Acute Flare Of Ulcerative Colitis Research Articles

A diagnostic dilemma: cytomegalovirus colitis as an uncommon comorbidity in inflammatory bowel disease: a case report

BackgroundThe role of cytomegalovirus infection as an opportunistic pathogen in exacerbating ulcerative colitis and its response to treatment remain a topic of ongoing debate. Clinicians encounter numerous challenges, including the criteria for differentiating between an acute ulcerative colitis flare and true cytomegalovirus colitis, the diagnostic tests for identifying cytomegalovirus colitis, and determining the appropriate timing for initiating antiviral therapy.Case presentationA 28-year-old Syrian female with a seven-year history of pancolitis presented with worsening bloody diarrhea, abdominal pain, and tenesmus despite ongoing treatment with azathioprine, mesalazine, and prednisolone. She experienced a new flare of acute severe ulcerative colitis despite recently completing two induction doses of infliximab (5 mg/kg) initiated four weeks prior for moderate-to-severe ulcerative colitis. She had no prior surgical history. Her symptoms included watery, bloody diarrhea occurring nine to ten times per day, abdominal pain, and tenesmus. Initial laboratory tests indicated anemia, leukocytosis, elevated C-reactive protein (CRP) and fecal calprotectin levels, and positive CMV IgG. Stool cultures, Clostridium difficile toxin, testing for Escherichia coli and Cryptosporidium, and microscopy for ova and parasites were all negative. Sigmoidoscopy revealed numerous prominent erythematous area with spontaneous bleeding. Biopsies demonstrated CMV inclusions confirmed by immunohistochemistry, although prior biopsies were negative. We tapered prednisolone and azathioprine and initiated ganciclovir at 5 mg/kg for ten days, followed by valganciclovir at 450 mg twice daily for three weeks. After one month, she showed marked improvement, with CRP and fecal calprotectin levels returning to normal. She scored one point on the partial Mayo score. The third induction dose of infliximab was administered on schedule, and azathioprine was resumed.ConclusionConcurrent cytomegalovirus infection in patients with inflammatory bowel disease presents a significant clinical challenge due to its associated morbidity and mortality. Diagnosing and managing this condition is particularly difficult, especially regarding the initiation or continuation of immunosuppressive therapies.

EXCESS DIETARY SUGAR ALTERS COLONOCYTE METABOLISM AND IMPAIRS THE EARLY PROLIFERATIVE RESPONSE TO DAMAGE

The colonic epithelium requires continuous renewal by crypt resident intestinal stem cells (ISCs) and transit amplifying (TA) cells to maintain barrier integrity, especially after inflammatory damage. An important regulator of ISC and TA cell function is dietary metabolites which can affect their proliferative capacity. Over the last 150 years, the diet of high-income countries contains increasing amounts of simple sugars, such as sucrose, but whether excess sugar affects the function of ISCs and TA cells directly is unknown. We used a combination of 3-dimensional colonoids and a mouse model of colon damage/repair (DSS colitis) to demonstrate the direct effect of sugar on the transcriptional, metabolic, and regenerative functions of crypt ISCs and TA cells. We demonstrate that high sugar conditions directly limit murine and human colonoid development, which is associated with a reduction in the expression of proliferative and key stem cell gene signatures. Further, high-glucose conditions led to the accumulation of glycolytic metabolite pyruvate in colonoids, with a concomitant decrease in ATP, suggesting impaired glycolytic fuel metabolism. Treatment of colonoids with DCA, which forces pyruvate into the TCA cycle, restored their growth, ATP levels, and the expression of proliferation and stem cell gene signatures. Similarly, DSS treatment of mice fed a high sugar diet led to massive irreparable damage that was independent of the colonic microbiota and its metabolites. Metabolic analyses of crypt cells from high-sucrose-fed mice revealed increased glycolytic potential without a commensurate increase in aerobic respiration. Rather, epithelium from high-sucrose-fed mice has increased mitochondrial content, without increased levels of ATP, further demonstrating impaired oxidative phosphorylation and fuel metabolism. Finally, we demonstrated impaired proliferative potential of ISCs and reduced number of TA direct daughter cells in high-sucrose-fed mice with DSS damage. Taken together, our results indicate that short-term, excess dietary sucrose can directly modulate intestinal crypt cell metabolism and inhibit ISC/TA cell regenerative proliferation. This knowledge may inform diets that better support the treatment of acute intestinal injury, as is seen in patients with an acute flare of Ulcerative Colitis.

