Αποτελέσματα αναζήτησης - "ГЕНЕТИЧЕСКИЕ ФАКТОРЫ РИСКА"

1

Academic Journal

Idiosyncratic Drug-Induced Liver Injury: From Pathogenesis to Risk Reduction ; Идиосинкратическая лекарственная гепатотоксичность — от патогенеза к снижению риска

Συγγραφείς: I. A. Mazerkina, И. А. Мазеркина

Συνεισφορές: The study reported in this publication was carried out as part of publicly funded research project No. 056-00052-23-00 and was supported by the Scientific Centre for Expert Evaluation of Medicinal Products (R&D public accounting No. 121022400082-4)., Работа выполнена в рамках государственного задания ФГБУ «НЦЭСМП» Минздрава России № 056-00052-23-00 на проведение прикладных научных исследований (номер государственного учета НИР 121022400082-4).

Πηγή: Safety and Risk of Pharmacotherapy; Том 11, № 2 (2023); 204-214 ; Безопасность и риск фармакотерапии; Том 11, № 2 (2023); 204-214 ; 2619-1164 ; 2312-7821

Θεματικοί όροι: человеческий лейкоцитарный антиген, drug-induced hepatotoxicity, iDILI, pathogenesis of idiosyncratic drug-induced hepatotoxicity, immune tolerance, T-cells, signalling pathway activation, genetic risk factors, human leukocyte antigen, HLA, лекарственное повреждение печени, патогенез лекарственной гепатотоксичности, иммунотолерантность, Т-клетки, сигнальные пути активации, генетические факторы риска

