Chronic Active Colitis Research Articles

Jejunal strongyloidiasis mimicking crohn's colitis: A diagnostic dilemma!

We report an unusual case of jejunal strongyloidiasis presenting as chronic malabsorption and intractable small bowel diarrhea in an immunocompetent adolescent boy who posed a diagnostic challenge for pathologists, radiologists, and gastroenterologists. Histopathology revealed chronic active colitis and was consistent with the clinicoradiological diagnosis of Crohn's colitis but nonresponse to immunomodulators warranted full-thickness jejunal biopsy through laparotomy which showed numerous larvae and eggs of Strongyloides. There is a need to increase the awareness of Strongyloides colitis given its high rate of misdiagnosis and mortality as the correct diagnosis can avoid a fatal outcome of this curable disease.

AYURVEDIC MANAGEMENT OF ULCERATIVE COLITIS (PITTAJA GRAHANI): A CASE REPORT

Ulcerative colitis (UC) is a form of chronic inflammatory bowel disease characterised by inflammation of the mucosa and submucosa in the colon, relapsing and remitting. It has a reported incidence of 9-20 cases per 100,000 people annually and can significantly impact both mental and physical health, causing distress to patients. Here is a case report of a 45-year-old female who presented with symptoms including increased frequency of defecation (7 times/day) with mucus discharge, bloody stool, abdominal pain, reduced appetite, general debility, weight loss (>5 kg) and mental distress persisting for one year. She was found to be anaemic (Hb 6.8 gm%), and her pulse rate was 105 bpm. The colonoscopy report showed multiple superficial ulcers with erythematous mucosa, and a biopsy confirmed chronic active colitis. This case was diagnosed as Pittaja Grahani with Pandu (anaemia). The study aimed to evaluate the efficacy of Ayurvedic management in treating ulcerative colitis (Pittaja Grahani). Therapeutic measures included Ayurvedic oral medications and procedures such as abhyanga (oil massage), parisheka (sudation), takradhara, takra basti (buttermilk enema), pathyahara and yoga. Clinical parameters were assessed on the 1st, 12th and 45th day using the Truelove and Witts severity index scale for Ulcerative Colitis and the Patient Health Questionnaire-9 (PHQ-9) depression severity score. Improvements were observed in the frequency of defecation, bloody stool, pulse rate, general debility, and appetite throughout treatment. The results indicate marked alleviation of Ulcerative colitis symptoms with Ayurvedic management, suggesting its potential as a practical therapeutic approach in managing this condition.

Redo IPAA for long rectal cuff syndrome after ileoanal pouch for inflammatory bowel disease.

BACKGROUND: When constructing an ileal pouch-anal anastomosis (IPAA), the rectal cuff should ideally be 1-2cm long to avoid subsequent complications. We identified patients from our IBD center who underwent redo IPAA for a long rectal cuff. Long rectal cuff syndrome (LRCS) was defined as a symptomatic rectal cuff ≥ 4cm. Forty patients met the inclusion criteria: 42.5% female, median age at redo surgery 42.5years. The presentation was ulcerative proctitis in 77.5% of the cases and outlet obstruction in 22.5%. The index pouch was laparoscopically performed in 18 patients (45%). The median rectal cuff length was 6cm. The pouch was repaired in 16 (40%) cases, whereas 24 (60%) required the creation of a neo-pouch. At the final pathology, the rectal cuff showed chronic active colitis in 38 (90%) cases. After a median follow-up of 34.5 (IQR 12-109) months, pouch failure occurred in 9 (22.5%) cases. The pouch survival rate was 78% at 3years. Data on the quality of life were available for 11 (27.5%) patients at a median of 75months after redo surgery. The median QoL score (0-1) was 0.7 (0.4-0.9). LRCS, a potentially avoidable complication, presents uniformly with symptoms of ulcerative proctitis or stricture. Redo IPAA was restorative for the majority.

Immune checkpoint inhibitor-related colitis in patients on immunotherapy for cancer.

Immune checkpoint inhibitors, a revolutionary class of cancer immunotherapy drugs, have transformed cancer treatment by bolstering antitumor immunity for various advanced-stage solid cancers. The US Food and Drug Administration has approved 7 immune checkpoint inhibitors that target 3 major immune checkpoint proteins: cytotoxic T-lymphocyte-associated protein 4, programmed cell death 1 protein, and programmed cell death 1 ligand 1. In addition to their remarkable efficacy, however, these inhibitors have been observed causing immune-related adverse events, particularly immune checkpoint inhibitor-related colitis, which often results in severe or life-threatening clinical issues. The diagnosis of immune checkpoint inhibitor-related colitis relies on incorporation of clinical evaluation as well as endoscopic and histopathologic examination, with exclusion of other potential etiologies. The common histopathologic manifestations of immune checkpoint inhibitor-related colitis are acute active colitis, chronic active colitis, microscopic colitis (collagenous or lymphocytic), and ischemic colitis, with patterns overlapping. Notably, enterocyte apoptosis is a unique feature of immune checkpoint inhibitor toxicity. The proposed mechanisms for the pathogenesis of immune checkpoint inhibitor-related colitis are primarily associated with autoimmune-type dysregulation and gut microbiome alteration. This review summarizes the clinical and pathologic characteristics of immune checkpoint inhibitor-related colitis and elucidates its underlying pathogenic mechanisms. Future successful management of this form of colitis relies on our comprehension of the intricate interplay between tumoral and systemic immune responses to immune checkpoint inhibitors and innovative approaches to modify these responses, along with specific immune cell populations, to preclude immune-related adverse events while achieving antitumor therapeutic outcomes.

