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Review The JAK attack: transforming the management of ulcerative colitis in India
Arshdeep Singh1orcid, Arshia Bhardwaj1orcid, Vandana Midha2orcid, Ajit Sood1orcid

DOI: https://doi.org/10.5217/ir.2025.00153
Published online: January 2, 2026

1Department of Gastroenterology, Dayanand Medical College and Hospital, Ludhiana, India

2Department of Internal Medicine, Dayanand Medical College and Hospital, Ludhiana, India

Correspondence to Ajit Sood, Department of Gastroenterology, Dayanand Medical College, Tagore Nagar, Ludhiana, Punjab 141001, India. E-mail: dr_ajit_sood@dmch.edu
• Received: July 26, 2025   • Revised: September 5, 2025   • Accepted: September 8, 2025

© 2026 Korean Association for the Study of Intestinal Diseases.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Inflammatory bowel disease is increasingly recognized as a significant clinical entity in India, reflecting the country’s ongoing epidemiological transition. With a rising incidence and an expanding disease spectrum, the limitations of conventional therapeutic agents, such as corticosteroids and thiopurines, have become increasingly evident. This review examines the transformative role of Janus kinase inhibitors, particularly tofacitinib, in redefining therapeutic goals and bridging the gap between medical innovation and real-world implementation in resource-limited settings. Tofacitinib represents a pivotal advancement in the therapeutic landscape of ulcerative colitis (UC) in India, offering the advantages of oral administration, rapid onset of action, predictable pharmacokinetics, and cost-effective generic formulations–thereby overcoming several longstanding barriers to the adoption of advanced therapies. Accumulating real-world evidence from India supports its clinical utility across various phenotypes of UC, including corticosteroid-dependent or refractory disease, acute severe UC, ulcerative proctitis, elderly-onset UC, and in achieving deeper remission endpoints such as histologic healing. Furthermore, its incorporation into routine clinical practice has contributed to a measurable reduction in corticosteroid reliance, thereby aligning treatment strategies with international standards of care. By combining efficacy, safety, accessibility, and ease of use, tofacitinib has catalyzed a paradigm shift in the management of UC in the Indian context.
  • Keywords: Developing countries; Inflammatory bowel diseases; Janus kinase inhibitors; Tofacitinib; Ulcerative colitis
Just five decades ago, inflammatory bowel disease (IBD) was virtually unheard of in India. Inflammatory diarrhea was largely attributed to infectious causes: bacterial, parasitic, or viral. At the time, IBD was perceived as a Western disease, rarely diagnosed and largely considered irrelevant to routine clinical practice in the Indian subcontinent. Over the years, this perception has changed dramatically. IBD has firmly established itself in India as a growing health challenge [1]. What was once a clinical rarity is now an increasingly common diagnosis in gastroenterology clinics across the country. This transition is not an isolated phenomenon, but part of a broader global trend: an epidemiological shift unfolding across low- and middle-income countries (LMICs) [2]. A recent analysis tracing the global evolution of IBD over the past century reveals that countries move through a series of well-defined epidemiological stages [3]. Improved hygiene, sanitation, urban development, and the adoption of Western dietary patterns herald the emergence of IBD [4,5]. India is in the midst of a phase marked by a rapid acceleration in the incidence of IBD [2]. While the crude prevalence of IBD may still be lower than that in North America and Europe, India’s vast population size suggests that the absolute number of individuals living with IBD could be among the highest in the world [6].
With the rising burden of IBD, healthcare systems in India are increasingly confronted with complex challenges. The evolving epidemiology of IBD reflects not only an increase in incidence and prevalence but also a shift in the disease spectrum. Global evolutionary studies highlight that ulcerative colitis (UC) often emerges earlier in the epidemiological timeline, followed by a rise in Crohn’s disease (CD) [3,7,8]. This pattern suggests a temporal progression in both disease phenotype and clinical complexity.
The increasing complexity of IBD has necessitated continual innovation in therapeutic strategies. As the disease spectrum broadens and more patients present with moderate-to-severe or refractory disease, conventional therapies often fall short of achieving long-term remission or preventing complications. This clinical reality has driven the evolution of treatment paradigms over the decades, guided by both emerging scientific insights and unmet patient needs.
To date, there have been 3 major therapeutic milestones in the management of IBD, each representing a paradigm shift in the approach to treatment. The first breakthrough occurred in the 1950s with the introduction of corticosteroids. Truelove and Witts, in a seminal study, demonstrated that corticosteroids markedly decreased mortality among patients with UC, cementing their role as a cornerstone in the treatment of acute severe disease [9].
The second major breakthrough was heralded by the introduction of biologics, particularly anti-tumor necrosis factor (anti-TNF) agents, i.e., infliximab, adalimumab, and golimumab in the late 20th and early 21st centuries [10-13]. Anti-TNFs revolutionized the treatment landscape by targeting key inflammatory pathways, facilitating not only clinical remission but also mucosal healing, an endpoint previously unattainable with conventional therapies [14]. These agents demonstrated versatility, being employed as first-line advanced therapy in both UC and CD, as rescue therapy in acute severe UC (ASUC), and for the management of extraintestinal manifestations. This marked the beginning of a more targeted, mechanism-based approach to IBD care. Over the past decade, several novel biologic agents targeting distinct immune pathways such as, integrins and interleukins (ILs), have been developed, approved, and successfully integrated into clinical practice in many developed countries [15-18].
However, the transformative impact of biologics observed in Western countries has not been fully mirrored in developing nations. In India, their widespread adoption is constrained by multiple barriers, including high treatment costs, limited access within public healthcare systems, and heightened concerns about infectious complications, particularly tuberculosis reactivation [19-21]. Although newer biologics such as vedolizumab, with its gut-selective mechanism and favorable long-term safety profile, and ustekinumab, supported by robust efficacy and safety data, offer important therapeutic options, their clinical use remains restricted by economic limitations and practical considerations. These challenges are further compounded by sociocultural factors, including the stigma surrounding chronic illness and reluctance to commit to long-term injectable therapies (Fig. 1). Consequently, the real-world uptake of biologics in many LMICs has been low, limiting their ability to substantially alter the disease trajectory.
Therefore, although therapeutic options expanded globally, patients and clinicians in India continued to face limited choices, largely confined to conventional immunosuppressants and corticosteroids. The pressing need for a treatment that was both clinically effective and broadly accessible remained unmet, prolonging the search for a truly feasible and transformative therapeutic option.
This unmet need was addressed in 2018, a landmark year that witnessed the approval of tofacitinib, an oral small molecule, for the treatment of UC. This development constituted the third major milestone in the therapeutic landscape [22]. Tofacitinib exerts its therapeutic effect by targeting the JAK–STAT signaling pathway, a central mediator of cytokine-driven inflammation. It competitively binds to the ATP-binding site of JAKs, thereby preventing STAT phosphorylation and subsequent transcription of pro-inflammatory genes. Through this mechanism, it inhibits signaling of multiple cytokines, including IL-6, IL-12, IL-23, interferon-γ, and common γ-chain cytokines, leading to attenuation of T-cell activation and mucosal inflammation. In contrast to biologics that selectively block individual cytokines, JAK inhibitors provide simultaneous suppression of diverse cytokine pathways, resulting in a rapid and broad anti-inflammatory response [23]. Its oral formulation, rapid onset of action, short half-life, and predictable pharmacokinetic and pharmacodynamic properties make it a particularly attractive therapeutic option. The convenience of oral administration eliminated the need for cold-chain infrastructure, infusion centers, or training in self-injection techniques, rendering tofacitinib suitable for use in resource-constrained and rural settings. Importantly, the availability of cost-effective generic formulations in India addressed one of the most significant barriers to the adoption of advanced therapies: affordability.
The approval of tofacitinib marked not only a scientific breakthrough but also a potential solution to several longstanding barriers in IBD care within India. By addressing issues of accessibility, affordability, and practicality, tofacitinib aligned well with the unmet clinical needs of a diverse patient population. Despite its promising profile, the integration of this novel therapy into routine practice was not immediate. As with any paradigm shift, the introduction of tofacitinib was met with cautious optimism, and its early use remained selective and measured. In the subsequent sections, we discuss the broader challenges in the management of UC and highlight how tofacitinib has influenced therapeutic decision-making and contributed to overcoming several of these hurdles.
1. Management of Corticosteroid Dependent/Refractory UC
For decades, the management of moderate-to-severe UC relied predominantly on corticosteroids to induce remission. In the Indian context, early clinical experience and observational studies established the efficacy of thiopurines, particularly azathioprine, in maintaining remission among patients with steroid-dependent disease [24-26]. Consequently, azathioprine emerged as the cornerstone of long-term immunosuppressive therapy. However, thiopurines presented several limitations, including high relapse rates, poor drug persistence, and frequent discontinuation due to adverse events. Notable safety concerns included hepatotoxicity, myelotoxicity, and idiosyncratic pancreatitis. Their use further necessitated pre-treatment screening for thiopurine methyl transferase (TPMT) and Nudix hydrolase (NUDT15) polymorphisms to mitigate the risk of severe myelotoxicity, as well as therapeutic drug monitoring to guide dosing and assess response [27].
The introduction of tofacitinib has progressively transformed treatment paradigms, offering a viable therapeutic option for both thiopurine-naive patients and those with intolerance or an inadequate response to thiopurines. Growing evidence from India has validated tofacitinib’s effectiveness across the patient subgroups (Table 1) [28-36]. Consequently, reliance on thiopurines is diminishing, especially in urban centers and academic institutions where tofacitinib is increasingly being used as a more predictable and manageable alternative.
2. Acute Severe Ulcerative Colitis

