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- Clinical features of active tuberculosis that developed during anti-tumor necrosis factor therapy in patients with inflammatory bowel disease
- Jang Wook Lee, Chang Hwan Choi, Ji Hoon Park, Jeong Wook Kim, Sang Bum Kang, Ja Seol Koo, Young-Ho Kim, You Sun Kim, Young Eun Joo, Sae Kyung Chang
- Intest Res 2016;14(2):146-151. Published online April 27, 2016
- DOI: https://doi.org/10.5217/ir.2016.14.2.146
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Abstract
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ePub <b>Background/Aims</b><br/> Anti-tumor necrosis factor (TNF) therapy for active ulcerative colitis (UC) and Crohn's disease (CD) is associated with increased risks of tuberculosis (TB) infection. We analyzed the incidence and clinical features of Korean patients with inflammatory bowel disease (IBD) who developed active TB during anti-TNF therapy.
Methods Ten cases of active TB developed in patients treated with infliximab (n=592) or adalimumab (n=229) for UC (n=160) or CD (n=661) were reviewed. We analyzed demographics, interval between start of anti-TNF therapy and active TB development, tests for latent TB infection (LTBI), concomitant medications, and the details of diagnosis and treatments for TB.
Results The incidence of active TB was 1.2% (10/821): 1.5% (9/592) and 0.4% (1/229) in patients receiving infliximab and adalimumab, respectively. The median time to the development of active TB after initiation of anti-TNF therapy was three months (range: 2–36). Three patients had past histories of treatment for TB. Positive findings in a TB skin test (TST) and/or interferon gamma releasing assay (IGRA) were observed in three patients, and two of them received anti-TB prophylaxis. Two patients were negative by both TST and IGRA. The most common site of active TB was the lungs, and the active TB was cured in all patients.
Conclusions Active TB can develop during anti-TNF therapy in IBD patients without LTBI, and even in those with histories of TB treatment or LTBI prophylaxis. Physicians should be aware of the potential for TB development during anti-TNF therapy, especially in countries with a high prevalence of TB.
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Citations
Citations to this article as recorded by
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Russian Journal of Evidence-Based Gastroenterology.2023; 12(3): 29. CrossRef - Five-Year Efficacy and Safety of Ustekinumab Treatment in Crohn’s Disease: The IM-UNITI Trial
William J. Sandborn, Rory Rebuck, Yuhua Wang, Bin Zou, Omoniyi J. Adedokun, Christopher Gasink, Bruce E. Sands, Stephen B. Hanauer, Stephan Targan, Subrata Ghosh, Willem J.S. de Villiers, Jean-Frederic Colombel, Brian G. Feagan, John P. Lynch
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Qin Yu Yang, Yi Juan Liu, Ye Xu, Lin Zhang, Cheng Dang Wang
Journal of Digestive Diseases.2021; 22(8): 473. CrossRef - Clinical Features and Outcomes of Tuberculosis in Inflammatory Bowel Disease Patients Treated with Anti-tumor Necrosis Factor Therapy
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The Korean Journal of Gastroenterology.2020; 75(1): 29. CrossRef - Increased Risk of Herpes Zoster in Young and Metabolically Healthy Patients with Inflammatory Bowel Disease: A Nationwide Population-Based Study
Hosim Soh, Jaeyoung Chun, Kyungdo Han, Seona Park, Gukhwan Choi, Jihye Kim, Jooyoung Lee, Jong Pil Im, Joo Sung Kim
Gut and Liver.2019; 13(3): 333. CrossRef - Discontinuation of Biological Treatments in Inflammatory Bowel Disease
Shomron Ben-Horin, Ren Mao, Yun Qiu, Minhu Chen
Journal of Clinical Gastroenterology.2018; 52(1): 6. CrossRef - Asian Organization for Crohn's and Colitis and Asia Pacific Association of Gastroenterology consensus on tuberculosis infection in patients with inflammatory bowel disease receiving anti-tumor necrosis factor treatment. Part 2: management
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The Korean Journal of Internal Medicine.2018; 33(1): 20. CrossRef - Nonimmunity against hepatitis B virus infection in patients newly diagnosed with inflammatory bowel disease
Seong Jae Yeo, Hyun Seok Lee, Byung Ik Jang, Eun Soo Kim, Seong Woo Jeon, Sung Kook Kim, Kyeong Ok Kim, Yoo Jin Lee, Hyun Jik Lee, Kyung Sik Park, Yun Jin Jung, Eun Young Kim, Chang Heon Yang
