15289-s-bos

7 103 | Latest developments in the treatment of lipoprotein (a) estrogens will even be used as Lp(a) lowering medication. Thyroid hormone analogues Abnormal thyroid function has serious consequences for lipoprotein levels and body composition [15]. These effects can be explained by the interaction of thyroid hormone with the thyroid hormone receptor. This receptor has two major isoforms, the α and the β isoform. The α isoform is predominantly present in heart and bone, whereas the β isoform is predominantly present in the liver. The thyroid hormone β-receptor analogue eprotirome (Karo Bio, Huddinge, Sweden) has been studied in two RCTs [15]. Eprotirome was found to lower Lp(a) levels by 43% from baseline, without any change in body weight, heart rate, blood pressure, or bone turnover [15]. This effect seems to be synergistic to either statins or ezetimibe because administration of eprotirome as monotherapy does not influence Lp(a) levels [16]. The proposed mechanism of Lp(a) lowering is that activation of the β isoform leads to a decreased apo-B synthesis. However, because of cartilage damage in toxicology studies in dogs and recent reports that elevation in liver function tests were observed in patients randomized to eprotirome, the trials were prematurely terminated [17]. To our knowledge there are no new thyroid analogues under development. Statins Statins are prescribed for over 20 years for treating dyslipidaemia to prevent CVD. Their effect is mainly due to lowering of LDL-C. Previous studies have reported either a lowering, no effect, or an increase in Lp(a) levels after statin treatment [18, 19]. It seems clear that Lp(a) cannot be cleared by the LDL-receptor. The mechanisms by which statins may affect Lp(a) levels, if they do, remain to be clarified. Two recent studies evaluated the effect of statins on Lp(a) levels [20, 21]. In the first study patients who were receiving a standard statin dose were switched to the maximum dosage of rosuvastatin, i.e. 40mg [20]. In this study, optimizing statin dose led to a decrease of LDL-C (23%), but did not show an effect on Lp(a)[20]. In the second study the effect of morning and evening dosages of simvastatin were compared, in previously untreated patients [21]. In this study, the use of simvastatin led to a decrease in LDL-C (36-38%), but to no changes in Lp(a). In addition, there was no difference in morning or evening dosages on any lipoprotein[21]. In conclusion, the effect of statins on Lp(a) levels, if present, is most likely not clinically significant.