1) Improving Response Rates to Intravenous Corticosteroids in ASUC

ASUC remains a medical emergency characterized by high morbidity and a substantial risk of colectomy. Intravenous corticosteroids (IVCS) have long been the first-line therapy, yet up to 30%–40% of patients fail to achieve an adequate clinical response, necessitating escalation to rescue therapies such as infliximab, cyclosporine, or surgical intervention [37]. Delayed therapeutic responses not only prolong hospitalization but also contribute to complications and increased healthcare burden. Efforts to improve early response rates to IVCS are critical to modifying the disease trajectory, reducing colectomy risk, and improving overall outcomes in ASUC. Despite advances in rescue strategies, optimizing initial therapy remains a key unmet need.
Tofacitinib has been investigated for enhancing primary response rates in ASUC when used in combination with IVCS [38]. The TACOS trial, a randomized controlled study, evaluated high-dose tofacitinib (30 mg/day) alongside standard IVCS therapy. The combination resulted in an absolute increase of nearly 25% in day 7 clinical response, suggesting that early, dual immunosuppression increases the response to IVCS and reduce the need for escalation to rescue therapy or surgery [32]. Although the dose employed was off-label, this study marked an important step toward optimizing early management strategies in ASUC.
The TACOS trial led to cautious, selective adoption of upfront combination strategy in ASUC in a select tertiary care centers. Importantly, a head-to-head randomized controlled trial comparing 20 mg versus 30 mg of tofacitinib in combination with IVCS is currently underway (CTRI/2024/10/075098), and is expected to provide further clarity on the optimal induction dosing for this indication.

2) Rescue Therapy in ASUC

As previously discussed, 30%–40% of patients fail to respond to IVCS alone, necessitating timely initiation of rescue therapy to prevent disease progression, reduce complications, and avoid colectomy. Conventional rescue strategies include infliximab, cyclosporine, or early colectomy. In resource-limited settings such as India, the use of infliximab is constrained by high cost, limited public healthcare access, and concerns regarding reactivation of latent tuberculosis [39]. Although cyclosporine remains an effective option, its use is challenged by a narrow therapeutic window, risk of nephrotoxicity and neurotoxicity, and the need for close monitoring of serum drug levels. Furthermore, cyclosporine requires transition to a long-term maintenance agent, typically azathioprine, which limits its utility in patients who are either azathioprine-experienced or intolerant, a scenario frequently encountered in Indian clinical practice.
Given the limitations of infliximab and cyclosporine, tofacitinib has emerged as a promising alternative for rescue therapy in patients refractory to IVCS [40]. Early real-world data from India have demonstrated encouraging outcomes with tofacitinib, including clinical response, avoidance of colectomy, and a manageable safety profile [36,41]. These findings have generated interest in integrating tofacitinib more broadly into ASUC treatment algorithms.
The effect of tofacitinib on perioperative outcomes represents another evolving area of clinical investigation. A recent study comparing ASUC patients undergoing colectomy found that those pre-treated with tofacitinib had a significantly lower rate of postoperative complications compared to those receiving infliximab [42]. Additionally, the short half-life of tofacitinib (approximately 3 hours) offers a distinct advantage, allowing for rapid drug clearance in patients requiring surgery, thereby minimizing the risks associated with perioperative immunosuppression. This pharmacokinetic profile makes tofacitinib particularly suitable as a bridging agent in patients at risk of requiring colectomy.

