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    1. E. A. Vagner Perm State Medical University (614990, Perm, Russia)

    Keywords: colorectal cancer, alkaline phosphatase, electrochemical method, biochips

    Abstract: Objective: To evaluate (morphologically) the eff ectiveness of the electrochemical method with biosensors applying to study the content of ALP in biopsies of tumors and intact colon mucosa. Materials and methods: Using the electrochemical method with nanotechnological biosensors, the concentration of alkaline phosphatase in biopsy specimens of colorectal carcinomas and intact colon mucosa, obtained from endoscopy from 24 patients were examined. Based on the results of a subsequent histological and immunohistochemical study of biopsy specimens, the eff ectiveness of the electrochemical method was evaluated. Results: The average value of the current, obtained in the study of fresh tumor biopsies was 0.0492 ± 0. 0007 μA, in case of biopsy specimens of the intact colon mucosa was 0.1197 ± 0.019 μA. Similar results were obtained in the study of biopsies, fi xed in formalin: tumor tissue — 0.033 ± 0.0005 μA, intact mucosa — 0.0596 ± 0.0008 μA. The histological structure of tumors corresponded to adenocarcinoma of various degrees of diff erentiation. A positive correlation of the results of electrochemical and histological / immunohistochemical studies was observed in all patients. Immunohistochemical study of biopsy specimens with antibodies to non-specifi c alkaline phosphatase revealed high expression of enzyme in the cell membranes of the glandular crypt’s colon epithelium and a weak “background” staining of the cytoplasm and cell membranes of tumor cells. Conclusion: An electrochemical study with biosensors can be used to assess the alkaline phosphatase content in tumor biopsies and intact colon mucosa. Diff erences in the content of alkaline phosphatase in the tissue of colon adenocarcinoma and the unmodifi ed mucosa are statistically signifi cant. The existing diff erences in the study of fresh and fi xed in formalin biopsy samples indicate the advisability of non-fi xed material using.

      1. Cancer facts and fi gures: estimated cases of new cancer cases in 2017 year (newsletter) / American Cancer Society. New York. 2017. P. 10.
      2. Kaprin A. D., Starinsky V. V., Petrova G. V. Zlokachestvennyye novoobrazovaniya v Rossii 2015 godu (zabolevayemost’ i smertnost’) [Malignant neoplasms in Russia in 2015 (morbidity and mortality)] P. A. Gertsen – branch of the Federal State Budgetary Institution “NMIRTS” of the Ministry of Health of Russia Publ., Moscow, 2017, 14 p.
      3. Wang J. Electrochemical biosensors: towards point-ofcare cancer diagnostics / J. Wang // Biosensors and Bioelectronics. – 2006. – no. 21(10). – P. 1887–1892.
      4. Kabbat E. A. A histochemical study of distribution of alkaline phosphatase in various normal and neoplastic tissues / E. A. Kabbat, J. Furth // American journal of pathology. – 1940. – № 27. – P. 40–61.
      5. Barnard J. A. Butyrate rapidly induces growth inhibition and diff erentiation in HT-29 cells / J. A. Barnard, G. Warwick // Cell Growth and Diff erentiation. – 1993. – № 4. – P. 495–501.
      6. Hinnebusch B. F. Enterocyte differentiation marker intestinal alkaline phosphatase is a target gene of the gut-enriched Kruppel-like factor / B. F. Hinnebusch // American Journal of Physiology. – № 286 (1). – P. 23–30.
      7. Giatromanolaki A. Downregulation of intestinal-type alkaline phosphatase in the tumor vasculature and stroma provides a strong basis for explaining amifostine selectivity / A. Giatromanolaki, E. Sivridis, E. Maltezos, M. Koukourakis // Seminars in Oncology. – 2002. – № 29. – P. 14.
      8. Mendonka M. S. Characterization of intestinal alkaline phosphatase expression and the tumorigenic potential of gamma-irradiated HeLa X fi broblast cell hybrids / M. S. Mendonka // Cancer research. – 1991. – № 51(16). – P. 4455–62.
     


