UC-duodenitis was first described in 1960 and has been repeatedly reported especially in the last few decades [3–10, 17]. While many of these reports demonstrate the cases of UC-duodenitis developed after colectomy, it appears to be still uncommon. Although it is still a rare condition, the clinical significance of this manifestation in patients with UC is based on the fact that the number of reported UC-duodenitis cases have been increasing in recent years despite the rate of colectomy in patients with UC reducing [5, 6, 24–28, 7, 9, 18–23] [29]. However, it is important to first establish a rationale for a rare but significant complication in UC which is now a globally emergence disease. In this study, we sought to determine the incidence, clinical course, and risk factors of UC-duodenitis developed after colectomy in patients with UC. We identified 11 cases of UC-duodenitis among 152 patients with UC who received colectomy due to treatment failure in our cohort. Higher disease activity and the use of anti-TNF-α at the time of colectomy are found to be the risks for UC-duodenitis. Most UC-duodenitis patients responded to 5-ASA or corticosteroids and did not experience relapses but additional biologics were needed if concomitant pouchitis existed. A better understanding of disease behavior, effective treatments, and risk factors of UC-duodenitis will help improve the management of patients with UC, especially severe cases that require colectomy.
The pathogenesis of UC-duodenitis remains to be elucidated. Consequently, there have not been any clinical measures to predict and prevent the development of UC-duodenitis in patients with UC undergoing colectomy. This study is the first to identify that disease status and a specific treatment of UC at the time of colectomy are associated with the development of UC-duodenitis. Higher disease activity in patients with UC may lead to a systemic inflammatory milieu, which remains active after colectomy while the inflammatory site is gone. Different from the surgical procedures of colorectal cancer, colectomy for UC due to treatment failure normally leaves the regional lymph nodes, which can be the reserver of activated lymphocytes and macrophages capable of homing to other parts of the intestine. The use of anti-TNF-α at the time of colectomy was the other possible risk factor of UC-duodenitis. Interestingly, it has been shown that the anti-TNF-α treatment, especially etanercept may induce intestinal inflammation when used for other autoimmune diseases than IBD [30, 31]. Similarly, anti-TNF-α agents are known to induce psoriatic skin lesions despite them being often used to treat psoriasis [32]. The psoriatic lesions caused by anti-TNF-α tend to distribute different body regions compared to ordinal psoriasis and thus called “inverse psoriasis” [32]. It is possible that artificial manipulations of unbalanced immune responses may paradoxically lead to another abnormal immune activations in different areas of the body. This hypothesis links the inverse psoriasis and the pathogenesis of UC-duodenitis that involve anti-TNF-α treatment. Therefore, activated lymphocytes and macrophages that have lost an effector site and uniquely manipulated immunity are plausible mechanisms underlying the development of UC-duodenitis after colectomy.
The treatment of UC-duodenitis has not been established. Previous case reports have shown the treatment experiences of UC-duodenitis with medications for UC such as powdered mesalazine, corticosteroids, tacrolimus, and anti-TNF-α agents [5, 6, 8–10]. The response to ordinal medications for UC implies the pathogenesis of UC-duodenitis may be similar to that in UC. However, our results show that the relapse of UC-duodenitis is uncommon and the maintenance therapy may not be necessary unless it is complicated with pouchitis. In the setting of status post colectomy, absence of effector site, transient immune rebooting by ordinal medications for UC may be enough to control UC-duodenitis.
UC-duodenitis is a relatively uncommon disease but its incidence appears to be increasing. Accumulating case reports have gradually revealed the clinical characteristics of UC-duodenitis. Because all of the previous reports including this study had retrospectively analyzed the cases, there are limitations to achieve definitive conclusions regarding the factors predispose to the development of UC-duodenitis. However, our results have characterized this rare condition to be able to at least develop clinical hypotheses. By identifying clinically applicable risk factors for the development of UC-duodenitis, our results may allow us to provide more efficient screening of UC-duodenitis and consequently improve the overall outcome of colectomy in patients with UC.