3) Optimal Maintenance Therapy in Corticosteroid Responsive ASUC

Despite initial response to IVCS, many patients with ASUC remain at high risk of early relapse, colectomy, or recurrent hospitalizations if not transitioned to an effective maintenance strategy [43-45]. However, there is a paucity of robust evidence to guide optimal maintenance therapy in this setting. Current guidelines recommend either thiopurines or anti-TNF agents, yet both approaches have limitations [46-48]. In a propensity matched-cohort study from India, tofacitinib demonstrated superior outcomes to azathioprine, with an event-free survival rate of 75% at 1 year [29]. This was significantly higher than the 50% event-free survival observed in the ACTIVE trial with infliximab [49]. These findings provide preliminary, but compelling, evidence supporting the role of tofacitinib as maintenance therapy in the continuum of ASUC management.
3. Frequent Corticosteroid Use
The use of systemic corticosteroids is increasingly recognized as an auditable quality metric in the management of IBD, with international guidelines emphasizing the importance of minimizing steroid exposure [50]. Persistent or repeated reliance on corticosteroids is associated with suboptimal disease control and a range of systemic complications, including metabolic disturbances, osteoporosis, adrenal suppression, and increased infection risk. Therefore, reducing corticosteroid dependency is now a key benchmark of high-quality IBD care.
The ORCHID study, a randomized controlled trial, demonstrated that tofacitinib was non-inferior to systemic corticosteroids for induction of remission at 8 weeks in patients with moderate-to-severe UC [33]. Importantly, this comparable efficacy was coupled with a more favorable safety profile, as tofacitinib avoided many of the metabolic, skeletal, and endocrine toxicities typically associated with systemic steroid use. An additional advantage of tofacitinib is its dual utility for both induction and maintenance of remission, thereby obviating the need to transition between agents and reducing treatment complexity.
In outpatients with severe UC, requiring prednisolone, we have adopted a novel strategy involving the use of tofacitinib in combination with budesonide. Budesonide, owing to its high first-pass metabolism and limited systemic exposure, offers a safer induction alternative with significantly lower risk of long-term adverse effects compared to prednisolone. This combined approach, administering tofacitinib with budesonide for 8 weeks, followed by withdrawal of budesonide while continuing tofacitinib as maintenance appears promising and has led to a nearly 50% reduction in the use of prednisolone at our center (unpublished data). This shift represents a significant advancement in aligning clinical practice with the overarching goal of steroid-free disease control and improving the long-term safety and quality of life for patients with UC.
4. Refractory Ulcerative Proctitis
Ulcerative proctitis (UP), a limited yet symptomatically burdensome phenotype of UC, presents a common and often frustrating challenge in clinical practice. Despite its confined anatomical extent, UP can produce disproportionately severe symptoms such as rectal bleeding, urgency, and tenesmus, significantly affecting patients’ quality of life. It is not an uncommon presentation, yet it remains underrepresented in clinical trials of advanced therapies, including biologics. Conventional topical and systemic therapies often provide only partial or short-lived relief, and many patients fail to achieve sustained remission
Tofacitinib has demonstrated efficacy in corticosteroid dependent/refractory UP. In a prospective cohort study comparing outcomes among patients with UP, left-sided colitis (LSC), and pancolitis (PC), clinical remission at week 8 was highest in the UP group (47%) compared to LSC (24%) and PC (43%). By week 48, patients with UP continued to show superior corticosteroid-free remission (59%) and the highest probability of sustained response [35].
These findings not only bridge a critical evidence gap but have influenced clinical decision-making in India, with tofacitinib being increasingly considered even in patients with limited disease extent but refractory symptoms, thus broadening the spectrum of patients eligible for advanced therapy.
5. Advanced Therapy in the Elderly
Elderly patients represent another underrepresented group in IBD clinical trials, largely due to concerns regarding comorbidities, polypharmacy, and immunosenescence. These factors not only increase the risk of adverse events but also complicate therapeutic decision-making, as the use of immunosuppressants and biologics is often limited in this population due to safety concerns. In a real-world cohort of 57 biologic-naive elderly UC patients, tofacitinib demonstrated favorable outcomes. Clinical remission was observed in 31.6% to 40.4% of patients across different timepoints, with clinical response rates ranging from 47.4% to 64.9%. Among patients who achieved clinical remission at week 8, 83% were corticosteroid-free, and all patients in remission at week 52 remained corticosteroid-free [30]. By enabling corticosteroid-free remission in a substantial proportion of patients, tofacitinib has helped reshape therapeutic strategies in elderly-onset or elderly-persistent UC.
6. Histologic Remission in Real World
Achieving sustained clinical remission has long been the primary goal in the management of UC; however, mounting evidence now supports the pursuit of deeper levels of disease control, including endoscopic and histologic healing [51,52]. These objective markers are associated with reduced relapse rates, hospitalization, and long-term complications. However, in routine clinical practice, achieving such stringent endpoints remains a challenge and conventional therapies often fall short of delivering durable mucosal and histologic remission [53-55]. Tofacitinib’s role in achieving deeper levels of disease control was evaluated in a prospective cohort assessing histologic and endoscopic remission. Among 77 patients with moderate-to-severe UC who responded to induction therapy, 28.6% achieved combined endoscopic-histologic remission at week 48, with endoscopic and histologic remission observed in 38.9% and 37.6% of patients, respectively [31]. These findings reinforce tofacitinib’s ability to meet evolving therapeutic goals, including histologic healing.
