JOURNAL CONTENT
CONTACT

Submission of the manuscript is online via e-mail
ecgarticle@gmail.com or
cholerez@mail.ru

Tel: +7 903 250 5288

Editorial Correspondence e-mail
gastrossr@gmail.com


Publishing, Subscriptions, Sales and Advertising, Correspondence e-mail
journal@cniig.ru

Tel: +7 917 561 9505

THE RULES OF SUBMITTING AN ARTICLE

READ

Scimago Journal & Country Rank

SCImago Journal & Country Rank

CLINICAL GASTROENTEROLOGY

    1. North-West Federal Medical Research Center named after V. A. Almazov (St. Petersburg, Russian Federation)
    2. The Leningrad Regional State Budgetary Healthcare Institution “Children’s Clinical Hospital” (St. Petersburg, Russian Federation)

    Abstract:The aim was to study the spectrum of gastroenterological diseases in adolescents with morbid obesity. Materials and methods: The study 34adolescents with a BMI> 35, and 20 adolescents with a BMI of 25 to 34. EGD, US, Fibromax test, lipidogram, the level of blood glucose and insulin was studied. Results. When morbid obesity more often were diagnosed esophagitis (26 % and 11,3 %, p <0,05), hiatal hernia (6 % and 0 %, p <0,05), NAFLD (71 % and 42,5 %, p <0,001), chronic gastritis (59 % and 35 %, p <0,05) and duodenal ulcer (6 % and 0 %, p <0,05). The positive correlations between gastrointestinal diseases and BMI, hyperinsulinemia and dyslipidemia were found. Thus Gastroenterological incidence of teenage obesity increases with increasing BMI and progression of metabolic disorders.

      1. Желудочно-кишечный тракт и ожирение у детей / под ред. В. П. Новиковой, М. М. Гуровой. СПб: СпецЛит, 2016. - 302 с.
      2. Метаболический синдром у детей и подростков: взгляд педиатра: учебное пособие / Захарова И. Н., Малявская С. И., Звенигородская Л. А., Боровик Т. Э., Творогова Т. М., Дмитриева Ю. А., Васильева С. В. Российская медицинская академия последипломного образования. Москва; Киров, 2016.
      3. Aaron S. Kelly, Sarah E. Barlow, Goutham Rao, Thomas H. Inge, Laura L. Hayman, Julia Steinberger, Elaine M. Urbina, Linda J. Ewing, Stephen R. Daniels. Severe Obesity in Children and Adolescents: Identification, Associated Health Risks, and Treatment Approaches. A Scientific Statement From the American Heart Association. Circulation. 2013; 128(15): 1689-1712
      4. Bahk J, Khang YH. Trends in childhood obesity and central adiposity between 1998-2001 and 2010-2012 according to household income and urbanity in Korea. BMC Public Health. 2016 Jan 7; 16:18.
      5. Bervoets L, Massa G. Defining morbid obesity in children based on BMI 40 at age 18 using the extended international (IOTF) cut-offs. Pediatr Obes. 2014 Oct; 9(5): e94-8.
      6. Ice CL, Murphy E, Cottrell L, Neal WA. Morbidly obese diagnosis as an indicator of cardiovascular disease risk in children: results from the CARDIAC Project. Int J Pediatr Obes. 2011 Apr; 6(2): 113-9.
      7. Koebnick C, Smith N, Coleman KJ, Getahun D, Reynolds K, Quinn VP, Portеr AH, Der-Sarkissian JK, Jacobsen SJ. Prevalence of extreme obesity in a multiethnic cohort of children and adolescents. J Pediatr. 2010; 157:26-31.e2
      8. Van Emmerik NMA, Redners CM, van de Veer M, van Buuren S, van der Baan-Slootweg OH, Holthe JEK, et al. High cardiovascular risk in severely obese young children and adolescents. Arch Dis Child 2012; 97(9): 818-21
      9. Wang YC, Gortmaker SL, Taveras EM. Trends and racial/ethnic disparities in severe obesity among US children and adolescents, 1976-2006. Int J Pediatr Obes 2011; 6: 12-20.
     


    Full text is published :
    Novikova V.P., Kalashnikova V.A., Burnysheva I.A., Usychenko E.A. STATE OF THE DIGESTIVE SYSTEM IN ADOLESCENTS WITH MORBID OBESITY. Experimental and Clinical Gastroenterology Journal. 2017;143(07):51-53
    Read & Download full text

    1. Federal State Government-financed Educational Institution of Higher Education “Stavropol State Medical University” (Stavropol, Russian Federation)

    Keywords:NERD and FD overlap syndrome,gastric motility disorders,myoelectric activity of the stomach,electrogastrography

    Abstract:The aim of this study was to investigate the motility of the stomach through the study of myoelectric activity in patients with the overlap syndrome of the gastroesophageal reflux disease and functional dyspepsia. Sixty-two patients with the overlap syndrome of the of gastroesophageal reflux disease and functional dyspepsia were examined. The control group consisted of 46 healthy volunteers. The diagnosis of the overlap syndrome of the of gastroesophageal reflux disease and functional dyspepsia was established on symptoms, data of esophagogastroduodenoscopy, 24-hour pH-meter or 24-hour impedance-pH-metry, Roman criteria III. Myoelectric activity of the stomach (MAS) was assessed by 24-hour electrogastrography (EGG) on an empty stomach and after taking a standard test breakfast (430 kcal, Nutri Drink). In preprandial and postprandial periods of detection of MAS, motility disorders were detected: a decrease in the dominant frequency of slow stomach waves, an increase in the coefficient of its instability. Chronotropic MAS dysfunction was characterized by a decrease in normogastric activity, an increase in bradygastric and tachigastric activities. Food intake led to a partial correction of MAS: an increase in normogastry and a decrease in bradygastria. The revealed disturbances are one of the mechanisms of the development of gastric motility disorders that cause the development of the overlap syndrome of the gastroesophageal reflux disease and functional dyspepsia.