EXCESS DIETARY SUGAR ALTERS COLONOCYTE METABOLISM AND IMPAIRS THE EARLY PROLIFERATIVE RESPONSE TO DAMAGE

Abstract The colonic epithelium requires continuous renewal by crypt resident intestinal stem cells (ISCs) and transit amplifying (TA) cells to maintain barrier integrity, especially after inflammatory damage. An important regulator of ISC and TA cell function is dietary metabolites which can affect their proliferative capacity. Over the last 150 years, the diet of high-income countries contains increasing amounts of simple sugars, such as sucrose, but whether excess sugar affects the function of ISCs and TA cells directly is unknown. We used a combination of 3-dimensional colonoids and a mouse model of colon damage/repair (DSS colitis) to demonstrate the direct effect of sugar on the transcriptional, metabolic, and regenerative functions of crypt ISCs and TA cells. We demonstrate that high sugar conditions directly limit murine and human colonoid development, which is associated with a reduction in the expression of proliferative and key stem cell gene signatures. Further, high-glucose conditions led to the accumulation of glycolytic metabolite pyruvate in colonoids, with a concomitant decrease in ATP, suggesting impaired glycolytic fuel metabolism. Treatment of colonoids with DCA, which forces pyruvate into the TCA cycle, restored their growth, ATP levels, and the expression of proliferation and stem cell gene signatures. Similarly, DSS treatment of mice fed a high sugar diet led to massive irreparable damage that was independent of the colonic microbiota and its metabolites. Metabolic analyses of crypt cells from high-sucrose-fed mice revealed increased glycolytic potential without a commensurate increase in aerobic respiration. Rather, epithelium from high-sucrose-fed mice has increased mitochondrial content, without increased levels of ATP, further demonstrating impaired oxidative phosphorylation and fuel metabolism. Finally, we demonstrated impaired proliferative potential of ISCs and reduced number of TA direct daughter cells in high-sucrose-fed mice with DSS damage. Taken together, our results indicate that short-term, excess dietary sucrose can directly modulate intestinal crypt cell metabolism and inhibit ISC/TA cell regenerative proliferation. This knowledge may inform diets that better support the treatment of acute intestinal injury, as is seen in patients with an acute flare of Ulcerative Colitis.

S844 Inpatient Outcomes and Healthcare Utilization in Obese vs Non-Obese Patients Hospitalized with an Acute Ulcerative Colitis Flare - A Nationwide Cohort Study

Introduction: Ulcerative colitis (UC) remains a leading cause of patient morbidity and in severe cases, mortality. Given the rise in prevalence of obesity in the United States, the goal of this study is to illustrate the impact of obesity in hospitalized patients admitted for acute flares of ulcerative colitis (UC). Our primary outcome was adjusted odds of inpatient mortality. Secondary outcomes included length of hospitalization (LOS), total hospital charge (THC), and complications including sepsis, upper and lower GI bleed (UGIB)(LGIB), and acute kidney injury (AKI). Methods: The National Inpatient Sample (NIS, 2016-2018) was sourced for hospitalization data from adult patients admitted for UC flares. The queried pool of patients was stratified into obese (BMI ≥ 30), and non-obese cohorts using International Classification of Diseases, Tenth Revision (ICD-10) codes. After performing descriptive analysis on the involved cohorts, linear and multivariate regression was used to evaluate study outcomes. STATA 14 was used for data analysis. Results: Of 142,094 admissions for UC flare, 12,989 (9.14%) had comorbid obesity. Compared to non-obese-UC patients, obese-UC patients were significantly older (51.2 vs 48.5 years, p < 0.0001), were more often female (63.9% vs 53.0%, p < 0.0001), had greater Caucasian and African American representation (73.0% vs 71.5%, p < 0.0001), (13.8% vs 11.3%, p < 0.0001) compared to non-obese patients. Obese-UC patients had more comorbid disease as measured by a Charlson Comorbidity Index score ≥3 (16.4% vs 9.62, p < 0.0001), and had more patients belonging to the poorest quartile of family income (27.9% vs 23.9%, p< 0.0001). Obese-UC patients as compared to those without obesity had a nonsignificant increase in adjusted odds of inpatient mortality (aOR 1.17; 95% CI 0.67-2.03, p=0.583). Obese-UC had higher rates of complications including LGIB (OR 1.79, p = 0.017), Shock (OR 1.48, p = 0.017), AKI (OR 1.42, p = 0.001). Additionally, Obese-UC patients had an increased LOS (5.48 vs 5.18 days, p = 0.007) and higher THC ($54,194 vs $49,957, p = 0.005). Conclusion: Obesity did not significantly increase inpatient mortality. However Obese-UC patients had increased complications (LGIB, Shock, AKI), LOS, and THC relative to UC patients without obesity. Additional studies are needed to further investigate the effects of obesity in UC, and to help reduce the economic burden obesity places on the healthcare system.

