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Chronic pancreatitis (CP) is a quite common disease with an annual incidence of up to 30 new cases per 100,000 persons in Russia, and 9.6 cases per 100,000 persons abroad. Idiopathic pancreatitis associated with genetic mutations ranks second in frequency. When conservative therapy is ineffective, surgical intervention is considered. Total pancreatectomy reduces pain, but leads to pancreatogenic diabetes mellitus. In case of hereditary pancreatitis caused by mutations in the PRSS1 , CFTR , SPINK1 genes, pancreatectomy becomes advisable, including for prevention of pancreatic cancer. Isolation of Langerhans islets from the excised pancreas and their autotransplantation (total pancreatectomy with islet autotransplantation, TPIAT) provides additional treatment options. Such surgical interventions are not performed in Russia as of yet. The aim of the study was to assess the effectiveness of total pancreatectomy followed by restoration of glucose tolerance in treatment of patients with chronic genetically determined pain pancreatitis., Materials and Methods: Two patients with chronic pain pancreatitis with the SPINK1 and PRSS1 genetic mutations were examined and underwent surgical total pancreatectomy. Islets were isolated from the excised glands and implanted into the liver. Postoperative followup included an assessment of quality of life and pain intensity based on questionnaires, as well as determination of the glycemic level., Results: Following total pancreatoduodenectomy and autotransplantation, a significant decrease in pain and an improvement in quality of life were noted. Transplanted islets' function was reduced, due to their insufficient number, which required administration of exogenous insulin., Conclusion: The described experience demonstrates the TPIAT effectiveness in treatment of chronic pancreatitis, which can become a basis for further research and introduction of the technique into domestic clinical practice., Competing Interests: Conflict of interest: The authors declare no conflict of interest.

Background: 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., Aims: 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 occurance 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).