      1. Xiao Y. L., Peng S., Tao J. et al. Prevalence and symptom pattern of pathologic esophageal acid reflux in patients with functional dyspepsia based on the Rome III criteria. American Journal of Gastroenterology, 2010, vol. 105, no. 12, pp. 2626-2631.
      2. Noh Y. W., Jung H. K., Kim S. E., and Jung S. A. Overlap of erosive and non-erosive reflux diseases with functional gastrointestinal disorders according to Rome III criteria. Neurogastroenterology and Motility, 2010, vol. 16, no. 2, pp. 148-156.
      3. Mittal R. K., Holloway R. H., Penagini R., Blackshaw L. A., Dent J. Transient lower esophageal sphincter relaxation. Gastroenterology, 1995, vol. 109, pp, 601-610.
      4. Пасечников В. Д., Слинько Е. Н., Ковалева Н. А. Гастроэзофагеальная рефлюксная болезнь с атипичными клиническими проявлениями. Гедеон Рихтер в СНГ, 2000, № 3, c. 36-40.
      5. Выскребенцева С. А., Алфёров В. В., Ковалева Н. А., Пасечников В. Д. Нарушения моторики желудка при гастроэзофагеальной рефлюксной болезни. Российский журнал гастроэнтерологии, гепатологии, колопроктологии, 2005, Том 5, № 6, c. 35-39.
      6. Sha W., Pasricha P., Chen J. D. Correlations among electrogastrogram, gastric dysmotility, and duodenal dysmotility in patients with functional dyspepsia. Journal of Clinical Gastroenterology, 2009, vol. 43, no. 8, pp.716-722.
      7. Chen J. D., Pan J., McCallum R. W. Clinical significance of gastric myoelectrical dysrhythmias. Dig Dis Sci., 1995, vol.40, pp.275-290.
      8. Hasler W. L., Soudah H.C, Dulai G., et al. Mediation of hyperglycemia-evoked gastric slow wave dysrhythmias by endogenous prostaglandin. Gastroenterology. 1995, vol.108, pp.727-736.
      9. Quigley E. M., Lacy B. E. Overlap of functional dyspepsia and GERD-diagnostic and treatment implications. Nat Rev Gastroenterol Hepatol., 2013, vol. 10(3), pp.175-86.
      10. Lundell L. R., Dent J., Bennett J. R. et al. Endoscopic assessment of esophagitis: clinical and functional correlates and further validation of the Los Angeles classification. Gut, 1999, vol. 45, pp. 172-180.
      11. Suzuki H., Nishizawa T., Hibi T. Therapeutic strategies for functional dyspepsia and the introduction of the Rome III classification. J. Gastroenterol. 2006, vol. 41, pp. 513-523.
      12. Parkman H. P., Hasler W. L., Barnett J. L., Eaker E. Y. Electrogastrography: a document prepared by the gastric section of the American Motility Society Clinical GI Motility Testing Task Force. Neurogastroenterol Motil, 2003, vol. 15, pp.89-102.
      13. Lin Z., Eaker E. Y., Sarosiek I., et al. Gastric myoelectrical activity and gastric emptying in patients with functional dyspepsia. Am J Gastroenterol., 1999, vol.94, pp.2384-2389.
      14. Parkman H. P., Miller M. A., Trate D., et al. Electrogastrography and gastric emptying scintigraphy are complementary for assessment of dyspepsia. J Clin Gastroenterol., 1997, vol.24, pp.214-219.
      15. Chey W. Y., You C. H., Lee K. Y., et al. Gastric dysrhythmias: clinical aspects.// Chey WY, ed. Functional Dyspepsia of the Digestive Tract. New York: Raven Press; 1983, pp.175-181.
      16. Riezzo G., Pezzolla F., Darconza G., Giorgio I. Gastric myoelectrical activity in the first trimester of pregnancy: a cutaneous electrogastrographic study. American Journal of Gastroenterology, 1992, vol. 87, no. 6, pp. 702-707.
      17. Bortolotti M., Sarti P., Barbara L., et al. Gastric myoelectric activity in patients with chronic idiopathic gastroparesis. J Gastrointest Motil., 1993, vol.5, pp.41-47.
      18. Telander R. L., Morgan K. G., Kreulen D. L., et al. Human gastric atony associated with tachygastria and gastric retention. Gastroenterology, 1978, vol.45, pp.495-501.
     


    Full text is published :
    Pasechnikov V.D., Golub I.V. DISTURBANCE OF GASTRIC MOTILITY IN PATIENTS WITH THE OVERLAP SYNDROME OF THE OF GASTROESOPHAGEAL REFLUX DISEASE AND FUNCTIONAL DYSPEPSIA. Experimental and Clinical Gastroenterology Journal. 2017;143(07):54-57
    Read & Download full text

    1. Multidisciplinary medical center Bank of Russia (Moscow, Russian Federation)

    Keywords:Barrett’s esophagus,metabolic syndrome,and comorbid pathology

    Abstract:The purpose of the study is to examine the degree of influence of metabolic syndrome (MS) on the course of Barrett’s esophagus (SP) depending on gender characteristics and morphological patterns. Materials and methods. The study included 151 patients with Barrett’s esophagus (men 75 (49,6 %) and 76 women (50,3 %) aged 26 to 90 years). The patients were divided into two groups depending on the presence/ absence of metabolic syndrome. Flow analysis of PB was carried out taking into account gender characteristics and severity of morphological changes of the mucosa in segments of Barrett’s in two groups before and after treatment. Methods of research were endoscopy in various versions, data of morphological research of biopsy material, clinical and laboratory parameters. Results. The main peak of the presence of comorbid pathology, including PB and MS account for the age between 50-70 years, mainly in women in postmenopausal period. Before the start of the treatment the more pronounced morphological changes were revealed in the 2nd group of patients (PB+MS), but in the same group were obtained and better treatment results: epithelialization segment squamous epithelium occurred in 43,5 % and 48 % respectively. Conclusion. The presence of PB patients with comorbid pathology, particularly of the metabolic syndrome, contributes to more pronounced morphological changes in the mucosa of the esophagus. However, adequate therapy of concomitant pathology allows to achieve the best results. This fact confirms the claim that PB is a condition which can depend on many factors, including the presence of comorbid pathology. In this regard, the therapy “is not illness, but patient” can help to optimize the treatment of the most severe complications of gastroesophageal reflux disease, recognized as a disease of the XXI century.

