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Crohn’s disease: Etiology, pathogenesis and treatment strategies

Yıl 2023, , 249 - 254, 31.05.2023
https://doi.org/10.5472/marumj.1307982

Öz

Crohn’s disease (CD), which can be localized in any part of the gastrointestinal tract, is a disease characterized by an irregular immune
response to normal and/or abnormal microbial antigens. Recent studies show many extensive data about the roles of genetic and
environmental factors, immune function, and gut microbiota in CD. Although, less invasive biomarkers are currently being developed,
the diagnosis of the disease is still based on the endoscopy and histological evaluation of biopsy samples. The most common symptoms
are diarrhea, abdominal pain, weight loss, and fatigue. Despite the improvements in the treatment methods in the last decade, there
is no definitive treatment since the etiology of CD is not known exactly. Therapeutic strategies focus on reducing inflammation and
symptoms, maintaining clinical remission, and improving quality of life.

Kaynakça

  • [1] Balmus IM, Ciobica A, Trifan A, Stanciu C. The implications of oxidative stress and antioxidant therapies in inflammatory bowel disease: Clinical aspects and animal models. Saudi J Gastroenterol 2016;22:3-17. doi:10.4103/1319-3767.173753.
  • [2] Ng SC, Shi HY, Hamidi N, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies. Lancet 2017;390:2769-78. doi: 10.1016/S0140-6736(17)32448-0.
  • [3] GBD-2017 Inflammatory Bowel Disease Collaborators. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol 2020;5:17-30. doi: 10.1016/S2468-1253(19)30333-4.
  • [4] Saka M, Koseler E, and Metin S. Gastrointestinal system diseases and nutrition therapy. In: Tufekci Alphan E, ed. Nutrition therapy in diseases. Ankara: Hatiboğlu Yayıncılık, 2018:541-638.
  • [5] Buran T. Inflammatory bowel disease; epidemiology, prevalence, incidence. Turkiye Klinikleri J Gastroenterohepatol-Special Topics 2017;10:15-7.
  • [6] Demir N, Erzin YZ. Clinical signs in inflammatory bowel diseases. Güncel Gastroenteroloji 2014;18:423-39.
  • [7] Mazal J. Crohn disease: pathophysiology, diagnosis, and treatment. Radiol Technol 2014;85:297-316.
  • [8] Porth CM. Essentials of pathophysiology: Concepts of altered health states 4th Ed. Philadelphia: Wolters Kluwer, 2015: 696- 723.
  • [9] Akbulut G. Nutrition therapy in gastrointestinal system diseases. 1st Ed. Ankara: Nobel Tıp Kitabevi, 2017: 327-32
  • [10] Kaplan GG. Ng SC. Epidemiology, pathogenesis, and diagnosis of inflammatory bowel diseases, In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. Philadelphia: Elsevier/Saunders,2020:1868-97.
  • [11] Veauthier B, Hornecker JR. Crohn’s disease: Diagnosis and management. Am Fam Physician 2018;98:661-9.
  • [12] Mills JC, Ciorba MA. Gastrointestinal disease, In: Hammer GD, McPhee SJ, eds. Pathophysiology of Disease: An Introduction to Clinical Medicine. 8th Ed.. New York: McGraw- Hill Education, 2019: 369-420.
  • [13] Roda G, Chien Ng S, Kotze PG, et al. Crohn’s disease. Nat Rev Dis Primers 2020;6:22. doi: 10.1038/s41572.020.0156-2.
  • [14] Younis N, Zarif R, Mahfouz R. Inflammatory bowel disease: between genetics and microbiota. Mol Biol Rep 2020;47:3053- 63. doi:10.1007/s11033.020.05318-5.
  • [15] Lauro ML, Burch JM, Grimes CL. The effect of NOD2 on the microbiota in Crohn’s disease. Curr Opin Biotechnol 2016;40:97-102. doi:10.1016/j.copbio.2016.02.028.