A177 AUTOIMMUNE ENTEROPATHY – AN UNCOMMON CAUSE OF MALNUTRITION

Abstract Background Autoimmune Enteropathy is a rare condition characterized by clinical symptoms of intractable diarrhea, vomiting, and weight loss that often results in malnutrition. It is associated with other autoimmune conditions from primary sclerosing cholangitis to type 1 diabetes and autoimmune thyroid disease. The epidemiology of AIE in adults is not well described. It is detailed more in the pediatric population, particularly early in life, the incidence is estimated at less than 1 in 100,000 infants. Aims Aims: To review a case of malnutrition secondary to Autoimmune enteropathy seen at our centre, and review the limited literature for treatment. Methods We did a case report presentation on an inpatient seen at our Tertiary care center in Hamilton, Ontario We reviewed the limited literature regarding treatment of autoimmune enteropathy in adults and modelled our treatment based on this. Results We describe the case of a 63-year-old male in Ontario, Canada whereby he was initially diagnosed with ulcerative colitis, but did not respond to therapy – with the final diagnosis being autoimmune enteropathy. He was first consulted to Gastroenterology with colonoscopy consistent with mayo III disease, and biopsies showing chronic active colitis. He did not improve despite 5-ASA compounds, oral steroids, and trials of IV steroids. He underwent multiple admissions for chronic watery diarrhea, and subsequent treatment with IV steroids. He was started on an Infliximab biosimilar with little to no clinical response, and subsequently referral to our centre for evaluation of worsening malnutrition. Our patient’s symptoms mirrored much of what was initially described in the literature in 1985 with significant unremitting diarrhea, and dependence on TPN due to malabsorption. He underwent an EGD which demonstrated villous blunting, and apoptotic bodies – reviewed by a GI-specialized pathologist who found it was consistent with autoimmune enteropathy. His serology testing revealed a weakly positive TTG, HLA testing was completed showed a HLA DQ2 positivity and a gluten free diet was reccomended. His symptoms improved drastically from 10-12 bowels movements daily, to 1-2 daily within two weeks of treatment. The limited literature surrounding treatment of autoimmune enteropathy was reviewed and the patient was started on oral budesonide in a tapering dose with significant clinical improvement as described in a retrospective case-control study in 2017. Conclusions Autoimmune enteropathy is a rare cause of malnutrition in adult patients. It is often associated with other autoimmune conditions, withsmall bowel histology showing villous atrophy, villous blunting, apoptotic bodies, and a relatively low amount of lymphocytic infiltration. The literature on treatment is limited, our patient responded to initial treatment of gluten removal for underlying celiac disease combined with oral budesonide. Funding Agencies None

Histopathologic Features of Unmasked Inflammatory Bowel Disease Following Immune Checkpoint Inhibitor Therapy in Colon Biopsies

Typical immune checkpoint inhibitor-induced colitis (T-ICI) has significant histomorphologic overlap with inflammatory bowel disease (IBD), a distinction further complicated in ICI-treated patients with pre-existing inflammatory bowel disease (P-IBD) and those with potentially "unmasked" inflammatory bowel disease (U-IBD) after ICI therapy. This study describes histopathologic findings seen in U-IBD colonic biopsies and assesses for distinguishing features from T-ICI and P-IBD biopsies. Initial colon biopsies after symptom onset from 34 patients on ICI therapy were reviewed, and histopathologic features were tabulated. U-IBD patients were identified clinically based on rapid toxicity development post-ICI treatment with multiple recurrences after immune suppression, frequently with regional colitis (versus pancolitis). The study cohort was classified into T-ICI (n= 20), P-IBD (n= 9), and U-IBD (n= 5) groups. The predominant histological patterns were diffuse active colitis (35%) in the T-ICI, and chronic active colitis in both the P-IBD (67%) and U-IBD (60%) groups (overall P= .003, P > .05 between the two IBD groups). None of the T-ICI biopsies demonstrated chronicity features (ie, architectural distortion score 2, basal lymphoplasmacytosis, or Paneth cell metaplasia). Only U-IBD biopsies demonstrated basal lymphoplasmacytosis (60% vs 0% in T-ICI/P-IBD, P= .002). Among available follow-up biopsies, chronicity features were present in all (4/4) U-IBD patients, including those without chronicity seen in the initial biopsy, but none (0/7) of T-ICI patients. These early results show that no definite features of chronicity were seen in colon biopsies from T-ICI patients, suggesting that the presence of those features may be a clue to U-IBD in patients without a known IBD diagnosis. Frequent basal lymphoplasmacytosis seen in U-IBD may support a recent onset of mucosal injury and early architectural remodeling.