      1. Бондаренко Е.Ю., Звенигородская Л. А., Чикунов Б.З и соав. Гастроэзофагеальнаярефлюксная болезнь у больных с метаболическим синдромом.
      2. Бокова Т. А. Факторы риска формирования ожирения и метаболического синдрома у детей // Врач. № 8, - 2016 г. -С 5-8.
      3. Бокова Т. А. Современный взгляд на этиопатогенез метаболического синдрома у детей // Лечащий врач № 8 2013 г.
      4. Дьяконов С. А. Метаболический синдром и репродуктивная система женщин (обзор литературы) //Проблемы репродукции № 2, Том 22. 2016 г. С 37-43.
      5. Ефремов Л.И., Комиссаренко И. А. Метаболический континуум и полиморбидность в гериатрии // Экспериментальная и клиническая гастроэнтерология. - № 6. 2014 г. С. 4-7.
      6. Лазебник Л.Б., Звенигородская Л. А. Метаболический синдром и органы пищеварения /М.: Анахарис, 2009. 181 с.
      7. Метаболический синдром. Под ред. Г. Е. Ройтберга / М.: Медпресс-информ, 2007;223 с.
      8. Метаболический синдром. Под ред. В. Фонсеки. Пер.с англ.-М.: «Практика», 2011.-272 с.
      9. Новгородцева Т.П, Денисенко Ю.К, Антонюк М.В, и соав. Жирные кислоты крови в формировании коррекции метаболического синдрома // Терапевтический архив.-№ 8, Том 88, 2016. С. 30-34.
      10. Пищевод Барретта. Клинические рекомендации. Москва - 2014
      11. American Gastroenterological Association Medical Position Statement on the Management of Barrett’s Esophagus. Gastroenterology. 2011;140:1-1091
      12. British Society of Gastroenterology guidelines on the diagnosis and management of Barrett’s oesophagus, 2013
      13. British Society of Gastroenterology guidelines on the diagnosis and management of Barrett’s oesophagus, 2014
     


    Full text is published :
    Belova G.V., Rudenko O.S. BARRETT’S ESOPHAGUS; THE IMPACT OF METABOLIC SYNDROME ON DISEASE. Experimental and Clinical Gastroenterology Journal. 2017;143(07):58-64
    Read & Download full text

    1. The Consultative and Diagnostic Centre with Polyclinic of the Administration of the President of the Russian Federation (Moscow, Russian Federation)
    2. First Saint Petersburg State Medical University n. a. I. P. Pavlov (St. Petersburg, Russian Federation)

    Keywords:habitual miscarriage,hepatopancreatobiliary system,metabolic syndrome

    Abstract:Introduction: To date, among the somatic and gynecological diseases in women of childbearing age, habitual miscarriage (PNP) is considered as a multifactorial problem. The aetiology of PNP remains completely unknown, and the role of general somatic pathology in the development of PND is poorly understood. Chronic liver diseases, leading to a disruption of its detoxification function and metabolic disorders, are one of the causes of PNP in the first trimester of pregnancy. Study Aims. To study the state of the hepatopancreatobiliary system in patients with PNP Methods. The study involved 74 women, aged 20-44 years (mean age = 32.5 ± 1.13). Group I (n = 53) included women with PNP (main group), group II (n = 21) - women with normal pregnancy in the history (control group). All women underwent a clinical examination, a biochemical blood test, ultrasound of the abdominal cavity, echo cholystography. Results. In the 1 group, a significant increase in cytolysis and cholestasis, fasting glucose, insulin and HOMA-IR index, atherogenic lipoprotein fractions, atherogenicity index. According to the data of ultrasound in the main group, the change in liver size, hepatic structure by the type of steatosis, enlargement of the gallbladder and thickening of its walls, sediment in the gall bladder was detected more often. Evaluation of the motor-evacuation function of the gallbladder indicated a predominance in the main group of hypomotor dysfunction of the gallbladder. Conclusions. In patients with PNP, changes in hepatic, lipid and carbohydrate metabolism, hepatomegaly with signs of steatosis of the liver, changes in the state and content of the gallbladder with a violation of its function predominate, which confirms the opinion of the influence of the pathology of the hepatobiliary system on the development of PNP, both in isolation and in metabolic syndrome.

