A novel serum biomarker of endoscopic mucosal healing in inflammatory bowel disease

Article information

Intest Res. 2024;22(1):3-4
Publication date (electronic) : 2024 January 29
doi : https://doi.org/10.5217/ir.2023.00198
Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Korea
Correspondence to Hyoun Woo Kang, Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, 20 Boramae-ro 5-gil, Dongjak-gu, Seoul 07061, Korea. Tel: +82-2-870-2234, Fax: +82-2-870- 3866, E-mail: gangmali@naver.com
Received 2023 December 19; Accepted 2023 December 22.

Inflammatory bowel disease (IBD) is widely recognized as a condition that progressively worsens, leading to ongoing and increasing damage to the bowel [1,2]. There is a growing consensus that early, personalized treatments aimed at specific goals can prevent this bowel damage and the associated physical disability in IBD. However, it is still uncertain what the best targets for these treatments are. The ideal target should be (1) well-defined, (2) achievable with current treatments, and (3) linked to positive long-term outcomes [3]. Previously, clinical remission was the goal, but with the development of effective biological treatments, the focus has shifted towards achieving endoscopic healing [4]. Questions have arisen about the benefits of aiming for even deeper healing, including histological and transmural healing. Technological advancements, like fecal calprotectin tests [5] and bedside cross-sectional imaging [6], have further supported this shift from just managing symptoms to normalizing objective signs of gut inflammation. While many observational studies suggest that deeper healing correlates with better outcomes, randomized controlled trials (RCTs) are needed to prove that treating to achieve these specific endpoints leads to meaningful clinical results. Additionally, proving that an extended treatment goal is superior isn’t enough to adopt it; the significant additional benefits of this new goal, compared to previous ones, must outweigh the extra costs and risks involved in achieving it. Choosing the most appropriate targets is challenging due to the limited number of RCTs examining the balance between cost, safety, and effectiveness.

The study “Ischemia-modified albumin: a novel blood marker of endoscopic mucosal healing in inflammatory bowel disease” explores ischemia-modified albumin (IMA) as a biomarker for assessing disease activity in IBD [7]. It includes 48 patients with IBD and examines the correlation between fecal calprotectin, serum IMA, and endoscopic findings. The study finds significant associations between elevated levels of fecal calprotectin and serum IMA with endoscopic non-mucosal healing. These findings suggest the potential of IMA as a noninvasive serum biomarker for predicting endoscopic mucosal healing in IBD, offering an alternative to current invasive methods. The study underscores the need for reliable, noninvasive biomarkers in IBD management, which could enhance patient care by reducing the need for invasive procedures.

As previously described, for IMA to be validated as an ideal treatment target for IBD, further research is necessary. This research should be large-scale and long-term, focusing on 4 key aspects: (1) being clearly defined, (2) reliable, (3) achievable with available therapies, and (4) directly linked to favorable long-term outcomes.


Funding Source

The author received no financial support for the research, authorship, and/or publication of this article.

Conflict of Interest

Kang HW is an editorial board member of the journal but was not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflicts of interest relevant to this article were reported.

Data Availability Statement

Not applicable.

Author Contributions

Writing and approval of the final manuscript: Kang HW.


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