In Poland there are still nearly 20 million individuals with hypercholesterolaemia, most of them are unaware of their condition; that is also why only ca. 5% of patients with familial hypercholesterolaemia have been diagnosed; that is why other rare cholesterol metabolism disorders are so rarely diagnosed in Poland. Let us hope that these guidelines, being an effect of work of experts representing 6 main scientific societies, as well as the network of PoLA lipid centers being a part of the EAS lipid centers, certification of lipidologists by PoLA, or the growing number of centers for rare diseases, with a network planned by the Ministry of Health, improvements in coordinated care for patients after myocardial infarction (KOS-Zawał), reimbursement of innovative agents, as well as introduction in Poland of an effective primary prevention program, will make improvement in relation to these unmet needs in diagnostics and treatment of lipid disorders possible.

Statin intolerance is a clinical syndrome whereby adverse effects (AEs) associated with statin therapy [most commonly statin-associated muscle symptoms (SAMS)] result in the discontinuation of therapy and consequently increase the risk of adverse cardiovascular outcomes. However, complete statin intolerance occurs in only a small minority of treated patients (estimated prevalence of only 3-5%). Many perceived AEs are misattributed (e.g. physical musculoskeletal injury and inflammatory myopathies), and subjective symptoms occur as a result of the fact that patients expect them to do so when taking medicines (the nocebo/drucebo effect)-what might be truth even for over 50% of all patients with muscle weakness/pain. Clear guidance is necessary to enable the optimal management of plasma in real-world clinical practice in patients who experience subjective AEs. In this Position Paper of the International Lipid Expert Panel (ILEP), we present a step-by-step patient-centred approach to the identification and management of SAMS with a particular focus on strategies to prevent and manage the nocebo/drucebo effect and to improve long-term compliance with lipid-lowering therapy.

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IntroductionThe relationship between inflammatory and anti-inflammato�ry markers and telomere length (TL), a biological index of aging, is still poor�ly understood. By applying a 2-sample Mendelian randomization (MR), we investigated the causal associations between adiponectin, bilirubin, C-reac�tive protein (CRP), leptin, and serum uric acid (SUA) with TL.Material and methodsMR was implemented by using summary-level data from the largest ever genome-wide association studies (GWAS) conducted on our interested exposure and TL. Inverse variance weighted method (IVW), weighted median (WM)-based method, MR-Egger, MR-Robust Adjusted Pro�file Score (RAPS), and MR-Pleiotropy RESidual Sum and Outlier (PRESSO) were applied. Sensitivity analysis was conducted using the leave-one-out method.ResultsWith regard to adiponectin, CRP, leptin, and SUA levels, we found no effect on TL for all 4 types of tests (all p > 0.108). Results of the MR-Egger (p = 0.892) and IVW (p = 0.124) showed that bilirubin had no effect on telomere maintenance, whereas the results of the WM (p = 0.030) and RAPS (p = 0.022) were negative, with higher bilirubin concentrations linked to shorter TL. There was a low likelihood of heterogeneity for all the estima�tions, except for bilirubin (IVW p = 0.026, MR Egger p = 0.018). MR-PRESSO highlighted no outlier. For all the estimations, we observed negligible inter�cepts that were indicative of low likelihood of the pleiotropy (all p > 0.161). The results of leave-one-out method demonstrated that the links are not driven because of single nucleotide polymorphisms (SNPs).ConclusionsOur results highlight that neither the anti-inflammatory nor pro-inflammatory markers tested have any significant causal effect on TL. The casual role of bilirubin on TL still needs to be investigated.