      1. Доброхотова Ю. Э. Актуальные вопросы невынашивания беременности. - М., 2007. - 96. - с. 3.
      2. Сидельникова В. М. Невынашивание беременности - современный взгляд на проблему // Российский вестник акушера-гинеколога. - 2007. - № 2. - С. 62-65.
      3. Allison JL, Schust DJ Recurrent first trimester pregnancy loss: revised definitions and novel causes // Curr Opin Endocrinol Diabetes Obes. - 2009. - Vol. 16(6). - P. 446-50
      4. Holly B Ford, Danny J Schust. Recurrent Pregnancy Loss: Etiology, Diagnosis, and Therapy // Rev Obstet Gynecol. - 2009. - Vol. 2(2). - P. 76-83.
      5. Вдовиченко Ю. П. Профилактика невынашивания и недонашивания у женщин старших возрастных групп с патологией печени и желевыводящих путей // Репродуктивное здоровье женщины. - 2006. - № 2 (26). - С. 50-52.
      6. Нагорная В. Ф. Структура причин невынашивания беременности в Одесской области // Репродуктивное здоровье женщины. - 2006. - № 2 (26). -С. 58-62.
      7. Лоскутова И. В., Бичевская Р. Г., Германов В. Т. Функциональная активность печени и желчевыводящих путей у женщин с обычным невынашиванием. Проблеми екологічної та медичної генетики і клінічної імунології. - Издательство Государственное заведение Луганский государственный медицинский университет. - 2009. - С. 482-488.
      8. Савельева. И.В. Беременность и метаболический синдром: состояние проблемы // Российский вестник акушера-гинеколога. - 2010. - № 2. - С. 28-31.
      9. Wannamethee S. G., Lowe G. D.O., Shaper A. G., Rumley A., Lennon L., Whincup P. H. Insulin resistance, haemostatic and inflammatory markers and coronary heart disease risk factors in type 2 diabetes with and without coronary heart disease // Diabetologia. - 2004. - Vol. 47. - P. 1557-65.
      10. Звенигородская, Л. А. Метаболический синдром и органы пищеварения / Л. А. Звенигородская, Л. Б. Лазебник. - М.: Анахарсис, 2009. - 184 с.
      11. Тихомиров А. Л., Лубнин Д. М. Привычное невынашивание беременности. Методическое пособие для врачей акушеров-гинекологов. - М., 2008. - 44 с. 172
      12. Balkwill F. Cytokine Cell Biology. - Oxford University Press, Oxford, England, 2001. - 272 p.
      13. Mohamed A. K., Bierhaus A., Schiekofer S. et al. The role of oxidative stress and NF-kB activation in late diabetic complications // BioFactors. - 1999. - Vol. 10. - P. 157-167.
      14. Méndez-Sánchez N., Arrese M., Zamora-Valdés D., Uribe M. Current concepts in the pathogenesis of nonalcoholic fatty liver disease // Liver Int. - 2007. - Vol. 27. - P. 423-33.
      15. Mandang S., Manuelpillai U., Wallace E. M. Oxidative stress increases placental and endothelial cell activin A secretion // J. Endocrinol. 2007. - Vol. 192.-P. 485-493.
      16. Chekanina L. I. Measures pregravidarum training and antenatal care for women living in rural areas. // Український журнал клінічної та лабораторної медицини. - 2012. -Т. 7. № 2. - С. 134-140.
      17. Макацария А. Д., Передеряева Е. Б., Пшеничникова Т. Б. Метаболический синдром и низкомолекулярные гепарины // Consilium medicum. - 2006. - № 8 (6). - С. 35-41
      18. Кравченко Е. Н., Марковская О. А. К вопросу о холестатическом гепатозе беременных. - Мат-лы ХII Российского форума «Мать и дитя». - М., 2012. - с. 99-100.
      19. Holly B Ford, Danny J Schust. Recurrent Pregnancy Loss: Etiology, Diagnosis, and Therapy // Rev Obstet Gynecol. - 2009. - Vol. 2(2). - P. 76-83.
     


    Full text is published :
    Karpeev S.A., Karpeeva Yu.S., Balukova E.V. CHRONIC DISEASES OF THE HEPATOPANCREATOBILIARY SYSTEM IN THE GENESIS OF THE HABITABLE INJECTION PREGNANCY. Experimental and Clinical Gastroenterology Journal. 2017;143(07):65-70
    Read & Download full text

    1. Saint-Petersburg state pediatric medical University (St. Petersburg, Russian Federation)
    2. North-Western state medical University n. a. I. I. Mechnikov (St. Petersburg, Russian Federation)

    Abstract:Objectives: The aim of our study was to evaluate bone mineralization and metabolism in children with Crohn’s Disease (CD) and ulcerative colitis (UC). Material and methods: 113 patients with inflammatory bowel disease (IBD) (2-17 years) and 40 healthy children were included in the present study. We assessed markers of IBD activity. Bone mineral density (BMD) of lumbar spine (DEXA), serum osteocalcin (OC), C-terminal telopeptides (CTT), parathyroid hormone (PTH), serum calcium, alkaline phosphatase and 25 (OH) vitamin D were measured. Results: BMD in patients with CD and UC were lower than in control group (Zscore -1,4 SD, -1,3 SD and 0,31 SD, p=0,00001, respectively). Differences in level of PTH (39,4 pg/ml, 41,7 pg/ml и 24,8 pg/ml, p=0,04), and CTT (1,09 pg/ml, 1,08 pg/ml, 0,84 ng/ml, p=0,03) between CD, UC and healthy patients respectively have been found. There were no differences in serum OC between groups. Positive correlation between BMD and albumin, OC concentration and linear growth have been detected. IBD activity and duration, cumulative steroid dose were negatively associated with BMD. Vitamin D deficiency was observed in 98 % and 94,1 % of children with CD and UC respectively. Conclusions: patients IBD have low bone mineral density with increased bone resorption due to systemic inflammation, steroids side effect, vitamin D and calcium deficiency.