Colonic Malakoplakia in Renal Transplant Patient: Case Report and Literature Review

Abstract Introduction/Objective Malakoplakia is a relatively rare inflammatory condition defined by histiocytic infiltration with pathognomonic intracytoplasmic inclusions known as Michaelis-Gutmann bodies. The lesion has been strongly associated with immunosuppressed states. Although the exact mechanism is unknown, an infectious component, such as impaired bactericidal activity in macrophages is highly implicated which leads to deposition of calcium and iron on residual bacterial glycolipid. Although commonly identified in the genitourinary tract, malakoplakia has been found in virtually all organ systems. Methods/Case Report We hereby present a 44-year-old male with a history of renal transplantation, presenting with a history of chronic diarrhea for one year. Colonoscopy was performed which identified diverticulosis in the sigmoid colon and a 5 mm sessile rectal polyp. Histopathological examination of the polyp biopsy demonstrated chronic active colitis, histiocyte aggregates and numerous intracellular, basophilic, concentric, laminated and targetoid calcified structures that were highlighted by Von Kossa and iron stains. These structures are known as Michaelis-Gutmann bodies which are pathognomonic of malakoplakia. A literature review of 45 cases was completed by utilizing the PubMed database. The cases reviewed included involvement of the allograft, host kidney, bladder, colon, prostate, thyroid, submandibular gland, lung, and testicles. Many of the patients were managed with either long term antibiotics, reduction of immunosuppression, or excision of the lesion with improvement in symptoms and/or renal function. Results (if a Case Study enter NA) NA Conclusion Our case highlights the importance of diagnosing this benign entity on histology examination to allow early treatment and improvement in symptoms.

Checkpoint Inhibitor-Induced Colitis: An Update.

Immunotherapy with immune checkpoint inhibitors (ICIs) nowadays has indications for several solid tumors. The current targets for ICIs are CTLA-4, PD-1, and PD-L1 receptors. Despite the clinical advantages derived from ICIs, a variety of side effects are linked to overstimulation of the immune system. Among these, ICI-related colitis is one of the most common, with a disabling impact on the patient. Diarrhea, abdominal pain, abdominal distension, cramping, and hematochezia are the most common ICI enterocolitis presenting symptoms. The most frequently used grading system for assessment of the severity of ICI enterocolitis is called the Common Terminology Criteria for Adverse Events (CTCAE) grading. With regard to the histological picture, there is no specific feature; however, microscopic damage can be classified into five types: (1) acute active colitis, (2) chronic active colitis, (3) microscopic colitis-like, (4) graft-versus-host disease-like, and (5) other types. Supportive therapy (oral hydration, a bland diet without lactose or caffeine, and anti-diarrheal agents) is indicated in mild colitis. Symptomatic treatment alone or with loperamide, a low-fiber diet, and spasmolytics are recommended for low-grade diarrhea. In more severe cases, corticosteroid treatment is mandatory. In refractory cases, off-label use of biological therapies (infliximab or vedolizumab) was proposed.

Molecular characterization of visible low-grade dysplastic lesions in patients with inflammatory bowel disease

We studied pathogenic gene mutations and tumor mutation burden (TMB) in visible low-grade dysplastic lesions in patients with inflammatory bowel disease (IBD). The dysplastic lesions with histologically normal mucosa in the background (group 1) were compared with dysplastic lesions occurring either in a background of chronic active colitis (group 2) or associated with synchronous carcinomas regardless of the status of the background mucosa (group 3). The TMB in group 3 was consistently higher in comparison to the group 1 and group 2 lesions, although the difference was not statistically significant. There also seemto be different mutation profiles between the groups, indicating different pathways of tumor pathogenesis. More frequent APC mutations were seen in group 1 as compared to other groups and TP53 mutations were seen in groups 2 and 3, but none in group 1. Molecular characterization could potentially be used as an ancillary prognostic marker in challenging cases to guide the further management of IBD patients with visible dysplastic lesions.

Isolated small bowel disease and multiple lung nodules: an unusual initial presentation of pediatric Crohn’s disease

Crohn’s disease (CD) is a chronic idiopathic inflammatory disorder of the gastrointestinal tract characterized by transmural inflammation, skip lesions, and architectural changes. Isolated small bowel involvement is seen in approximately 1% of patients with CD at diagnosis. Extraintestinal manifestations can occur, with pulmonary involvement seen in <1% of all CD. We report an unusual case of a previously healthy 12-year old male who presented to hospital with acute abdominal pain, emesis, and fever. He had microcytic anemia, thrombocytosis, elevated C-reactive protein, hypoalbuminemia, digital clubbing, and poor growth. Interestingly, initial upper endoscopy and ileocolonoscopy were unremarkable. Pathology revealed colonic nonnecrotizing granulomas without inflammation. He incidentally was found to have multiple lung nodules despite the absence of respiratory symptoms, and MRE revealed five small bowel strictures. This prompted work-up for alternative etiologies including infectious and rheumatologic, which were negative. Ultimately, five months later, double balloon enteroscopy revealed ileal ulcerations at the strictures and several small aphthous ulcers in the transverse and sigmoid colon. Biopsies showed active ileitis and chronic active colitis with nonnecrotizing granulomas. He developed perianal disease, confirmed on MR pelvis, and a diagnosis of CD was made. The patient started infliximab therapy and is clinically in remission. This is a rare and unique phenotype of CD with initial presentation of multiple lung nodules and isolated small bowel disease. This case highlights the importance of recognizing that pulmonary manifestations should be considered in the absence of respiratory symptoms and that a normal first endoscopy does not preclude a diagnosis of CD.