S2748 Necrobiotic Lung Nodules in Patient With Ulcerative Colitis

Introduction: Ulcerative colitis and Crohn’s disease are two forms of inflammatory bowel disease (IBD). 25-40% of IBD patients have extra-intestinal manifestations (EIM). Pulmonary manifestations are one of the rarest forms of EIM, particularly necrobiotic nodules. It is a challenge to diagnose as it presents with symptoms similar to autoimmune, vasculitis, or infectious pathologies. We present a rare case of a patient who was found to have necrobiotic lung nodules during an acute ulcerative colitis flare. Case Description/Methods: 44-year-old male with newly diagnosed ulcerative pancolitis, presented with diarrhea and hematochezia for 8 weeks and 4 weeks of leg ulcers. He denied any other symptoms. 4 months ago, he was started on high dose steroids and switched to vedolizumab, however began to relapse after steroids were tapered. On admission, vitals significant for tachycardia at 118 bpm. Physical exam was significant for lower extremity ulcers consistent with pyoderma gangrenosum. Labs significant for leukocytosis (16,500/µL), Hg of 6.8, and elevated CRP at 160.26. Findings were suggestive of IBD flare and he also underwent chest x-ray which showed multifocal nodular airspace opacities, which appeared to have developed cavitations. CT chest revealed bilateral pulmonary nodules. He underwent infectious, autoimmune and vasculitis work up including HIV, tuberculosis, bacterial, viral, endocarditis, ANA, ANCA as well as fungal serologies which were all negative. He had CT guided biopsies, which were suggestive of necrobiotic lung nodules. Repeat CT chest showed interval improvement in solid and cavitary nodules. Given extensive negative infectious work up and improvement with steroids and infliximab, his presentation was consistent with necrobiotic lung nodules secondary to uncontrolled inflammatory bowel disease. (Figure) Discussion: We describe a rare case of necrobiotic lung nodules as an extra-intestinal manifestation of uncontrolled ulcerative colitis. Histologically, these nodules are sterile aggregates of neutrophils, that can cavitate and have a high degree of resemblance to pyoderma gangrenosum in cases of IBD. Few cases of necrobiotic lung nodules with IBD have been reported and most of them had respiratory symptoms but our case did not present with respiratory manifestations. In conclusion, necrobiotic lung nodules should be considered as a differential diagnosis of lung nodules in patients with IBD while excluding any infectious etiologies as mandatory before starting treatment with steroids and biologics.Figure 1.: CT guided biopsy suggestive of necrobiotic lung nodule.

P272 Tofacitinib as salvage therapy for patients hospitalized with refractory severe active ulcerative colitis: a GETAID multicenter prospective/retrospective cohort