      1. Duricova D, Fumery M, Annese V, Lakatos P, Peyrin-Biroulet L, Gower-Rousseau C. The natural history of Crohn’s disease in children: a review of population-based studies. Eur J Gastroenterol Hepatol. 2017 Feb;29(2):125-134. doi: 10.1097/MEG.0000000000000761.
      2. Virta L, Saarinen M, Kolho K. Inflammatory bowel disease incidence is on the continuous rise among all paediatric patients except for the very young: A Nationwide Registry-based Study on 28-Year Follow-up. Crohns Colitis 2017 Feb 23;11(2):150-156. Epub 2016 Aug 23.
      3. Malmborg P, Hildebrand H. The emerging global epidemic of paediatric inflammatory bowel disease - causes and consequences. J Intern Med. 2016 Mar;279(3):241-58. doi: 10.1111/joim.12413. Epub 2015 Sep 10.
      4. Gasparetto M, Guariso G. Highlights in IBD epidemiology and its natural history in the paediatric age. Gastroenterol Res Pract. 2013;2013:829040. doi: 10.1155/2013/829040. Epub 2013 Dec 24.
      5. Корниенко Е. А. Воспалительные заболевания кишечника у детей. Москва, 2014.
      6. Marineaţă A, Rezuş E, Mihai C, Prelipcean C. Extraintestinal manifestations and complications in inflammatory bowel disease. Rev Med Chir Soc Med Nat Iasi. 2014 Apr-Jun;118(2):279-88.
      7. Ley D, Duhamel A, Behal H, Vasseur F, Sarter H, Michaud L, Gower-Rousseau C, Turck D. Growth pattern in paediatric Crohn disease is related to inflammatory status. J Pediatr Gastroenterol Nutr. 2016 Dec;63(6):637-643.
      8. Compston JE, Judd D, Crawley EO, Evans WD, Evans C, Church HA, Reid EM, Rhodes J. Osteoporosis in patients with inflammatory bowel disease. Gut 1987;28:410-5.
      9. Dinca M, Fries W, Luisetto G, Peccolo F, Bottega F, Leone L, Naccarato R, Martin A. Evolution of osteopenia in inflammatory bowel disease. Am J Gastroenterol 1999;94:1292-7.
      10. Bjarnason I1, Macpherson A, Mackintosh C, Buxton-Thomas M, Forgacs I, Moniz C. Reduced bone density in patients with inflammatory bowel disease. Gut 1997;40:228-33.
      11. Pollak RD, Karmeli F, Eliakim R, Ackerman Z, Tabb K, Rachmilewitz D. Femoral neck osteopenia in patients with inflammatory bowel disease. Am J Gastroenterol 1998;93:1483-90.
      12. Jahnsen J, Falch JA, Mowinckel P, Aadland E. Bone mineral density in patients with inflammatory bowel disease: a population-based prospective two-year follow-up study. Scand J Gastroenterol 2004;39:145-53.
      13. Ardizzone S, Bollani S, Bettica P, Bevilacqua M, Molteni P, Bianchi Porro G. Altered bone metabolism in inflammatory bowel disease: there is a difference between Crohn’s disease and ulcerative colitis. J Intern Med 2000;247:63-70.
      14. Bernstein CN, Blanchard JF, Leslie W, Wajda A, Yu BN. The incidence of fracture among patients with inflammatory bowel disease. A population-based cohort study. Ann Intern Med 2000;133:795-9.
      15. Card T, West J, Hubbard R, Logan RF. Hip fractures in patients with inflammatory bowel disease and their relationship to corticosteroid use: a population based cohort study. Gut 2004;53:251-5.
      16. Ruemmele FM, Veres G, Kolho KL, Griffiths A, Levine A, Escher JC, Amil Dias J, Barabino A, Braegger CP, Bronsky J, Buderus S, Martín-de-Carpi J, De Ridder L, Fagerberg UL, Hugot JP, Kierkus J, Kolacek S, Koletzko S et al. Consensus guidelines of ECCO/ESPGHAN on the medical management of pediatric Crohn’s disease. J Crohns Colitis. 2014 Oct;8(10):1179-207. doi: 10.1016/j.crohns.2014.04.005. Epub 2014 Jun 6.
      17. Turner D, Levine A, Escher JC, Griffiths AM, Russell RK, Dignass A, Dias JA, Bronsky J, Braegger CP, Cucchiara S, de Ridder L, Fagerberg UL, Hussey S, Hugot JP, Kolacek S, Kolho KL, Lionetti P, Paerregaard A, Potapov A, Rintala R, Serban DE, Staiano A, Sweeny B, Veerman G, Veres G, Wilson DC, Ruemmele FM. Management of pediatric ulcerative colitis: joint ECCO and ESPGHAN evidence-based consensus guidelines. J Pediatr Gastroenterol Nutr. 2012 Sep;55(3):340-61.
      18. Баранов А. А., Намазова- Баранова Л. С., Потапов А. С., Алиева Э. И., Габрузская Т. В., Горелов А. В., Захарова И. Н., Корниенко Е. А., Панфилова В. Н., Печкуров Д.В, Ратникова М.А, Ревнова М. О., Ситникова Е. П., Урсов Н. И., Федулова Э. Н., Цимбалова Е.Г, Шумилов П. В., Щербакова О.В, Щиголева Н. Е. и др. Клиническая картина, диагностика и лечение язвенного колита у детей: Российский педиатрический консенсус. Вопросы современной педиатрии. 2013; 12 (3): 18-30
      19. Потапов А. С. Болезнь Крона у детей и подростков. Клинические рекомендации по диагностике и лечению. М., 2010, 13 с.
      20. Semeao E, Stallings V, Peck S, Piccoli D. Vertebral compression fractures in pediatric patients with Crohn’s disease. Gastroenterology. 1997; 112(5): 1710-1713.
      21. Johnell O1, Kanis JA, Oden A, Johansson H, De Laet C, Delmas P, Eisman JA, Fujiwara S, Kroger H, Mellstrom D, Meunier PJ, Melton LJ 3rd, O’Neill T, Pols H, Reeve J, Silman A, Tenenhouse A. Predictive value of BMD for hip and other fractures. J Bone Miner Res 2005;20:1185-94
