History Of Ulcerative Colitis Research Articles

Myositis as a de-novo extraintestinal manifestation of ulcerative colitis in a pediatric patient developing post-colectomy: a case report

This report presents the case of a 13-year-old female with a history of ulcerative colitis who underwent ileostomy closure after total colectomy. Postoperatively, she developed right leg paresis and extensive swelling of the lower extremities. Imaging investigations revealed myositis with avascular necrosis in the distal femoral condyles. These findings were consistent with myositis as an extraintestinal complication of ulcerative colitis.

Clinical usefulness of image-enhanced endoscopy for the diagnosis of ulcerative colitis-associated neoplasia.

Patients with a long history of ulcerative colitis (UC) are at risk of developing a significant complication known as UC-associated neoplasia (UCAN). To reduce the risk of UCAN and the associated mortality, the current guidelines recommend initiating surveillance colonoscopy 8-10 years after confirmation of UC diagnosis. In recent years, advancements in endoscopic diagnostic technologies, including magnifying and image-enhancing techniques, have allowed for the production of high-contrast images that emphasize mucosal structures, vascular patterns, and color tones. Recently, image-enhanced endoscopy technologies have become available and offer the potential to improve the qualitative endoscopic assessment of UCAN. The use of high-definition chromoendoscopy enables the evaluation of subtle mucosal patterns in the colon. Magnifying narrow-band imaging facilitates the visualization of mucosal vascular structures. Texture and color enhancement imaging processes structure, color tone, and brightness aspects more appropriately, whereas linked color imaging optimizes the emphasis on mucosal and vascular redness. Both techniques are expected to excel in the depiction of subtle color variations and mucosal changes characteristic of UCAN. This article provides an overview of the current status and future challenges regarding the use of various image-enhanced endoscopytechniques in the diagnosis of UCAN.

An Unusual Hiccup: Severe Singultus as a Symptom in Ulcerative Colitis

ABSTRACT Inflammatory bowel disease encompasses a group of chronic inflammatory conditions associated with both intestinal and extraintestinal manifestations. We present a 26-year-old man with a history of ulcerative colitis who presented with a disease exacerbation associated with severe intractable hiccups. We report a unique clinical symptom associated with severe ulcerative colitis and the diagnostic dilemma associated with this presentation. This case highlights the importance of recognizing unusual symptoms that can be associated with inflammatory bowel disease exacerbations and demonstrates the therapeutic potential of effective therapy of the underlying inflammatory disease.

Bickerstaff’s brainstem encephalitis: a rare case of neurologic complication in Ulcerative Colitis

Bickerstaff’s brainstem encephalitis is a rare autoimmune disorder that presents with ataxia, ophthalmoplegia, disturbance of consciousness and quadriplegia. A 45-year-old man with a history of ulcerative colitis (UC) taking mesalazine (5-aminosalicylic acid) visited the emergency room presenting with ataxia, ophthalmoplegia and a progressively worsening cognitive impairment. Cerebrospinal fluid analysis showed mild elevation in protein and white blood cell count and increased intracranial pressure. Anti-GQ1b autoantibodies were found positive in the patient’s serum and contrast-enhanced brain magnetic resonance imaging showed diffuse leptomeningeal enhancement and pontine lesions. Based on these findings and the patient’s clinical course and history, he was diagnosed with Bickerstaff’s brainstem encephalitis. Mesalazine was discontinued and high-dose steroid pulse therapy was started, followed by intravenous immunoglobulin, which resulted in gradual improvement of the neurologic symptoms. When an ulcerative colitis patient presents with progressive cognitive impairment, quadriplegia and disturbance of consciousness and gait, Bickerstaff brainstem encephalitis should be considered in the differential diagnosis and prompt immunotherapy may lead to favorable prognosis.

Dissemination and genome characterization of a human adenovirus F41 in a patient with B-Cell lymphoma

Adenovirus (HAdV) F41 is a common cause of gastroenteritis and has rarely been reported associated with disseminated disease. In this report, an adult patient with a history of ulcerative colitis, cryptogenic cirrhosis, stage III adenocarcinoma, high-grade diffuse large B-cell lymphoma on chemotherapy was diagnosed with disseminated adenovirus infection. HAdV DNA was quantified in stool, plasma, and urine with viral loads of 7, 4, and 3 log10 copies/mL, respectively. The patient’s course was rapidly progressive and he passed away 2 days after initiation of antiviral therapy. The patient’s infecting virus was characterized as HAdV-F41 by whole genome sequencing.