7. Safety
Biologic and small molecule therapies, while effective, are associated with potential risks, including serious infections, malignancies, thromboembolic events, and adverse cardiovascular outcomes. These concerns are especially pertinent in real-world settings, where patients often present with comorbidities, prior immunosuppressant exposure, or other risk-enhancing factors not fully represented in clinical trials. In India and other LMICs, the burden of latent infections, such as tuberculosis, complicates risk mitigation strategies. Consequently, the safety profile of any advanced therapy must be carefully evaluated in local contexts to ensure both efficacy and long-term tolerability.
The safety profile of tofacitinib in Indian clinical practice has been largely favorable, with the majority of adverse events reported as mild and manageable. Across multiple real-world studies, commonly observed side effects included herpes zoster, acne, transient transaminitis, and hair loss–events that were generally self-limited and did not necessitate permanent drug discontinuation [28,29,33-35]. Thromboembolic risk remains an area of clinical attention. In an elderly cohort, a single case of central retinal vein occlusion was reported, and one instance of dural venous sinus thrombosis was noted in the TACOS study, highlighting the importance of careful risk stratification, particularly in patients with a predisposition to thrombotic complications [30,32]. Despite these isolated events, no major adverse cardiovascular events, malignancies, or serious opportunistic infections were observed, and no new safety signals emerged.
Currently, there are no published data from India specifically evaluating the long-term safety of tofacitinib in UC; however, in the authors’ clinical experience, no major safety concerns have been encountered. Globally, long-term extension studies in UC have likewise not demonstrated an increased incidence of thromboembolic events at recommended doses, although careful monitoring is advised in patients with additional risk factors [56]. The most consistently reported adverse event is herpes zoster infection, for which the current guidelines recommend vaccination in patients initiating or receiving JAK inhibitors [57]. Prophylactic low-molecular-weight heparin is not routinely indicated in patients receiving tofacitinib, but standard venous thromboembolism prophylaxis is advised during hospitalization, irrespective of therapy[ 58].
As discussed, affordability remains one of the most decisive determinants of therapeutic choice in UC across India. Evidence from Western cohorts has consistently demonstrated the cost-effectiveness of tofacitinib relative to other advanced therapies, even when evaluated at the price point of the originator formulation [59-62]. In the Indian context, this economic advantage is further amplified by the availability of generic formulations. While the originator product is priced on par with biologics in high-income countries, the availability of generics has significantly reduced treatment costs, thereby facilitating access to advanced therapy for a larger proportion of patients. Current estimates suggest that the annual cost of generic tofacitinib is only one-eighth to one-tenth that of biologics, making it a uniquely affordable option in routine clinical practice.
From a budget impact perspective, this substantial cost differential reduces the out-of-pocket expenditure borne by patients, thereby making long-term maintenance therapy and sustained treatment adherence more feasible. Improved affordability not only enhances persistence with therapy but also translates into a reduction in disease relapses, hospitalizations, and the indirect costs associated with loss of productivity. Consequently, the economic implications of tofacitinib extend beyond the individual patient to the broader healthcare system, with potential to reduce overall resource utilization. Thus, in addition to its well-established clinical efficacy and safety, generic tofacitinib emerged as a pragmatic and scalable solution to the economic barriers that have historically hindered the uptake of advanced therapies for UC in India.
Tofacitinib has quietly but significantly transformed the therapeutic landscape of UC in India (Fig. 2). Its ability to induce rapid and sustained remission has contributed to a notable reduction in corticosteroid dependence, thereby aligning clinical practice more closely with international quality standards for IBD care. The drug’s oral administration, short half-life, non-immunogenic profile, and absence of therapeutic drug monitoring requirements render it especially suitable for routine use in resource-constrained settings. Indian real-world data have further substantiated its favorable safety profile, with no new safety signals related to serious infections, malignancy, or cardiovascular events when used with appropriate clinical monitoring. The availability of affordable generic formulations has expanded access across socioeconomic strata, positioning tofacitinib as a cost-effective and pragmatic alternative to biologics. The paradigm shift it has enabled is reminiscent of the transformative impact of sofosbuvir in hepatitis C therapy–converting a complex and costly treatment landscape into one that is more manageable, scalable, and broadly accessible. With the advent of upadacitinib and its expanding indications across both UC and CD, the therapeutic relevance of this class of drugs is poised to grow further. By integrating efficacy, safety, and affordability, tofacitinib has redefined the treatment trajectory for UC in India, enabling personalized, contemporary, and scalable care that effectively bridges the gap between medical innovation and real-world implementation.

