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Start Over Author "Michopoulos, S." Topic crohn disease
4 results on '"Michopoulos, S."'

1. Case Report: Malignant melanoma in a patient with Crohn's disease treated with ustekinumab.

Author

Axiaris G, Ioannou A, Papoutsaki M, Marinos L, Liontos M, Michopoulos S, and Zampeli E

Subjects
Male, Humans, Child, Preschool, Adult, Ustekinumab therapeutic use, Adalimumab therapeutic use, Antibodies, Monoclonal, Humanized therapeutic use, Melanoma, Cutaneous Malignant, Crohn Disease complications, Crohn Disease drug therapy, Melanoma complications, Melanoma drug therapy, Skin Neoplasms complications, Skin Neoplasms drug therapy
Abstract

The cornerstone of inflammatory bowel disease (IBD) treatment is immunomodulators. IBD patients are at increased risk of intestinal and extraintestinal malignancy. Ustekinumab is a fully humanized monoclonal anti-IL12/23 antibody with a good safety profile. Malignancies of breast, colon, head and neck, kidney, prostate, thyroid, and non-melanoma skin cancer have been reported among patients who received ustekinumab. We report the case of a 42-year-old Crohn's patient on long-term treatment with ustekinumab, who developed achromatic malignant melanoma. Crohn's was diagnosed at the age of 15, with upper and lower gastrointestinal involvement and was initially treated with azathioprine (2mg/kg for 4 years) and infliximab (5mg/kg for 6 weeks). Due to ileal obstruction, the patient underwent stricturoplasty and received adalimumab (40mg every other week) for two years. He then discontinued therapy and a year later underwent right hemicolectomy. Adalimumab was reinstituted (40mg every other week) and the patient remained in clinical remission for two years. His overall exposure to adalimumab was four years. Ustekinumab was initiated due to a relapse and after 3 years, an incident of scalp itching led to the diagnosis metastatic achromatic malignant melanoma bearing BRAF V600E mutation. He received targeted therapy with an initial good response. We aim to point out the risk of dermatologic malignancy in IBD patients on long-term immunosuppression and the lifelong and meticulous evaluation that is required., Competing Interests: No competing interests were disclosed., (Copyright: © 2023 Axiaris G et al.)

Published
2023
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2. The natural history of COVID-19 in vaccinated inflammatory bowel disease patients.

Author

Viazis N, Drygiannakis I, Karmiris K, Theodoropoulou A, Zampeli E, Tzouvala M, Bamias G, Liatsos C, Theocharis G, Vrakas S, Tsironi E, Mathou N, Mantaka A, Christidou A, Koustenis K, Veretanos C, Papathanasiou E, Zacharopoulou E, Tribonias G, Kitsou V, Kartsoli S, Theodoulou A, Michopoulos S, Thomopoulos K, Koutroubakis IE, and Mantzaris GJ

Subjects
Humans, Male, Adult, COVID-19, Inflammatory Bowel Diseases, Colitis, Ulcerative diagnosis, Crohn Disease diagnosis
Abstract

Aim: Assess the characteristics of break through COVID-19 in Inflammatory Bowel Disease (IBD) patients, despite complete vaccination., Methods: Patients who reported a COVID-19 at least 3 weeks after complete vaccination were asked to answer an on-line anonymous questionnaire which included patient and disease characteristics, vaccination history, and the evolution of COVID-19., Results: Among 3240 IBD patients who reported complete vaccination between 1st May 2021 and 30thJune 2022, 402 (12.4%) were infected by SARS Cov-2 [223 male, 216 Crohn's disease (CD), 186 Ulcerative Colitis (UC), mean (SD) age 42.3 (14.9) years, mean (SD) IBD duration 10.1 (9.7) years]. Three hundred and sixty-nine patients (91.8%) were infected once and 33 (8.2%) twice. The mean (SD) time between last vaccination and infection was 4.1 (1.6) months. Overall, 351 (87.3%) patients reported mild constitutional and/or respiratory symptoms, 34 (8.4%) were asymptomatic and only 17 patients (4.2%) required hospitalization. Of hospitalized patients, 2 UC patients died of COVID-19 pneumonia. The remaining hospitalized patients did not need high flow oxygen supply or ICU admission., Conclusions: A minority of completely vaccinated IBD patients developed COVID-19 which evolved with mild symptoms and a favorable outcome. These results reinforce the importance of vaccination especially in vulnerable populations., Competing Interests: Conflict of Interest There are no conflicts of interest to declare regarding this study, (Copyright © 2023 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.)

