scholarly journals S2477 Ocular Melanoma: A Rare Complication of TNF-α Antagonist Therapy in Ulcerative Colitis

2021 ◽  
Vol 116 (1) ◽  
pp. S1045-S1046
Author(s):  
Alla Turshudzhyan ◽  
Haleh Vaziri
Keyword(s):  
Ulcerative Colitis ◽  
Rare Complication ◽  
Ocular Melanoma ◽  
Antagonist Therapy ◽  
Tnf Α

scholarly journals Vedolizumab as a Potential Culprit in the Development of Ovarian Teratoma?

2017 ◽  
Vol 11 (3) ◽  
pp. 786-790 ◽  
Author(s):  
Judy A. Trieu ◽  
Mohammad Bilal ◽  
Gurinder Luthra
Keyword(s):  
Ulcerative Colitis ◽  
Monoclonal Antibody ◽  
Opportunistic Infections ◽  
Ovarian Teratoma ◽  
Antagonist Therapy ◽  
Humanized Monoclonal Antibody ◽  
Increased Risk ◽  
Tnf Α ◽  
Integrated Studies ◽  
Meta Analyses

Vedolizumab is a new humanized monoclonal antibody that has been reserved for those with moderate-to-severe Crohn’s disease and ulcerative colitis who have failed immunomodulator and TNF-α antagonist therapy, and for those who have an increased risk for developing progressive multifocal leukoencephalopathy. Because it targets gastrointestinal tract-specific lymphocytes, meta-analyses and integrated studies have shown that vedolizumab causes fewer extraintestinal adverse effects, such as opportunistic infections and malignancies, compared with anti-TNF therapies. We present the case of a patient who developed an ovarian teratoma after initiation of vedolizumab therapy.

Anti-TNF-α therapy in ulcerative colitis

2008 ◽  
Vol 149 (20) ◽  
pp. 921-927
Author(s):  
Péter László Lakatos ◽  
László Lakatos
Keyword(s):  
Ulcerative Colitis ◽  
Colitis Ulcerosa ◽  
Tnf Α

A colitis ulcerosa kezelését meghatározó legfontosabb tényezők a betegség kiterjedése és súlyossága. Az enyhe és középsúlyos betegek nagy többsége ma is a hagyományos gyógyszereket kapja (orális-topicalis 5-ASA, sulfasalazin). A hagyományos terápiára (szteroid, azathioprin, 5-ASA) rezisztens és a súlyos, akut colitis ulcerosa kezelése ugyanakkor nincs megoldva. Az újabb adatok alapján az infliximab indukciós vagy fenntartó kezelés formájában mindkét betegcsoportban hatékony kezelési alternatívát jelenthet, így az esetek egy részében elkerülhetővé válik a colectomia. Az összefoglalóban a szerzők colitis ulcerosában az anti-TNF-α-kezeléssel kapcsolatos eredményeket foglalták össze.

scholarly journals Inflammatory cytokines-stimulated human muscle stem cells ameliorate ulcerative colitis via the IDO-TSG6 axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shengchao Zhang ◽  
Jiankai Fang ◽  
Zhanhong Liu ◽  
Pengbo Hou ◽  
Lijuan Cao ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokines ◽  
Human Muscle ◽  
Enzyme Linked Immunosorbent Assay ◽  
Muscle Stem Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Anti Inflammatory

Abstract Background Muscle stem cells (MuSCs) are absolutely required for the formation, repair, and regeneration of skeletal muscle tissue. Increasing evidence demonstrated that tissue stem cells, especially mesenchymal stem cells (MSCs), can exert therapeutic effects on various degenerative and inflammatory disorders based on their immunoregulatory properties. Human mesenchymal stem cells (hMSCs) treated with interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) were reported to possess anti-inflammatory functions by producing TNF-stimulated gene 6 (TSG-6). However, whether human muscle stem cells (hMuSCs) also possess TSG-6 mediated anti-inflammatory functions has not been explored. Methods The ulcerative colitis mouse model was established by subjecting mice to dextran sulfate sodium (DSS) in drinking water for 7 days. hMuSCs were pretreated with IFN-γ and TNF-α for 48 h and were then transplanted intravenously at day 2 of DSS administration. Body weights were monitored daily. Indoleamine 2,3-dioxygenase (IDO) and TSG-6 in hMuSCs were knocked down with short hairpin RNA (shRNA) and small interfering RNA (siRNA), respectively. Colon tissues were collected for length measurement and histopathological examination. The serum level of IL-6 in mice was measured by enzyme-linked immunosorbent assay (ELISA). Real-time PCR and Western blot analysis were performed to evaluate gene expression. Results hMuSCs treated with inflammatory factors significantly ameliorated inflammatory bowel disease (IBD) symptoms. IDO and TSG-6 were greatly upregulated and required for the beneficial effects of hMuSCs on IBD. Mechanistically, the tryptophan metabolites, kynurenine (KYN) or kynurenic acid (KYNA) produced by IDO, augmented the expression of TSG-6 through activating their common receptor aryl hydrocarbon receptor (AHR). Conclusion Inflammatory cytokines-treated hMuSCs can alleviate DSS-induced colitis through IDO-mediated TSG-6 production.

Ulcerative colitis is not a rare complication of Takayasu arteritis

2013 ◽  
Author(s):  
Ryu Watanabe ◽  
Tomonori Ishii ◽  
Kyohei Nakamura ◽  
Tsuyoshi Shirai ◽  
Hiroshi Fujii ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Takayasu Arteritis ◽  
Rare Complication

Oat β-glucan ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice

2015 ◽  
Vol 6 (11) ◽  
pp. 3454-3463 ◽  
Author(s):  
Bo Liu ◽  
Qinlu Lin ◽  
Tao Yang ◽  
Linna Zeng ◽  
Limin Shi ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tnf Α

Oral administration of oat β-glucan ameliorates DSS induced colitis in mice by decreasing the expression of inflammatory cytokines TNF-α, IL-1β, IL-6 and iNOS.

