair testosterone production either by reducing availability of its preferred substrate, that is, locally produced de novo cholesterol in the gonads and elsewhere, or by inhibiting steps in the steroidogenesis process,but this concern has been considered of little clinical significance.
In our study there were a significant reduction in total cholesterol, LDL and TGs in both low dose and high dose groups, but the effect on testosterone was quite different between them, the reduction in testosterone was about 33% from the baseline in the high dose group while in the low dose there was no significant reduction in the testosterone level.
Not only the testosterone and the lipid profile were affected in the high dose group, there was a significant increase in the liver enzymes (ALT & AST) in the high dose group, while in the low dose group there was also significant statistically increase in the mean levels of AST but of no clinical value as this rise was within normal range.
As regard the CK total levels, there was also noticeable increase in CK total level in the high dose group, while in the low dose group there was only significant statistically increase in the mean levels of CK total but again of no clinical value as this rise was within normal range.
In our study we have reported that statins lower serum testosterone in men in the high dose statin group, a potentially important finding. Unfortunately, the clinical implications of this observation are less clear than they could be because the only data available to us were the average changes in testosterone induced by statins. While the average changes may be small, the range of changes in individuals, potentially, might be much more substantial.
So our study raises the following question ”why don’t we use the low to moderate doses of statins for primary and secondary prevention of CAD ? ” the effect on the lipid profile was the same between high and low doses but the side effect of the high doses was marked on the testosterone level, liver enzymes and CK levels.