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    Belkin A. N., Freynd G. G. Morphological evaluation of eff ectiveness of electochemical method with nanotechnological biosensors using for alkaline phosphotase detection in colorectal carcinoma biopsies. Experimental and Clinical Gastroenterology. 2018;156(8): 64–67. DOI: 10.31146/1682-8658-ecg-156-8-64-67
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    1. E. A. Vagner Perm State Medical University (614990, Perm, Russia)
    2. Perm State National Research University (Perm, Russia)
    3. Perm Institute of the Federal Penal Service (Perm, Russia)

    Keywords: interleukin-2 receptor expression, NSAID-pancreatopathy, nimesulide

    Abstract: Objective: to study the involvement of regulatory cytokine-interleukin-2 in the pathogenesis of NSAID-pancreatopathy induced by prolonged intake of nimesulide, using immunohistochemical methods. Materials and methods: the study was carried out on laboratory animals (rats) who received nimesulide by the oral route for 21 days at diff erent dosages: 0.5 mg / kg (therapeutic), 2.5 mg / kg and 5 mg / kg. Evaluation of the eff ect of the drug was made on the basis of histological examination of pancreatic tissue and manifestation of immunohistochemical expression of interleukin-2 (IL-2Rα) receptors. To identify the expression of receptors, labeled antibodies IL-2Rα (poly), species-specifi c to rat tissue antigens, were used. Results: histological studies revealed pathomorphological changes characteristic of toxic pancreatic lesions. Assessment of the degree of lesions showed a pronounced dose-dependent eff ect. The manifestation of immunohistochemical expression of IL-2Rα was determined by semi-quantitative methods, the intensity of staining and the number of positively stained cells were evaluated. It was found that the expression of IL-2Rα is localized in the endocrine islets of Langerhans. In animals of experimental groups receiving high doses of nimesulide, a signifi cant increase in the intensity of staining of endocrine islets as well as connective tissue components was revealed, which is due to the high intensity of expression of IL-2Rα. Conclusion: increased expression of IL-2Rα, refl ecting islet cell damage, may be due to deterioration of tissue nutrition of islands due to hemodynamic disorders and dystrophic processes in the parenchyma of the gland and the development of an autoimmune component of the infl ammatory process.