Endometriosis ofthe Appendix: When Appendicitis Is Less Than Straightforward.

We present a case report of a 49-year-old female with a history of ulcerative colitis who originally presented to the general surgery clinic after an incidental finding on computed tomography was concerning for a dilated, fluid-filled appendix. She ultimately underwent a laparoscopic appendectomy. The pathology returned consistent with early acute appendicitis, with endometrial tissue along the outer wall of the appendix. We then performed a literature review regarding appendiceal masses and the occurrence of endometriomas and/or endometriosis of the appendix. A PubMed search was performed using the key words of appendix and appendicitis and endometrioma. Specific articles were examined mentioning the occurrence of endometriomas of the appendix and isolated endometriosis of the appendix. Between 2% and 6% of cases of appendicitis present due to an appendiceal mass, usually an inflammatory phlegmon. A variety of other causes, including primary malignancy, secondary malignancy, and combinations of pathologies, may lead to the eventual removal of the appendix. Specifically, endometriosis of the appendix is reported in less than 1% of females on post-appendectomy pathologic analysis. Although specific symptoms may guide a provider, there are few distinguishing symptoms that would point a provider toward a different etiology, to include malignancy, for appendicitis. Further information is needed to determine when a patient has an increased risk for an underlying pathology when presenting with appendicitis. This information will help drive continued treatment and lead to improved screening for appendiceal masses.

DP10 A relapsing–remitting rash with associated neurological symptoms: a rare presentation of ​­neuro-Sweet syndrome

Abstract A 46-year-old woman presented with an 8-week history of an asymptomatic eruption on her upper extremities and back. She had a history of ulcerative colitis, asthma and hyposplenism. There had been no changes to her regular medications. Over the next 3 years, she developed a relapsing and remitting course of headaches, pyrexia and feeling unwell with the associated rash. She further developed deafness and vertigo and was admitted with headaches, blurred vision and paraesthesia of the fingers. Physical examination revealed multiple erythematous, asymptomatic, annular plaques present on her upper extremities and back with no oral, genital or ophthalmological lesions. Skin biopsy from the lesion on the upper back showed a neutrophilic dermatosis with mildly acanthotic epidermis, superficial dermal collection of acute inflammatory cells, dermal oedema and endothelial swelling, with no evidence of vasculitis. This was considered in keeping with Sweet syndrome. Magnetic resonance imaging of the brain revealed meningoencephalitis and focal cerebritis. A lumbar puncture performed for infection was negative. Following this, a diagnosis of neuro-Sweet syndrome (NSS) was made. She has responded well to oral steroids and is currently well controlled on dapsone. To date, extensive malignancy screens have been negative. Sweet syndrome, or acute febrile neutrophilic dermatosis, is characterized by fever, malaise, leucocytosis and painful distinctive skin lesions and may be associated with malignancies, drugs and infection. Skin biopsy shows dense dermal infiltration of neutrophils without any histological signs of vasculitis. Sweet syndrome is known to involve multiple organs; however, involvement of the central nervous system (CNS) is rare. When the CNS is involved, it is referred to as NSS and is defined as the coexistence of characteristic skin lesions of Sweet syndrome with encephalitis or meningitis (Suh HB, Kim HJ. Recurrent neuro-Sweet disease associated with preceding upper respiratory infection: a case study. iMRI 2018; 22:187–93). Although the condition is usually steroid responsive, disease recurrences have been reported in 50% of cases in the literature (Hisanaga K, Iwasaki Y, Itoyama Y, Neuro-Sweet Study Group. Neuro-Sweet disease: clinical manifestations and criteria for diagnosis. Neurology 2005; 64:1756–61). It is important to note that the clinical features and imaging results in NSS are similar to those of neuro-Behçet disease (NBD), and it is important to distinguish between the two as CNS involvement in NSS is often transient, whereas NBD often follows a more progressive course. We report a rare case of NSS and highlight that NSS should be considered by dermatologists in patients presenting with recurrent skin lesions of Sweet syndrome and associated neurological symptoms.