Abstract Background Up to 25% of patients with ulcerative colitis (UC) will require hospitalization for severe flare. In UC patients admitted who have already experienced multiple drug failures, including steroids and anti-TNF agents, new quick-acting medical options are needed. Tofacitinib is effective in refractory UC and has a rapid mechanism of action. It could be considered in this setting. We aimed to evaluate the efficacy and safety of tofacitinib in patients hospitalized for an acute UC flare. Methods We conducted an observational and multicenter study with both retrospective and prospective collections in 14 GETAID tertiary IBD centers. The primary objective was to assess the survival without colectomy following tofacitinib initiation. We determined rates of clinical response, clinical remission, and clinical steroid-free remission at week 6 and week 14 and safety. Results Fifty-eight patients were included. All but one patient with active lupus were exposed to antiTNF. 50 (86.2%) patients have received infliximab and 18 (31%) to ciclosporin. Patients were previously exposed to a median of 2.5 lines of biologic treatment before tofacitinib.Median Lichtiger at inclusion was 11.5 (interquartile range IQR[9 - 13]), median CRP was 17 mg/l (IQR[6.5 - 67]) and total Mayo score was 10 (IQR[9.3 - 11]). Deep ulcerations were observed in 10 patients (17.2%).With a median follow-up of 6.5 months (IQR [2.9-12.4]), colectomy-free survival rates were estimated at 80.1% (95CI [70.1-91.4]) at 3 months and at 75.1% (95CI[64.1-88.1]) at 6 months. Rates of clinical response, clinical remission and clinical steroid-free remission were 60.3%, 46.6% and 37.9% at week 6 an, 48.1%, 37% and 35.2% at week 14, respectively. At the end of follow-up, 29 patients (50%) were still treated with tofacitinib. The survival without tofacitinib discontinuation was estimated at 82.8% (95CI[73.6-93.1), 67.8% (95CI[56.6-81.4]) and 46.2% (95CI[34.2-62.4]) at 1, 3, and 6 months (Figure 3).Regarding safety, no death was observed, three patients withdrew tofacitinib due to adverse events. Two herpes zosters occurred in patients aged over 60 years old. No thrombotic event occurred. Conclusion Tofacitinib appears as a promising option in patients hospitalized with a severe UC flare that needs further validation in prospective and controlled trials.

A Microsimulation Model to Project the 5-Year Impact of Using Hyperbaric Oxygen Therapy for Ulcerative Colitis Patients Hospitalized for Acute Flares

Hyperbaric oxygen therapy (HBOT) improves short-term outcomes for ulcerative colitis (UC) patients hospitalized for acute flares. Longer-term impacts and cost-effectiveness are unknown. We compared disease outcomes and cost-effectiveness of HBOT in addition to standard ofcare versus standard of care alonefor UC patients hospitalized for acute flares using a microsimulation model. Published literature was used for transition probabilities, costs, and quality-adjusted life year (QALY) estimates. We modeled 100,000 individuals in each group over a 5-year horizon and compared rates of re-hospitalization, rescue medical therapy, colectomy, death, and cost-effectiveness at a willingness-to-pay of $100,000/QALY. Probabilistic sensitivity analyses were performed with 500 samples and 250 trials, in addition to multiple microsimulation sensitivity analyses. The use of HBOT at the time of index hospitalization for an acute UC flare is projected to reduce the risk of re-hospitalization, inpatient rescue medical therapy, and inpatient emergent colectomy by over 60% (p < 0.001) and mortality by over 30% (p <0.001), during a 5-year horizon. The HBOT strategy costs more ($5600 incremental cost) but also yielded higher QALYs (0.13 incremental yield), resulting in this strategy being cost-effective ($43,000/QALY). Results were sensitive to HBOT costs and rates of endoscopic improvement with HBOT. Probabilistic sensitivity analyses observed HBOT to be more cost-effective than standard of care in 95% of iterations. The use of HBOT to optimize response to steroids during the index hospitalization for an acute UC flare is cost-effective and is projected to result in significant reductions in disease-related complications in the long term.

2077 A Rare Case of Migratory Urticaria Causing Dysphagia During an Acute Flare of Ulcerative Colitis

INTRODUCTION: Ulcerative colitis (UC) is characterized by chronic mucosal inflammation limited to the colon. The most common manifestation of UC is progressively worsening hematochezia that may be accompanied by extraintestinal manifestations including, peripheral arthritis, uveitis, primary sclerosing cholangitis, fatty liver, venous/arterial thromboembolism, and pulmonary disease. Erythema nodosum (EN) and pyoderma gangrenosum (PG) are the most common dermatologic manifestations. Uncommonly, UC may present with unpredictable urticaria and angioedema that may be life threatening. We present a rare care of acute UC flare with migratory urticaria as the initial presenting symptom. CASE DESCRIPTION/METHODS: A 25-year-old woman with UC presented with 1 week of abdominal pain, bloody stools, bilateral ankle and knee pain with non-blanching rash over her right shoulder, left armpit, and left groin. GI PCR and C. difficile assay were negative. Rheumatoid factor, double stranded DNA, anti-cyclic citrullinated peptide antibodies, anti-Smith antibody, anti-ribonuclear protein, and C1 esterase inhibitor were negative. The patient was started on cetirizine with resolution of the arthralgia. However, new rashes were noted under right axilla and left antecubital fossa over a two day period. Patient subsequently developed dysphagia and left sided mandibular swelling. Indirect laryngoscopy was unremarkable. She was immediately treated with IV methylprednisolone and transitioned to a slow oral steroid taper over 3 months with improvement of gastrointestinal and dermatologic symptoms. Skin biopsies revealed superficial and mid-dermal perivascular lymphocytic infiltrate consistent with urticaria. DISCUSSION: This patient presented with unpredictable migratory skin lesions involving multiple mucosal surfaces that brought concerns of possible airway involvement. The etiology was initially unclear as limited infectious and rheumatologic work up was negative, as well as negative allergen and medication exposure. Cutaneous vasculitis was considered, however biopsy showed urticaria. Patient’s symptoms significantly improved after the initiation of oral steroids. Migratory urticaria with associated angioedema can be a manifestation of an acute flare of UC that warrants evaluation by otolaryngologist and prompt initiation of steroids. Glucocorticoids may address symptoms of a pro-inflammatory state while allowing for more time to rule out other etiologies of extraintestinal manifestations of a patient’s presentations.