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Genetic susceptibility to diclofenac-induced hepatotoxicity: contribution of UGT2B7, CYP2C8, and ABCC2 genotypes. Gastroenterology. 2007;132(1):272–81. https://doi.org/10.1053/j.gastro.2006.11.023; Wattanapokayakit S, Mushiroda T, Yanai H, Wichukchinda N, Chuchottawon C, Nedsuwan S, et al. NAT2 slow acetylator associated with anti-tuberculosis drug-induced liver injury in Thai patients. Int J Tuberc Lung Dis. 2016;20(10):1364–9. https://doi.org/10.5588/ijtld.15.0310; Sharma SK, Jha BK, Sharma A, Sreenivas V, Upadhyay V, Jaisinghani C, et al. Genetic polymorphisms of N-acetyltransferase 2 & susceptibility to antituberculosis drug-induced hepatotoxicity. Indian J Med Res. 2016;144(6):924–8. https://doi.org/10.4103/ijmr.IJMR_684_14; Du H, Chen X, Fang Y, Yan O, Xu H, Li L, et al. Slow N-acetyltransferase 2 genotype contributes to anti-tuberculosis drug-induced hepatotoxicity: a meta-analysis. Mol Biol Rep. 2013;40(5):3591–6. https://doi.org/10.1007/s11033-012-2433-y; Suvichapanich S, Fukunaga K, Zahroh H, Mushiroda T, Mahasirimongkol S, Toyo-Oka L, et al. NAT2 ultra-slow acetylator and risk of anti-tuberculosis drug-induced liver injury: a genotype-based meta-analysis. Pharmacogenet Genomics. 2018;28(7):167–76. https://doi.org/10.1097/FPC.0000000000000339; Zhang M, Wang S, Wilffert B, Tong R, van Soolingen D, van den Hof S, Alffenaar JW. The association between the NAT2 genetic polymorphisms and risk of DILI during anti-TB treatment: a systematic review and meta-analysis. Br J Clin Pharmacol. 2018;84(12):2747–60. https://doi.org/10.1111/bcp.13722; Li YJ, Phillips EJ, Dellinger A, Nicoletti P, Schutte R, Li D, et al. Human leukocyte antigen B*14:01 and B*35:01 are associated with trimethoprim-sulfamethoxazole induced liver injury. Hepatology. 2021;73(1):268–81. https://doi.org/10.1002/hep.31258; Hirata K, Takagi H, Yamamoto M, Matsumoto T, Nishiya T, Mori K, et al. Ticlopidine-induced hepatotoxicity is associated with specific human leukocyte antigen genomic subtypes in Japanese patients: a preliminary case-control study. Pharmacogenomics J. 2008;8(1):29–33. https://doi.org/10.1038/sj.tpj.6500442; Li C, Rao T, Chen X, Zou Z, Wei A, Tang J, et al. HLA-B*35:01 allele is a potential biomarker for predicting Polygonum multiflorum-induced liver injury in humans. Hepatology. 2019;70(1):346–57. https://doi.org/10.1002/hep.30660; Yang WN, Pang LL, Zhou JY, Qiu YW, Miao L, Wang SY, et al. Single-nucleotide polymorphisms of HLA and Polygonum multiflorum-induced liver injury in the Han Chinese population. World J Gastroenterol. 2020;26(12):1329–39. https://doi.org/10.3748/wjg.v26.i12.1329; O’Donohue J, Oien KA, Donaldson P, Underhill J, Clare M, MacSween RN, Mills PR. Co-amoxiclav jaundice: clinical and histological features and HLA class II association. Gut. 2000;47(5):717–20. https://doi.org/10.1136/gut.47.5.717; Aithal GP, Ramsay L, Daly AK, Sonchit N, Lea thart JB, Alexander G, et al. Hepatic adducts, circulating antibodies, and cytokine polymorphisms in patients with diclofenac hepatotoxicity. Hepatology. 2004;39(5):1430–40. https://doi.org/10.1002/hep.20205; Uffelmann E, Huang QQ, Munung NS, Vries J, Okada Y, Martin AR, et al. Genome-wide association studies. Nat Rev Methods Primers. 