Case report: intraperitoneal tattoo ink pigmentation associated with endometriosis

A 50-year-old female with a history of ulcerative colitis and autoimmune pancreatitis on monoclonal antibody therapy was found to have dispersed, small ‘black spots’ or pigment on uterine, peritoneal and bowel surfaces during a routine total laparoscopic hysterectomy and bilateral salpingo-oophorectomy for treatment of endometriosis. Histological examination of the ‘black spots’ revealed pigment-laden macrophages. These were frequently seen adjacent to and directly associated with endometriosis.

Cushing's syndrome, pheochromocytoma, or both?

Abstract Clinical Case A 45-year-old woman presented to the emergency department with weakness and was found to have a Hb level of 68 g/l. She was also tachycardic (pulse 118 x/min) and hypertensive with a BP of 210/108 mmhg. She had a history of ulcerative colitis, menorrhagia and seronegative arthritis for which she had been using 5mg prednisolone daily for several years. The patient had suffered and episode of heart failure 4 years earlier of unknown etiology, during which she was tachycardic, hypertensive and her LVEF was decreased to 35%. In 2016 the patient had undergone an abdominal CT that had shown an incidental finding of a mass in the right adrenal gland, but she did not show up for additional investigations. During the previous year, the patient had developed symptoms of decreased physical fitness, increased weight, livedo reticularis-type skin changes (Figure), agitation, hirsutism and swelling on the neck. Gastroscopy revealed esophageal candidiasis and abdominal CT-scan showed a mass in the right adrenal gland that had increased in size from 2 cm to 3.8 cm compared to the previous CT in 2016 with a density of 21 HU. The patient had clinical Cushing's syndrome, that was confirmed in the lab tests (Table). In addition, lab tests showed an excess production of catecholamines. MRI of the sellar region was performed, that showed a 3×4×3 mm size Rathke's cleft cyst/microadenoma. A CRH stimulation test with inferior petrosal sinus sampling was performed and results were consistent with ectopic ACTH production. The clinical studies were consistent with pheochromocytoma that was also producing ACTH. The patient underwent unilateral adrenalectomy after having been treated with metyrapone and phenoxybenzamine preoperatively. Histopathology was compatible with pheochromcytoma. ACTH staining was negative, but CRH staining was not available. MIB-1 proliferation index was ≤3%. Postoperatively hypercortisolism and catecholamine excess have subsided. The patient has stopped diabetic and antihypertensive medication and she also been cured of the notable livedo reticularis-type skin changes (Figure). Conclusion The clinical presentation of pheochromocytoma in our patient was atypical with coexistence of ACTH-dependent Cushing's syndrome. Furthermore, the patient had a mass in the hypophysis that could have been a potential cause for ACTH-secretion. The clinical and biochemical signs were completely reversed with adrenalectomy, compatible with ectopic Cushing's syndrome due to a pheochromytoma that produced both catecholamines and most probably CRH. In summary pheochromocytomas can rarely also secrete other hormones such as interleukins, calcitonin, ACTH or CRH and this can significantly alter the clinical presentation of both Cushing's syndrome and pheochromocytoma. A recent meta-analysis (Elliott, JCEM 2021) reported 99 published cases of ACTH/CRH-producing pheochromocytomas.

