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A symposium organized by the Cochrane IBD Group and presented at the 2017 Digestive Disease Week annual meeting reviewed the recent literature on several controversial topics in inflammatory bowel disease (IBD) management including the efficacy of oral aminosalicylates for induction and maintenance of Crohn's disease (CD), the feasibility of drug withdrawal in patients with quiescent CD, and strategies for detecting colon cancer in patients with IBD. This article summarizes the data presented at that session.Copyright © 2018 Crohn's & Colitis Foundation. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

A symposium organized by the Cochrane IBD Group and presented at the 2017 Digestive Disease Week annual meeting reviewed the recent literature on several controversial topics in inflammatory bowel disease (IBD) management including the efficacy of oral aminosalicylates for induction and maintenance of Crohn's disease (CD), the feasibility of drug withdrawal in patients with quiescent CD, and strategies for detecting colon cancer in patients with IBD. This article summarizes the data presented at that session.Copyright © 2018 Crohn's & Colitis Foundation. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Background/Objectives:Delayed treatment failure occurs in a significant proportion of inflammatory bowel disease (IBD) patients treated with tumor necrosis factor-alpha (TNF) antagonists. Identification of predictors of loss of response (LOR) may help to optimize therapy. We sought to determine whether body composition parameters at the commencement of anti-TNF therapy were associated with earlier treatment failure.Subjects/Methods:A retrospective cohort study was performed on 68 patients who had undergone cross-sectional abdominal imaging coincident with the commencement of anti-TNF drugs. Analysis of the images at the third lumbar vertebra was performed using standard techniques to determine cross-sectional areas of skeletal muscle (SM), visceral adipose tissue, subcutaneous adipose tissue and intermuscular adipose tissue. Treatment failure was defined as: post-induction hospital admission or surgery for IBD, escalation of TNF dose or immunosuppressants for clinical LOR, emergence of a new fistula or Crohn's Disease Activity Index (CDAI) >150. Result(s):Two-thirds of patients had myopenia. Patients with less than gender-specific median SM area had a median time to failure of 520 (s.d. 135) days compared to 1100 (s.d. 151) days for those with more than median SM area (P=0.036). No difference was found in disease duration, inflammatory markers or CDAI between quartiles of SM area. No relation between outcomes and measures of adipose tissue, weight or body mass index was observed. Conclusion(s):Identifying low muscle mass at anti-TNF induction as a risk factor for treatment failure may contribute to a more tailored approach to IBD therapy.Copyright © 2017 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.

Goals: We sought to determine whether low muscle mass at commencement of anti-tumour necrosis factor (TNF) therapy was associated with earlier treatment failure. Background(s): Delayed treatment failure occurs in significant proportion of inflammatory bowel disease (IBD) patients treated with TNF-alpha antagonists. Identification of predictors of loss of response may help optimize therapy. Study: A retrospective cohort study was performed of 67 patients who had undergone cross-sectional abdominal imaging at a single centre coincident with commencement of anti-TNF drugs. Analysis of the images at the third lumbar vertebra was performed using standard techniques to determine cross-sectional areas of skeletal muscle (SM), visceral adipose tissue, subcutaneous adipose tissue, and intermuscular adipose tissue. Treatment failure was defined as follows: a post-induction hospital admission or surgery for IBD, escalation of TNF dose or immunosuppressants for clinical loss of response, emergence of a new fistula, or rising Crohn's Disease Activity Index >150. Result(s): Two-thirds of patients had sarcopenia. Patients with less than the gender-specific median SM area had a median time to failure of 520 (SD 135) days compared with 1100 (SD 151) days for those with greater than median SM area (P = 0.036). No difference was found in disease duration, inflammatory markers, or Crohn's Disease Activity Index between quartiles of SM area. No relation between outcomes and measures of adipose tissue, weight, or body mass index was observed. Conclusion(s): Identifying low muscle mass at anti-TNF induction as a risk factor for treatment failure may contribute to a more tailored approach to IBD therapy.