2021;(1):59. https://doi.org/10.1038/s43586-021-00056-9; Suvichapanich S, Wattanapokayakit S, Mushiroda T, Yanai H, Chuchottawon C, Kantima T, et al. Genomewide association study confirming the association of NAT2 with susceptibility to antituberculosis drug-induced liver injury in Thai patients. Antimicrob Agents Chemother. 2019;63(8):e02692–18. https://doi.org/10.1128/AAC.02692-18; Lucena MI, Molokhia M, Shen Y, Urban TJ, Aithal GP, Andrade RJ, et al. Susceptibility to amoxicillin-clavulanate-induced liver injury is influenced by multiple HLA class I and II alleles. Gastroenterology. 2011;141(1):338–47. https://doi.org/10.1053/j.gastro.2011.04.001; Nicoletti P, Barrett S, McEvoy L, Daly AK, Aithal G, Lucena MI, et al. Shared genetic risk factors across carbamazepine-induced hypersensitivity reactions. Clin Pharmacol Ther. 2019;106(5):1028–36. https://doi.org/10.1002/cpt.1493; Nicoletti P, Aithal GP, Bjornsson ES, Andrade RJ, Sawle A, Arrese M, et al. Association of liver injury from specific drugs, or groups of drugs, with polymorphisms in HLA and other genes in a genome-wide association study. Gastroenterology. 2017;152(5):1078–89. https://doi.org/10.1053/j.gastro.2016.12.016; Urban TJ, Nicoletti P, Chalasani N, Serrano J, Stolz A, Daly AK, et al. Minocycline hepatotoxicity: clinical characterization and identification of HLA-B*35:02 as a risk factor. J Hepatol. 2017;67(1):137–44. https://doi.org/10.1016/j.jhep.2017.03.010; Bruno CD, Fremd B, Church RJ, Daly AK, Aithal GP, Björnsson ES, et al. HLA associations with infliximab-induced liver injury. Pharmacogenomics J. 2020;20(5):681–6. https://doi.org/10.1038/s41397-020-0159-0; Daly AK, Donaldson PT, Bhatnagar P, Shen Y, Pe’er I, Floratos A, et al. HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin. Nat Genet. 2009;41(7):816–9. https://doi.org/10.1038/ng.379; Nicoletti P, Aithal GP, Chamberlain TC, Coulthard S, Alshabeeb M, Grove JI, et al. Drug-induced liver injury due to flucloxacillin: relevance of multiple human leukocyte antigen alleles. Clin Pharmacol Ther. 2019;106(1):245–53. https://doi.org/10.1002/cpt.1375; Kindmark A, Jawaid A, Harbron CG, Barratt BJ, Bengtsson OF, Andersson TB, et al. Genome-wide pharmacogenetic investigation of a hepatic adverse event without clinical signs of immunopathology suggests an underlying immune pathogenesis. Pharmacogenomics J. 2008;8(3):186–95. https://doi.org/10.1038/sj.tpj.6500458; Spraggs CF, Budde LR, Briley LP, Bing N, Cox CJ, King KS, et al. HLA-DQA1*02:01 is a major risk factor for lapatinib-induced hepatotoxicity in women with advanced breast cancer. J Clin Oncol. 2011;29(6):667–73. https://doi.org/10.1200/JCO.2010.31.3197; Parham LR, Briley LP, Li L, Shen J, Newcombe PJ, King KS, et al. Comprehensive genome-wide evaluation of lapatinib-induced liver injury yields a single genetic signal centered on known risk allele HLA-DRB1*07:01. Pharmacogenomics J. 2016;16(2):180–5. https://doi.org/10.1038/tpj.2015.40; Singer JB, Lewitzky S, Leroy E, Yang F, Zhao X, Klickstein L, et al. A genome-wide study identifies HLA alleles associated with lumiracoxib-related liver injury. 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Διαθεσιμότητα: https://www.risksafety.ru/jour/article/view/365
https://doi.org/10.30895/2312-7821-2023-11-2-204-214