PRIMARY EOSINOPHILIC COLITIS WITH CONCOMITANT NEWLY DIAGNOSED INFLAMMATORY BOWEL DISEASE – A DIAGNOSITIC CONUNDRUM

Abstract Eosinophilic colitis (EC) is a rare primary condition characterized by eosinophilic infiltration of the colon in the absence of secondary causes. Affecting only 0.003% of people in the United States, clinical manifestations of the disease can range from abdominal pain, bloody stools, and diarrhea to colonic obstruction, intussusception, volvulus, and perforation. The diagnosis is made upon histopathological analysis of colonic biopsies with the inflammatory infiltrate consisting predominantly or exclusively of eosinophils with focal collections greater than 100 per high-power field (hpf). Unlike inflammatory bowel disease (IBD), granulomas, crypt architectural distortion, pseudopyloric metaplasia, and fibrosis are not usually present with EC, but differentiating between the two conditions has proven to be difficult over the decades. A 33-year-old male with a history of ulcerative colitis since the age of 23 currently on mesalamine presented to the clinic for follow-up. He was officially diagnosed 10 years ago after being hospitalized with bloody bowel movements. Flexible sigmoidoscopy at the time showed confluent, erythematous, ulcerated mucosa suggestive of moderate to severe colitis seen extending from the rectum to 40cm. Rectosigmoid pathology showed distorted crypt architecture with increased lymphoplasmacytic infiltrate in the lamina propria and markedly increased neutrophils within crypt epithelial cells, indicative of ulcerative colitis. He was started on mesalamine and a prednisone taper but was poorly compliant. He presented again 5 months ago with abdominal pain and bloody diarrhea and was given steroids with follow-up colonoscopy. This time, findings showed scattered inflammation and aphthous ulcers throughout the colon with systemic loss of vascularity. Biopsies were negative for any evidence of active inflammatory bowel disease. Pathology showed mildly distorted crypts and significantly increased lamina propria eosinophils >100/hpf consistent with eosinophilic colitis. Bloodwork, including ESR and CRP, were normal. The patient was continued on mesalamine and as needed steroids with good symptom control. Our case highlights a rare phenomenon of primary eosinophilic colitis with newly diagnosed ulcerative colitis. It is difficult to ascertain which disease at which time contributed to our patient’s symptoms as the timeframe of both conditions likely overlap. His mild crypt architectural distortion and absence of lymphoplasmacytic infiltrate upon the repeat colonoscopy is indicative of well-controlled ulcerative colitis. There were no other etiologies ascertained for his colonic eosinophilia. Our case demonstrates the diagnostic obscurity of EC in its ability to masquerade as IBD. We aim to educate gastroenterologists on the timely diagnosis and effective management of this disease in order to prevent serious patient complications. Initial colonoscopy showing confluent, erythematous, ulcerated mucosa in the rectosigmoid region. Subsequent pathology confirmed ulcerative colitis. Rectosigmoid histopathology from second colonsocopy showing mildly distorted crypts and significantly increased lamina propria eosinophils >100/hpf consistent with well-controlled ulcerative colitis but active primary eosinophilic colitis. 400x magnification.

Abstract 15381: Phlegmasia Cerulea Dolens and Concurrent Gastrointestinal Bleeding: A Dangerous Combination With Challenging Management

Introduction: Phlegmasia cerulea dolens (PCD) is a rare and life-threatening complication related to extensive deep venous thrombosis (DVT) resulting in acute limb ischemia. Treatment options include anticoagulation, thrombolysis and thrombectomy. Case: A 31-year-old female with a history of ulcerative colitis (UC) on chronic steroids presented with acute dyspnea and tachycardia. She was hemodynamically stable. The initial workup included a lower extremity (LE) Doppler ultrasound (US) which showed an acute occlusive thrombus involving the left posterior tibial and popliteal veins, and a computerized tomography angiography (CTA) of her chest which showed bilateral pulmonary emboli. She was placed on heparin drip for 48 hours but due to an episode of acute gastrointestinal (GI) bleeding due to severe UC, anticoagulation was discontinued after an inferior vena cava filter placement and she was discharged from the hospital. After 1 month, she presented with severe diarrhea, hypotension and tachycardia. A chest CTA showed reduced clot burden compared to prior. On hospital day 2, the patient experienced acute onset of severe left LE pain, bluish skin discoloration and rapidly progressing edema. A repeat US showed progression of DVT to the left common femoral vein. The findings were consistent acute limb ischemia in the setting of PCD. She was managed with emergent thrombectomy, with significant amount of thrombus retrieved. Gastroenterology was consulted and GI bleeding did not recur. Discussion: Due to its rarity, there are limited data available to guide PCD management in the setting of elevated bleeding risk such as severe UC. However, after a risk-benefit assessment, we determined that this young patient should be treated with anticoagulation and undergo emergent thrombectomy, which resulted in significant improvement of her symptoms. We highlight the importance of multidisciplinary approach, early diagnosis and prompt treatment in these complex patients.