Funding Source

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

Conflict of Interest

Sood A received honoraria for speaker events from Pfizer India and Takeda India. He also serves as an editorial board member of this journal but was not involved in the selection of peer reviewers, evaluation, or decision-making for this article. No other potential conflicts of interest relevant to this article were reported. The remaining authors declare no conflicts of interest.

Data Availability Statement

Data sharing is not applicable as no new data were created or analyzed in this study.

Author Contributions

Conceptualization: Singh A, Sood A. Data curation: Bhardwaj A. Methodology: Bhardwaj A, Sood A. Project administration: Midha V, Sood A. Resources: Singh A, Bhardwaj A, Sood A. Software: Singh A, Bhardwaj A. Supervision: Midha V, Sood A. Visualization: all authors. Writing - original draft: Singh A. Writing - review & editing: all authors. Approval of final manuscript: all authors.

Fig. 1.
Determinants contributing to the paradox between rising disease burden and therapeutic complexity versus the limited uptake of biologics in India. IBD, inflammatory bowel disease.
ir-2025-00153f1.jpg
Fig. 2.
The role and impact of tofacitinib in the evolving therapeutic landscape of UC in India. UC, ulcerative colitis; ASUC, acute severe ulcerative colitis; IVCS, intravenous corticosteroids.
ir-2025-00153f2.jpg
Table 1.
Key Indian Studies Evaluating the Role of Tofacitinib in UC
Author Study design Patient population Tofacitinib use Outcomes Key findings
Bhati et al. (2025) [28] Prospective single center cohort Steroid dependent moderate to severe UC Biologic-naive adult patients Clinical remission and clinical response at weeks 8 and 24 Week 8
· Clinical remission: 19/53 (35.8%)
· Clinical response: 36/53 (67.92%)
· Endoscopic remission: 12/53 (22.64%)
Week 24
· Clinical remission: 35/53 (66.03%)
· Clinical response: 35/53 (66.03%)
· Endoscopic remission: 22/53 (41.50%)
Singh et al. (2025) [29] Retrospective single center propensity matched cohort Acute severe UC responsive to intravenous corticosteroids Compared to azathioprine for maintenance of remission after response to intravenous corticosteroids Cumulative event-free (rehospitalization, use of corticosteroids, colectomy, escalation of therapy) survival at 1 year Cumulative probability of event-free survival at 1 year
Azathioprine: 44.0%
Tofacitinib: 75.0%
Singh et al. (2025) [30] Prospective single center cohort Steroid dependent or refractory moderate to severe UC Biologic-naive elderly (> 60 years) patients Sustained corticosteroid-free remission from week 8 through week 52 Sustained corticosteroid-free remission from week 8 through week 52: 9/57 (15.78%)
Week 8
· Clinical remission: 18/57 (31.57%)
Clinical remission and clinical response at week 8, 16, and 52 · Clinical response: 37/57 (64.91%)
Week 16
· Clinical remission: 23/57 (40.35%)
· Clinical response: 35/57 (61.40%)
Week 52
· Clinical remission: 22/57 (38.59%)
· Clinical response: 27/57 (47.36%)
Singh et al. (2025) [31] Prospective single center cohort Steroid dependent or refractory moderate to severe UC Adult patients Combined EHR Combined EHR: 22/77 (28.6%)
ER ER: 30/77 (38.9%)
HR HR: 29/77 (37.6%)
HEMI HEMI: 32/77 (41.6%)
EIHR EIHR: 27/77 (35.1%)
Singh et al. (2024) [32] Randomized Controlled Trial Acute severe UC Upfront in combination with intravenous corticosteroids Clinical response at day 7 Day 7 clinical response
Cumulative probability of requiring initiation of rescue therapy or undergoing colectomy within 90 days following randomization · Tofacitinib: 44/53 (83.01%)
· Placebo: 30/51 (58.82%)
Cumulative probability of need for rescue therapy at day 90
· Tofacitinib: 13%
· Placebo: 38%
Singh et al. (2024) [33] Open label randomized controlled trial Steroid dependent or refractory moderate to severe UC Compared to prednisolone for induction of remission Composite remission (defined as total Mayo clinic score ≤2, with endoscopic sub-score of 0 and fecal calprotectin <100 μg/g) at week 8 Tofacitinib: 7/43 (16.28%)
Prednisolone: 3/35 (8.57%)
Giri et al. (2024) [34] Retrospective multicenter cohort Moderate to severe UC Biologic naive adult patients Clinical remission and clinical response at week 8, week 16 and week 24 Week 8
· Clinical remission: 33/47 (70.21%)
· Clinical response: 6/47 (12.76%)
Week 16
· Clinical remission: 30/47 (63.82%)
· Clinical response: 6/47 (12.76%)
Week 24
· Clinical remission: 28/47 (59.57%)
· Clinical response: 5/47 (10.63%)
Singh et al. (2024) [35] Prospective single center cohort Steroid dependent or refractory moderate to severe UC Compared the effectiveness in UP with LSC and PC Clinical remission in the 3 groups at weeks 8, 16 and 48 Week 8 Clinical remission
· UP: 15/32 (47%)
· LSC: 23/94 (24%)
· PC: 23/54 (43%)
Week 16 Clinical remission
· UP: 18/32 (56%)
· LSC: 35/94 (37%)
· PC: 30/54 (56%)
Week 48 Clinical remission
· UP: 19/32 (59%)
· LSC: 36/94 (38%)
· PC: 13/54 (24%)
Jena et al. (2021) [36] Case series Acute severe UC Rescue therapy after failure of intravenous corticosteroids Clinical response and avoidance of colectomy Clinical response: 3/4 (75%)
Colectomy: 1/4 (25%)

All studies used generic formulation of tofacitinib.

UC, ulcerative colitis; UP, ulcerative proctitis; LSC, left-sided colitis; PC, pancolitis; EHR, endoscopic-histologic remission; ER, endoscopic remission; HR, histologic remission; HEMI, histologic endoscopic mucosal improvement; EIHR, endoscopic improvement histologic remission.