VEDOLIZUMAB, USTEKINUMAB AND TOFACITINIB AS TRIPLE THERAPY FOR ULCERATIVE COLITIS

Abstract BACKGROUND Therapies for ulcerative colitis include mesalamine, immunomodulators, biologics, and small molecules. Unfortunately, patient response is not universal, and efficacy can diminish with time, postulated to be from increased drug clearance, anti-drug antibodies with biologics, and immune mediated pathogenesis changes. Biologic combinations have been investigated for producing synergistic drug effects and extending targeted therapy in patients lacking monotherapy response, with promise shown in two drug combinations (1), but not investigated using three. CASE A 20-year-old Caucasian male with UC presented in August 2015 following 1 month hospitalization for Clostridium difficile infection. He had 2 infusions of infliximab 10 mg/kg continued post-discharge, and started mesalamine 4.8gm qd, 6-mercaptopurpine (6MP) 100mg qd, and prednisone taper. By November 2015, colonoscopy showed severe Mayo 3 pancolitis. Due to insufficient response 6MP and infliximab were discontinued and he started vedolizumab. August 2016 colonoscopy had chronic colitis with Mayo 2 inflammation of the ascending, transverse, descending and rectosigmoid colon so prednisone 40mg was initiated and vedolizumab increased to vedolizumab q4 weeks. He responded well clinically and was tapered off prednisone by October 2016. November 2016 colonoscopy had right sided colitis resolution with residual proctosigmoiditis (Mayo 2); May 2017 colonoscopy still had rectosigmoid inflammation (Mayo 2) with chronic active colitis, so ustekinumab q8 weeks was added. December 2017 colonoscopy was unimproved so ustekinumab increased to q4 weeks, prednisone was increased, and he requested addition of budesonide and mesalamine. With clinical improvement, prednisone was tapered by February 2020. However, December 2020 colonoscopy showed severe (Mayo 3) recto-sigmoiditis with mild colitis in the descending to transverse colon, so tofacitinib XR 22 mg qd was added. He improved clinically, so budesonide was discontinued in February 2021. November 2021 colonoscopy showed complete endoscopic remission (Mayo 0) so he initiated de-escalation with initially discontinuing mesalamine and increasing ustekinumab initially to q8 week intervals and later vedolizumab to q8 weeks with maintenance of clinical remission. Given marginal effect, ustekinumab was discontinued initially and later, tofacitinib was discontinued. He remains in remission on vedolizumab q8 weeks monotherapy. CONCLUSION Combination therapies may be considered for suitable patients experiencing severe, refractory disease. Although patients with multiple comorbidities, frailty, immunosuppression or certain contraindications may not be well suited, this patient presents as an ideal candidate with no comorbidities and few other therapeutic options. REFERENCES (1) Privitera G et al. Combination therapy in IBD. Autoimmunity Reviews. 2021 Jun 1;20(6):102832.

S44 One Fell Swoop: Ozanimod for Ulcerative Colitis and Multiple Sclerosis

Background: Recent clinical trials have demonstrated the efficacy of ozanimod, a once-daily oral sphingosine-1-phosphate (S1P) receptor modulator, for the treatment of moderate-to-severe ulcerative colitis. S1P modulators attenuate the immune response by reducing circulating lymphocytes and targeting subtypes of T lymphocytes that have shown to play a role in autoimmune diseases. They offer beneficial effects such as neuroprotection and neuromodulation by targeting several pathophysiological pathways also implicated in multiple sclerosis. This case report describes the successful use of ozanimod for both ulcerative colitis and multiple sclerosis, achieving clinical remission in both diseases.\ Case Report: A 52-year-old White woman with a past medical history of psoriasis was diagnosed with ulcerative colitis after presenting with abdominal pain and bleeding; colonoscopy demonstrated severe left-sided inflammation and pathology consistent with chronic active colitis. Initial therapies included mesalamines, intermittent steroids and eventually adalimumab. She was switched to vedolizumab after reporting excessive fatigue and ‘low quality of life’ on adalimumab. Endoscopic remission was never achieved on this regimen. High-dose accelerated infliximab in combination with methotrexate and high-dose PO mesalamine got her into remission. Methotrexate was then stopped due to the patient reporting headache and ‘brain fog.’ Shortly after, she developed right foot tingling and foot drop and was diagnosed with demyelinating disease on MRI. Notably, upon further questioning, she did endorse central nervous system deficits dating back more than 10 years, starting with optic neuritis. After shared decision making and multi-disciplinary discussion, infliximab was discontinued and ozanimod was started. Since the initiation of ozanimod, the patient’s neurologic deficits have not progressed, GI-related symptoms are under control and colonoscopy after 6 months of therapy demonstrated only mild Mayo 1 left-sided disease. ESR and CRP are within normal limits. Her latest MRI was negative for any active demyelinating lesions. Her current maintenance regimen is ozanimod 0.92 mg daily and 4.8 g mesalamine daily, which she is tolerating well with no side effects. She has graduated from physical therapy and is back to jogging 2 miles 3 times per week. Discussion: Screening for neurologic diseases like multiple sclerosis influences drug selection in IBD patients, precluding use of medications like anti-TNFs. The increased risk of progressive multifocal leukoencephalopathy (PML) has led to medications such as natalizumab to require intensive prescribing programs to ensure appropriate training for prescribers. Use of an S1P receptor modulator like ozanimod has a unique potential to treat ulcerative colitis and multiple sclerosis, whose respective therapies are often contraindicated when they are comorbid diseases. Infrequently does an opportunity present itself to use one drug for both disease states, proving especially beneficial in the case of this patient intolerant of numerous established therapies for ulcerative colitis.