TUBERCULOUS PLEURAL EFFUSION MASQUERADING AS DRUG-INDUCED LUPUS

TUBERCULOUS PLEURAL EFFUSION MASQUERADING AS DRUG-INDUCED LUPUS

S2848 Massive Pseudo-Pneumoperitoneum After Endoscopic Necrosectomy

Introduction: Encapsulated peripancreatic fluid collection and walled-off necrosis are some of the complications of acute pancreatitis. Most resolve spontaneously but symptomatic pseudocysts or walled-off necrosis require drainage. The preferred therapeutic management is endoscopic ultrasound (EUS) guided drainage with stent placement. Known iatrogenic complications of the procedure include bleeding and perforation. Case Description/Methods: A 39-year-old woman with history of ulcerative colitis, in remission on certrolizumab presented with symptomatic walled-off necrosis after idiopathic necrotizing pancreatitis. EUS-guided drainage and stent placement was successfully performed. On subsequent upper endoscopy for necrosectomy, post-procedure large pneumoperitoneum was noted on imaging leading to emergent surgical evaluation with laparoscopy. However, no perforation or pancreatic fluid contamination was seen. On post-operative day 1, patient was asymptomatic and tolerating diet. She was discharged on post-operative day 2. At 3-month follow-up, patient remained asymptomatic and plastic stents were removed. Discussion: Pneumoperitoneum is an uncommon but dreaded complication of EUS guided cystogastrostomy. This occurs when there is separation of the gastric wall and the wall of the pancreatic cyst or walled-off necrosis. If perforation is detected during cystgastrostomy, it may be possible to use a LAMS to close the defect by bridging the walls or close the gastric defect endoscopically with clips or sutures. Immediate surgery (such as cyst-enterotomy with closure of the wall defect) should be performed if there is generalized contamination of the peritoneum with cyst fluid content and subsequent signs of peritonitis. (Figure) Our case, to our knowledge, is the only one that describes pneumoperitoneum after endoscopic necrosectomy, two weeks after placement of LAMS. Our hypothesis is that the walled-off necrosis moved away from the gastric wall after removal of LAMS, which had aided apposition of the gastric wall and cyst wall due to its flanges and short saddle length. Pneumoperitoneum, in the absence of peritoneal findings, is referred to as benign peritoneum. Our case describes massive benign pneumoperitoneum after endoscopic necrosectomy without perforation. There is a paucity of literature on non-surgical management of post-endoscopic pneumoperitoneum and we hope that our case, will help endoscopists carefully select patients who will benefit from surgical management of pneumoperitoneum.Figure 1.: Figure A. CT abdomen showing pancreatic walled off necrosis containing turbid fluid and debris. Figure B. Massive pneumoperitoneum seen on CT abdomen after EUS-guided drainage and double pig-tailed stent placement for continued drainage.

S3430 Lactulose Works in the Large Bowel: But How Does It Improve Hepatic Encephalopathy in a Patient Without a Large Bowel?

Introduction: Lactulose is a non-absorbable disaccharide which acts in the large bowel, and is commonly used in the treatment of hepatic encephalopathy. We present an interesting case of altered mental status due to hepatic encephalopathy successfully managed with lactulose in a patient with history of total colectomy. Case Description/Methods: A 67-year-old male with non-alcoholic cirrhosis and inflammatory bowel disease (IBD) post total proctocolectomy with a continent ileostomy known as a “Kock-pouch” (K-pouch) presented to the hospital with flu like symptoms and altered mental status. He was subsequently found to be positive for COVID-19. At the time of initial evaluation, the patient was obtunded with an elevated ammonia level of 91 umol/L. Colorectal surgery was consulted as the patient was not able to empty his K-pouch. Recently, he complained of inability to catheterize and with bleeding from the stoma. Initial catheterization with a Water’s tube yielded 400 cc of effluent. Nasogastric tube was placed through which he was receiving lactulose 30 mg q8 hours. The patient’s mental status improved within 24 hours. The patient ultimately underwent flexible pouchoscopy with endoscopic dilation and placement of a 22 French mushroom catheter for decompression of the K-pouch. Discussion: Lactulose is a non-absorbable disaccharide composed of galactose and fructose. The small intestine does not have the enzymes required to breakdown lactulose so it reaches the large bowel in its original form. In the large bowel, it is metabolized by colonic bacteria into monosaccharides and then to volatile fatty acids, hydrogen and methane. Lactulose decreases both the production and absorption of ammonia mainly through the presence of gut bacteria. The question arises as to how lactulose decreased ammonia levels in this patient without a large bowel. One proposed mechanism is the translocation of bacteria normally found in the large bowel to the small intestine. Small Intestinal Bacterial Overgrowth (SIBO), is a condition causing an increased number of bacteria in the small intestine. Patients with IBD and structural abnormalities are at increased risk of developing SIBO. Lactulose is commonly used in the diagnosis through the administration of lactulose and subsequent measurements of hydrogen and methane gas in expired air. This condition, in our patient with history of ulcerative colitis and colectomy, is a proposed mechanism of the efficacy of lactulose in the treatment of hepatic encephalopathy.