      22. Clark E, Ness A, Bishop N, Tobias J. Association between bone density and fractures in children. Pediatrics. 2006 February; 117(2): e291-e297. doi:10.1542/peds.2005-1404.
      23. Laakso S, Valta H, Verkasalo M, Toiviainen-Salo S, Viljakainen H, Mäkitie O. Impaired bone health in inflammatory bowel disease: a case-control study in 80 pediatric patients. Calcif Tissue Int. 2012 Aug;91(2):121-30. doi: 10.1007/s00223-012-9617-2. Epub 2012 Jun 23.
      24. Burnham JM, Shults J, Semeao E, Foster B, Zemel BS, Stallings VA, Leonard MB. Whole body BMC in pediatric Crohn’s disease: independent effects of altered growth, maturation, and body composition. J Bone Miner Res. 2004;19:1961-1968.
      25. Sylvester F, Leopold S, Lincoln M, Hyams J, Griffiths A, Lerer T. A two-year longitudinal study of persistent lean tissue deficits in children with Crohn’s disease. Clin Gastroenterol Hepatol 2009;7:452-5.
      26. Schmidt S, Mellström D, Norjavaara E, Sundh S, Saalman R. Low bone mineral density in children and adolescents with inflammatory bowel disease: a population-based study from Western Sweden. Inflamm Bowel Dis. 2009 Dec;15(12):1844-50. doi: 10.1002/ibd.20962. Epub 2009 Apr 30
      27. Schmidt S, Mellström D, Norjavaara E, Sundh V, Saalman R. Longitudinal assessment of bone mineral density in children and adolescents with inflammatory bowel disease. J Pediatr Gastroenterol Nutr. 2012 Nov;55(5):511-8. doi: 10.1097/MPG.0b013e31825817a0.
      28. Szumera M, Landowski P, Kamińska B, Góra-Gebka M, Popadiuk S, Renke J. Bone mineral density in inflammatory bowel diseases in children. Med Wieku Rozwoj.2006;10(2):445-51.
      29. Boot AM, Bouquet J, Krenning EP, de Muinck Keizer-Schrama SM. Bone Mineral Density and Nutritional Status in Children With Chronic Inflammatory Bowel Diseased Gut 1998;42(2), 188-194.
      30. Laakso S, Valta H, Verkasalo M, Toiviainen-Salo S, Makitie. Compromised peak bone Mass in Patients with Inflammatory Bowel Disease-A Prospective Study. Pediatr 2014;164:1436-43.
      31. Kappelman M., Galanko J., Porter C., Sandler S. The risk of diagnosed fractures in children with inflammatory bowel diseases. Inflamm Bowel Dis. 2011 May; 17(5): 1125-1130.
      32. Landin LA. Fracture patterns in children. Analysis of 8682 fractures with special reference to incidence, etiology and secular changes in a Swedish urban population 1950-1979. Acta Orthop Scand Suppl. 1983;202: 1-109.
      33. Khosla S, Melton LJ 3rd, Dekutoski M, Achenbach S, Ober A, Riggs B. Incidence of childhood distal forearm fractures over 30 years: population-based study. JAMA. 2003; 290:1479-85.
      34. Semeao E, Stallings V, Peck S, Piccoli D. Vertebral compression fractures in pediatric patients with Crohn’s disease. Gut. 2002; 51:654-8.
      35. Mauro M, Armstrong D. Juvenile onset of Crohn’s disease: a risk factor for reduced lumbar bone mass in premenopausal women. Bone. 2007 May;40(5):1290-3. Epub 2007 Jan 17.
      36. Pichler J, Huber W, Aufricht C, Bidmon-Fliegenschnee B. Growth and bone health in paediatric patients with Crohn’s disease receiving subcutaneous tumor necrosis factor antibody. World J Gastroenterol. 2015 Jun 7; 21(21): 6613-6620.
      37. Lindsay M. Griffin, Meena Thayu, Robert N. Baldassano, Mark D. DeBoer, Babette S. Zemel, Michelle R. Denburg, Lee A. Denson, Justine Shults, Rita Herskovitz, Jin Long, and Mary B. Leonard Improvements in Bone Density and Structure during Anti-TNF-α Therapy in Pediatric Crohn’s Disease. J Clin Endocrinol Metab. 2015 Jul; 100(7): 2630-2639.
      38. Sands BE. Biomarkers of Inflammation in Inflammatory Bowel Disease. Gastroenterology. 2015 Oct;149(5):1275-1285.e2. doi: 10.1053/j.gastro.2015.07.003.
      39. Ghosh S, Cowen S, Hannan WJ, Ferguson A. Low bone mineral density in Crohn’s disease, but not in ulcerative colitis, at diagnosis. Gastroenterology 1994; 107:1031-1039.
      40. Ryan JG, Morgan RK, Lavin PJ, Murray FE, O’Connell PG. Current management of corticosteroid-induced osteoporosis: variations in awareness and management. Ir J Med Sci. 2004 Jan-Mar;173(1):20-2.
      41. Bernstein C., Leslie W. Therapy insight: Osteoporosis in inflammatory bowel disease - advances and retreats. Nat Clin Pract Gastroenterol Hepatol. 2005 May;2(5):232-9.
      42. Veerappan S, Healy M, Walsh B, O’Morain C, Daly J, Ryan B. Adalimumab Therapy Has a Beneficial Effect on Bone Metabolism in Patients with Crohn’s Disease. Dig Dis Sci 2015; 60:2119-2129.
      43. Card T, West J, Hubbard R, Logan RF. Hip fractures in patients with inflammatory bowel disease and their relationship to corticosteroid use: a population based cohort study. Gut 2004; 53:251-255.
      44. van Staa TP. The pathogenesis, epidemiology and management of glucocorticoid-induced osteoporosis. Calcif Tissue Int 2006; 79:129-137.
      45. Bernstein C, Blanchard J, Metge C, Yogendran M. The association between corticosteroid use and development of fractures among IBD patients in a population-based database. Am J Gastroenterol 2003; 98:1797-1801.