S2228 A Segmental Colitis Associated With Diverticulosis versus Inflammatory Bowel Disease: A Diagnostic Dilemma Despite Total Proctocolectomy

Introduction: Patients with diverticular disease can develop segmental colitis associated with diverticulosis (SCAD). It can range from mild inflammatory changes to chronic active inflammation that mimics inflammatory bowel disease (IBD). SCAD usually presents a more benign outcome, with a low rate of complications. Here, we present a complex case in which a diagnosis was still unclear till the final stage of the management. Case Description/Methods: A 60-year-old female was admitted for hypovolemic shock. She was resuscitated, and the GI was consulted for the management of IBD. She was recently diagnosed with ulcerative colitis about 2 months ago. She has abdominal pain in the right lower side, and examination revealed mild abdominal tenderness. She was already on prednisone 60 mg daily for 2 weeks and infliximab maintenance dose (completed 2 doses) and mesalamine from the last admission. She has had 3 colonoscopies in the past. The first colonoscopy 6 months ago showed a normal rectum, unable to traverse the sigmoid colon due to stricture and diverticulosis. The biopsy showed a normal rectum and a very focal area of cryptitis. The last colonoscopy 2 months ago showed a severely inflamed ulcerated mucosa in the sigmoid colon (Figure, left). Colon biopsy showed mild acute cryptitis and distorted and branched crypts. No crypt abscesses or granulomas were seen. On this admission, CT enterography showed pancolitis. Serology for Crohn's disease (CD) was negative, including ASCA IgA and ASCA IgG. The strong differential diagnosis was SCAD vs.IBD. The decision was to continue with the medical treatment (i.e., completion of steroid course, infliximab, and follow the response) and was discharged. The patient again presented with a shock one month after this admission. Unfortunately, she had colonic perforation and had total proctocolectomy with ileostomy creation. Pathology of surgical specimens revealed mild chronic active colitis and severe diverticular disease with associated transmural inflammation (Figure, right). Ileum excision showed no significant pathologic changes unlikely to be CD. The patient was doing well till the last follow-up. Discussion: This is a unique case where the diagnosis of SCAD vs. IBD was unclear regardless of the availability of serology, endoscopic, surgery, and histopathological examinations. In this complex case, we suggest a multidisciplinary team approach to improve patient-centered care.Figure 1.: Left: colonoscopy showing inflamed ulcerated mucosa in the sigmoid colon. Right: Pathology shows mild chronic active colitis and severe diverticular disease.

S2164 An Unusual Case of Diarrhea in an Immunosuppressed Patient

Introduction: Amoebic Colitis, a frequent clinical manifestation of invasive intestinal infection due to Entamoeba histolytica, is a common cause of diarrhea mostly prevalent in developing countries due to unsanitary conditions. Although 90% of the cases may be asymptomatic carriers, one of the most common clinical manifestations include dysentery. It carries an excellent prognosis if diagnosed promptly and treated. However, establishing a diagnosis of Amoebic Colitis is often challenging. We highlight a unique case of Amoebic Colitis in a 73-year-old female in a setting of immunosuppression. Case Description/Methods: A 73-year-old female from Qatar with ESRD, DM, HTN, and Renal cell carcinoma was admitted for abdominal pain, bloody diarrhea, and on and off a fever for 3 months. She was on tacrolimus, mycophenolate, and prednisone for her renal transplant. Diffuse abdominal tenderness was noted on examination but vitals were normal. CT scan showed ascending and transverse colon colitis and colonoscopy showed congested rectal, rectosigmoid, and sigmoid colon mucosa with multiple ulcers in descending, transverse, and ascending colon and rectum. Stool calprotectin was >3000 mg/kg Biopsy results showed active colitis with ulcers. Intravenous steroids were started and she showed improvement but abdominal pain and bloody diarrhea recurred with rise in CRP (from 6.9 to 15.5 mg/kg) when she was switched to oral steroids. A repeat CT scan showed an increase in the involvement of the right colon and piperacillin-tazobactam was started. Repeat colonoscopy showed a vascular pattern in mucosa diffusely decreased and nonbleeding ulcerated mucosa. Meanwhile, the E. histolytica antibody was positive. Antibiotics were switched to oral metronidazole. Pathology showed chronic active colitis with ulcer and increase apoptotic crypt epithelial cells. The clinical condition continued to improve and she was discharged home on steroid taper with a plan to repeat the scope in 3 months. She is doing well and on regular follow-up (Figure). Discussion: Amoebic colitis should be a differential diagnosis for individuals from eastern countries where the prevalence of Entamoeba histolytica continues to be high as a delay in diagnosis may lead to adverse outcomes. Diagnosis often requires a combination of different modalities including stool microscopy, stool antigen testing, and colonic biopsies. Treatment with metronidazole, tinidazole, paromomycin, diiodohydroxyquin, or diloxanide furoate is often highly safe and effective.Figure 1.: A- Ascending and transverse colonic wall thickening consistent with colitis B - Congested, friable, and ulcerated mucosa C- The mucosa vascular pattern in the descending colon was diffusely decreased- after treatment.