      1. Flamenbaum M.; Abergel A.; Marcato N. et al. Regressive fulminant hepatitis, acute pancreatitis and renal insuffi ciency aft er taking ketoprofen // Gastroenterol. Clin. Biol. 1998. № 22. P. 975–976.
      2. Carrillo-Jimenez R., Nurnberger M. Celecoxib-induced acute pancreatitis and hepatitis: A case report // Arch. Intern. Med. 2000. № 160. P. 553–554.
      3. Lee S.C., Dalia S. M. Drug-induced chronic pancreatitis // Med Health R I. – 2012. № 95(1). P. 19–20.
      4. Mete D., Milon A., Belon G., Gatina J. H. Acute pancreatitis and ketoprofen // Gastroenterol. Clin. Biol. 2001. № 25. P. 721–722.
      5. Mennecier D., Ceppa F., Sinayoko L. et al. Acute pancreatitis aft er treatment by celecoxib // Gastroenterol. Clin. Biol. 2007. № 31. P. 668–669.
      6. Testoni P. A. Therapy: can rectal NSAIDs prevent post-ERCP pancreatitis? // Nat Rev. Gastroenterol. Hepatol. 2012. № 9(8). P. 429–430.
      7. Pezzilli R., Morselli-Labate A.M., Corinaldesi R. NSAIDs and Acute Pancreatitis: A Systematic Review // Pharmaceuticals. 2010. № 3. P. 558–571.
      8. Parfenov I. P., Belousov V. A., Yarosh A. L. Sovremennye predstavleniya o roli citokinov v patogeneze ostrogo pankreatita [Modern concepts of the role of cytokines in the pathogenesis of acute pancreatitis]. Nauchnye vedomosti BelGU. Seriya: Medicina. Farmaciya. – [Scientifi c statements of BelSU. Series: Medicine. Pharmacy], 2011, no. 16 (111), pp. 40–45.
      9. Firsova V. G., Parshikov V. V., Gradusov V. P. Ostry`j pankreatit: sovremennye aspekty patogeneza i klassifi kacii [Acute pancreatitis: modern aspects of pathogenesis and classifi cation]. Sovremennye texnologii v medicine. – [Modern technologies in medicine], 2011, no. 2, pp. 127–134.
      10. Smith K. A. Interleukin-2: inception, impact, and implications // Science. – 1988. Vol. 240, № 4856. P. 1169–1176.
      11. Kopylova O. I., Kuraeva T. L., Lavrikova E. Yu. Polimorfnye markery genov IL2RA i IL2: populyacionnye razlichiya v associacii s saxarnym diabetom [Polymorphic gene markers ILRA and IL2: population distinctions in association with diabetes mellitus]. Saxarny`j diabet – [Diabetes mellitus], 2012, no. 1, pp. 14–18.
      12. Kramer S., Schimpl A., Hünig T. Immunopathology of interleukin (IL) 2-defi cient mice: thymus dependence and suppression by thymus-dependent cells with an intact IL-2 gene // J Exp Med. – 1995. Vol. 182, № 6. P. 1769–1776.
      13. Shevach E. M. Certifi ed professionals: CD4(+) CD25(+) suppressor T cells // J Exp Med. – 2001. Vol. 193, № 11. F41–46.
      14. Kozlova I. V., Lipatova T. E., Afonina N. G., Kvetnoj I. M. Gastropatiya, inducirovannaya nesteroidnymi protivovospalitelnymi preparatami, u bolnyx osteoartrozom: rol nekotoryx faktorov diffuznoj endokrinnoj sistemy zheludka v vozniknovenii [Gastropathy induced by non-steroidal anti-infl ammatory drugs in patients with osteoarthritis: the role of some factors of the diff use endocrine system of the stomach in its occurrence]. Rossijskij zhurnal gastroe`nterologii, gepatologii,Hepatology, Coloproctology], 2006, no. 1, pp. 47–53.
      15. Kogan E. A., Nizyaeva N. V., Demura T. A. Avtonomnost rosta ochagov adenomioza: immunogistoximicheskie osobennosti ekspressii markerov [Th e autonomy of the growth of foci of adenomyosis: immunohistochemical characteristics of expression of markers]. Immunologiya – [Immunology], 2011, no. 12, pp. 311–325.
      16. Lazarenko L. V., Kosareva P. V., Samodelkin E.I, Horinko V. P. Patomorfologicheskie izmeneniya tkani podzheludochnoj zhelezy krys pri dlitelnom prieme nimesulida [Pathomorphological changes in rat pancreatic tissues caused by long administration of nimesulide]. Permskij medicinskij zhurnal. – [Perm medical journal], 2016, vol. 33, no. 4, pp. 78–81.
      17. Belot M-P, Fradin D, Mai N. et al. CpG Methylation Changes within the IL2RA Promoter in Type 1 Diabetes of Childhood Onset // PLoS ONE. – 2013. № 8 (7). e68093.
      18. Van Belle T. L., Coppiters K. T., Von Herrath M. G. Type 1 diabetes: etiology, immunology, and therapeutic strategies // Physiol Rev. – 2011. № 91(1). P. 79–118.
      19. Wolf M., Schimpl A., Hunig T. Control of T cell hyperactivation in IL-2-defi cient mice by CD4(+)CD25(–) and CD4(+) CD25(+) T cells: evidence for two distinct regulatory mechanisms // Eur J Immunol. № 31(6). P. 1637–1645.
      20. Rudensky A. Y. Regulatory T cells and Foxp3 // Immunol. Rev. 2011. № 241(1). P. 260–268.
      21. Bluestone J.A., Tang Q., Sedwick C. E. T regulatory cells in autoimmune diabetes: past challenges, future prospects // J. Clin. Immunol. – 2008. – Vol. 28. – P. 677–684.
      22. Sitrin J., Ring A., Garcia K. C. et al. Regulatory T cells control NK cells in an insulitic lesion by depriving them of IL-2 // JEM. 2013. № 210 (6) P. 1153–1165.
      23. Todd J.A., Walker N. M., Cooper J. D. et al. Robust associations of four new chromosome regions from genome-wide analyses of type 1 diabetes // Nat Genet. – 2007. № 39(7). P. 857–864.
      24. Maier L.M., Lowe C. E., Cooper J., Downes K. et al. IL2RA genetic heterogeneity in multiple sclerosis and type 1 diabetes susceptibility and soluble interleukin-2 receptor production // PLoS Genet. – 2009. № 5(1) e1000322.
      25. Vinokurova L. V., Drozdov V. N., Berezina O. I. Osobennosti techeniya saxarnogo diabeta pri xronicheskom pankreatite [Features of the course of diabetes in chronic pancreatitis]. Eksperimentalnaya i Klinicheskaya gastroenterologiya – [Experimental and Clinical Gastroenterology Journal], 2011, no. 7, pp. 59–63.
     


