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The Onset of Ulcerative Colitis Upon Helicobacter Pylori Eradication in a 72‑Year‑Old Woman: Report of a Rare Case with a 3‑Year Follow‑Up J

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The Onset of Ulcerative Colitis Upon Helicobacter Pylori Eradication in a 72‑Year‑Old Woman: Report of a Rare Case with a 3‑Year Follow‑Up J Homolak et al. BMC Gastroenterol (2021) 21:303 https://doi.org/10.1186/s12876-021-01876-5 CASE REPORT Open Access The onset of ulcerative colitis upon Helicobacter pylori eradication in a 72-year-old woman: report of a rare case with a 3-year follow-up J. Homolak1, M. Nikolić2,3*, D. Potoč3, M. Živković2, D. Bakula2, I. Budimir2,4, I. Pavić5, D. Hrabar2,4, N. Ljubičić2,3,4 and D. Vražić6 Abstract Background: Epidemiological studies suggest an inverse association between H. pylori infection/exposure and infammatory bowel disease prevalence/incidence, however, there are no reports of individual patients who devel- oped a "non-transient” ulcerative colitis (UC) following H. pylori eradication. Case presentation: We report a case of a 72-year-old female with an elderly-onset UC developed upon H. pylori eradication and a 3-year follow-up of the progression to steroid-dependent colitis complicated with enteropathic arthritis and fnal containment of the disease with golimumab. In our patient, H. pylori eradication was associated with the development of pancolitis that evolved into clinically, endoscopically, and pathohistologically confrmed UC. Conclusions: The case of our patient provides a unique clinical context for a growing body of literature suggesting molecular mechanisms involved in the interaction of genes, environment, and microbiota to be of critical importance in the etiopathogenesis of UC, and thus, provides a valuable set of complementary translational information for pre- clinical and epidemiological research on the topic. Keywords: Case report, Helicobacter pylori, Ulcerative colitis, Infammatory bowel disease, Golimumab Background Parkinson’s disease [2]. Increasing understanding of the Helicobacter pylori (H. pylori) is an important human serious pathophysiological consequences of H. pylori pathogen with 50–90% prevalence depending on the infection led to a general recommendation published in stage of economic development [1]. H. pylori causes the Kyoto global consensus report that even individuals active gastritis associated with peptic ulcers, atrophic without clinically manifest disease should undergo eradi- gastritis, gastric adenocarcinoma, and MALT lymphoma cation [3]. Interestingly, a growing body of research also [2]. Furthermore, it is associated with unexplained iron reported a negative association of H. pylori and some dis- defciency anemia, idiopathic thrombocytopenic pur- eases such as asthma [4] and infammatory bowel disease pura, vitamin B12 defciency and there is some early (IBD) [5], however, the causality of these associations, evidence for atherosclerosis, stroke, Alzheimer’s and their clinical relevance, and mechanisms of action are yet to be elucidated. *Correspondence: [email protected] IBD is an umbrella term representing a group of 2 Gastroenterology and Hepatology Unit, University Hospital Centre chronic infammatory diseases of the gastrointestinal “Sestre Milosrdnice”, Vinogradska 29, 10000 Zagreb, Croatia Full list of author information is available at the end of the article tract. Ulcerative colitis (UC) and Crohn’s disease (CD) © The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. The Creative Commons Public Domain Dedication waiver (http:// creat iveco mmons. org/ publi cdoma in/ zero/1. 0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Homolak et al. BMC Gastroenterol (2021) 21:303 Page 2 of 7 are the most important clinical entities of IBD character- the H. pylori infection rates, so the observed association ized by episodes of mucosal infammation accompanied might "merely be a proxy for the hygiene hypothesis” [18]. by abdominal pain, diarrhea, bloody stools, and weight Interestingly, in contrast to extensive epidemiological loss [6]. In UC, the disease usually afects the rectum and studies, case reports of patients developing IBD upon the part of the colon, but in severe cases, the entire colon H. pylori eradication that would provide a “proof-of- can be infamed. Pathohistological fndings usually reveal concept” are scarce. Jovanovic reported an onset of CD infammation limited to the mucosa and submucosa with in a 28-year-old upon H. pylori eradication [19]. Tursi