S2790 A Sweet Response: Crohn’s Flare Leading to Sweet Syndrome

Introduction: Sweet’s syndrome, or acute febrile neutrophilic dermatosis (AFND), is a rare extraintestinal manifestation of inflammatory bowel disease (IBD). It presents with fever, malaise, and erythematous papules that are tender, edematous, and, rarely, bullous. It is associated with underlying diseases including IBD, infections, cancer, autoimmune disorders, medications, and pregnancy. Case Description/Methods: A 79-year-old male with colonic Crohn’s disease (on Infliximab), NSAID-related peptic ulcer disease, and recurrent Clostridium Difficile infection presented with sudden onset, exquisitely painful, bullous rash with fevers to 102oF. The blistering eruptions started on his left wrist and spread to his arms and legs, including extensor and flexor surfaces and soles of his feet. His laboratory results were significant for white blood cell count of 18.5 K/uL, erythrocyte sedimentation rate of 130 mm/hr, c-reactive protein of 185.5 mg/L, and positive ANA titer 1:320. Gastroenterology was consulted for concern for IBD associated dermatological manifestation such as erythema nodosum (EN) or pyoderma gangrenosum (PG); however, given atypical appearance and distribution, dermatology consultation was recommended, and punch biopsy was obtained. Skin biopsy revealed nodular dermal neutrophilic infiltrate, consistent with Sweet’s syndrome. Given association with IBD, colonoscopy was performed revealing significant inflammation with large ulcers throughout the colon. Simple Endoscopic Score for Crohn’s disease was 25 with biopsies consistent with severe chronic active colitis. He was started on IV steroids with immediate improvement in pain and flattening of lesions. Ultimately, his infectious workup was negative, and it was concluded that his presentation was from severe Crohn’s flare. (Figure) Discussion: EN and PG are commonly associated with IBD; however, Sweet’s syndrome is rarely associated with IBD itself, and can also develop as a result of immunosuppressant medications or opportunistic infections. This case of Sweet’s syndrome was unique as it was secondary to uncontrolled IBD, the lesions were bullous, and the patient was male, as classically it is more common in females. It is prudent in patients with atypical appearance of skin lesions, to consider a multidisciplinary approach with dermatology consultation to diagnose and treat appropriately. Understanding the vast array of skin manifestations of IBD is key in providing comprehensive care to IBD patients.Figure 1.: Left: Bullous lesions noted on patient's arm Right: Fingernail changes.

S2772 Subcutaneous Sweet Syndrome Successfully Treated With Ustekinumab in Patient With Ulcerative Colitis

Introduction: Extraintestinal manifestations (EIMs) of inflammatory bowel disease (IBD) are well-established. Sweet syndrome (SS), or acute febrile neutrophilic dermatosis, is a reactive mucocutaneous manifestation of IBD presenting as erythematous papules/plauqes with associated fever and arthomyalgias. There is limited evidence regarding efficacy of Ustekinumab in management of EIMs of UC, particularly SS. Case Description/Methods: The patient is a 50-year-old woman with left-sided UC (Montreal classification E2) that previously failed several therapies, including mesalamine, azathioprine, infliximab, adalimumab, vedolizumab, and a fecal microbiota transplant trial. She presented with worsening abdominal pain, diarrhea/hematochezia, and bilateral lower extremity pain. She was febrile and tachycardic with tender, violaceous, and ulcerated subcutaneous nodules on the bilateral ankles with hemorrhagic bullae (FigureA). Labs revealed negative C. diff, elevated ESR/CRP, thrombocytosis, and borderline leukocytosis with neutrophilic predominance. Lower extremity MR imaging and bone biopsy revealed multifocal sterile osteomyelitis with adjacent abscess; skin biopsy demonstrated dense granulomatous/neutrophilic infiltrate in the deep dermis/subcutis without microorganisms, consistent with subcutaneous SS (FigureB). A restaging colonoscopy demonstrated severe proctosigmoid ulcerative colitis (FigureC). Given that the patient had failed several immunomodulators and biologic therapies, she was started on prednisone and Ustekinumab. Four months later, she reported complete resolution of her cutaneous SS off steroids and improving UC symptoms (less frequent and more formed stools, minimal hematochezia). Repeat MRI demonstrated resolution of the sterile osteomyelitis and abscess. Discussion: Our case highlights the novel use of Ustekinumab in the treatment of subcutaneous SS with sterile osteomyelitis in a patient with flaring UC. SS is a neutrophilic dermatosis that is a rare EIM of IBD, classically characterized by tender cutaneous lesions. There is limited evidence supporting the use of Ustekinumab in treating EIMs of CD, and a lack of data regarding its efficacy in treating EIMs of UC. Our case fills a major gap in the literature and highlights the clinical efficacy of Ustekinumab for SS and UC especially in patients that have a contraindication to, failed previous treatment with, or otherwise cannot tolerate corticosteroids and TNF-alpha antagonists.Figure 1.: 1A. Right lateral malleolus with 2.5 cm shallow erosion with slightly violaceous borders and central bright yellow fibrinous debris. There was slight atrophy of surrounding skin with mild edema and hyperpigmentation (left image). Left medial malleolus/dorsal foot with grouped irregular shallow ulcers with surrounding mild violaceous erythema (middle and right image). 1B. Left ankle biopsies showed mixed septal and lobular panniculitis with granulomatous and neutrophilic inflammation. Histologic sections show a mildly spongiotic epidermis with dense granulomatous and neutrophilic inflammatory infiltrate in the deep dermis and subcutis (left image). The inflammatory infiltrate, which consists of prominent neutrophils, histiocytes, and scattered lymphocytes, surrounds vascular and adnexal structures, as well as adipocyte lobules. Definitive features of vasculitis are not seen. PASd (periodic acid-Schiff-diastase), GMS (Grocott’s methenamine silver), Gram, and Fite staining fail to highlight microorganisms (right image). 1C. Colonoscopy demonstrated severe (Mayo Endoscopy Score 3) proctosigmoid ulcerative colitis to 30 cm (left image). Sigmoid biopsies showed significant immune cell infiltration with crypt architectural distortion concerning for severe chronic active colitis. No evidence of granulomas, dysplasia or cytomegalovirus (right image).