Intestinal Research.2018; 16(3): 400. CrossRef - Asian Organization for Crohn's and Colitis and Asia Pacific Association of Gastroenterology consensus on tuberculosis infection in patients with inflammatory bowel disease receiving anti‐tumor necrosis factor treatment. Part 2: Management
Dong Il Park, Tadakazu Hisamatsu, Minhu Chen, Siew Chien Ng, Choon Jin Ooi, Shu Chen Wei, Rupa Banerjee, Ida Normiha Hilmi, Yoon Tae Jeen, Dong Soo Han, Hyo Jong Kim, Zhihua Ran, Kaichun Wu, Jiaming Qian, Pin‐Jin Hu, Katsuyoshi Matsuoka, Akira Andoh, Yasu
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Clinics and Research in Hepatology and Gastroenterology.2017; 41(6): 693. CrossRef
- (Re-)introduction of TNF antagonists and JAK inhibitors in patients with previous tuberculosis: a systematic review
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- The Changes of Non-steroidal Anti-inflammatory Drug Induced Gut Damage, Bacterial Overgrowth, Bacterial Translocation and Organ Weights in Rat Model
- Eun Jeong Kim, Jeong Wook Kim
- Intest Res 2006;4(1):45-52. Published online June 30, 2006
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Abstract
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- Background/Aims
NSAIDs induce gut damage throughout the entire gastrointestinal tract and bacterial translocation. The aim of this study was to exam the change of NSAID induced gut damage, enteric bacterial overgrowth, bacterial translocation and organ weight in the animals. Methods: Rats were utilized in 4 group; control group, diclofenac 60 mg/kg group, diclofenac 120 mg/kg group and diclofenac 60 mg/kg group. Gut injury was induced by oral administration of a single dose of diclofenac. Intestinal permeability (24 hour urinary excretion of pheonolsulfonphthalein), intestinal adhesion and number of stool pallet were measured to evaluate gut injury. Enteric aerobic total and gram negative bacterial counts in distal ileum and cecum were measured to evaluate enteric bacterial overgrowth. Bacterial counts of gram negatives in mesenteric lymph nodes, liver, spleen, kidney and heart were measured to evaluate bacterial translocation. Also, the organ weight change of liver, spleen, kidney and heart was measured. Results: Diclofenac caused the increase in intestinal permeability, intestinal adhesion, enteric bacterial numbers, bacterial translocation to mesenteric lymph nodes, liver, spleen, kidney and heart and hepatomegaly, and the decrease in numbers of stool pellet. Conclusions: Diclofenac induced gut damage, enteric bacterial overgrowth, bacterial translocation and hepatomegaly. (Intestinal Research 2006;4:45-52)
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- The Changes of Intestinal Permeability in Patients with Acute Viral Hepatitis B and Toxic Hepatitis
- Jeong Wook Kim, Woo Kyu Jeon
- Intest Res 2005;3(1):74-79. Published online June 30, 2005
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Abstract
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- Background/Aims
The changes of intestinal permeability have been investigated in patients with chronic liver disease such as alcoholic liver disease. However, the changes of intestinal permeability had not been reported in patients with acute hepatitis except acute hepatitis A. This study aimed to investigate the changes of intestinal permeability and examine correlations between the intestinal permeability and clinical characteristics in patients with acute hepatitis. Methods: The intestinal permeability were measured in 15 normal heathy controls, 30 patients with acute hepatitis (acute hepatitis B 15 , acute toxic hepatitis 15) by measuring 24 hour urine excretion of 51Cr-EDTA (51Cr-ethylenediaminetetraacetic acid) for evaluation of the gut barrier dysfunction. We compared the intestinal permeability with clinical characteristics of patients. Results: The increase in intestinal permeability in patients with acute hepatitis B was more higher than patients with acute toxic hepatitis (p＜0.05). The increase in intestinal permeability showed significant correlation with erythrocyte sedimentation rate and prothrombin time (p＜0.05). Conclusions: The increase in intestinal permeability was more in patients with acute hepatitis B than acute toxic hepatitis and may be related to erythrocyte sedimentation rate and prothrombin time. (Intest Res 2005;3:74-79)
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