Дислипидемия часто встречается у пациентов с гипотиреозом, в связи с чем встает вопрос о применении статинов в лече-нии. В то же время как гипотиреоз, так и прием статинов могут приводить к развитию миопатии и рабдомиолиза, что обусловливает озабоченность безопасностью применения этих препаратов у различных групп пациентов с гипотиреозом. Настоящая статья представляет собой обзор статей, клинических рекомендаций, инструкций к лекарственным препаратам, относящимся к проблеме назначения статинов у пациентов с гипотиреозом. На основании проанализированного материала даются рекомендации по применению статинов у пациентов с компенсированным и некомпенсированным гипотиреозом. Клю че вые сло ва: гипотиреоз, дислипидемия, статины, миопатия, рабдомиолиз.Dyslipidemia is a frequent condition in patients with hypothyroidism which determines possible need for statin use in treatement. However, both hypothyroidism and statin use can lead to myopathy and rhabdomyolysis so safety concerns are important for clinical decision. Current article is a review of publications, clinical guidelines and drug labels which are related to the problem of statin safety in patients with hypothyroidism. Recommendations are given for use of statin in patients with compensated and decompensated hypothyroidism based on review of data.

Цель исследования -оценить влияние компенсированного гипотиреоза и полиморфизма гена SLCO1B1*5 (c.521T>C) на клинико-лабораторные признаки поражения мышц на фоне терапии статинами. Методы. Оценка симптомов и маркеров мышечного поражения, генотипирование по аллельному варианту SLCO1B1*5 (c.521T>C) проведены у 33 пациентов с первичным гипотиреозом, получающих статины, у 31 пациента без гипотиреоза, получающих статины, и у 33 пациентов с первичным гипотиреозом, не получающих статины. Результаты. В группе пациентов с компенсированным гипотиреозом на фоне приема статинов мышечные боли регистри-ровались чаще по сравнению с другими группами (45,5, 16,1 и 30,3% соответственно, р = 0,048). Только в этой группе боли ассоциировались с повышением креатининфосфокиназы (171,0 ± 108,12 и 110,0 ± 43,81 Е/д при наличии и отсут-ствии болей, р = 0,049), лактатдегидрогеназы (369,5 ± 66,22 и 305,6 ± 41,98 Е/д, р = 0,007), титра миоглобина (90,7 ± 109,89 и 41,1 ± 28,56, р = 0,005), повышением частоты встречаемости аллельных вариантов ТС и СС гена SLCO1B1*5 (c.521T>C) -68,4 и 28,6%, р = 0,0027. Заключение. Пациенты с компенсированным гипотиреозом имеют повышенный риск статин-индуцированной миопа-тии, который возрастает при наличии аллельных вариантов ТС и СС гена SLCO1B1*5 (c.521T>C), что требует тщательно-го мониторинга клинико-биохимических признаков мышечного поражения в случае их выявления. Клю че вые сло ва: компенсированный гипотиреоз, статины, миопатия, полиморфизм гена SLCO1B1*5 (c.521T>C).Aim: to assess the influence of compensated hypothyroidism and SLCO1B1*5 (c.521T>C) gene polymorphism on the clinical and laboratory signs of the muscle damage during statin therapy. Methods. Assessment of symptoms and markers of the muscle damage and SLCO1B1*5 (c.521T>C) genotyping were performed in 33 patients with primary hypothyroidism taking statins, in 31 patients taking statins without hypothyroidism and in 33 patients with primary hypothyroidism without statins taking. Results. Muscle pain was observed more often in the group of the patients with compensated hypothyroidism on the background of statins taking compared with other groups (45,5, 16,1 and 30,3%, respectively, p = 0.048). Only in this group the pain was associated with increased levels of creatine-kinase (171.0 ± 108.12 and 110.0 ± 43.81U/L, in the presence and absence of the pain, p = 0.049), LDH (369.5 ± 66.22 and 305.6 ± 41.98 U/L, р = 0.007), myoglobin titer (90.7 ± 109.89 and 41.1 ± 28.56, р = 0.005), and more frequent occurrence of TC and CC genotypes of SLCO1B1*5 (c.521T>C) (68.4 и 28.6%, р = 0.0027). Conclusions. The patients with compensated hypothyroidism have a higher risk of statin-induced myopathy increasing if the TC heterozygotes or CC homozygotes of SLCO1B1*5 (c.521T>C) gene are present, which requires thorough monitoring of clinical and biochemical muscle damage signs in case of its detection.

Statin-associated muscle symptoms are one of the statin-induced side effects. The incidence of the condition is increased by the presence of associated risk factors, one of which is hypothyroidism. The paper reports clinical case of statin-associated muscle symptoms in patient with compensated hypothyroidism carrying a SLCO1B1 mutation. Optimal assessment and treatment algorithms are discussed.

Abstract There is no unequivocal opinion regarding the safety of statin in patients with hypothyroidism. However, based on some new data, it can be assumed that hypothyroidism, even in a stage of compensation, may cause muscle damage in patients receiving statins. As part of this study, this hypothesis was tested, and was confirmed. Aim To study the possibility of muscle damage and the nature of muscle metabolism in patients with compensated hypothyroidism who takes statin. Materials and methods The study is transverse and observational with the inclusion of 120 women, subdivided on three groups (n=40). The main group of patients with hypothyroidism who took statins (group 1) was compared with two control groups, including those who took statins without hypothyroidism (group 2), and who did not take statins with hypothyroidism (group 3). Results Patients taking statins and have compensated hypothyroidism are more likely to develop complaints of muscle pain, which are often associated with the elevation of muscle lesion markers, as well as the presence of the C allele in the SLCO1B1 * 5 gene (c.521T C). In patients with compensated hypothyroidism, relative frequency of occurrence of muscle pain syndrome associated with CPK elevation increases with TSH levels above 2.86 mU / L. Compensated hypothyroidism increases the possibility of development of SPM-ATP by 2.7 times. Conclusions Compensated hypothyroidism is not a contraindication for statin therapy. However, the presence of even compensated hypothyroidism in patients taking statins increases the possibility of the development of muscle symptoms associated with taking statins, and requires additional monitoring of the clinical and biochemical parameters of muscle metabolism (especially the level of CPK).

Aim. To develop and implement a method for isolating the islets of Langerhans from pancreatic tissue after pancreatectomy with islet autotransplantation.Materials and Methods. The study used ten Wiesenau miniature pig pancreases, 30 Wistar rat pancreases, eight resected human pancreases, and five human pancreases from extensive resection or pancreatectomy.Results. Islets of Langerhans completely devoid of human and experimental animals’ acinar tissue were obtained. When using the protocol for mechanical isolation, the efficiency of isolating the islets of Langerhans in humans and experimental animals was 50%. The research proved that the isolated cells belonged to the islets of Langerhans. Additionally, their purity was confirmed. The survival of the isolated islets exceeded 90%. The enzyme immunoassay for insulin synthesis showed that the isolated islets of Langerhans remained functionally active. The sterility of the isolated islet cells was confirmed.Conclusion. This proven isolation technology makes it possible to obtain pure, sterile, viable, and functionally active islet cells suitable for further autotransplantation.