      46. Ford AC 1, Bernstein CN, Khan KJ, Abreu MT, Marshall JK, Talley NJ, Moayyedi P. Glucocorticosteroid therapy in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. 2011 Apr;106(4):590-9; quiz 600. doi: 10.1038/ajg.2011.70. Epub 2011 Mar 15.
      47. Gudbjornsson B, Juliusson UI, Gudjonsson FV. Prevalence of long term steroid treatment and the frequency of decision making to prevent steroid induced osteoporosis in daily clinical practice. Ann Rheum Dis, 2002, 61(1):32-36.
      48. van Staa T, Leufkens H, Cooper C. The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporos Int, 2002, 13(10):777-787
      49. Van Staa T, Leufkens H, Abenhaim L, Zhang B, Cooper C (2000) Use of oral corticosteroids and risk of fractures. J Bone Miner Res 15(6):993-1000
      50. Dubner SE, Shults J, Baldassano RN, Zemel BS, Thayu M, Burnham JM, Herskovitz RM, Howard KM, Leonard MB. Longitudinal assessment of bone density and structure in an incident cohort of children with Crohn’s disease. Gastroenterology. 2009; 136:123-30.
      51. Lopes L, Sdepanian V, Szejnfeld V, de Morais M, Fagundes-Neto U. Risk factors for low bone mineral density in children and adolescents with inflammatory bowel disease. Dig Dis Sci 2008; 53: 2746-53.
      52. Boot A, Bouquet J, Krenning E, de Munck Kezer-Schrama S. Bone mineral density in children and adolescents with inflammatory bowel disease: a population-based study from Western Swede. Inflamm Bowel Dis Sci 2008; 53: 2746-53.
      53. van Staa, Leufkens HG, Cooper C. The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis.Osteoporosis Int. 2002.;13 777-787
      54. Levine A, Broide E, Stein M, Bujanover Y, Weizman Z, Dinari G, Pacht A, Branski D, Zahavi I. Evaluation of oral budesonide for treatment of mild and moderate exacerbations of Crohn’s disease in children. J Pediatr 2002;140:75-80.
      55. Holick M, Binkley N, Bischoff-Ferrari H, Gordon C, Hanley D, Heaney R. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2011;96:1911-30.
      56. Priemel M, von Domarus C, Klatte TO, Kessler S, Schlie J, Meier S, Proksch N, Pastor F, Netter C, Streichert T, Püschel K, Amling M. Bone mineralization defects and vitamin D deficiency: histomorphometric analysis of iliac crest bone biopsies and circulating 25- hydroxyvitamin D in 675 patients. J Bone Miner Res 2010;25:305-12.
      57. Alkhouri R, Hashmi H, Baker R, Gelfond D, Baker S. Vitamin and mineral status in patients with inflammatory bowel disease. J Pediatr Gastroenterol Nutr. 2013; 56:89-92.
      58. Leslie W, Miller N, Rogala L, Bernstein C. Vitamin D status and bone density in recently diagnosed inflammatory bowel disease: the Manitoba IBD Cohort Study. Am J Gastroenterol. 2008; 103:1451-9.
      59. Gilman J, Shanahan F, Cashman KD. Determinants of vitamin D status in adult Crohn’s disease patients, with particular emphasis on supplemental vitamin D use. Eur J Clin Nutr. 2006; 60:889-96.
      60. McCarthy D, Duggan P, O’Brien M, Kiely M, McCarthy J, Shanahan F, Cashman KD. Seasonality of vitamin D status and bone turnover in patients with Crohn’s disease. Aliment Pharmacol Ther. 2005; 21:1073-83.
      61. Levin A, Wadhera V, Leach S, Woodhead H, Lemberg D, Mendoza-Cruz A, Day A. Vitamin D deficiency in children with inflammatory bowel disease. Dig Dis Sci. 2011; 56:830-6.
      62. Ulitsky A, Ananthakrishnan AN, Naik A, Skaros S, Zadvornova Y, Binion DG, Issa M. Vitamin D deficiency in patients with inflammatory bowel disease: association with disease activity and quality of life. JPEN J Parenter Enteral Nutr. 2011;35(3):308-16.
      63. Leslie W, Miller N, Rogala L, Bernstein C. Vitamin D status and bone density in recently diagnosed inflammatory bowel disease: the Manitoba IBD Cohort Study. Am J Gastroenterol. 2008; 103:1451-9.
      64. Gilman J, Shanahan F, Cashman K. Determinants of vitamin D status in adult Crohn’s disease patients, with particular emphasis on supplemental vitamin D use. Eur J Clin Nutr. 2006; 60:889-96.
      65. de Bruyn О, van Heeckeren R, Ponsioen С, van den Brink G, Löwenberg M, Bredenoord AJ, Frijstein G. Vitamin D deficiency in Crohn’s disease and healthy controls: A prospective case-control study in the Netherlands J Crohns Colitis. 2014 Mar 22. pii: S 1873-9946(14)00099-3. doi: 10.1016/j.crohns.2014.03.004
      66. Торшин И.Ю, Громова О. А., Лиманова О. А., Сардарян И. С., Малявская С. И., Галустян А. Н., Волков А. Ю., Калачева А. Г., Гришина Т. Р., Громов А. Н., Рудаков К. В. Обеспеченность витамином D детей и подростков 7-14 лет и взаимосвязь дефицита витамина D с нарушениями здоровья детей. Анализ крупномасштабной выборки пациентов посредством интеллектуального анализа данных. Педиатрия им. Сперанского, 2015, No2., 175-185.
      67. Захарова И. Н., Мальцев С. В., Боровик Т. Э., Яцык Г. В., Малявская С. И., Вахлова И. В., Шуматова Т. А., Романцова Е. Б., Романюк Ф. П., Климов.Я., Елкина Т. Н., Пирожкова Н. И., Колесникова С. М., Курьянинова В. А., Васильева С. В., Мозжухина М. В., Евсеева Е. А. Недостаточность витамина D у детей раннего возраста в России (результаты многоцентрового исследования - зима 2013-2014 гг.) // Педиатрия. -2014. - Том 93. - No2. - 75-80.