Kaposi Sarcoma Mimicking Acute Flare of Ulcerative Colitis.

Besides an AIDS-defining illness, Kaposi sarcoma (KS) is also seen in individuals on long-term immunosuppressant therapy. We report KS in a 70-year-old immunocompetent man, which initially mimicked acute flare of ulcerative colitis (UC). He was hospitalized multiple times for complaints of watery diarrhea and tenesmus. Despite treatment with mesalamine, short courses of methylprednisolone, and one dose of infliximab, his symptoms improved only partially. He underwent colonoscopy, which revealed mild active colitis and a mass in the ascending colon. After treatment of acute flare with methylprednisone and mesalamine, he underwent total colectomy with end ileostomy. The histopathology confirmed stage I adenocarcinoma of colon. He continued to experience watery diarrhea, which was attributed to intractable UC, and he underwent protectomy several weeks later. The histopathology of rectum revealed KS. After surgery, watery diarrhea resolved completely. Review of literature suggests KS has been rarely reported in immunocompetent individuals with inflammatory bowel disease.

A Case of Kaposi's Sarcoma of the Rectum in a Homosexual Male with HIV–AIDS

Kaposi sarcoma (KS) is a locally aggressive endothelial tumor, commonly diagnosed among individuals with acquired immunodeficiency syndrome (AIDS). The most typical site of involvement by KS is the skin, but in some cases, it can also affect other tissues and organs. Most patients with gastrointestinal involvement of Kaposi's sarcoma remain asymptomatic and they are often diagnosed on endoscopy or autopsy. However, there are cases of KS mimicking ulcerative colitis (UC), whereby clinical manifestations can confuse physicians. We report a 31 y old homosexual man who presented with rectal pain and bleeding. Patient was diagnosed eight years ago with HIV/ AIDS, and despite highly active retroviral therapy, he developed extensive skin lesions. Because of expressive rectal pain and bleeding, he underwent rectoscopy, which revealed ulcerous and hemorrhagic lesions. The rectoscopic and clinical presentation mimicked acute flare of UC, which was patient initial diagnosis. Tissue samples were collected for microscopical examination. After histological, histochemical and immunhistochemical examination of the sampled tissue, KS diagnosis was confirmed. The clinical manifestations of Kaposi sarcoma can be confused with acute exacerbation of ulcerative colitis often delaying the diagnosis. Therefore, early endoscopic evaluation with adequate biopsies could help in timely diagnosis and management of gastrointestinal KS (GI-KS) in patients with HIV/AIDS, even if they do not have skin lesions.

The Utility of Fecal Calprotectin in an Acute Flare of Inflammatory Bowel Disease