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2

Academic Journal

The role of occupational factors and individual susceptibility in the development and course of bronchopulmonary diseases ; Профессиональные факторы и роль индивидуальной восприимчивости к развитию и течению бронхолегочных заболеваний

Συγγραφείς: Olga S. Vasilieva, Lyudmila P. Kuzmina, Alexandr V. Chernyak, Natalia Yu. Kravchenko, Marina M. Koljaskina, О. С. Васильева, Л. П. Кузьмина, А. В. Черняк, Н. Ю. Кравченко, М. М. Коляскина

Πηγή: PULMONOLOGIYA; Том 31, № 4 (2021); 463-468 ; Пульмонология; Том 31, № 4 (2021); 463-468 ; 2541-9617 ; 0869-0189

Θεματικοί όροι: динамические наблюдения, occupational asthma, chronic obstructive pulmonary disease, genetic risk factors, individual sensitivity, long-term observations, профессиональная бронхиальная астма, хроническая обструктивная болезнь легких, генетические факторы риска, индивидуальная чувствительность

Περιγραφή αρχείου: application/pdf

Relation: https://journal.pulmonology.ru/pulm/article/view/2407/1858; De Matteis S., Heederik D., Burdorf A. et al. Current and new challenges in occupational lung diseases. Eur. Respir. Rev. 2017; 26 (146): 170080. DOI:10.1183/16000617.0080-2017.; Baur X., Sigsgaard T., Aasen T.B. et al. Guidelines for the management of work-related asthma. Eur. Respir. J. 2012; 39 (3): 529–545. DOI:10.1183/09031936.00096111.; Suganuma N., Natori Y., Kurosawa H. et al. Update of occupational lung disease. J. Occup. Health. 2019; 61 (1): 10–18. DOI:10.1002/1348-9585.12031.; Thirteenth Session of the Joint ILO/WHO Committee on Occupational Health. Report of the Committee, JCOH/XIII/D.4. Geneva, 9–12 December, 2003. Available at: http://www.icohweb.org/site/multimedia/asbestos/Enclosure_5.pdf [Accessed: July 1, 2021].; Kobayashi S., Hanagama M., Yamanda S. et al.Impact of a large-scale natural disaster on patients with chronic obstructive pulmonary disease: the aftermath of the 2011 Great East Japan Earthquake. Respir. Investig. 2013; 51 (1): 17–23. DOI:10.1016/j.resinv.2012.10.004.; Tarlo S.M. Occupational lung diseases. Can. J. Respir. Crit. Care Sleep Med. 2020; 4 (Suppl. 1): S6–8. DOI:10.1080/24745332.2020.1726231.; Cullinan P., Muñoz X., Suojalehto H. et al. Occupational lung diseases: from old and novel exposures to effective preventive strategies. Lancet Respir. Med. 2017; 5 (5): 445–455. DOI:10.1016/S2213-2600(16)30424-6.; European Lung White Book. Occupational risk factors. Available at: https://www.erswhitebook.org/chapters/occupational-risk-factors/ [Accessed: July 1, 2021].; Burge P.S. Recent developments in occupational asthma. Swiss. Med. Wkly. 2010; 140 (9–10): 128–132.; Schulte P., Howard J. Genetic susceptibility and the setting of occupational health standards. Annu. Rev. Public. Health. 2011; 32: 149–159. DOI:10.1146/annurev-publhealth-031210-101144.; Васильева О.С., Кузьмина Л.П., Кулемина Е.А., Коляскина М.М. Клинические и молекулярно-генетические аспекты формирования бронхиальной астмы мясоупаковщиков. Пульмонология. 2012; (3): 39–44. DOI:10.18093/0869-0189-2012-0-3-39-44.; Кузьмина Л.П., Хотулева А.Г. Молекулярные механизмы нозологической синтропии профессиональной бронхиальной астмы. В кн.: Измеров Н.Ф., ред. Профессиональные заболевания органов дыхания: национальное руководство. М.: ГЭОТАРМедиа; 2015: 180–187.; Park D., Moore V.C., Burge C.B.S. et al. Serial PEF measurement is superior to cross-shift change in diagnosing occupational asthma. Eur. Respir. J. 2009; 34 (3): 574–578. DOI:10.1183/09031936.00150108.; Васильева О.С., Соркина Н.С. Профессиональная бронхиальная астма. В кн.: Измеров Н.Ф., Чучалин А.Г., ред. Профессиональные заболевания органов дыхания. М.: ГЭОТАР-Медиа; 2015: 338–363.; Васильева О.С., Черняк А.В., Неклюдова Г.В. и др. Клиникофункциональные методы обследования в диагностике профессиональных бронхолегочных заболеваний. В кн.: Измеров Н.Ф., ред. Профессиональные заболевания органов дыхания: национальное руководство. М.: ГЭОТАР-Медиа; 2015: 607–634.; Burge S. Management of an individual worker with occupational asthma. In: Sigsgaard T., Heederik D., eds. Occupational Asthma. Progress in Inflammation Research. Birkhäuser Basel. 2010: 249–270. DOI:10.1007/978-3-7643-8556-9_14.; Trivedi V., Apala D.R., Iyer V.N. Occupational asthma: diagnostic challenges and management dilemmas. Curr. Opin. Pulm. Med. 2017; 23 (2): 177–183. DOI:10.1097/MCP.0000000000000352.; Lemiere C., Bernstein D. Occupational asthma: Management, prognosis and prevention. UpToDate. November 07, 2019. Available at: https://www.uptodate.com/contents/occupational-asthma-management-prognosis-and-prevention [Accessed: July 1, 2021].; British Thoracic Society. British Guidelines on the Management of Asthma. Revised 2017. Available at: https://www.brit-thoracic.org.uk [Accessed: July 6, 2018].; Mehta A.J., Miedinger D., Keidel D. et al. Occupational exposure to dusts, gases and fumes and incidence of chronic obstructive pulmonary disease in the swiss cohort study on air pollution and lung and heart diseases in adults. Am. J. Respir. Crit. Care Med. 2012; 185 (12): 1292–1300. DOI:10.1164/rccm.201110-1917OC.; Kurth L., Doney B., Weinmann S. Occupational exposures and chronic obstructive pulmonary disease (COPD): comparison of a COPD-specific job exposure matrix and expert-evaluated occupational exposures. Occup. Environ. Med. 2017; 74 (4): 290–293. DOI:10.1136/oemed-2016-103753.; https://journal.pulmonology.ru/pulm/article/view/2407