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    Lazarenko L. V., Kosareva P. V., Samodelkin E. I. Pathogenetic aspects of experimental pancreatopathy induced by nimesulid. Experimental and Clinical Gastroenterology. 2018;156(8): 68–72. DOI: 10.31146/1682-8658-ecg-156-8-68-72
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    1. E Federal Scientifi c Center for Medical and Preventive Health Risk Management Technologies (614990, Perm, Russia)
    2. E. A. Vagner Perm State Medical University (614990, Perm, Russia)

    Keywords: Oxidative stress, malondialdehyde, glutathione transferase, catalase, glutathione reductase, glutathione peroxidase, chronic hepatitis

    Abstract: Aims. The paper studies the polymorphism of antioxidant system genes, CAT, GSTP1, GPX4, in patients with chronic hepatitis C. Materials and methods. The paper examines 83 patients in the age from 18 to 70 with chronic hepatitis C in the reactivation phase and 30 healthy individuals. Real-time PCR methods are used to analyze polymorphic types of the studied genes, the DNA sequence of catalase genes CAT (rs1001179), glutathione-S-transferase GSTP1 (rs1695), glutathione peroxidase-4 GPX4 (rs713041) was used as the primers. Results. Correlative relationships between separate polymorphisms of genes and indicators of biochemical analysis of blood were found. For example, a polymorphic type of the gene GPX4 is associated with the lowest level of activity of glutathione reductase in heterozygotes, the activity of alkaline phosphatase is linked with the GSTP1 gene polymorphism, the level of catalase activity in blood serum correlates with the presence of a polymorphic type of the gene catalase CAT. Conclusions. Identifi cation of candidate genes in patients with HCV is predictive for changes in the activity of several enzymes of the antioxidant system (GR, catalase) and enzymes that characterize toxic liver damage (AST, gamma-GTP), and therefore allows to predict the course of HCV in these patients.