Introduction: Fecal calprotectin (FC) is a noninvasive biomarker of inflammation used to predict relapse and trend remission in inflammatory bowel disease (IBD). Its predictive value is higher in ulcerative colitis (UC) than in Crohn's disease (CD). FC has been studied over the course of weeks to months. In this trial we aim to study how intensive therapy for an acute flare changes FC in a short time period. Methods: In this prospective pilot study, we enrolled adult patients with an acute IBD flare requiring treatment adjustment. Stool calprotectin was obtained at the beginning of a flare and after change in therapy. T-tests were performed as statistical analyses. Symptoms were assigned a numerical score before and after treatment. For UC, a partial Mayo Score was used: episodes of diarrhea and number of bloody bowel movements were each assigned a score from 0 to 3, in order of increasing severity (maximum score 6). For CD, a partial Harvey-Bradshaw index was used: pain, diarrhea, fevers, presence of fistula, and presence of extra-intestinal manifestations were each assigned a score from 0 to 2, in order of increasing severity (maximum score 10). Results: Of 23 enrolled patients, 18 were hospitalized and 5 were outpatients. Median age was 40 years and 65% were men. Nine (39%) had UC and 14 (61%) had CD. Initial mean FC was 867 μg/g; after median 10 days, repeat mean FC was 540 μg/g, p = 0.03. Treatments are summarized in Table 1. In UC, there was a mean decline of 617 μg/g, from 924 μg/g to 307 μg/g over 8 days, p = 0.02. Initial partial Mayo median was 4, improving to 2 at time of second FC. For CD patients, mean FC decreased by 141 μg/g, from 831 μg/g to 689 μg/g over 15 days, p = 0.27. Initial partial Harvey-Bradshaw median was 4, improving to 1 at time of second FC.Table 1: TreatmentSix patients had increasing FC despite clinical improvement, 5 of these had CD. Of the 4 CD patients who had surgical resection, 75% had improvement of FC, as early as 2 days post-op. The UC group was comprised of medical management only. Conclusion: Our findings suggest that it is useful to trend FC as a marker of improvement in an acute UC flare. In CD, FC is not reliable in acute disease, except perhaps post-operatively. In UC, FC can be employed as a noninvasive marker of inflammation and response to treatment in less than 10 days.

Magnetic resonance colonography for assessment of acute severe colitis in pregnancy

Serial plain abdominal radiography is important in the assessment of the extent and severity of disease in acute severe colitis and assists in identifying complications, such as toxic dilatation. The need to avoid exposure to ionising radiation during pregnancy makes the assessment of acute severe colitis in pregnancy more challenging. The development of protocols for magnetic resonance colonography (MR-C) has yielded an interesting diagnostic option. We present the case of a 38-year-old female transferred at 20 weeks of her second pregnancy with an acute flare of ulcerative colitis (UC). The patient reported a history of steroid induced psychosis and had been hospitalised after her first pregnancy with acute severe UC which responded to infliximab infusion. The current flare had failed to respond to two doses of infliximab at 5 mg/kg and the patient reported [20 motions per day. Haemoglobin was measured as 9.1 g/dL, CRP 84 mg/dL and albumin 12 g/L. The patient experienced recurrent fevers, raising concern for colonic perforation or intra-abdominal collection. MRC was performed for assessment of disease severity and identification of complications. Multiplanar T1and T2weighted sequences with diffusion weighted imaging (DWI) were performed on 1.5 T magnet following intravenous (iv) administration of buscopan. No iv, rectal or oral contrast was given. Continuous circumferential thickening from rectum to distal transverse colon was noted with DWI demonstrating marked restricted diffusion in the involved bowel segment, consistent with active colitis. There were no fluid collections and no evidence of toxic dilatation or perforation (Fig. 1). In the absence of radiological evidence of colonic perforation, she was given two doses of infliximab 10 mg/kg at an interval of 5 days and showed a gradual improvement. On discharge from hospital, she was passing 3-formed stools/day and received further infliximab (10 mg/kg) at weeks 24 and 30 of pregnancy and remains

Pyogenic Granuloma of Gastrointestinal Tract: A Large Case Series and Review of Literature