  • 1. Dharni K, Singh A, Sharma S, et al. Trends of inflammatory bowel disease from the Global Burden of Disease Study (1990-2019). Indian J Gastroenterol 2024;43:188–198.ArticlePubMedPDF
  • 2. Kaplan GG, Windsor JW. The four epidemiological stages in the global evolution of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol 2021;18:56–66.ArticlePubMedPDF
  • 3. Hracs L, Windsor JW, Gorospe J, et al. Global evolution of inflammatory bowel disease across epidemiologic stages. Nature 2025;642:458–466.PubMedPMC
  • 4. Piovani D, Danese S, Peyrin-Biroulet L, Nikolopoulos GK, Lytras T, Bonovas S. Environmental risk factors for inflammatory bowel diseases: an umbrella review of meta-analyses. Gastroenterology 2019;157:647–659.ArticlePubMed
  • 5. Ananthakrishnan AN, Bernstein CN, Iliopoulos D, et al. Environmental triggers in IBD: a review of progress and evidence. Nat Rev Gastroenterol Hepatol 2018;15:39–49.ArticlePubMedPDF
  • 6. Singh P, Ananthakrishnan A, Ahuja V. Pivot to Asia: inflammatory bowel disease burden. Intest Res 2017;15:138–141.ArticlePubMedPMCPDF
  • 7. Cosnes J, Gower-Rousseau C, Seksik P, Cortot A. Epidemiology and natural history of inflammatory bowel diseases. Gastroenterology 2011;140:1785–1794.ArticlePubMed
  • 8. Lakatos PL. Recent trends in the epidemiology of inflammatory bowel diseases: up or down? World J Gastroenterol 2006;12:6102–6108.ArticlePubMedPMC
  • 9. Truelove SC, Witts LJ. Cortisone in ulcerative colitis; final report on a therapeutic trial. Br Med J 1955;2:1041–1048.ArticlePubMedPMC
  • 10. van Dullemen HM, van Deventer SJ, Hommes DW, et al. Treatment of Crohn’s disease with anti-tumor necrosis factor chimeric monoclonal antibody (cA2). Gastroenterology 1995;109:129–135.ArticlePubMed
  • 11. Present DH, Rutgeerts P, Targan S, et al. Infliximab for the treatment of fistulas in patients with Crohn’s disease. N Engl J Med 1999;340:1398–1405.ArticlePubMed
  • 12. Danese S, Colombel JF, Peyrin-Biroulet L, Rutgeerts P, Reinisch W. Review article: the role of anti-TNF in the management of ulcerative colitis: past, present and future. Aliment Pharmacol Ther 2013;37:855–866.ArticlePubMed
  • 13. Rutgeerts P, Sandborn WJ, Feagan BG, et al. Infliximab for induction and maintenance therapy for ulcerative colitis. N Engl J Med 2005;353:2462–2476.ArticlePubMed
  • 14. D’haens G, Van Deventer S, Van Hogezand R, et al. Endoscopic and histological healing with infliximab anti-tumor necrosis factor antibodies in Crohn’s disease: a European multicenter trial. Gastroenterology 1999;116:1029–1034.ArticlePubMed
  • 15. Feagan BG, Rutgeerts P, Sands BE, et al. Vedolizumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med 2013;369:699–710.ArticlePubMed
  • 16. Sands BE, Sandborn WJ, Panaccione R, et al. Ustekinumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med 2019;381:1201–1214.ArticlePubMed
  • 17. Rubin DT, Allegretti JR, Panés J, et al. Guselkumab in patients with moderately to severely active ulcerative colitis (QUASAR): phase 3 double-blind, randomised, placebo-controlled induction and maintenance studies. Lancet 2025;405:33–49.PubMed
  • 18. Louis E, Schreiber S, Panaccione R, et al. Risankizumab for ulcerative colitis: two randomized clinical trials. JAMA 2024;332:881–897.PubMedPMC
  • 19. Banerjee R, Pal P, Mak JW, Ng SC. Challenges in the diagnosis and management of inflammatory bowel disease in resource-limited settings in Asia. Lancet Gastroenterol Hepatol 2020;5:1076–1088.ArticlePubMed
  • 20. Sood A, Kaur K, Mahajan R, et al. Colitis and Crohn’s Foundation (India): a first nationwide inflammatory bowel disease registry. Intest Res 2021;19:206–216.ArticlePubMedPDF
  • 21. Rogler G, Bernstein CN, Sood A, et al. Role of biological therapy for inflammatory bowel disease in developing countries. Gut 2012;61:706–712.ArticlePubMed
  • 22. Sandborn WJ, Su C, Sands BE, et al. Tofacitinib as induction and maintenance therapy for ulcerative colitis. N Engl J Med 2017;376:1723–1736.ArticlePubMed
  • 23. Danese S, Grisham M, Hodge J, Telliez JB. JAK inhibition using tofacitinib for inflammatory bowel disease treatment: a hub for multiple inflammatory cytokines. Am J Physiol Gastrointest Liver Physiol 2016;310:G155–G162.ArticlePubMed
  • 24. Sood A, Midha V, Sood N, Avasthi G. Azathioprine versus sulfasalazine in maintenance of remission in severe ulcerative colitis. Indian J Gastroenterol 2003;22:79–81.PubMed
  • 25. Sood A, Midha V, Sood N, Bansal M. Long term results of use of azathioprine in patients with ulcerative colitis in India. World J Gastroenterol 2006;12:7332–7336.ArticlePubMedPMC
  • 26. Sood A, Kaushal V, Midha V, Bhatia KL, Sood N, Malhotra V. The beneficial effect of azathioprine on maintenance of remission in severe ulcerative colitis. J Gastroenterol 2002;37:270–274.ArticlePubMedPDF
  • 27. Singh A, Mahajan R, Kedia S, et al. Use of thiopurines in inflammatory bowel disease: an update. Intest Res 2022;20:11–30.ArticlePubMedPDF
  • 28. Bhati R, Yadav A, Mitrolia B, Saini V, Dadhich SK, Bhargava N. Real-world experience with tofacitinib in steroid-dependent patients with moderate-to-severe ulcerative colitis on immunomodulators. Cureus 2025;17:e79456.ArticlePubMedPMC
  • 29. Singh A, Bhardwaj A, Sharma R, et al. Azathioprine or tofacitinib as maintenance therapy in corticosteroid-responsive acute severe ulcerative colitis. Aliment Pharmacol Ther 2025;62:722–731.ArticlePubMed
  • 30. Singh A, Bhardwaj A, Sharma R, Jain D, Midha V, Sood A. Effectiveness and safety of tofacitinib in biologic-naïve elderly patients with ulcerative colitis. Clin Gastroenterol Hepatol 2025;23:2045–2047.ArticlePubMed
  • 31. Singh A, Bhardwaj A, Jain D, et al. Endo-histologic outcomes in patients with ulcerative colitis responding to tofacitinib. Indian J Gastroenterol 2025;Jun 24 [Epub]. https://doi.org/10.1007/s12664-025-01779-3.Article
  • 32. Singh A, Goyal MK, Midha V, et al. Tofacitinib in acute severe ulcerative colitis (TACOS): a randomized controlled trial. Am J Gastroenterol 2024;119:1365–1372.ArticlePubMed
  • 33. Singh A, Midha V, Kaur K, et al. Tofacitinib versus oral prednisolone for induction of remission in moderately active ulcerative colitis [ORCHID]: a prospective, open-label, randomized, pilot study. J Crohns Colitis 2024;18:300–307.ArticlePubMedPDF
  • 34. Giri S, Bhrugumalla S, Kamuni A, et al. Upfront tofacitinib in patients with biological-naïve ulcerative colitis: an Indian multicentric experience. Indian J Gastroenterol 2024;43:237–243.ArticlePubMedPDF