Background/Objectives:Delayed treatment failure occurs in a significant proportion of inflammatory bowel disease (IBD) patients treated with tumor necrosis factor-alpha (TNF) antagonists. Identification of predictors of loss of response (LOR) may help to optimize therapy. We sought to determine whether body composition parameters at the commencement of anti-TNF therapy were associated with earlier treatment failure.Subjects/Methods:A retrospective cohort study was performed on 68 patients who had undergone cross-sectional abdominal imaging coincident with the commencement of anti-TNF drugs. Analysis of the images at the third lumbar vertebra was performed using standard techniques to determine cross-sectional areas of skeletal muscle (SM), visceral adipose tissue, subcutaneous adipose tissue and intermuscular adipose tissue. Treatment failure was defined as: post-induction hospital admission or surgery for IBD, escalation of TNF dose or immunosuppressants for clinical LOR, emergence of a new fistula or Crohn's Disease Activity Index (CDAI) >150. Result(s):Two-thirds of patients had myopenia. Patients with less than gender-specific median SM area had a median time to failure of 520 (s.d. 135) days compared to 1100 (s.d. 151) days for those with more than median SM area (P=0.036). No difference was found in disease duration, inflammatory markers or CDAI between quartiles of SM area. No relation between outcomes and measures of adipose tissue, weight or body mass index was observed. Conclusion(s):Identifying low muscle mass at anti-TNF induction as a risk factor for treatment failure may contribute to a more tailored approach to IBD therapy.Copyright © 2017 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.

Goals: We sought to determine whether low muscle mass at commencement of anti-tumour necrosis factor (TNF) therapy was associated with earlier treatment failure. Background(s): Delayed treatment failure occurs in significant proportion of inflammatory bowel disease (IBD) patients treated with TNF-alpha antagonists. Identification of predictors of loss of response may help optimize therapy. Study: A retrospective cohort study was performed of 67 patients who had undergone cross-sectional abdominal imaging at a single centre coincident with commencement of anti-TNF drugs. Analysis of the images at the third lumbar vertebra was performed using standard techniques to determine cross-sectional areas of skeletal muscle (SM), visceral adipose tissue, subcutaneous adipose tissue, and intermuscular adipose tissue. Treatment failure was defined as follows: a post-induction hospital admission or surgery for IBD, escalation of TNF dose or immunosuppressants for clinical loss of response, emergence of a new fistula, or rising Crohn's Disease Activity Index >150. Result(s): Two-thirds of patients had sarcopenia. Patients with less than the gender-specific median SM area had a median time to failure of 520 (SD 135) days compared with 1100 (SD 151) days for those with greater than median SM area (P = 0.036). No difference was found in disease duration, inflammatory markers, or Crohn's Disease Activity Index between quartiles of SM area. No relation between outcomes and measures of adipose tissue, weight, or body mass index was observed. Conclusion(s): Identifying low muscle mass at anti-TNF induction as a risk factor for treatment failure may contribute to a more tailored approach to IBD therapy.

Background: In Australia, infliximab (IFX) and adalimumab (ADA) are available for the treatment of moderate-severe Crohn disease (CD) refractory to conventional therapies, with minimal local data comparing their efficacy. Aim(s): The aim of this study was to compare clinical and biochemical outcomes at 3 and 12 months between patients receiving induction and maintenance therapy with IFX versus ADA. Method(s): Retrospective single-centre audit of all patients commenced on IFX or ADA as their first anti-tumour necrosis factor agent between July 2007 and May 2012. Clinical and biochemical parameters were compared pre-commencement, 3 and 12 months post-commencement. Result(s): A total of 81 patients was included in the study; 63 IFX-treated and 18 ADA-treated. Significant Crohn disease activity index (CDAI) reductions were noted within both groups at 3 months (P < 0.001) and 12 months (P < 0.001). Similarly, significant reductions were noted in steroid doses within groups at 3 months (P < 0.05) and 12 months (P < 0.05), with notable reductions in C-reactive protein (CRP) at 3 months within groups (P < 0.05). Adverse events occurred in 14.3% of IFX and 11.1% of ADA patients. Comparing IFX with ADA, no difference was shown between groups in CDAI reductions at 3 months (P = 0.94) and 12 months (P = 0.95), steroid dosing at 3 months (P = 0.23) and 12 months (P = 0.81), and CRP reduction at 3 months (P = 0.33) and 12 months (P = 0.62). Fistula-related admissions were significantly reduced in IFX patients (100% reduction post-IFX vs 66.7% post-ADA) (P = 0.01). Conclusion(s): Clinical and biochemical outcomes were similar in patients treated with IFX or ADA as induction and maintenance therapy for CD. However, significant reductions were noted in admissions relating to fistulising disease in IFX patients.Copyright © 2016 Royal Australasian College of Physicians