Purpose: To report all available cases of PG of intestinal tract, diagnosed at our hospital in the last 10 years and to review previously reported cases in the literature. Methods: A retrospective review of the pathology database was performed on all gastrointestinal biopsies in the last 10 years using diagnostic and pathology codes searching for PG of the gastrointestinal tract. Results: A total of 23 cases of pathologically proven PG were diagnosed over a 10 year period. The median age of patients was 64 (±9) years with 47.8% men and 52.2 % women. The most common location of the PG was the colon - 19 (82.6%) cases (14 cases in sigmoid colon, 3 cases in transverse colon and 1 case in splenic flexure) followed by esophagus - 4 cases (17.4%) and rectum - 1 case (4.3%). PG presented as a polyp in 16 patients (69.6%) and as an erythematous inflamed edematous mucosa in 6 patients (26%). The polyp was Sessile in most cases - 13 patients (81.3%) and pedunculated in the rest - 3 patients (18.7%). The size of polyp was <1 cm in 8 patients and >1 cm in the rest. Endoscopically, most lesions appeared as inflammatory pseudopolyps without features suggestive of adenoma. The most common indication for endoscopy was screening/surveillance colonoscopy (82.6% cases) with a family history of colon cancer or polyp in a first degree relative in 5 patients, a personal history of adenoma in the past in 4 cases and colorectal cancer in 3 cases. Other indications for endoscopy were melena in 4 cases (17.4%), iron deficiency anemia in 2 cases (8.7%) and acute flare of ulcerative colitis in 1 patient (4.3%). Conclusion: PG of gastrointestinal tract is rare. To date, only about 15-20 cases have been reported in the literature mainly from Japan and Korea. To our knowledge this is the largest case series (23 cases) of this rare pathological lesion of gastrointestinal tract. In our series, most cases of PG were incidental findings in an asymptomatic patient who had an endoscopy done for an unrelated reason, unlike previously reported cases which were mostly associated with gastrointestinal bleeding. In summary, PG is a rare pathological lesion in GI tract excluding the oral cavity and can present in various ways ranging from an asymptomatic polyp to a life threatening GI bleeding.

Pregnancy-associated Sweet’s Syndrome in an Acute Episode of Ulcerative Colitis

A 33-year old pregnant patient (pregnancy week 15) with a past medical history of ulcerative colitis with onset of the disease following the birth of her first child was admitted to the hospital with symptoms of weight loss, pyrexia, leukocytosis and bloody and mucous diarrhoea. Total ileocolonoscopy revealed an acute flare of ulcerative colitis. Within a few days, tender erythematous skin lesions occurred and were histologically proven to be neutrophilic dermatosis. Treatment with highly-dosed prednisone led to a complete remission of both cutaneous and intestinal manifestations. Both pathogenic entities are associated with similar immunological alterations, such as comparable cytokine and chemokine release patterns and recruitment of inflammatory cells. Recent data also indicates that proinflammatory cytokine levels are elevated in pregnancy, which might be pivotal in the pathogenesis and the severity of intestinal and extraintestinal symptoms. We present and discuss a diagnostic algorithm and an overall therapeutic rationale for Sweet's syndrome.

Pneumocystis jiroveci pneumonia and pneumomediastinum in an anti-TNFα naive patient with ulcerative colitis

We report the case of a 21-year-old man who was noted to have pneumomediastinum during an admission for an acute flare of ulcerative colitis. At that time, he was on maintenance treatment with azathioprine at a dose of 1.25 mg/kg per day, and had not received supplementary steroids for 9 mo. He had never received anti-tumor necrosis factor (TNF)alpha therapy. Shortly after apparently effective treatment with intravenous steroids and an increased dose of azathioprine, he developed worsening colitic and new respiratory symptoms, and was diagnosed with Pneumocystis jiroveci (carinii) pneumonia (PCP). Pneumomediastinum is rare in immunocompetent hosts, but is a recognized complication of PCP in human immunodeficiency virus (HIV) patients, although our patient's HIV test was negative. Treatment of PCP with co-trimoxazole resulted in resolution of both respiratory and gastrointestinal symptoms, without the need to increase the steroid dose. There is increasing vigilance for opportunistic infections in patients with inflammatory bowel disease following the advent of anti-TNFalpha therapy. This case emphasizes the importance of considering the possibility of such infections in all patients with inflammatory bowel disease, irrespective of the immunosuppressants they receive, and highlights the potential of steroid-responsive opportunistic infections to mimic worsening colitic symptoms in patients with ulcerative colitis.

Schwere Colitis ulcerosa und Infektion mit Cytomegalieviren, Herpes-simplex-Viren und Clostridium difficile

The treatment of severe flares of ulcerative colitis is based on systemic corticosteroids, immunomodulators such as cyclosporine and azathioprine and in some cases TNF-alpha-antagonists, respectively. These immunosuppressed patients are susceptible for infectious pathogens. Here we report the case of a patient with a severe flare of ulcerative colitis that was first treated with systemic corticosteroids combined with immunomodulators and subsequent with infliximab. The patient then experienced an infection with Clostridium difficile and cytomegalovirus of the colon and a Herpes simplex esophagitis, respectively. After specific treatment the patient responded well to the immunosuppressive therapy. This case illustrates that infections have to be considered before systemic treatment of an acute flare of ulcerative colitis is instituted especially in the case of disease activation during immunosuppressive treatment.