Διαθεσιμότητα: https://journal.pulmonology.ru/pulm/article/view/2407
https://doi.org/10.18093/0869-0189-2021-31-4-463-468

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SINGLE NUCLEOTIDE POLYMORPHISMS WITHIN GENES REGULATING IMMUNE RESPONSE AND ANTIOXIDANT DEFENCE IN PATIENTS WITH COLORECTAL AND GASTRIC CANCER

Συγγραφείς: Асия Дамировна Падюкова, Арсений Евгеньевич Южалин, Антон Геннадьевич Кутихин, Алексей Николаевич Волков, Юлия Александровна Попова, Алексей Станиславович Животовский, Юрий Абрамович Магарилл, Евгений Анатольевич Цитко, Елена Борисовна Брусина

Πηγή: Медицина в Кузбассе, Vol 16, Iss 1, Pp 50-56 (2017)

Θεματικοί όροι: колоректальный рак, рак желудка, гены, полиморфизмы, генетические факторы риска, Medicine

Περιγραφή αρχείου: electronic resource

Relation: http://mednauki.ru/index.php/MK/article/view/64; https://doaj.org/toc/1819-0901

Σύνδεσμος πρόσβασης: https://doaj.org/article/0cb0fc33ed8a4bf796a8445efaacc0b0

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GENETIC DIAGNOSIS AND MECHANISMS OF CHRONIC BRONCHITIS IN CHILDREN ; ГЕНЕТИЧЕСКИЕ МЕХАНИЗМЫ ФОРМИРОВАНИЯ И ДИАГНОСТИКИ ХРОНИЧЕСКОГО БРОНХИТА У ДЕТЕЙ ; ГЕНЕТИЧНІ МЕХАНІЗМИ ФОРМУВАННЯ ТА ДІАГНОСТИКИ ХРОНІЧНОГО БРОНХІТУ В ДІТЕЙ

Συγγραφείς: Shamsiev, A. M., Yusupov, Sh. A., Muhammadieva, L. A., Yuldashev, B. A.

Πηγή: Bulletin of Scientific Research; No 1 (2017) ; Вестник научных исследований; № 1 (2017) ; Вісник наукових досліджень; № 1 (2017) ; 2415-8798 ; 1681-276X ; 10.11603/2415-8798.2017.1

Θεματικοί όροι: chronic bronchitis, children, genetic risk factors, matrix metalloproteinases, хронический бронхит, дети, генетические факторы риска, матричные металлопротеиназы, хронічний бронхіт, діти, генетичні фактори ризику, матричні металопротеїнази

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Relation: https://ojs.tdmu.edu.ua/index.php/visnyk-nauk-dos/article/view/7468/7122; https://repository.tdmu.edu.ua//handle/123456789/12410

Διαθεσιμότητα: https://repository.tdmu.edu.ua//handle/123456789/12410
https://ojs.tdmu.edu.ua/index.php/visnyk-nauk-dos/article/view/7468
https://doi.org/10.11603/2415-8798.2017.1.7468

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Сочетание полиморфизмов генов PAI-1 -675 5G>4G, FXIII: Val34Leu G>T и ITGA2: 807 С>T у женщин с бесплодием может рассматриваться как предиктор неудач вспомогательных репродуктивных технологий: The combination of polymorphisms of genes PAI-1 -675 5G>4G, FXIII: Val34Leu G>T and ITGA2: 807 C>T in women with infertility can be considered as a predictor of failures of assisted reproductive technologies

Πηγή: Тромбоз, гемостаз и реология.