  • [16] Tuvlin JA, Raza SS, Bracamonte S, et al. Smoking and inflammatory bowel disease: trends in familial and sporadic cohorts. Inflamm Bowel Dis 2007:573-9. doi: 10.1002/ ibd.20043.
  • [17] Baumgart DC, Carding SR. Inflammatory bowel disease: cause and immunobiology. Lancet 2007;369:1627-40. doi:10.1016/ S0140-6736(07)60750-8.
  • [18] Baumgart DC, Sandborn WJ. Crohn’s disease. Lancet 2012; 380:1590-605. doi: 10.1016/S0140-6736(12)60026-9.
  • [19] Birrenbach T, Böcker U. Inflammatory bowel disease and smoking: a review of epidemiology, pathophysiology, and therapeutic implications. Inflamm Bowel Dis 2004;10:848-59. doi:10.1097/00054.725.200411000-00019.
  • [20] Hou JK, Abraham B, El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol 2011;106:563-73. doi:10.1038/ajg.2011.44.
  • [21] Sakamoto N, Kono S, Wakai K, et al. Epidemiology Group of the Research Committee on Inflammatory Bowel Disease in Japan. Dietary risk factors for inflammatory bowel disease: a multicenter case-control study in Japan. Inflamm Bowel Dis 2005;11:154-63. doi: 10.1097/00054.725.200502000-00009.
  • [22] Zheng JJ, Zhu XS, Huangfu Z, Gao ZX, Guo ZR, Wang Z. Crohn’s disease in mainland China: a systematic analysis of 50 years of research. Chin J Dig Dis 2005;6:175-81. doi: 10.1111/j.1443-9573.2005.00227.x.
  • [23] Zeng L, Hu S, Chen P, Wei W, Tan Y. Macronutrient intake and risk of Crohn’s Disease: systematic review and doseresponse meta-analysis of epidemiological studies. Nutrients 2017;9:500. doi: 10.3390/nu9050500.
  • [24] Boyko EJ, Theis MK, Vaughan TL, Nicol-Blades B. Increased risk of inflammatory bowel disease associated with oral contraceptive use. Am J Epidemiol 1994;140:268-78. doi:10.1093/oxfordjournals.aje.a117246.
  • [25] Ananthakrishnan AN, Higuchi LM, Huang ES, et al. Aspirin, nonsteroidal anti-inflammatory drug use, and risk for Crohn disease and ulcerative colitis: a cohort study. Ann Intern Med 2012;156:350-9. doi: 10.7326/0003-4819-156-5- 201203.060.00007.
  • [26] Ananthakrishnan AN. Epidemiology and risk factors for IBD. Nat Rev Gastroenterol Hepatol 2015;12:205-17. doi: 10.1038/ nrgastro.2015.34. Epub 2015 Mar 3.
  • [27] Ohkusa T, Nomura T, Sato N. The role of bacterial infection in the pathogenesis of inflammatory bowel disease. Intern Med 2004;43:534-39. doi:10.2169/internalmedicine.43.534.
  • [28] Bernstein CN, Hitchon CA, Walld R, et al. Increased Burden of Psychiatric Disorders in Inflammatory Bowel Disease. Inflamm Bowel Dis 2019;25:360-68. doi: 10.1093/ibd/izy235.
  • [29] Mikocka-Walus A, Knowles SR, Keefer L, Graff L. Controversies revisited: A systematic review of the comorbidity of depression and anxiety with inflammatory bowel diseases. Inflamm Bowel Dis 2016;22:752-62. doi:10.1097/MIB.000.000.0000000620.
  • [30] Benjamin JL, Sumpter R Jr, Levine B, Hooper LV. Intestinal epithelial autophagy is essential for host defense against invasive bacteria. Cell Host Microbe 2013;13:723-34. doi:10.1016/j.chom.2013.05.004.
  • [31] Jostins L, Ripke S, Weersma RK, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 2012;491:119-24. doi: 10.1038/nature11582.
  • [32] Uhlig HH, Powrie F. Translating Immunology into Therapeutic Concepts for Inflammatory Bowel Disease. Annu Rev Immunol 2018;36:755-81. doi:10.1146/annurevimmunol- 042.617.053055.
  • [33] de Souza HS, Fiocchi C. Immunopathogenesis of IBD: current state of the art. Nat Rev Gastroenterol Hepatol 2016;13:13-27. doi:10.1038/nrgastro.2015.186.