cryptitis and crypt abscesses [6], and molecular studies described a 34-year-old man and a 39-year-old woman indicate increased TH1 and/or TH17 responses accom- who developed CD upon H. pylori eradication [20]. Nag- panied by enhanced production of tumor necrosis factor ami reported a patient requiring a subtotal colectomy α, interleukin 1-β, interferon γ, interleukin-17, interleu- following a relapse of UC associated with H. pylori eradi- kin-6, and IL-23 [7]. Diagnosis of IBD is usually done by cation [21, 22], and Chiba reported a case of a 63-year- colonoscopy combined with pathohistological examina- old developing a transient UC upon eradication therapy tion of colonic biopsies, however exciting new diagnos- [22]. To the best of our knowledge no published reports tic approaches such as virtual computed tomography describe the course of H. pylori eradication therapy- (CT) colonoscopy (CT colonography) [8] and difusion- induced UC that required initiation of biological therapy weighted imaging techniques [9] have also been pro- to achieve satisfactory disease control. posed recently. Etiopathogenesis of UC is still unknown We report a case of a 72-year-old woman who devel- and recent evidence suggests pathophysiological pro- oped UC upon H. pylori eradication with a 3-year fol- cesses arise as a consequence of a complex interaction low-up, and fnal containment of the disease following of genetic predisposition, dysbiosis, environmental and initiation of golimumab (Fig. 1). immunological factors [6]. An inverse association between H. pylori infection/ Case presentation exposure and prevalence/incidence of IBD has been A 72-year-old Caucasian female (height-161 cm; reported by many epidemiological studies [5, 10–12]. weight-82 kg; BMI-31.6 kg/m2) presented with a year- A comprehensive meta-analysis on the prevalence of long history of dyspeptic symptoms in 2017. Te patient H. pylori infection in IBD (including UC subgroup) and reported she was diagnosed with chronic gastritis and non-IBD controls suggested a negative association after gastroesophageal refux disease in 2016 (Fig. 2A). Past accounting for ethnicity, age, detection methods, and medical history included untreated osteoporosis diag- previous use of drugs (e.g. aminosalicylates and cor- nosed in 2005, thyroidectomy (toxic multinodular goiter ticosteroids) [5]. Furthermore, an inverse association in 2013 and a history of Hashimoto’s thyroiditis), hyper- between H. pylori prevalence and disease severity was tension, and Reinke’s edema-induced hoarseness. Fam- reported [13]. Several mechanisms have been proposed ily history and physical examination were unremarkable. for the potential protective efect. It has been shown that Te patient admitted to a 50-pack-year of cigarette smok- Hp(2–20), an H. pylori ribosomal peptide reduces infam- ing. She was regularly taking levothyroxine, rabeprazole, mation and upregulates mucosal damage repair in a rat amlodipine, and reported penicillin allergy. model of colitis [14, 15]. Microbiota, an important player Esophagogastroduodenoscopy (EGD) and pathohistol- in IBD [16] is modulated by H. pylori [17]. H. pylori has ogy were suggestive of moderate chronic active gastritis been shown to reduce the gastric secretion of the pro- with incomplete intestinal metaplasia and H. pylori inva- infammatory satiety hormone leptin (increased in UC), sion in concordance with fndings from 2016 (Fig. 2B). and increase tolerogenic dendritic cells and suppressive Eradication therapy with rabeprazole, clarithromycin, regulatory T cells through IL-18 [5]. metronidazole, and a probiotic was initiated. Te patient Although accumulating evidence suggests H. pylori was encouraged to stop smoking. might provide some benefcial anti-infammatory efects, Seven days in eradication, the patient reported to the the results should be interpreted with caution. Observa- emergency department due to redness and tongue swell- tional retrospective studies are susceptible to bias, and ing. Te symptoms were resolved with intravenous appropriate adjustments are not always possible. Te methylprednisolone and intramuscular chloropyramine. incidence of IBD is associated with economic develop- Eradication was discontinued. ment and "westernization” e.g. increased use of anti- Two months later the patient underwent EGD with biotics, hygiene, cigarette smoking and consumption biopsy samples subjected to H. pylori antibiotic sensi- of processed foods, and decreased family size [18]. Te tivity
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