S2791 A Rare Etiology for Ulcerative Colitis Flare

Introduction: Prior to colonoscopy, it is well understood that patients must undergo bowel cleansing. Based on the type of laxative, colonoscopy preparations fall into two categories – polymer-based formulas (PEG) and saline-based formulas (NaP). Both types of bowel preparations are deemed to be relatively safe and part of routine practice. However, we describe the rare case of an ulcerative colitis (UC) flare due to the bowel preparation formula. Case Description/Methods: A 29-year-old female with diagnosis of UC, presently in clinical and biochemical remission on oral mesalamine, contracted COVID-19 and had reactivation of UC symptoms. After being on budesonide tablets and rectal foam for two months, patient achieved clinical remission, and a surveillance colonoscopy was performed which revealed normal colon and terminal ileum except mild congestion in the cecum (Figure A). Pathology revealed unremarkable mucosa in the entire colon except for chronic active colitis in the cecum. Immediately following this colonoscopy, the patient started to experience another severe UC flare requiring hospitalization. The patient’s laboratory work-up was normal except for an elevated fecal calprotectin (1710). Stool infectious work-up was negative and the patient denied any NSAID or antibiotic use. The patient underwent a repeat colonoscopy which revealed severe Mayo 3 pancolitis (Figure B) in comparison to a stable colonoscopy a few weeks prior. It was revealed that for her initial colonoscopy, she had used SUPREP bowel prep kit. On prior colonoscopies she had used MiraLAX bowel prep with no adverse effects. During hospitalization, the patient was started on biologic therapy with good effect. Discussion: There are no clear guidelines on appropriate bowel preparation formula for the inflammatory bowel disease (IBD) population. Sufficient literature exists to confirm that NaP can irritate the intestinal mucosal wall. Moreover, numerous animal experiments have employed dextran sodium sulfate for chemical induction of intestinal inflammation to mimic UC flares in humans [1]. Thus, it can be surmised that because SUPREP ingredients contain sodium sulfate, the potential for UC flare is higher. It is pertinent for practitioners to be aware of the possible rare adverse effects of saline-based formulas, especially when treating the IBD population.Figure 1.: (A) Colon (04/19/2022) and (B) Colon (05/09/2022).

S2722 Cytomegalovirus Colitis in an Immunocompetent Patient Presenting With New Onset Ulcerative Colitis: A Clinical Vignette

Introduction: Cytomegalovirus (CMV) colitis is a rare disease among immunocompetent patients presenting with inflammatory bowel disease (IBD). CMV can cause steroid-refractory IBD, which may require antiviral and infliximab (IFX) combination therapy. Case Description/Methods: A 23-year-old woman was admitted for dehydration and poor oral intake in the setting of eight bloody bowel movements per day, tenesmus, and weight loss. She presented to an outside hospital 5-weeks prior with abdominal cramps and bright red blood per rectum. The CT scan showed bowel wall thickening and mucosal enhancement in the rectosigmoid and descending colon. A colonoscopy 2-weeks prior to admission was suggestive of severe ulcerative colitis (UC) and she was started on mesalamine/budesonide. Due to poor clinical response, she was switched to prednisone 40 mg for 5 days. Outpatient medical management failed and, upon admission, she was converted to methylprednisolone 20 mg every eight hours. Serum CMV PCR was positive at 1,758 IU/mL and colonic biopsies showed scattered CMV inclusions by immunohistochemical staining. She was started on ganciclovir 5mg/kg/dose IV in addition to the steroid regimen and IFX infusions were deferred. By day 2 of ganciclovir IV and day 7 of methylprednisolone IV, IBD symptoms began to resolve. On discharge at hospital day 12, patient was transitioned to twice daily oral valganciclovir 900 mg for a 3-week course and an oral prednisone taper. CMV PCR was 1,185 IU/mL on discharge and < 100 IU/mL at one week follow up. IFX therapy was initiated 45 days post discharge with improved symptoms, as characterized by a 17-lb weight gain at 3-month follow-up. (Figure) Discussion: CMV colitis is a rare diagnosis in immunocompetent patients with early, steroid naïve IBD. Serum PCR positive infection has been reported more commonly after 2-3 weeks of steroid therapy. CMV infection is a recognized complication and marker of poor prognosis in moderate to severe UC, especially those who present with steroid refractory disease. It is believed that the inflammatory mediators associated with UC play a synergistic role in CMV reactivation and subsequent disease. In addition, local corticosteroid induced immunosuppression may further facilitate CMV gene transcription, resulting in disease progression and poor steroid response. There remains no consensus for management of UC with concomitant CMV colitis however, in our patient the use of antiviral and biologic therapy (IFX) promoted disease regression and clinical improvement.Figure 1.: H&E Stain (20x) demonstrating active chronic colitis (left). Immunohistochemical staining (40x) showing CMV immunoreactivity (right).