      1. Pimenov N. N., Chulanov V. P., Komarova S. V. Gepatit S v Rossii: ehpidemiologicheskaya harakteristika i puti sovershenstvovaniya diagnostiki i nadzora. [Hepatitis C in Russia: epidemiological characteristics and ways to improve diagnosis and supervision]. Ehpidemiologiya i infekcionnye bolezni – [Epidemiology and infectious diseases], 2012, no. 3, pp. 4–10.
      2. Liu G, Zhou W, Wang LI, Park S, Miller DP, Xu LL, Wein JC, Lyneh TJ, Christiani DC. MPO and SOD2 polymorhisms gender and the risk of non-small cell lung carcinoma. // Cancer Lett. 2004; 214:69–79.
      3. Nemoto M., Nishimura R., Sasaki T. et al. Genetic association of glutathione peroxidase-1 with coronary artery calcifi cation in type 2 diabetes: a case control study with multi-slice computed tomography. // Cardiovasc Diabetol. 2007 Sep 7; 6:23.
      4. Ivanov V. P., Polonikov A. V., Solodilova M. A., Panfi lov V. I. Fermenty antioksidantnoj sistemy i mul'tifaktorial'nye zabolevaniya: rol' gena selenzavisimoj glutationperoksidazy v formirovanii predraspolozhennosti k allergicheskoj forme bronhial'noj astmy. [Antioxidant enzymes and multifactorial diseases: the role of the gene of the antioxidant glutathione peroxidase in the formation of the allergic form of asthma]. Kurskij nauchno-prakticheskij vestnik “Chelovek i ego zdorov'e” – [Kursk scientifi c and practical Bulletin “Man and his health”], 2006, no. 4, pp. 39–45.
      5. Plahtij L. YA., Nagoev B. S., Otaraeva B. I., Tadeeva A. K., Ckhovrebov A. CH. Perekisnoe okislenie lipidov i antioksidantnaya zashchita u bol'nyh hronichesikm virusnym gepatitom S. [Lipid peroxidation and antioxidant protection in patients with hronicheskiy hepatitis C].Uspekhi sovremennogo estestvoznaniya – [Successes of modern natural science], 2010, no. 9, pp.141-143.
      6. Bulatova I. A., Shchekotova A. P., Krivcov A. V. Metabolicheskie narusheniya i polimorfi zm genov ?-2-adrenergicheskogo receptora i apolipoproteina V pri hronicheskom gepatite S i nealkogol'noj zhirovoj bolezni pecheni. [Metabolic disorders and polymorphism of the genes of ?-2-adrenergic receptor and apolipoprotein B in chronic hepatitis C and nonalcoholic fatty liver disease]. Klinicheskaya medicina – [Clinical medicine], 2015, v. 93, no. 1, pp. 35–41.
     


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    Krivtsov A. V., Ulitina P. V. Genes of the antioxidant system of CAT, GSTP1, GPX4 at patients with chronic viral hepatitis C. Experimental and Clinical Gastroenterology. 2018;156(8): 73–77. DO I: 10.31146/1682-8658-ecg-156-8-73-77
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    1. E. A. Vagner Perm State Medical University (614990, Perm, Russia)
    2. Federal Research Center of preventive health management health risk Rospotrebnadzor (Perm, Russia)

    Keywords: ulcerative colitis, vascular endothelial growth factor, polymorphism of the vascular endothelial growth factor gene

    Abstract: Objective. To assess the functional signifi cance of the –634G/C polymorphism of the vascular endothelial growth factor gene VEGFA (rs 2010963) in the progression of ulcerative colitis (UC) in patients in the Perm Krai. Materials and methods. 70 patients with UC in the active phase of the disease and 50 healthy donors were examined. The level of serum VEGF and the polymorphism of the VEGFA gene in the –634G/C region were studied. Results. The signifi cant increase of vascular endothelial growth factor VEGF, whose concentration was 239,40 (137,70– 554,30) pg/ml was determined; it was 2.8 times higher than in the control group. A signifi cant relationship between the level of VEGF in the serum and the severity of the attack of the UC and the index of endoscopic activity (IEA) (r = 0.39 and r = 0.45, respectively) was revealed. The distribution of genotypes and alleles of the –634G/C region of the VEGFA gene at position rs 2010963 did not reveal signifi cant diff erences in patients with UC and healthy individuals in the Perm Krai. However, in assessing the occurrence of allelic variations of the VEGFA gene with diff erent endoscopic activity of the UC, a minor allele C and an unfavorable homozygote CC associated with severe progressive UC fl ow are established. Conclusions. The risk of developing an unfavorable course of the UC, prone to relapse and progression, is associated with the carriage of allele C and homozygotes CC of the VEGFA –634 G/C gene, which should be taken into account in predicting the course of the disease and choosing a treatment strategy.