  • [34] Huether SE. Alterations of digestive function, In: McCance KL, Huether SE, eds. Study guide for Pathophysiology: The Biologic Basis for Disease in Adults and Children. St. Louis, Missouri: Elsevier, 2019:1321-72.SE
  • [35] Özbek M, Hitit M, Ergün E, Beyaz F, Ergün L. Toll-like receptors. MAKÜ Sag Bil Enst Derg 2017;5: 180-92.
  • [36] Kostic AD, Xavier RJ, Gevers D. The microbiome in inflammatory bowel disease: current status and the future ahead. Gastroenterology 2014;146:1489-99. doi:10.1053/j. gastro.2014.02.009.
  • [37] Quévrain E, Maubert MA, Michon C, et al. Identification of an anti-inflammatory protein from Faecalibacterium prausnitzii, a commensal bacterium deficient in Crohn’s disease. Gut 2016;65:415-25. doi: 10.1136/gutjnl-2014-307649.
  • [38] Lapaquette P, Glasser AL, Huett A, Xavier RJ, Darfeuille- Michaud A. Crohn’s disease-associated adherent-invasive E. coli are selectively favoured by impaired autophagy to replicate intracellularly. Cell Microbiol 2010;12:99-113. doi:10.1111/ j.1462-5822.2009.01381.x.
  • [39] Darfeuille-Michaud A, Boudeau J, Bulois P, et al. High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology 2004;127:412-21. doi: 10.1053/j.gastro.2004.04.061.
  • [40] Virta L, Auvinen A, Helenius H, Huovinen P, Kolho KL. Association of repeated exposure to antibiotics with the development of pediatric Crohn’s disease—a nationwide, register-based finnish case-control study. Am J Epidemiol 2012;175:775-84. doi:10.1093/aje/kwr400.
  • [41] Kronman MP, Zaoutis TE, Haynes K, Feng R, Coffin SE. Antibiotic exposure and IBD development among children: a population-based cohort study. Pediatrics 2012;130:e794-e803. doi:10.1542/peds.2011-3886.
  • [42] Sartin J. Gastrointestinal disorders, In: Banasik JL, Copstead L. eds. Pathophysiology. St. Louis, Missouri: Elsevier, 2019:721-41.
  • [43] Glassner KL, Abraham BP, Quigley EMM. The microbiome and inflammatory bowel disease. J Allergy Clin Immunol 2020;145:16-27. doi:10.1016/j.jaci.2019.11.003.
  • [44] Bak SH, Choi HH, Lee J, et al. Fecal microbiota transplantation for refractory Crohn’s disease. Intest Res 2017;15:244-48. doi: 10.5217/ir.2017.15.2.244.
  • [45] Suskind DL, Brittnacher MJ, Wahbeh G, et al. Fecal microbial transplant effect on clinical outcomes and fecal microbiome in active Crohn’s disease. Inflamm Bowel Dis 2015;21:556-63. doi: 10.1097/MIB.000.000.0000000307.
  • [46] Lochs H, Dejong C, Hammarqvist F, et al. ESPEN Guidelineson Enteral Nutrition: Gastroenterology. Clin Nutr 2006; 25:260-74.
  • [47] Cresci G, Escuro A. Medical nutrition therapy for lower gastrointestinal tract disorders, In: Mahan LK, Raymond JL, eds. Krause’s Food and Nutrition Therapy. Elsevier,2017:541-49.
  • [48] Bischoff SC, Escher J, Hébuterne X, et al. ESPEN practical guideline: Clinical Nutrition in inflammatory bowel disease. Clin Nutr 2020;39:632-53. doi: 10.1016/j.clnu.2019.11.002.
  • [49] Brown AC, Rampertab SD, Mullin GE. Existing dietary guidelines for Crohn’s disease and ulcerative colitis. Expert Rev Gastroenterol Hepatol 2011;5:411-25. doi: 10.1586/egh.11.29.
  • [50] Naseer M, Poola S, Ali S, Samiullah S, Tahan V. Prebiotics and Probiotics in Inflammatory Bowel Disease: Where are we now and where are we going? Curr Clin Pharmacol 2020;15:216- 33. doi: 10.2174/157.488.4715666.200.312100237.
Yıl 2023, , 249 - 254, 31.05.2023
https://doi.org/10.5472/marumj.1307982