S2728 From Shortness of Breath to Bowel Unrest: COVID-19-Induced Ulcerative Colitis

Introduction: COVID-19 is recognized for its respiratory complications, but it can also cause extrapulmonary manifestations such as gastrointestinal complaints. Usually, GI manifestations are transient and rarely progress to chronic disease. We highlight a rare case of newly diagnosed ulcerative colitis triggered by COVID-19 infection. Case Description/Methods: A 49-year-old female with history of GERD presented with bloody diarrhea and abdominal pain that persisted six weeks after recent COVID-19 infection with otherwise complete resolution of other disease related symptoms. CT abdomen/pelvis showed colonic wall thickening from the hepatic flexure to the rectum concerning for colitis. Labs were significant for leukocytosis 13,600/microliter with elevated CRP 39.1 mg/L. Infectious workup and celiac panel were negative. Colonoscopy was performed and revealed pancolitis with pathology showing architectural distortion with crypt abscesses and chronic inflammatory cells in lamina propria. She was started on a steroid taper with rapid resolution of symptoms for presumed COVID-induced colitis. Unfortunately, upon completion of the taper, her symptoms recurred. Repeat labs showed CRP 8.7 mg/L with imaging negative for colitis. Repeat colonoscopy showed pseudopolyps at the hepatic flexure with segmental biopsies showing moderately active chronic colitis in the right colon. Patient was ultimately diagnosed with ulcerative colitis triggered by COVID-19 infection. She was started on Mesalamine with Prednisone induction eventually requiring Ustekinumab for disease control. Discussion: Incidence of gastrointestinal manifestations in COVID-19 are variable ranging anywhere from 3-50% of cases. However, COVID-19 induced inflammatory bowel disease is exceedingly rare with only a handful of case reports documenting such occurrence. While not completely understood, the pathophysiology behind COVID-19 related gastrointestinal manifestations likely involves binding of ACE-2 receptors along the epithelium, disrupting the gut barrier. In most patients this disruption is self-resolving; however, patients who develop inflammatory bowel disease likely have underlying genetic predisposition that results in chronic intestinal inflammation. Our case demonstrates the importance of recognizing the extrapulmonary manifestations of COVID-19 which can have life altering implications as seen in our patient.

S2175 Now You See Me, Now You Don’t: A Case of Campylobacter Jejuni Colitis Presenting as a Colonic Mass

Introduction: Campylobacter jejuni is responsible for 3-6% of diarrheal illnesses in the United States. Inoculation follows ingestion of a contaminated source such as poultry, unpasteurized milk, or drinking water. The presentation of a C. jejuni infection may radiographically and endoscopically mimic other pathologies such as colonic malignancy and inflammatory bowel disease (IBD). Case Description/Methods: A 66-year-old man with a past medical history of prostate cancer in remission and a 6mm colonic polyp removed 5 years prior presented to the emergency department with 5 days of watery diarrhea. He complained of 6 watery bowel movements per day associated with colicky abdominal pain and bloating. He was hemodynamically stable with a physical exam notable for severe tenderness in the right lower quadrant. Serum chemistries did not reveal any abnormalities. Computed tomography revealed severe, focal bowel wall thickening in the ascending colon and a 1.7cm hypodense lesion in the right hepatic lobe which was confirmed on magnetic resonance of the abdomen. The radiologist’s interpretation emphasized concern for colonic malignancy with metastasis to the liver (Figure). Endoscopic evaluation revealed diffusely erythematous, granular and ulcerated mucosa throughout the colon with concern for infectious vs inflammatory colitis. Histologic evaluation of ascending colonic mucosal biopsy revealed moderately active chronic colitis with extensive cryptitis and crypt abscesses. Stool polymerase chain reaction was notable for C. jejuni infection and the patient achieved clinical and endoscopic remission without antimicrobial therapy. Discussion: In patients with C. jejuni enterocolitis, radiographic imaging may reveal signs of bowel wall edema or ulcerations which may resemble colonic malignancy or IBD. Endoscopic findings of campylobacter enterocolitis are non-specific, however, may reveal edematous, erythematous, and friable mucosa which may be associated with hemorrhage. Inflamed mucosa can be either isolated or discontinuous. Colonic ulcers may present as either aphthous or linear (may resemble cobblestoning as seen in Crohn's Disease). Histologic evaluation can reveal cryptitis and crypt abscess formation similar to findings of ulcerative colitis. This case highlights the range of radiographic and endoscopic presentations of C. jejuni Colitis. Infectious colitis should remain on the differential for radiographic evidence of colonic edema in the right clinical setting.Figure 1.: A and B: CT Abdomen/Pelvis showing ascending colon wall thickening resembling mass; C: CT of Hypoechoic liver mass; D: T2-weighted MRI Abdomen of ascending colon wall thickening resembling a mass; E: Colonoscopy image revealing inflamed mucosa of ascending colon; F: Ulcerated mucosa of the sigmoid colon.