ReviewAnnals of gastroenterology
Evaluating spleen volume in inflammatory bowel disease.
Review in Annals of gastroenterology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Beyond the Gut: Extra-Enteric Digestive Manifestations of Inflammatory Bowel Disease-A Personalized Medicine Perspective and Comprehensive Review.Journal of personalized medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crohn's disease (CD) and ulcerative colitis (UC), known as inflammatory bowel disease (IBD), are characterized by immune system dysregulation. The spleen holds a primary role in systemic inflammation and immune responses. Splenic involvement or splenomegaly in IBD patients may result from secondary causes, such as portal hypertension, myeloproliferative diseases, amyloidosis, splenic abscesses or granulomas. Current research on the direct association between IBD and spleen volume (SV) has expanded significantly. In CD, SV is predominantly increased, and is associated with worsen clinical outcomes. Successful treatment with infliximab often leads to a reduction in the elevated SV. Patients with UC often present spleens with invariant SV, or smaller spleens than those observed in CD, as UC typically affects a more limited part of the gastrointestinal tract compared to CD. However, reduction of SV in UC can also indicate relapsing pancolitis. Recent genetic data also suggest that an increased SV serves as a potential risk factor for the development of IBD, emphasizing the possible bidirectional causal relationship between IBD and SV. Shared pathogenic pathways, including intestinal immune activation, tumor necrosis factor-α activation, bowel toxin absorption and lymphatic tissue involvement, might explain the splenic and intestinal immune dysfunction. Thus, the measurement of SV and its adjustment for body mass index or weight, factors that affect the spleen size, may serve as a potential indicator for IBD monitoring, predicting disease-related flares and complications, and evaluating the response to current biologics. Nonetheless, further insights into the underlying pathogenic pathways linking SV and IBD are considered imperative.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.