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Abstract

The present study was undertaken to highlight the influence of simvastatin administration on hepatocyte morphology, proliferation, and apoptosis. The study included 48 gilts aged 3 months (weighing ca. 30 kg) divided into groups I (control; n=24) and II, receiving 40 mg/animal simvas- tatin orally (simavastatin; n=24) for 29 days. The animals were euthanized on days subsequent to the experiment. The livers were sampled, fixed, and processed routinely for histopathology, histochemistry, and immunohistochemistry (for proliferating cell nuclear antigen, Bcl-2, and caspase-3). Apoptosis was visualized by terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL). Simvastatin administration caused acute hepatocyte swelling, glycogen de- pletion, hyperaemia, multifocal hepatocyte proliferation with occasional pseudoacinar formation, connective tissue hyperplasia, eosinophil infiltration, and interface hepatitis. The proliferating cell nuclear antigen index, mean diameter of argyrophilic nucleolar organizer regions, and Bcl-2 immunoexpression were lower compared to control, and mean caspase-3 immunoexpression was higher in group II compared to control. On day 25 and 29 single hepatocytes in the simvasta- tin-treated group were TUNEL-positive. Simvastatin caused morphological alteration which became more intense over time. The results from the present study suggest that simvastatin treat- ment may cause glycogen, lipid metabolism and cell membrane permeability distortion, fibrosis, interface hepatitis, reduction in hepatocyte proliferation and transcriptional activity, and enhanced vulnerability to apoptosis. Summing up the results, it can be concluded that simvastatin caused liver damage with similar morphological changes seen in autoimmune-like liver injury, which may indicate that simvastatin may induce autoimmune-like drug induced liver injury.

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Authors and Affiliations

M. Mikiewicz
I. Otrocka-Domagała
K. Paździor-Czapula
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Abstract

Background: Cardiovascular diseases are the first cause of death globally. Hypercholester-olemia is the most important factor responsible for atherosclerotic plaque formation and increasing cardiovascular risk. Reduction of LDL-C level is the most relevant goal for reduction of cardiovascular risk.
Aims: Real life adherence to guidelines concerning statin therapy in one center study population. Methods: We analyzed data collected in the Department of Internal Diseases from September 2019 to February 2020, obtained from 238 patients hospitalized in this time period. We assessed application of the new 2019 ESC/EAS Guidelines for the Management of Dyslipidaemias in daily clinical practice and compared effectiveness of LLT according to 2016 and 2019 guidelines.
Results: Only 1 in 5 patients with dyslipideamia achieve the 2019 ESC/EAS guideline-recommended levels of LDL-C with relation to their TCVR. We noticed that 20 of patients who did not achieve proper 2019 LDL level, meet the therapy targets established in year 2016. We observed that higher patient TCVR resulted in better compliance with guidelines and ordination of proper LLT. Most patients were on monotherapy with statins.
Conclusions: It could be beneficial to start treatment with double or even triple therapy especially in group with the highest LDL-C levels.
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Authors and Affiliations

Patrycja Cecha
1
Anna Chromik
1
Ilona Piotrowska
1
Michał Zabojszcz
1
Magdalena Dolecka-Ślusarczyk
1
Zbigniew Siudak
1

  1. Collegium Medicum, Jan Kochanowski University, Kielce, Poland

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