      1. Shimshoni E., Yablecovitch D., Liran Baram, Dotan I., Sagi I. ECM remodelling in IBD: innocent bystander or partner in crime? Th e emerging role of extracellular molecular events in sustaining intestinal infl ammation. Gut, 2015, vol. 64, no. 3, pp. 367–372. doi: 10.1136/gutjnl-2014–308048
      2. Akbari S., Hosseini M., Rezaei-Tavirani M., Rezaei-Tavirani M. et al. Common and diff erential genetically pathways between ulcerative colitis and colon adenocarcinoma. Gastroenterol Hepatol Bed Bench, 2017, vol. 10, no. 1, pp. 93–101.
      3. Stepina E. A., Khlynova O. V., Tuev A. V. Diagnosticheskaya i prognosticheskaya znachimost’ markerov endotelial’noy disfunktsii u patsientov s yazvennym kolitom [Diagnostic and prognostic signifi cance of markers of endothelial dysfunction in patients with ulcerative colitis]. Kazanskiy meditsinskiy zhurnal – [Kazan Medical Journal], 2016, vol. 97, no. 2, pp. 187–191 (in Russian).
      4. Kajdaniuk D., Marek B., Borgiel -Marek H., Kos-Kudła B. Vascular endothelial growth factor (VEGF) in physiology and pathophysiology. Polish Journal of Endocrinology, 2011, vol. 62, no. 5, pp. 444–455.
      5. Zdravkovic N. D., Jovanovic I. P., Radosavljevic G. D., Arsenijevic A. N. et al. Potential Dual Immunomodulatory Role of VEGF in Ulcerative Colitis and Colorectal Carcinoma. Int J Med Sci, 2014, vol. 11, no 9, pp. 936–947. doi: 10.7150 / ijms.8277
      6. Alkim C., Alkim H., Koksal A., Boga S. et al. Angiogenesis in Infl ammatory Bowel Disease. Int J Infl am, 2015: 970890. Available at https://www.ncbi.nlm.nih.gov/pmc/ articles/PMC4709626/ (Accessed 29 December 2015). doi: 10.1155/2015/970890
      7. Alkim C., Savas B., Ensari A. Expression of p53, VEGF, microvessel density, and cyclin-D1 in noncancerous tissue of infl ammatory bowel disease. Digestive Diseases and Sciences, 2009, vol. 54, no. 9, pp. 1979–1984. doi: 10.1007/s10620–008–0554-x
      8. Cromer W. E, Mathis J. M.,.Granger D. N., Chaitanya G. V. et al. Role of the endothelium in infl ammatory bowel diseases. World J Gastroenterol, 2011, vol. 17, no. 5, pp. 578–593. doi: 10.3748 / wjg.v17.i5.578
      9. McGovern D.P., Gardet A., Törkvist L., Goyette P. et al. Genome-wide association identifi es multiple ulcerative colitis susceptibility loci. Nat Genet, 2010, vol. 42, no. 4, pp. 332–7. doi: 10.1038/ng.549
      10. Shevchenko A. V., Konenkov V. I. Funktsional’nyy polimorfi zm genov semeystva VEGF [Functional polymorphism of genes of the VEGF family] Tsitokiny i vospalenie – [Cytokines and infl ammation], 2012, vol. 11, no. 4, pp. 14–20 (in Russian).
      11. Ferrante M., Pierik M., Henckaerts L. Th e role of vascular endothelial growth factor (VEGF) in inflammatory bowel disease. Inflammatory Bowel Diseases, 2006, vol. 12, no. 9, pp. 870–878. doi: 10.1097/01. mib.0000235095.01608.10.
      12. Ivashkin V. T., Shelygin Yu.A., Khalif I. L. et al. Klinicheskie rekomendatsii Rossiyskoy gastroenterologicheskoy assotsiatsii i assotsiatsii koloproktologov Rossii po diagnostike i lecheniyu yazvennogo kolita [Clinical recommendations of the Russian gastroenterological association and association of coloproctologists of Russia on the diagnosis and treatment of ulcerative colitis]. Koloproktologiya – [Coloproctology], 2017, vol. 59, no. 1, pp. 6–30 (in Russian).
      13. Shelud’ko V.S., Podluzhnaya M. Ya. Teoreticheskie osnovy meditsinskoy statistiki [Th eoretical bases of medical statistics]. Perm, 2001. 36 р. (in Russian).
     