  • 35. Singh A, Mahajan R, Midha V, et al. Effectiveness of tofacitinib in ulcerative proctitis compared to left sided colitis and pancolitis. Dig Dis Sci 2024;69:1389–1402.ArticlePubMedPDF
  • 36. Jena A, Mishra S, Sachan A, Singh H, Singh AK, Sharma V. Tofacitinib in acute severe ulcerative colitis: case series and a systematic review. Inflamm Bowel Dis 2021;27:e101–e103.ArticlePubMedPDF
  • 37. Rivière P, Li Wai Suen C, Chaparro M, De Cruz P, Spinelli A, Laharie D. Acute severe ulcerative colitis management: unanswered questions and latest insights. Lancet Gastroenterol Hepatol 2024;9:251–262.ArticlePubMed
  • 38. Berinstein JA, Sheehan JL, Dias M, et al. Tofacitinib for biologic-experienced hospitalized patients with acute severe ulcerative colitis: a retrospective case-control study. Clin Gastroenterol Hepatol 2021;19:2112–2120.ArticlePubMedPMC
  • 39. Puri AS, Desai D, Sood A, Sachdeva S. Infliximab-induced tuberculosis in patients with UC: Experience from India: a country with high prevalence of tuberculosis. J Gastroenterol Hepatol 2017;32:1191–1194.ArticlePubMedPDF
  • 40. Huang CW, Yen HH, Chen YY. Rescue therapies for steroid-refractory acute severe ulcerative colitis: a systemic review and network meta-analysis. J Crohns Colitis 2024;18:2063–2075.
  • 41. Singh A, Luthra M, Bhardwaj A, et al. Clinical spectrum of acute severe ulcerative colitis in the biologic era: a prospective cohort study from India. Intest Res 2025;Jun 9 [Epub]. https://doi.org/10.5217/ir.2024.00189.Article
  • 42. Larson C, Berinstein JA, Tedesco N, et al. Postoperative outcomes in tofacitinib-treated patients with acute severe ulcerative colitis undergoing colectomy. Clin Gastroenterol Hepatol 2025;23:2263–2271.ArticlePubMed
  • 43. Bojic D, Radojicic Z, Nedeljkovic-Protic M, Al-Ali M, Jewell DP, Travis SP. Long-term outcome after admission for acute severe ulcerative colitis in Oxford: the 1992-1993 cohort. Inflamm Bowel Dis 2009;15:823–828.ArticlePubMed
  • 44. Lynch RW, Lowe D, Protheroe A, Driscoll R, Rhodes JM, Arnott ID. Outcomes of rescue therapy in acute severe ulcerative colitis: data from the United Kingdom inflammatory bowel disease audit. Aliment Pharmacol Ther 2013;38:935–945.ArticlePubMed
  • 45. Festa S, Scribano ML, Pugliese D, et al. Long-term outcomes of acute severe ulcerative colitis in the rescue therapy era: a multicentre cohort study. United European Gastroenterol J 2021;9:507–516.ArticlePubMedPMCPDF
  • 46. Moran GW, Gordon M, Sinopolou V, et al. British Society of Gastroenterology guidelines on inflammatory bowel disease in adults: 2025. Gut 2025;74:s1–s101.PubMed
  • 47. Spinelli A, Bonovas S, Burisch J, et al. ECCO guidelines on therapeutics in ulcerative colitis: surgical treatment. J Crohns Colitis 2022;16:179–189.ArticlePubMedPDF
  • 48. Chen JH, Andrews JM, Kariyawasam V, et al. Review article: acute severe ulcerative colitis: evidence-based consensus statements. Aliment Pharmacol Ther 2016;44:127–144.ArticlePubMed
  • 49. Amiot A, Seksik P, Meyer A, et al. Top-down infliximab plus azathioprine versus azathioprine alone in patients with acute severe ulcerative colitis responsive to intravenous steroids: a parallel, open-label randomised controlled trial, the ACTIVE trial. Gut 2025;74:197–205.ArticlePubMed
  • 50. Blackwell J, Selinger C, Raine T, Parkes G, Smith MA, Pollok R. Steroid use and misuse: a key performance indicator in the management of IBD. Frontline Gastroenterol 2021;12:207–213.ArticlePubMed
  • 51. Peyrin-Biroulet L, Sandborn W, Sands BE, et al. Selecting Therapeutic Targets in Inflammatory Bowel Disease (STRIDE): determining therapeutic goals for treat-to-target. Am J Gastroenterol 2015;110:1324–1338.ArticlePubMedPDF
  • 52. Turner D, Ricciuto A, Lewis A, et al. STRIDE-II: An Update on the Selecting Therapeutic Targets in Inflammatory Bowel Disease (STRIDE) Initiative of the International Organization for the Study of IBD (IOIBD): determining therapeutic goals for treat-to-target strategies in IBD. Gastroenterology 2021;160:1570–1583.ArticlePubMed
  • 53. Bryant RV, Burger DC, Delo J, et al. Beyond endoscopic mucosal healing in UC: histological remission better predicts corticosteroid use and hospitalisation over 6 years of follow-up. Gut 2016;65:408–414.ArticlePubMed
  • 54. Cushing KC, Tan W, Alpers DH, Deshpande V, Ananthakrishnan AN. Complete histologic normalisation is associated with reduced risk of relapse among patients with ulcerative colitis in complete endoscopic remission. Aliment Pharmacol Ther 2020;51:347–355.ArticlePubMedPDF
  • 55. Narang V, Kaur R, Garg B, et al. Association of endoscopic and histological remission with clinical course in patients of ulcerative colitis. Intest Res 2018;16:55–61.ArticlePubMedPMCPDF
  • 56. Panés J, D’Haens GR, Sands BE, et al. Analysis of tofacitinib safety in ulcerative colitis from the completed global clinical developmental program up to 9.2 years of drug exposure. United European Gastroenterol J 2024;12:793–801.ArticlePubMedPMC
  • 57. Farraye FA, Melmed GY, Lichtenstein GR, et al. ACG clinical guideline update: preventive care in inflammatory bowel disease. Am J Gastroenterol 2025;120:1447–1473.ArticlePubMed
  • 58. Olivera PA, Zuily S, Kotze PG, et al. International consensus on the prevention of venous and arterial thrombotic events in patients with inflammatory bowel disease. Nat Rev Gastroenterol Hepatol 2021;18:857–873.ArticlePubMedPMCPDF
  • 59. Milev S, DiBonaventura MD, Quon P, et al. An economic evaluation of tofacitinib for the treatment of moderately-to-severely active ulcerative colitis: modeling the cost of treatment strategies in the United States. J Med Econ 2019;22:859–868.ArticlePubMedPDF
  • 60. Gil F, Juliao-Baños F, Amador L, Castano N, Reyes JM. Cost effectiveness of tofacitinib for the treatment of moderate to severe active ulcerative colitis in Colombia. Pharmacoecon Open 2022;6:837–846.ArticlePubMedPMCPDF
  • 61. Kobayashi T, Hoshi M, Yuasa A, et al. Cost-effectiveness analysis of tofacitinib compared with biologics in biologic-naïve patients with moderate-to-severe ulcerative colitis in Japan. Pharmacoeconomics 2023;41:589–604.ArticlePubMedPMCPDF
  • 62. Diamantopoulos A, Lohan C, LeReun C, Wright E, Bohm N, Sawyer L. PGI29 An economic evaluation of tofacitinib in the treatment of moderately to severely active ulcerative colitis in the United Kingdom. Value Health 2019;22(Suppl 3): S621.Article