Öz

Kaynakça

  • [1] Balmus IM, Ciobica A, Trifan A, Stanciu C. The implications of oxidative stress and antioxidant therapies in inflammatory bowel disease: Clinical aspects and animal models. Saudi J Gastroenterol 2016;22:3-17. doi:10.4103/1319-3767.173753.
  • [2] Ng SC, Shi HY, Hamidi N, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies. Lancet 2017;390:2769-78. doi: 10.1016/S0140-6736(17)32448-0.
  • [3] GBD-2017 Inflammatory Bowel Disease Collaborators. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol 2020;5:17-30. doi: 10.1016/S2468-1253(19)30333-4.
  • [4] Saka M, Koseler E, and Metin S. Gastrointestinal system diseases and nutrition therapy. In: Tufekci Alphan E, ed. Nutrition therapy in diseases. Ankara: Hatiboğlu Yayıncılık, 2018:541-638.
  • [5] Buran T. Inflammatory bowel disease; epidemiology, prevalence, incidence. Turkiye Klinikleri J Gastroenterohepatol-Special Topics 2017;10:15-7.
  • [6] Demir N, Erzin YZ. Clinical signs in inflammatory bowel diseases. Güncel Gastroenteroloji 2014;18:423-39.
  • [7] Mazal J. Crohn disease: pathophysiology, diagnosis, and treatment. Radiol Technol 2014;85:297-316.
  • [8] Porth CM. Essentials of pathophysiology: Concepts of altered health states 4th Ed. Philadelphia: Wolters Kluwer, 2015: 696- 723.
  • [9] Akbulut G. Nutrition therapy in gastrointestinal system diseases. 1st Ed. Ankara: Nobel Tıp Kitabevi, 2017: 327-32
  • [10] Kaplan GG. Ng SC. Epidemiology, pathogenesis, and diagnosis of inflammatory bowel diseases, In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. Philadelphia: Elsevier/Saunders,2020:1868-97.
  • [11] Veauthier B, Hornecker JR. Crohn’s disease: Diagnosis and management. Am Fam Physician 2018;98:661-9.
  • [12] Mills JC, Ciorba MA. Gastrointestinal disease, In: Hammer GD, McPhee SJ, eds. Pathophysiology of Disease: An Introduction to Clinical Medicine. 8th Ed.. New York: McGraw- Hill Education, 2019: 369-420.
  • [13] Roda G, Chien Ng S, Kotze PG, et al. Crohn’s disease. Nat Rev Dis Primers 2020;6:22. doi: 10.1038/s41572.020.0156-2.
  • [14] Younis N, Zarif R, Mahfouz R. Inflammatory bowel disease: between genetics and microbiota. Mol Biol Rep 2020;47:3053- 63. doi:10.1007/s11033.020.05318-5.
  • [15] Lauro ML, Burch JM, Grimes CL. The effect of NOD2 on the microbiota in Crohn’s disease. Curr Opin Biotechnol 2016;40:97-102. doi:10.1016/j.copbio.2016.02.028.
  • [16] Tuvlin JA, Raza SS, Bracamonte S, et al. Smoking and inflammatory bowel disease: trends in familial and sporadic cohorts. Inflamm Bowel Dis 2007:573-9. doi: 10.1002/ ibd.20043.
  • [17] Baumgart DC, Carding SR. Inflammatory bowel disease: cause and immunobiology. Lancet 2007;369:1627-40. doi:10.1016/ S0140-6736(07)60750-8.
  • [18] Baumgart DC, Sandborn WJ. Crohn’s disease. Lancet 2012; 380:1590-605. doi: 10.1016/S0140-6736(12)60026-9.
  • [19] Birrenbach T, Böcker U. Inflammatory bowel disease and smoking: a review of epidemiology, pathophysiology, and therapeutic implications. Inflamm Bowel Dis 2004;10:848-59. doi:10.1097/00054.725.200411000-00019.
  • [20] Hou JK, Abraham B, El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol 2011;106:563-73. doi:10.1038/ajg.2011.44.
  • [21] Sakamoto N, Kono S, Wakai K, et al. Epidemiology Group of the Research Committee on Inflammatory Bowel Disease in Japan. Dietary risk factors for inflammatory bowel disease: a multicenter case-control study in Japan. Inflamm Bowel Dis 2005;11:154-63. doi: 10.1097/00054.725.200502000-00009.
  • [22] Zheng JJ, Zhu XS, Huangfu Z, Gao ZX, Guo ZR, Wang Z. Crohn’s disease in mainland China: a systematic analysis of 50 years of research. Chin J Dig Dis 2005;6:175-81. doi: 10.1111/j.1443-9573.2005.00227.x.
  • [23] Zeng L, Hu S, Chen P, Wei W, Tan Y. Macronutrient intake and risk of Crohn’s Disease: systematic review and doseresponse meta-analysis of epidemiological studies. Nutrients 2017;9:500. doi: 10.3390/nu9050500.
  • [24] Boyko EJ, Theis MK, Vaughan TL, Nicol-Blades B. Increased risk of inflammatory bowel disease associated with oral contraceptive use. Am J Epidemiol 1994;140:268-78. doi:10.1093/oxfordjournals.aje.a117246.
  • [25] Ananthakrishnan AN, Higuchi LM, Huang ES, et al. Aspirin, nonsteroidal anti-inflammatory drug use, and risk for Crohn disease and ulcerative colitis: a cohort study. Ann Intern Med 2012;156:350-9. doi: 10.7326/0003-4819-156-5- 201203.060.00007.
  • [26] Ananthakrishnan AN. Epidemiology and risk factors for IBD. Nat Rev Gastroenterol Hepatol 2015;12:205-17. doi: 10.1038/ nrgastro.2015.34. Epub 2015 Mar 3.
  • [27] Ohkusa T, Nomura T, Sato N. The role of bacterial infection in the pathogenesis of inflammatory bowel disease. Intern Med 2004;43:534-39. doi:10.2169/internalmedicine.43.534.