Background: In Australia, infliximab (IFX) and adalimumab (ADA) are available for the treatment of moderate-severe Crohn disease (CD) refractory to conventional therapies, with minimal local data comparing their efficacy. Aim(s): The aim of this study was to compare clinical and biochemical outcomes at 3 and 12 months between patients receiving induction and maintenance therapy with IFX versus ADA. Method(s): Retrospective single-centre audit of all patients commenced on IFX or ADA as their first anti-tumour necrosis factor agent between July 2007 and May 2012. Clinical and biochemical parameters were compared pre-commencement, 3 and 12 months post-commencement. Result(s): A total of 81 patients was included in the study; 63 IFX-treated and 18 ADA-treated. Significant Crohn disease activity index (CDAI) reductions were noted within both groups at 3 months (P < 0.001) and 12 months (P < 0.001). Similarly, significant reductions were noted in steroid doses within groups at 3 months (P < 0.05) and 12 months (P < 0.05), with notable reductions in C-reactive protein (CRP) at 3 months within groups (P < 0.05). Adverse events occurred in 14.3% of IFX and 11.1% of ADA patients. Comparing IFX with ADA, no difference was shown between groups in CDAI reductions at 3 months (P = 0.94) and 12 months (P = 0.95), steroid dosing at 3 months (P = 0.23) and 12 months (P = 0.81), and CRP reduction at 3 months (P = 0.33) and 12 months (P = 0.62). Fistula-related admissions were significantly reduced in IFX patients (100% reduction post-IFX vs 66.7% post-ADA) (P = 0.01). Conclusion(s): Clinical and biochemical outcomes were similar in patients treated with IFX or ADA as induction and maintenance therapy for CD. However, significant reductions were noted in admissions relating to fistulising disease in IFX patients.Copyright © 2016 Royal Australasian College of Physicians

Aims: In Inflammatory Bowel Disease (IBD), large registration studies have not shown a significant difference in clinical endpoints in patients treated with anti-tumour necrosis factor alpha (anti-TNF) monoclonal antibody alone versus with immunomodulator co-therapy, however from recent data, there is a trend towards co-therapy to reduce immunogenicity to anti-TNFs. Given the risks of immunomodulators, particularly thiopurines, we queried the long-term therapeutic benefits of immunomodulator co-therapy. Our aim was to assess whether anti-TNF monotherapy was associated with earlier loss of response (LOR) in patients with Inflammatory Bowel Disease (IBD) versus combination therapy in a real world cohort. Method(s): A retrospective audit was conducted of all patients with IBD receiving anti-TNF therapy in a tertiary centre. All patients on anti-TNF therapy with an accurate date for TNF commencement and adequate correspondence to determine end-points were included. Patients with prior exposure to any anti-TNF agent were excluded. Outcomes measured included weight and body mass indices pre and post anti-TNF and days to first loss of response; defined by an admission or surgery post-induction, escalation of TNF dose or concurrent immunomodulators for clinical LOR, emergence of a new fistula or rising Crohn's Disease Activity Index > 150 (CDAI). Statistical analysis was performed with GraphPad Prism v6. Result(s): A total of 94 patients were included for analysis; 53 induced with Infliximab (IFX) and 41 induced with Adalimumab (ADA). 91 patients were treated for Crohn's Disease and 3 patients treated for Ulcerative Colitis. 81 patients received co-therapy and 13 patients received monotherapy. 42 (45%) patients had loss of response during follow-up; 23 (55%) IFX patients and 19 (45%) ADA patients (p = ns). Causes for LOR included hospital admission (n = 13, 31%), clinical LOR (n = 21, 50%), surgery (n = 6, 14%) or new fistula (n = 2, 5%). The median time to loss of response