We read with great interest the brief communication by Yamamoto-Furusho et al.,1 describing eight Mexican patients initially diagnosed with ulcerative colitis (UC), who later developed Crohn’s disease (CD)-like features, and so were considered to represent the proposed “UC2CD” phenotype. The authors are to be commended for highlighting a clinically relevant and insufficiently studied challenge in inflammatory bowel disease (IBD), namely the subgroup of patients whose disease classification appears to evolve over time. Their report adds useful real-world observations and may encourage further discussion on phenotypic heterogeneity in IBD.

A key issue, however, is whether these cases should be interpreted as a truly distinct biologic phenotype or as a diagnostic reclassification within the established spectrum of IBD. In routine practice, the diagnosis and classification of UC and CD rely on a combination of clinical symptoms, laboratory tests, endoscopy with biopsies, histology, and imaging assessment of bowel involvement.2 The later appearance of ileal strictures, fistulas, or perianal disease is certainly noteworthy, but does not, by itself, establish biologic transformation from UC to CD. An alternative explanation is that some patients may have had CD or IBD-unclassified features that were not fully recognized at the time of the initial diagnosis. Current consensus documents likewise emphasize careful diagnostic adjudication before assigning a definitive disease category.2

Therefore, additional details regarding the original diagnostic assessment would have been highly informative. A clearer description of baseline histologic findings, initial small-bowel evaluation, and whether pathology was re-reviewed after the phenotypic shift would help readers better assess how confidently “UC2CD” can be distinguished from delayed diagnostic revision. This point is particularly important because the concept of UC2CD, as cited by the authors, appears to derive primarily from a conference abstract rather than a full peer-reviewed validation study.3 Consequently, the authors’ report may be better viewed as a descriptive observation consistent with an emerging hypothesis, rather than confirmatory evidence of a separate IBD subtype.

In addition, several features emphasized in the manuscript, including extraintestinal manifestations, anti-TNF refractoriness, elevated globulin levels, and the need for surgery, are clinically important but may not be specific to UC2CD. Extraintestinal manifestations are well recognized across the broader IBD population, and refractoriness to therapy or surgical intervention may also reflect severe disease, referral bias, or long disease duration in a tertiary care setting.4 Furthermore, although elevated globulin levels were noted in most patients, other serologic markers proposed in the original UC2CD model were not routinely assessed in this cohort, limiting the extent to which that framework can be examined here.

Overall, this report makes a valuable contribution by drawing attention to a clinically challenging subgroup. We respectfully suggest that slightly more cautious wording of the conclusions would further strengthen the article. At present, these cases may be more appropriately interpreted as patients with late CD-like reclassification after an initial UC diagnosis, whose shared features warrant prospective, multicenter investigation.