  • [28] Bernstein CN, Hitchon CA, Walld R, et al. Increased Burden of Psychiatric Disorders in Inflammatory Bowel Disease. Inflamm Bowel Dis 2019;25:360-68. doi: 10.1093/ibd/izy235.
  • [29] Mikocka-Walus A, Knowles SR, Keefer L, Graff L. Controversies revisited: A systematic review of the comorbidity of depression and anxiety with inflammatory bowel diseases. Inflamm Bowel Dis 2016;22:752-62. doi:10.1097/MIB.000.000.0000000620.
  • [30] Benjamin JL, Sumpter R Jr, Levine B, Hooper LV. Intestinal epithelial autophagy is essential for host defense against invasive bacteria. Cell Host Microbe 2013;13:723-34. doi:10.1016/j.chom.2013.05.004.
  • [31] Jostins L, Ripke S, Weersma RK, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 2012;491:119-24. doi: 10.1038/nature11582.
  • [32] Uhlig HH, Powrie F. Translating Immunology into Therapeutic Concepts for Inflammatory Bowel Disease. Annu Rev Immunol 2018;36:755-81. doi:10.1146/annurevimmunol- 042.617.053055.
  • [33] de Souza HS, Fiocchi C. Immunopathogenesis of IBD: current state of the art. Nat Rev Gastroenterol Hepatol 2016;13:13-27. doi:10.1038/nrgastro.2015.186.
  • [34] Huether SE. Alterations of digestive function, In: McCance KL, Huether SE, eds. Study guide for Pathophysiology: The Biologic Basis for Disease in Adults and Children. St. Louis, Missouri: Elsevier, 2019:1321-72.SE
  • [35] Özbek M, Hitit M, Ergün E, Beyaz F, Ergün L. Toll-like receptors. MAKÜ Sag Bil Enst Derg 2017;5: 180-92.
  • [36] Kostic AD, Xavier RJ, Gevers D. The microbiome in inflammatory bowel disease: current status and the future ahead. Gastroenterology 2014;146:1489-99. doi:10.1053/j. gastro.2014.02.009.
  • [37] Quévrain E, Maubert MA, Michon C, et al. Identification of an anti-inflammatory protein from Faecalibacterium prausnitzii, a commensal bacterium deficient in Crohn’s disease. Gut 2016;65:415-25. doi: 10.1136/gutjnl-2014-307649.
  • [38] Lapaquette P, Glasser AL, Huett A, Xavier RJ, Darfeuille- Michaud A. Crohn’s disease-associated adherent-invasive E. coli are selectively favoured by impaired autophagy to replicate intracellularly. Cell Microbiol 2010;12:99-113. doi:10.1111/ j.1462-5822.2009.01381.x.
  • [39] Darfeuille-Michaud A, Boudeau J, Bulois P, et al. High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology 2004;127:412-21. doi: 10.1053/j.gastro.2004.04.061.
  • [40] Virta L, Auvinen A, Helenius H, Huovinen P, Kolho KL. Association of repeated exposure to antibiotics with the development of pediatric Crohn’s disease—a nationwide, register-based finnish case-control study. Am J Epidemiol 2012;175:775-84. doi:10.1093/aje/kwr400.
  • [41] Kronman MP, Zaoutis TE, Haynes K, Feng R, Coffin SE. Antibiotic exposure and IBD development among children: a population-based cohort study. Pediatrics 2012;130:e794-e803. doi:10.1542/peds.2011-3886.
  • [42] Sartin J. Gastrointestinal disorders, In: Banasik JL, Copstead L. eds. Pathophysiology. St. Louis, Missouri: Elsevier, 2019:721-41.
  • [43] Glassner KL, Abraham BP, Quigley EMM. The microbiome and inflammatory bowel disease. J Allergy Clin Immunol 2020;145:16-27. doi:10.1016/j.jaci.2019.11.003.
  • [44] Bak SH, Choi HH, Lee J, et al. Fecal microbiota transplantation for refractory Crohn’s disease. Intest Res 2017;15:244-48. doi: 10.5217/ir.2017.15.2.244.
  • [45] Suskind DL, Brittnacher MJ, Wahbeh G, et al. Fecal microbial transplant effect on clinical outcomes and fecal microbiome in active Crohn’s disease. Inflamm Bowel Dis 2015;21:556-63. doi: 10.1097/MIB.000.000.0000000307.
  • [46] Lochs H, Dejong C, Hammarqvist F, et al. ESPEN Guidelineson Enteral Nutrition: Gastroenterology. Clin Nutr 2006; 25:260-74.
  • [47] Cresci G, Escuro A. Medical nutrition therapy for lower gastrointestinal tract disorders, In: Mahan LK, Raymond JL, eds. Krause’s Food and Nutrition Therapy. Elsevier,2017:541-49.
  • [48] Bischoff SC, Escher J, Hébuterne X, et al. ESPEN practical guideline: Clinical Nutrition in inflammatory bowel disease. Clin Nutr 2020;39:632-53. doi: 10.1016/j.clnu.2019.11.002.
  • [49] Brown AC, Rampertab SD, Mullin GE. Existing dietary guidelines for Crohn’s disease and ulcerative colitis. Expert Rev Gastroenterol Hepatol 2011;5:411-25. doi: 10.1586/egh.11.29.
  • [50] Naseer M, Poola S, Ali S, Samiullah S, Tahan V. Prebiotics and Probiotics in Inflammatory Bowel Disease: Where are we now and where are we going? Curr Clin Pharmacol 2020;15:216- 33. doi: 10.2174/157.488.4715666.200.312100237.
Toplam 50 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Klinik Tıp Bilimleri
Bölüm Review Article
Yazarlar