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      The JAK attack: transforming the management of ulcerative colitis in India
      Image Image
      Fig. 1. Determinants contributing to the paradox between rising disease burden and therapeutic complexity versus the limited uptake of biologics in India. IBD, inflammatory bowel disease.
      Fig. 2. The role and impact of tofacitinib in the evolving therapeutic landscape of UC in India. UC, ulcerative colitis; ASUC, acute severe ulcerative colitis; IVCS, intravenous corticosteroids.

      Fig. 1.

      Fig. 2.

      The JAK attack: transforming the management of ulcerative colitis in India
      Author Study design Patient population Tofacitinib use Outcomes Key findings
      Bhati et al. (2025) [28] Prospective single center cohort Steroid dependent moderate to severe UC Biologic-naive adult patients Clinical remission and clinical response at weeks 8 and 24 Week 8
      · Clinical remission: 19/53 (35.8%)
      · Clinical response: 36/53 (67.92%)
      · Endoscopic remission: 12/53 (22.64%)
      Week 24
      · Clinical remission: 35/53 (66.03%)
      · Clinical response: 35/53 (66.03%)
      · Endoscopic remission: 22/53 (41.50%)
      Singh et al. (2025) [29] Retrospective single center propensity matched cohort Acute severe UC responsive to intravenous corticosteroids Compared to azathioprine for maintenance of remission after response to intravenous corticosteroids Cumulative event-free (rehospitalization, use of corticosteroids, colectomy, escalation of therapy) survival at 1 year Cumulative probability of event-free survival at 1 year
      Azathioprine: 44.0%
      Tofacitinib: 75.0%
      Singh et al. (2025) [30] Prospective single center cohort Steroid dependent or refractory moderate to severe UC Biologic-naive elderly (> 60 years) patients Sustained corticosteroid-free remission from week 8 through week 52 Sustained corticosteroid-free remission from week 8 through week 52: 9/57 (15.78%)
      Week 8
      · Clinical remission: 18/57 (31.57%)
      Clinical remission and clinical response at week 8, 16, and 52 · Clinical response: 37/57 (64.91%)
      Week 16
      · Clinical remission: 23/57 (40.35%)
      · Clinical response: 35/57 (61.40%)
      Week 52
      · Clinical remission: 22/57 (38.59%)
      · Clinical response: 27/57 (47.36%)
      Singh et al. (2025) [31] Prospective single center cohort Steroid dependent or refractory moderate to severe UC Adult patients Combined EHR Combined EHR: 22/77 (28.6%)
      ER ER: 30/77 (38.9%)
      HR HR: 29/77 (37.6%)
      HEMI HEMI: 32/77 (41.6%)
      EIHR EIHR: 27/77 (35.1%)
      Singh et al. (2024) [32] Randomized Controlled Trial Acute severe UC Upfront in combination with intravenous corticosteroids Clinical response at day 7 Day 7 clinical response
      Cumulative probability of requiring initiation of rescue therapy or undergoing colectomy within 90 days following randomization · Tofacitinib: 44/53 (83.01%)
      · Placebo: 30/51 (58.82%)
      Cumulative probability of need for rescue therapy at day 90
      · Tofacitinib: 13%
      · Placebo: 38%
      Singh et al. (2024) [33] Open label randomized controlled trial Steroid dependent or refractory moderate to severe UC Compared to prednisolone for induction of remission Composite remission (defined as total Mayo clinic score ≤2, with endoscopic sub-score of 0 and fecal calprotectin <100 μg/g) at week 8 Tofacitinib: 7/43 (16.28%)
      Prednisolone: 3/35 (8.57%)
      Giri et al. (2024) [34] Retrospective multicenter cohort Moderate to severe UC Biologic naive adult patients Clinical remission and clinical response at week 8, week 16 and week 24 Week 8
      · Clinical remission: 33/47 (70.21%)
      · Clinical response: 6/47 (12.76%)
      Week 16
      · Clinical remission: 30/47 (63.82%)
      · Clinical response: 6/47 (12.76%)
      Week 24
      · Clinical remission: 28/47 (59.57%)
      · Clinical response: 5/47 (10.63%)
      Singh et al. (2024) [35] Prospective single center cohort Steroid dependent or refractory moderate to severe UC Compared the effectiveness in UP with LSC and PC Clinical remission in the 3 groups at weeks 8, 16 and 48 Week 8 Clinical remission
      · UP: 15/32 (47%)
      · LSC: 23/94 (24%)
      · PC: 23/54 (43%)
      Week 16 Clinical remission
      · UP: 18/32 (56%)
      · LSC: 35/94 (37%)
      · PC: 30/54 (56%)
      Week 48 Clinical remission
      · UP: 19/32 (59%)
      · LSC: 36/94 (38%)
      · PC: 13/54 (24%)
      Jena et al. (2021) [36] Case series Acute severe UC Rescue therapy after failure of intravenous corticosteroids Clinical response and avoidance of colectomy Clinical response: 3/4 (75%)
      Colectomy: 1/4 (25%)
      Table 1. Key Indian Studies Evaluating the Role of Tofacitinib in UC

      All studies used generic formulation of tofacitinib.

      UC, ulcerative colitis; UP, ulcerative proctitis; LSC, left-sided colitis; PC, pancolitis; EHR, endoscopic-histologic remission; ER, endoscopic remission; HR, histologic remission; HEMI, histologic endoscopic mucosal improvement; EIHR, endoscopic improvement histologic remission.

      Table 1.

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