Publications by authors named "Mona Gundersen"

Background: The long-term outcomes of Ulcerative colitis (UC) after discontinuation of biological therapy are largely unknown. There is also a lack of accurate and validated markers that can predict outcome after withdrawal accurately. The aims of this study were to describe the long-term outcomes in UC patients following cessation of anti-TNF therapy and explore potential biomarkers as an approach towards precision medicine.

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Background And Aims: Biological therapy for inflammatory bowel disease is efficient in many cases but not all. The underlying molecular mechanisms behind non-response to biological therapy in inflammatory bowel disease are poorly described. Therefore, we aimed to characterize the mucosal cytokine transcript profile in non-immunogenic, non-responder patients with adequate trough level.

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Epithelial alarmins are gaining interest as therapeutic targets for chronic inflammation. The nuclear alarmin interleukin-33 (IL-33) is upregulated in the colonic mucosa of acute ulcerative colitis (UC) and may represent an early instigator of the inflammatory cascade. However, it is not clear what signals drive the expression of IL-33 in the colonic mucosa, nor is the exact role of IL-33 elucidated.

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Background: There are no accurate markers that can predict clinical outcome in ulcerative colitis at time of diagnosis. The aim of this study was to explore a comprehensive data set to identify and validate predictors of clinical outcome in the first year following diagnosis.

Methods: Treatment naive-patients with ulcerative colitis were included at time of initial diagnosis from 2004 to 2014, followed by a validation study from 2014 to 2018.

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Ulcerative colitis (UC) is a chronic inflammatory bowel disease. In UC, a wide range of criteria are used for disease remission, with few studies investigating the differences between disease remission and normal control groups. This paper compares known inflammatory and healing mediators in the mucosa of UC in clinical remission and normal controls, in order to better describe the remission state.

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Objectives: A healed intestinal mucosa is the aim of therapy in acute ulcerative colitis (UC). Disruption of mucosal wound healing may lead to severe complications including intestinal fibrosis. This study examined mucosal gene expression in the healing process of acute UC with a special focus on known mediators of fibrosis.

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Background: Anti-tumour necrosis factor (TNF) agents play a pivotal role in the treatment of moderate to severe ulcerative colitis (UC), and yet, no international consensus on when to discontinue therapy exists.

Objective: The aim of this study is to study the long-term performance of a treatment algorithm of repeated intensified induction therapy with infliximab (IFX) to remission, followed by discontinuation in patients with UC.

Patients And Methods: Patients with moderate to severe UC were enroled in an open prospective study design.

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Interleukin 33 (IL-33) is a cytokine preferentially elevated in acute ulcerative colitis (UC), inferring a role in its pathogenesis. The role of IL-33 in intestinal inflammation is incompletely understood, with both pro-inflammatory and regulatory properties described. There are also conflicting reports on cellular sources and subcellular location of IL-33 in the colonic mucosa, justifying a closer look at IL-33 expression in well-defined clinical stages of UC.

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Background: Biological agents such as anti-tumor necrosis factor (TNF) induce remission in ulcerative colitis. There is however no consensus regarding the discontinuation of this treatment.

Aim: The aim of this study is to assess whether clinical parameters and mucosal cytokine mRNAs in healed colonic mucosa can predict long-term remission in ulcerative colitis following discontinuation of infliximab (IFX) therapy.

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Most sporadic colorectal cancers (CRCs) develop from preformed adenomas. Cytokines are involved in the transition from adenoma to CRC. Interleukin-33 (IL-33) is a newly discovered proinflammatory cytokine belonging to the IL-1 cytokine family and involved in the development of chronic inflammation and cancer.

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Background: To determine the annual incidence rate and clinical features of amyotrophic lateral sclerosis (ALS) in Møre and Romsdal County, Norway, in the 20-year period from 1988 to 2007.

Methods: We recruited ALS patients retrospectively from the patient database of the two neurological departments in Møre and Romsdal County, Norway. The patients were identified by use of the international classification code for diseases.

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