      68. Яблокова Е. А. Клинические особенности и нарушение минерализации костной ткани у детей с воспалительными заболеваниями кишечника. Диссертация на соискание ученой степени кандидата медицинских наук. Москва, 2006.
      69. Abraham B, Prasad P, Malaty H. Vitamin D deficiency and corticosteroid use are risk factors for low bone mineral density in inflammatory bowel disease patients. Dig Dis Sci. 2014 Aug;59(8):1878-84. doi: 10.1007/s10620-014-3102-x. Epub 2014 Mar 12.
      70. Панкратова Ю. В., Пигарова Е. А., Дзеранова Л. К. Витамин К-зависимые белки: остеокальцин, матриксный Gla-белок и их внекостные эффекты. Ожирение и метаболизм, № 2, 2013: 11-18.
      71. Sánchez Cano D, Ruiz-Villaverde R, Olvera Porcel M, Callejas Rubio JL, Pérez CC, García MG, Calvin JG, Ortego Centeno N. Evaluation of bone mineral density, bone turnover markers, the OPG/RANKL system and sTNF-RI in Crohn’s disease. Gastroenterol Hepatol. 2011 Jan;34(1):3-9. doi: 10.1016/j.gastrohep.2010.10.006. Epub 2011 Jan 8
      72. Silvennoinen J, Risteli L, Karttunen T, Risteli J. Increased degradation of type I collagen in patients with inflammatory bowel disease Gut 1996; 38: 223-228.
      73. Park J, Jung S, Noh Y, Kang M, Jung J, Kim S, Jung H, Shim K, Kim T, Yoo K, Moon I, Hong Y. Analysis of risk factors for low bone mineral density in patients with inflammatory bowel disease. Korean J Gastroenterol. 2010 Apr;55(4):237-44.
      74. Gokhale R, Favus M, Karrison T, Sutton M, Rich B, Kirschner B. Bone mineral density assessment in children with inflammatory bowel disease. Gastroenterology. 1998 May;114(5):902-11.
      75. Veerappan S, Healy M, Walsh B, O’Morain C, Daly J, Ryan B. A 1-year prospective study of the effect of infliximab on bone metabolism in inflammatory bowel disease patients. Eur J Gastroenterol Hepatol. 2016 Nov;28(11):1335-44. doi: 10.1097/MEG.0000000000000719
      76. Veerappan S, Healy M, Walsh B, O’Morain C, Daly J, Ryan B. Adalimumab Therapy Has a Beneficial Effect on Bone Metabolism in Patients with Crohn’s Disease Dig Dis Sci. 2015 Jul;60(7):2119-29. doi: 10.1007/s10620-015-3606-z. Epub 2015 Mar 3
      77. Franchimont N, Putzeys V, Collette J, Vermeire S, Rutgeerts P, De Vos M, Van Gossum A, Franchimont D, Fiasse R, Pelckmans P, Malaise M, Belaiche J, Louis E. Rapid improvement of bone metabolism after infliximab treatment in Crohn’s disease. Aliment Pharmacol Ther. 2004 Sep 15;20(6):607-14
      78. Miheller P1, Muzes G, Zágoni T, Tóth M, Rácz K, Tulassay Z. Improvement of bone metabolism after infliximab therapy in Crohn’s disease. Orv Hetil. 2005 Jul 10;146(28):1477-80.
      79. Szabó D, Hosszú É, Arató A, Müller K, Béres N, Lakatos P, Papp M, Dezsőfi A, Szabó A, Szűcs D, Veres G. Seasonal variabilit of vitamin D and bone metabolism in infliximab-treated paediatric Crohn’s disease. Dig Liver Dis. 2015 Aug;47(8):652-7 doi: 10.1016/j.dld.2015.05.006. Epub 2015 May 1
      80. Griffiths A, Baldassano R, Walters T. Improvements of markers of bone metabolism with adalimumab in children with moderetly to severe active crohn disease: results from IMAgINE. European Gastroenterology Week, 12-16 October 2013, Berlin.
      81. Visvanathan S, van der Heijde, Deodhar A, Wagner C, Baker D, Han J, Braun J. Effects of infliximab on markers of inflammation and bone turnover and associations with bone mineral density in patients with ankylosing spondylitis. Ann Rheum Dis. 2009 Feb; 68(2): 175-182. Published online 2008 May 21. doi: 10.1136/ard.2007.084426
      82. Walters T, Gilman A, Griffiths A. Linear growth improves during infliximab therapy in children with chronically active severe Crohn’s disease. Inflamm Bowel Dis. 2007 Apr;13(4):424-30.
      83. Tilg H, Moschen A, Kaser A, Pines A, Dotan I. Gut, inflammation and osteoporosis: basic and clinical concepts. Gut 2008;57:684-694.
      84. Theill L, Boyle W, Penninger J. RANK-L and RANK: T cells, bone loss, and mammalian evolution. Annu Rev Immunol 2002;20:795-823.
      85. Silveonnoinen O, Risteli O, Karttunen T, Risteli O. Increased degradation oftype I collagen in patients with inflammatory bowel disease Gut 1996; 38: 223-228
      86. Bischoff S, Herrmann A, Göke M, Manns M, von zur Mühlen A, Brabant G., Orv Hetil. Altered bone metabolism in inflammatory bowel disease. Am J Gastroenterol. 1997 Jul;92(7):1157-63.
      87. Miheller P, Tóth M, Molnár E, Zágoni T, Rácz K, Tulassay Z. Serum bone marker measurements in bone metabolism disorders associated with inflammatory bowel diseases. Orv Hetil. 2001 Jul 22;142(29):1557-60
      88. Thayu et al. Improvement in Biomarkers of Bone Formation During Infliximab Therapy in Pediatric Crohn’s Disease: Results of the REACH Study. Clinical gastroenterology and hepatology 2008;6:1378-1384.
     


    Full text is published :
    Gabrusskaya T.V., Revnova M.O., Kuzmina D.A., Kostik M.M. ASSESSMENT OF BONE MINERALIZATION AND BONE METABOLISM IN CHILDREN WITH INFLAMMATORY BOWEL DISEASE. Experimental and Clinical Gastroenterology Journal. 2017;143(07):71-81
    Read & Download full text