Published
2023
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3. Differential expression of the TL1A/DcR3 system of TNF/TNFR-like proteins in large vs. small intestinal Crohn's disease.

Author

Bamias G, Kaltsa G, Siakavellas SI, Gizis M, Margantinis G, Zampeli E, Vafiadis-Zoumboulis I, Michopoulos S, Daikos GL, and Ladas SD

Subjects
Adolescent, Adult, Aged, Crohn Disease pathology, Enzyme-Linked Immunosorbent Assay, Female, Humans, Intestinal Mucosa metabolism, Intestinal Mucosa pathology, Intestine, Large pathology, Intestine, Small pathology, Male, Middle Aged, RNA, Messenger metabolism, Real-Time Polymerase Chain Reaction, Receptors, Tumor Necrosis Factor, Member 6b blood, Tumor Necrosis Factor Ligand Superfamily Member 15 blood, Up-Regulation, Young Adult, Crohn Disease metabolism, Intestine, Large metabolism, Intestine, Small metabolism, Receptors, Tumor Necrosis Factor, Member 6b metabolism, Tumor Necrosis Factor Ligand Superfamily Member 15 metabolism
Abstract

Background: TNF-like cytokine 1A provides co-stimulatory signals to activated lymphocytes through binding to death-domain receptor-3. Decoy receptor-3 inhibits death-domain receptor-3 signalling, rendering immunocytes resistant to apoptosis. These functions may be important for the pathogenesis of Crohn's disease., Aims: To study the mucosal and systemic expression of Decoy receptor-3 and TNF-like cytokine 1A in Crohn's disease, in relation to disease activity, localization, and response to treatment., Methods: Soluble Decoy receptor-3 and TNF-like cytokine 1A were measured by ELISA in active or quiescent Crohn's disease. Relative mRNA expression in non-affected and inflamed intestinal mucosa was determined by real-time RT-PCR., Results: We found significant upregulation of Decoy receptor-3 and its ligands TNF-like cytokine 1A and FasL in inflamed intestinal mucosa of Crohn's disease patients. During active disease, Decoy receptor-3 and TNF-like cytokine 1A were detected in the serum in the majority of patients. Intestinal inflammation was strongly associated with these elevations as they were absent during remission and significantly reduced with anti-inflammatory treatment. Regional diversity was observed as Decoy receptor-3 was upregulated in colonic and ileal sites, whereas TNF-like cytokine 1A was preferentially induced in the large bowel mucosa and systemic circulation of patients with colonic involvement., Conclusions: TNF-like cytokine 1A and Decoy receptor-3 are upregulated during active Crohn's disease and may participate in disease pathogenesis and offer novel therapeutic opportunities., (Copyright © 2011 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.)

Published
2012
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4. Is there any association between IgA nephropathy, Crohn's disease and Helicobacter pylori infection?

Author

Pipili C, Michopoulos S, Sotiropoulou M, Mpakirtzi T, and Grapsa E

Subjects
Azathioprine therapeutic use, Crohn Disease diagnosis, Crohn Disease immunology, Drug Therapy, Combination, Follow-Up Studies, Glomerulonephritis, IGA diagnosis, Glomerulonephritis, IGA drug therapy, Glucocorticoids therapeutic use, Helicobacter Infections diagnosis, Helicobacter Infections immunology, Helicobacter pylori isolation & purification, Humans, Immunity, Innate, Immunosuppressive Agents therapeutic use, Intestinal Mucosa immunology, Intestinal Mucosa microbiology, Male, Middle Aged, Crohn Disease complications, Glomerulonephritis, IGA etiology, Helicobacter Infections complications
Abstract

A case of IgA nephropathy (IgAN) associated with Crohn's disease (CD) and preceded Helicobacter pylori (Hp) infection is described. Therapy with corticosteroids and azathioprine resulted in clinical improvement. The connection between IgAN and CD is well established, while tonsillar Hp is a potential antigen causative of IgAN. The three entities may reflect a common immunopathogenetic mechanism involving an IgA response to mucosal challenge.

Published
2012
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