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    Tretyakova Y. I., Bulatova I. A., Shchekotova A. P., Krivtsov A. V. The impact of polymorphism of the vascular endothelial growth factor gene VEGFA –634G/C (rs 2010963) on the progression of ulcerative colitis. Experimental and Clinical Gastroenterology. 2018;156(8): 78–82.DOI: 10.31146/1682-8658-ecg-156-8-78-82
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    1. E. A. Vagner Perm State Medical University (614990, Perm, Russia)
    2. Perm City Clinical Hospital № 4 (Perm, Russia)

    Keywords: procalcitonin, bile, cholangitis e

    Abstract: Procalcitonin concentration (PC) was determined in the simultaneously obtained samples of blood serum and bile. 56 patients were examined on 1–3 day after the operation. The subjects were divided into two groups. The main group contain of 31 patients with cholangitis and the comparison group includes 25 patients without infl ammation of the bile ducts. The PC level was determined by enzyme immunoassay method with the test systems with sensitivity according to the manufacturer — 0.01 ng/ml. The PC concentration in blood serum fl uctuated within wide limits: from 0.005 ng/ml to 10.11 ng/ml and was signifi cantly higher in the main group (p <0.000001). The PC level in bile was lower in comparison with serum and varied from undetectably low (

      1. Schneider HG, Lam QT. Procalcitonin for the clinical laboratory: a review// Pathology. – 2007. – Vol. 39, N. 4. – P. 383–390. doi: 10.1080/00313020701444564
      2. Gao Y., Yu K. J., Kang K. et al. Procalcitionin as a diagnostic marker to distinguish upper and lower gastrointestinal perforation//World J Gastroenterol. – 2017. – Vol. 23, N. 24. – P. 4422–4427. doi: 10.3748/wjg.v23.i24.4422
      3. Meisner M. Pathobiochemistry and clinical use of procalcitonin//Clin. Chim. Actaю. – 2002. – Vol. 323, N. 1–2. – P. 17–29. doi: 10.1016/S0009–8981(02)00101–8
      4. Meisner M. Biomarkers of sepsis: clinically useful?//Curr. Opin. Crit. Care. 2005. – Vol. 11, N. 5. – P. 473–480. doi: 10.1097/01.ccx.0000176694.92883.ce
      5. Chiappini F.M., Matita C., Sole P. et al. Urinary procalcitonin associated with a microbiologically diagnosed pneumonitis: preliminary result // Critical Care. – 1998. – N. 2(Suppl 1). – P038. doi: 10.1186/cc168
      6. Linssen C.F., Bekers O., Drent M., Jacobs J. A. C-reactive protein and procalcitonin concentrations in bronchoalveolar lavage fl uid as a predictor of ventilator-associated pneumonia // Ann. Clin. Biochem. – 2008. – Vol. 45, N. 3. – P. 293–298. doi: 10.1258/acb.2007.007133
      7. Determan R., Millo J., Gibot S. et. el. Serial changes in soluble triggering receptor expressed on myeloid cells in the lung during development of ventilator – associated pneumonia // Intensive Care Med. – 2005. – Vol. 31. – P. 1495–1500. doi: 10.1007/s00134–005–2818–7}
      8. Kon’kova A. Yu., Sosnin D. Yu., Gavrilova T. V., Chereshneva M. V. Issledovanie prokal’tsitonina v sleznoy zhidkosti i syvorotke krovi pri uveitakh. [Th e analysis of procalcitonin in lacrimal fl uid and blood serum under uveitis] Klin. lab. diagn. 2015; 60 (10):21–25
      9. Sosnin D. Yu., Zubareva N. A., Nenasheva O. Yu. et al. Kontsentratsiya prokal’tsitonina v eyakulyate i syvorotke krovi zdorovykh muzhchin i muzhchin s oligozooastenospermiey [Ejaculate and serum procalcitonin levels in healthy men and men with oligoasthenozoospermia]. Urologiya. 2017; 1:61–65. doi: 10.18565/urol.2017.1.61–65