Θεματικοί όροι: генетические факторы риска, полиморфизм, genetic risk factors, экстракорпоральное оплодотворение, in vitro fertilization, 3. Good health, polymorphism

Σύνδεσμος πρόσβασης: https://thrj.ru/index.php/thrj/article/view/196

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SINGLE NUCLEOTIDE POLYMORPHISMS WITHIN GENES REGULATING IMMUNE RESPONSE AND ANTIOXIDANT DEFENCE IN PATIENTS WITH COLORECTAL AND GASTRIC CANCER ; АНАЛИЗ ПОЛИМОРФИЗМОВ ГЕНОВ TOLL-ПОДОБНЫХ РЕЦЕПТОРОВ, ИНТЕРЛЕЙКИНОВ И АНТИОКСИДАНТНОЙ ЗАЩИТЫ У ПАЦИЕНТОВ С КОЛОРЕКТАЛЬНЫМ РАКОМ И РАКОМ ЖЕЛУДКА

Συγγραφείς: Падюкова, Асия Дамировна, Южалин, Арсений Евгеньевич, Кутихин, Антон Геннадьевич, Волков, Алексей Николаевич, Попова, Юлия Александровна, Животовский, Алексей Станиславович, Магарилл, Юрий Абрамович, Цитко, Евгений Анатольевич, Брусина, Елена Борисовна

Πηγή: Medicine in Kuzbass; Том 16, № 1 (2017): март; 50-56 ; Медицина в Кузбассе; Том 16, № 1 (2017): март; 50-56 ; 2588-0411 ; 1819-0901

Θεματικοί όροι: colorectalcancer, gastriccancer, genes, polymorphisms, genetic risk factors, колоректальный рак, рак желудка, гены, полиморфизмы, генетические факторы риска

Περιγραφή αρχείου: text/html; application/pdf

Relation: http://mednauki.ru/index.php/MK/article/view/64/131; http://mednauki.ru/index.php/MK/article/view/64/143; http://mednauki.ru/index.php/MK/article/view/64

Διαθεσιμότητα: http://mednauki.ru/index.php/MK/article/view/64

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FREQUENCY ASSESSMENT OF KEY HEMOSTATIC GENES POLYMORPHISMS AND OF FOLATE METABOLISM GENES IN PATIENTS WITH ISCHEMIC HEART DISEASE

Πηγή: Тромбоз, гемостаз и реология.

Θεματικοί όροι: ishemic heart disease, myocardial infarction, генетические факторы риска, полиморфизм, ишемическая болезнь сердца, genetic risk factors, инфаркт миокарда, 3. Good health, polymorphism

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SINGLE NUCLEOTIDE POLYMORPHISMS WITHIN GENES REGULATING IMMUNE RESPONSE AND ANTIOXIDANT DEFENCE IN PATIENTS WITH COLORECTAL AND GASTRIC CANCER

Πηγή: Медицина в Кузбассе, Vol 16, Iss 1, Pp 50-56 (2017)

Θεματικοί όροι: гены, полиморфизмы, колоректальный рак, генетические факторы риска, Medicine, рак желудка, 3. Good health

Σύνδεσμος πρόσβασης: https://doaj.org/article/0cb0fc33ed8a4bf796a8445efaacc0b0

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ПЕРИНАТАЛЬНЫЙ АНАМНЕЗ И ГЕНЕТИЧЕСКИЕ АСПЕКТЫ ФОРМИРОВАНИЯ БРОНХОЛЕГОЧНОЙ ДИСПЛАЗИИ У ГЛУБОКО НЕДОНОШЕННЫХ МЛАДЕНЦЕВ

Συγγραφείς: Панов, П., Ахмадеева, Э., Панова, Л., Байков, Д.

Θεματικοί όροι: БРОНХОЛЕГОЧНАЯ ДИСПЛАЗИЯ, НЕДОНОШЕННЫЕ МЛАДЕНЦЫ, ПЕРИНАТАЛЬНЫЕ И ГЕНЕТИЧЕСКИЕ ФАКТОРЫ РИСКА

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Διαθεσιμότητα: http://cyberleninka.ru/article/n/perinatalnyy-anamnez-i-geneticheskie-aspekty-formirovaniya-bronholegochnoy-displazii-u-gluboko-nedonoshennyh-mladentsev
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MODERN VIEWS ON ETIOLOGY OF CHRONIC PANCREATITIS AND CORRECTION OF FUNCTIONAL INSUFFICIENCY OF THE PANCREAS ; СОВРЕМЕННЫЕ ПРЕДСТАВЛЕНИЯ ОБ ЭТИОЛОГИИ ХРОНИЧЕСКОГО ПАНКРЕАТИТА И КОРРЕКЦИИ ФУНКЦИОНАЛЬНОЙ НЕДОСТАТОЧНОСТИ ПОДЖЕЛУДОЧНОЙ ЖЕЛЕЗЫ