Izel Aycan Basoglu Bu kişi benim 0000-0003-1199-3194

Berna Karakoyun Bu kişi benim 0000-0003-0929-4239

Yayımlanma Tarihi 31 Mayıs 2023
Yayımlandığı Sayı Yıl 2023

Kaynak Göster

APA Basoglu, I. A., & Karakoyun, B. (2023). Crohn’s disease: Etiology, pathogenesis and treatment strategies. Marmara Medical Journal, 36(2), 249-254. https://doi.org/10.5472/marumj.1307982
AMA Basoglu IA, Karakoyun B. Crohn’s disease: Etiology, pathogenesis and treatment strategies. Marmara Med J. Mayıs 2023;36(2):249-254. doi:10.5472/marumj.1307982
Chicago Basoglu, Izel Aycan, ve Berna Karakoyun. “Crohn’s Disease: Etiology, Pathogenesis and Treatment Strategies”. Marmara Medical Journal 36, sy. 2 (Mayıs 2023): 249-54. https://doi.org/10.5472/marumj.1307982.
EndNote Basoglu IA, Karakoyun B (01 Mayıs 2023) Crohn’s disease: Etiology, pathogenesis and treatment strategies. Marmara Medical Journal 36 2 249–254.
IEEE I. A. Basoglu ve B. Karakoyun, “Crohn’s disease: Etiology, pathogenesis and treatment strategies”, Marmara Med J, c. 36, sy. 2, ss. 249–254, 2023, doi: 10.5472/marumj.1307982.
ISNAD Basoglu, Izel Aycan - Karakoyun, Berna. “Crohn’s Disease: Etiology, Pathogenesis and Treatment Strategies”. Marmara Medical Journal 36/2 (Mayıs 2023), 249-254. https://doi.org/10.5472/marumj.1307982.
JAMA Basoglu IA, Karakoyun B. Crohn’s disease: Etiology, pathogenesis and treatment strategies. Marmara Med J. 2023;36:249–254.
MLA Basoglu, Izel Aycan ve Berna Karakoyun. “Crohn’s Disease: Etiology, Pathogenesis and Treatment Strategies”. Marmara Medical Journal, c. 36, sy. 2, 2023, ss. 249-54, doi:10.5472/marumj.1307982.
Vancouver Basoglu IA, Karakoyun B. Crohn’s disease: Etiology, pathogenesis and treatment strategies. Marmara Med J. 2023;36(2):249-54.