      10. Slavakis A, Papadimas J. Procalcitonin: does it play a role in male reproduction? // Fertil Steril. – 2000. – Vol. 74, N.6. – P. 1227–1228. doi: 10.1016/S0015–0282(00)01588–0
      11. Chereshnev V. A., Sosnin D. Yu., Zubareva N. A. et al. Kontsentratsiya prokal’tsitonina v krovi i enteral’nom otdelyaemom u patsientov v rannem posleoperatsionnom periode [Th e concentration of procalcitonin in blood and enteric exudation in patients at early post-operation period]. Klin. lab. diagn. 2014; 59(10):20–24.
      12. Bassim C. W., Redman R. S., De Nucci D. J. et. al. Salivary procalcitonin and periodontitis in diabetes//J. Dent. Res. – 2008. – Vol. 87, N. 7. – P. 630–634. doi: 10.1177/154405910808700707
      13. Yousefi manesh H., Robati M., Malekzadeh H. et al. Investigation of the association between salivary procalcitonin concentration and chronic periodontitis//Cell J. – 2015. – Vol. 17, N. 3. – P. 559–563. doi: 10.22074/cellj.2015.17
      14. Redman R., Kerr G., Payne J. et al. Salivary and serum procalcitonin and C-reactive protein as biomarkers of periodontitis in United States veterans with osteoarthritis or rheumatoid arthritis// Biotechnic & Histochemistry: Offi cial Publication of the Biological Stain Commission. – 2016. – Vol. 91, N. 2. – P. 77–85. doi: 10.3109/10520295.2015.1082625
      15. Boyer JL. Bile formation and secretion // Compr. Physiol. 2013. – Vol. 3, N3. – P. 1035–78. doi: 10.1002/cphy.c120027
      16. Reshetnyak VI. Physiological and molecular biochemical mechanisms of bile formation//World J Gasroenterol. 2013. – Vol. 19, N. 42. – P. 7341–60. doi: 10.3748/wjg.v19. i42.7341
      17. Podoprigorova V. G., Tsygankova G. M., Farashchuk N. F. Osobennosti tsitoliticheskogo sindroma u bol’nykh khronicheskimi diff uznymi zabolevaniyami pecheni v zavisimosti ot tyazhesti patologicheskogo protsessa [Features of the cytolytic syndrome in patients with chronic diff use liver diseases, depending on the severity of the pathological process]. Klin. lab. diagnostika. 2006;1:15–18.
      18. Sosnin D. Yu., Zubareva N. A. Aktivnost’ katalazy i laktatdegidrogenazy zhelchi u patsientov s zabolevaniyami pecheni i zhelchevyvodyashchikh putey [Catalase and lactate dehydrogenase activity of bile in patients with diseases of the liver and biliary tract]. Permskiy med. zhurnal. 2010;27(4):88–94.
      19. Shinya S., Sasaki T., Yamashita Y. et al. Procalcitonin as a useful biomarker for determining the need to perform emergency biliary drainage in cases of acute cholangitis//J Hepatobiliary Pancreat Sci., – 2014. – Vol.21, N. 10. – P. 777–785. doi: 10.1002/jhbp.132
      20. Umefune G., Kogure H., Hamada T. et al. Procalcitonin is a useful biomarker to predict severe acute cholangitis: a single-center prospective study//J Gastroenterol. 2017. – Vol. 52, N. 6. – P. 734–745. doi: 10.1007/s00535– 016–1278-x doi: 10.1007/s00535–016–1278-x
     


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    Sosnin D. Yu., Zubareva N. A., Popova N. N., Renzhin A. V. Blood and bile procalcitonin concentration in patients with acute cholangitis. Experimental and Clinical Gastroenterology. 2018;156(8): 83–87.
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