Clinical Case of Tofacitinib Therapy in Autoimmune Alopecia in Patient with Ulcerative Colitis.

This article presents the clinical case of a patient with a long history of ulcerative colitis. Seven years after the onset of the disease, other autoimmune disorders such as sacroiliitis and alopecia have manifested. Ulcerative colitis is characterized by severe exacerbations, development of steroid resistance, ineffectiveness of mesalazine therapy, and onset of leukopenia when taking azathioprine and 6-mercaptopurine. Janus kinase inhibitor (tofacitinib) administration leads to remission of the disease, reduced activity of ulcerative colitis and sacroiliitis, and a resumption of hair growth was also observed.

BEZLOTOXUMAB THERAPY FOR RECURRENT CLOSTRIDIUM DIFFICILE INFECTION IN AN ULCERATIVE COLITIS PATIENT

Abstract INTRODUCTION Clostridium difficile infection (CDI) is the most common infectious cause of nosocomial diarrhea, comprising 10-20% of all cases. CDI is a significant complication for IBD patients. Not only can CDI induce IBD flare, IBD patients also experience significantly higher CDI recurrence when compared to the general population. New monoclonal antibody (mAB) therapies, such as bezlotoxumab, have improved management of recurrent CDI (rCDI). The MODIFY I/II trial included 44 patients with known IBD, 28 of which received bezlotoxumab. Among these 28 patients, there was a 27.2% absolute reduction in the incidence of rCDI. Encouraged by these results, we recently prescribed bezlotoxumab in a UC patient with rCDI and herein report our experience. CASE REPORT A 21-year-old female with a history of ulcerative colitis (UC) diagnosed in 2017 presented for treatment of rCDI. Her first episode of CDI occurred in 2019 during an active UC flare treated with steroids and infliximab induction. CDI was successfully treated with a four-week course of 125mg oral vancomycin twice daily followed by once daily for an additional four weeks. She had a recurrent episode of CDI one year after her initial infection while on vedolizumab for UC treatment. She was treated with 125mg oral vancomycin, four times daily, and tapered down by one dose over a four-month period. Two years after her initial CDI, she developed worsening non-bloody diarrhea, nausea, and anorexia with weight loss. She again tested positive for C. difficile via glutamate dehydrogenase antigen and PCR for toxin B. Fecal calprotectin was 2190 mg/g. She was treated with 14-day course fidaxomicin 200mg BID and a single infusion of bezlotoxumab 10mg/kg. Treatment for UC was not adjusted. At follow up one month later, her symptoms had resolved and fecal calprotectin normalized (17 mg/g). Six months later, she remains asymptomatic. DISCUSSION Recurrent CDI is a frequent culprit for inducing IBD flares, and is difficult to manage. Fecal transplant (FMT) is an option for rCDI, but often entails logistical challenges and risks cross-contamination of endoscopic facilities. Bezlotoxumab is an appealing option for rCDI as a single dose medication with few reported side effects in the MODIFY clinical trials. While the number of IBD patients in the MODIFY trial was small, results were promising. In our patient, bezlotoxumab quickly resolved her rCDI and IBD flare without need for alteration or escalation of her biologic therapy, and she has remained asymptomatic for six months. This case corroborates the prospect that bezlotoxumab positively affects the clinical outcomes of UC patients with rCDI compared to those on repetitive antimicrobial therapy and/or FMT without mAB therapy. Further investigation into the long-term efficacy of this therapy is merited for the IBD patient population in the real-world setting.