Συγγραφείς: E. А. Kornienko, A. A. Yagupova, Е. А. Корниенко, А. А. Ягупова

Πηγή: Current Pediatrics; Том 11, № 4 (2012); 134-138 ; Вопросы современной педиатрии; Том 11, № 4 (2012); 134-138 ; 1682-5535 ; 1682-5527

Θεματικοί όροι: ферментотерапия, hereditary pancreatitis, genetic risk factors, enzyme therapy, наследственный панкреатит, генетические факторы риска

Περιγραφή αρχείου: application/pdf

Relation: https://vsp.spr-journal.ru/jour/article/view/467/372; Banks P. A. Classification and diagnosis of chronic pancreatitis. J. Gastroenterol. 2007; 42 (S XVII): 148–151.; Ma M. H., Bai H. X., Park A. J. et al. Risk factors associated with biliary pancreatitis in children. J. Pediatr. Gasreornterol. Nutr. 2012; 54 (5): 651–656.; Okazaki K., Chiba T. Autoimmune related pancreatitis. Gut. 2002; 51: 1–4.; Корниенко Е. А., Ягупова А. А., Лобода Т. Б., Фадина С. А. Аутоиммунный панкреатит в педиатрической практике. Фарматека. 2011; 1 (214): 47–54.; Sultan M., Werlin S., Venkatasubramani N. Genetic prevalence and characteristics in children with recurrent pancreatitis. J. Pediatr. Gastroenterol. Nutr. 2012; 54 (5): 645–650.; Witt H., Becker M. Genetics of chronic pancreatitis. J. Pediatr. Gastroenterol. Nutr. 2002; 34 (2): 125–136.; Scheele G. A., Bartelt D., Bieger W. Characterization of human exocrine pancreatic proteins by two-dimentional sequeces. Biochemistry. 1978; 17: 1669–1675.; Keiles S., Kammesheidt A. Identification of CFTR, PRSS1 and SPINK1 mutations in 381 patients with pancreatitis. Pancreas. 2006; 33: 221–227.; Matthew P., Wyllie R., Caulfield M. et al. Chronic pancreatitis in late childhood and adolescence. Clin. Pediatr. 1994; 33: 88–94.; Witt H., Luck W., Hennies H. C. et al. Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis. Nat. Genet. 2000; 25: 213–216.; Chen J. M., Mercier B., Audrezet M. P. et al. Mutations of the pancreatic secretory trypsin inhibitor gene in idiopathic chronic pancreatitis. Gastroenterology. 2001; 120: 1061–1064.; Del Rosario J. F., Putnam P. E., Orenstein D. M. Chronic pancreatitis in a patient with cystic fibrosis and clinical pancreatic insufficiency. J. Pediatr. 1995; 126: 951–952.; Freedman S. D., Blanco P., Shea J. C. et al. Mechanisms to explain pancreatic dysfunction in cystic fibrosis. Gastroenterol. Clin. North. Am. 2000; 84: 657–664.; Bishop M. D., Freedman S. D., Zielenski J. et al. The cystic fibrosis transmembrane conductance regulator gene and ion channel function in patients with idiopathic pancreatitis. Hum. Genet. 2005; 118: 372–381.; Whitcomb D. C., Gorry M. C., Preston R. A. et al. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene. Nat. Genet. 1996; 14: 141–145.

Διαθεσιμότητα: https://vsp.spr-journal.ru/jour/article/view/467
https://doi.org/10.15690/vsp.v11i4.372

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