Induction of remission with tacrolimus in a patient with severe acute, cortisone refractory ulcerative colitis and severe Covid-19 pneumonia: a case report

BackgroundTherapy regimens used in patients with inflammatory Bowel Disease (IBD) have been associated with enhanced risk of viral infections or viral reactivation. Moreover, it is uncertain whether IBD patients have increased risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection or infected patients may have an increased risk for severe coronavirus disease 2019 (Covid-19). Managing severe acute flare in ulcerative colitis during the Covid-19 pandemic is a challenge for clinicians and their patients. The results of the published studies mainly report on the role of the prior medication, but not how to treat severe acute flare of IBD patients with severe Covid-19 pneumonia.Case presentationWe report the case of a 68-year-old patient with a long history of ulcerative colitis. He was initially admitted to an external hospital because of severe acute flare. The initiation of a high-dose oral cortisone therapy did not improve the clinical symptoms. During the inpatient treatment, he was tested positive for SARS-CoV-2. At admission to our hospital the patient showed severe flare of his ulcerative colitis and increased Covid-19 symptoms. A cortisone-refractory course was noticed. After detailed multidisciplinary risk–benefit assessment, we initiated an intravenous tacrolimus therapy and dose of prednisolone was tapered gradually. After clinical response, the therapy was adjusted to infliximab. Additionally, the Covid-19 pneumonia was kept under control despite immunosuppression and the patient could be discharged in clinical remission.ConclusionsThis case suggest the use of tacrolimus as a bridging therapeutic option for severe acute, cortisone refractory ulcerative colitis in Covid-19 patients. Nevertheless, the best treatment strategy for IBD patients presenting a flare during the outbreak has yet to be defined. Further data for IBD patients under calcineurin inhibitor therapy are urgently needed.

Immunohistochemical signs of IgG4-related disease in patients with inflammatory bowel diseases

To determine immunohistochemical features of IgG4-related disease in patients with inflammatory bowel diseases (IBD). Immunohistochemical testing of colonic biopsy material from 35 patients with IBD (24 cases of ulcerative colitis and 11 cases of Crohn's disease) was carried out using IgG, IgG4 and CD138 antibodies. The number of IgG4- and CD138-positive cells was counted in high power field of microscope (×400). Patient selection was random. IgG4-positive cells were detected in the colonic mucosa of 5 patients with ulcerative colitis. The age of the patients ranged from 24 to 47 years. Two patients had a total, and three had a left-sided lesion of the colon. The anamnesis of the disease ranged from 3 to 13 years. The number of positively stained cells in the reaction with the antibody to IgG4 varied from 2 to 50 in high power field of microscope. We were able to detect over 10 IgG4-positive cells in 3 females aged 28, 30 and 31 years with a long history of ulcerative colitis (5, 4 and 3 years, respectively). Two patients had a total lesion of the colon, all three had an exacerbation of the disease, and a morphological study revealed chronic diffuse active erosive colitis. A high degree of histological activity and pronounced diffuse basal plasmacytosis were noted. In one of the cases, the infiltrate captured the muscular lamina of the mucosa and areas of the submucosa. IgG4-positive cells in the inflammatory infiltrate, including those with an excess of more than 10 in the field of view of the microscope at high magnification, can be observed in patients with ulcerative colitis with severe and prolonged course of the disease. To classify this colitis as a manifestation of an IgG4-related disease, the results of immunohistochemical studies alone are not enough. It is required to accumulate a larger number of observations, as well as to search for other diagnostic criteria for an IgG4-related disease in these patients.

S2433 Cutaneous Intestinal Metaplasia: A Rare Complication of an End Ileostomy

Introduction: Intestinal metaplasia (IM) is a known precursor to adenocarcinoma. Combinations of host genetic factors, responses within the mucosa, as well as dietary/environmental alterations, predispose to mucosal inflammation, leading to atrophy, metaplasia, and eventual dysplasia. Cutaneous involvement is very rare. Cutaneous IM is a pathologic diagnosis defined by scattered colonic crypts within an intact epidermis. We report a case of peristomal intestinal metaplasia in a patient with an ileostomy. Case description/methods: A 90 year-old male with a history of ulcerative colitis with subsequent total proctocolectomy with end ileostomy 67 years prior and in remission, presented to a dermatologist to evaluate a growing raised lesion around the stoma. He denied any abdominal pain, changes in stool output or consistency, weight loss, or changes in appetite. He did not have peristomal tenderness or bleeding from the site. Biopsy of the area revealed adenocarcinoma with tubulovillous origin and invasion into the lamina propria. Surgery was planned, but he opted for a second opinion at our institution. He underwent an ileoscopy to evaluate whether the adenocarcinoma extended into the ileum. Around the stoma, there was a well-demarcated raised, pink lesion that was not friable (Figure 1A); a separate lesion was seen extending to the right of the stoma (Figure 1B). The ileal mucosa was normal without any evidence of invading lesions (Figure 1C). Dermatology performed two punch biopsies from the lateral and medial lesion edges. The biopsies revealed intraepidermal growth of intestinal glandular tissue, consistent with IM, with dense chronic and scattered acute inflammation. No dysplasia or malignancy was seen. He opted to not pursue further investigation as he was otherwise asymptomatic. Discussion: Three other cases have documented cutaneous peristomal IM in patients with inflammatory bowel disease, all found via shave biopsy by dermatology. The proposed pathophysiology involves chronic inflammation due to bile acid exposure to the peristomal squamous tissue, inducing metaplasia and transforming the epithelium, similar to Barrett’s esophagus. Inflammation from IBD has been proposed as a pathway for cutaneous IM in reported cases, but our patient had been in remission for 67 years. Distinguishing dysplasia is critical, particularly in the setting of inflammation. Documented treatment includes electrocautery with repeat biopsies to evaluate for eradication.Figure 1.: A. Right colon showing >80 eosinophils per HPF (400x). B. Left colon showing >50 eosinophils per HPF (400x). C, D. Left colon biopsies showing lamina propria invasion by eosinophils with focal epithelial breakdown. Note how crypts are relatively intact with little to no eosinophilic presence. E. Colonoscopic view showing erythematous mucosa without ulcerations. F. Colonoscopic view showing normal colonic mucosa.

S2450 COVID-19-Associated Ulcerative Colitis Flare: A Bad Breakout

Introduction: COVID-19 can trigger autoimmune responses via molecular mimicry. Retrospective studies of COVID-19 patients have showed up to 50% prevalence of autoimmune disease related autoantibodies. We report a patient with a history of ulcerative colitis (UC) who presented with a UC flare and COVID-19 infection was later found during evaluation as a possible trigger. Case description/methods: A 31-year-old Black female presented to the hospital with abdominal pain and bloody diarrhea for 10 days. Patient also endorsed a cough productive of thick yellow sputum. Past history-ulcerative colitis on mesalamine. Physical exam-temperature-98.7F, blood pressure-138/92 mmHg, pulse-120/min, respiratory rate-18/min, O2 saturation-100%/room air, wheezing present in b/l lung fields, abdomen-nondistended, hypoactive bowel sounds, soft, tender to palpation in the left lower quadrant, no guarding/rebound or masses. Laboratory-hemoglobin 12.8 g/dL, C-reactive protein-77.8 mg/L (Ref: < 10), positive stool guaiac, SARS-CoV-2-positive, fecal calprotectin >3000 ug/g (Ref: < =49). CT of the abdomen/pelvis showed inflammatory/infectious thickening of the transverse colon likely reflecting a nonspecific colitis and a patchy area of pneumonic infiltrate in the posterior medial lung base. Intravenous fluids, Metronidazole 500 mg IV TID, Ciprofloxacin 400 mg IV Q12H and Solumedrol 60 mg IV Daily were started. Sigmoidoscopy with biopsy-moderate to severe colitis extending from the descending colon to the rectum without any dysplasia or granulomas. With IV steroids the patient reported improvement in her diarrhea and was able to tolerate her meals. Solumedrol was changed to prednisone 40 mg daily for 2 weeks and the patient was discharged with outpatient close gastroenterology follow up. Discussion: Viral infections including COVID-19 are known to trigger autoimmunity through molecular mimicry, activating immune responses to antigenic epitopes distinct from the disease causing epitopes (epitope spreading), activating T cells in an antigen independent manner (bystander activation) or exposing cryptic epitope's (epitope which is otherwise hidden). In turn, immunosuppressive therapies used to treat autoimmune disorders may increase the risk of COVID-19. Though it is now known that COVID-19 can trigger autoimmunity further studies are required to understand the exact immunopathogenesis. Such studies may provide more insights to prevent and treat diseases of the immune system.Figure 1.: Possible mechanisms of autoimmunity in viral infections like COVID-19.