A RARE ASSOCIATION OF CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY WITH ULCERATIVE COLITIS

2021 ◽  
pp. 18-19
Author(s):  
Nilima K. Shah ◽  
Ankita Patel ◽  
Umeshkumar Nakum ◽  
Ravindra Patel
Keyword(s):  
Ulcerative Colitis ◽  
Ulcerative Colitis Patient ◽  
Chronic Inflammatory Demyelinating Polyneuropathy ◽  
Rare Complication ◽  
Gastrointestinal Symptoms ◽  
Demyelinating Polyneuropathy ◽  
High Dose ◽  
Initial Symptom ◽  
Colitis Patient ◽  
Rare Association

Chronic inammatory demyelinating polyneuropathy (CIDP) is a rare complication of Ulcerative colitis and it is uncertain whether it is associated with Ulcerative colitis itself or with its treatment. We describe a case of CIDP-like neuropathy as an initial symptom of Ulcerative colitis. A 17 years old male patient presented with symmetrical weakness of both lower extremities with paresthesia of both hand and feet. With impression of AIDP patient was treated with plasmapheresis and discharged on tapering steroid therapy. After 3 months again presented with bilateral weakness of all four limbs associated with diarrhea and fever. Patient was diagnosed with Ulcerative colitis ,so considering previous episode as 1st episode of CIDP and with rare association with Ulcerative colitis . Patient was treated with high dose of steroids and immunosuppressive therapy. Neurological and gastrointestinal symptoms remarkably improved after treatment.

scholarly journals Inflammatory bowel disease: the role of inflammatory cytokine gene polymorphisms

2004 ◽  
Vol 13 (3) ◽  
pp. 181-187 ◽  
Author(s):  
Joanna Balding ◽  
Wendy J. Livingstone ◽  
Judith Conroy ◽  
Lesley Mynett-Johnson ◽  
Donald G. Weir ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Disease Incidence ◽  
Strong Association ◽  
Tnf Α ◽  
Genes Encoding ◽  
Inflammatory Processes ◽  
Inflammatory Bowel ◽  
Cytokine Gene Polymorphisms

THE mechanisms responsible for development of inflammatory bowel disease (IBD) have not been fully elucidated, although the main cause of disease pathology is attributed to up-regulated inflammatory processes. The aim of this study was to investigate frequencies of polymorphisms in genes encoding pro-inflammatory and anti-inflammatory markers in IBD patients and controls. We determined genotypes of patients with IBD (n=172) and healthy controls (n=389) for polymorphisms in genes encoding various cytokines (interleukin (IL)-1β, IL-6, tumour necrosis factor (TNF), IL-10, IL-1 receptor antagonist). Association of these genotypes to disease incidence and pathophysiology was investigated. No strong association was found with occurrence of IBD. Variation was observed between the ulcerative colitis study group and the control population for the TNF-α-308 polymorphism (p=0.0135). There was also variation in the frequency of IL-6-174 and TNF-α-308 genotypes in the ulcerative colitis group compared with the Crohn's disease group (p=0.01). We concluded that polymorphisms in inflammatory genes are associated with variations in IBD phenotype and disease susceptibility. Whether the polymorphisms are directly involved in regulating cytokine production, and consequently pathophysiology of IBD, or serve merely as markers in linkage disequilibrium with susceptibility genes remains unclear.

scholarly journals Chronic inflammation in ulcerative colitis causes long term changes in gobletcell function

2021 ◽  
Author(s):  
Varsha Singh ◽  
Kelli Johnson ◽  
Jianyi Yin ◽  
Sunny Lee ◽  
Ruxian Lin ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Active Sites ◽  
Mucus Secretion ◽  
Pcr Analysis ◽  
Mucus Layer ◽  
Percentage Decrease ◽  
Tnf Α ◽  
Long Term Changes ◽  
Reduced Rate

ABSTRACTObjectiveOne of the features of ulcerative colitis (UC) is a defect in the protective mucus layer. This has been attributed to a reduced number of goblet cells (GC). However, it is not known whether abnormal GC mucus secretion also contributes to the reduced mucus layer. Our aims were to test the hypothesis that GC secretion was abnormal in UC with the changes persistent in colonoids even in the absence of immune cells.DesignColonoids were established from intestinal stem cells of healthy subjects (HS) and from patients with UC (inactive and active sites). Colonoids were maintained as undifferentiated (UD) or induced to differentiate (DF) and studied as 3D or monolayers on Transwell filters. Total RNA was extracted for quantitative real-time PCR analysis. Carbachol and PGE2 mediated stimulation followed by examination of mucus layer by MUC2 IF/confocal microscopy and TEM were performed.ResultsColonoids derived from patients with UC can be propagated over many passages; however, they exhibit a reduced rate of growth and TEER compared with colonoids from HS. Differentiated UC colonoid monolayers form a thin and non-continuous mucus layer. UC colonoids have increased expression of secretory lineage markers: ATOH1 and SPDEF, including MUC2 positive GCs and ChgA positive enteroendocrine cells but failed to secrete mucin when exposed to the cholinergic agonist carbachol and PGE2, which caused increased secretion in HS. Exposure to TNF-α (5days), reduced the number of GC with a greater percentage decrease in UC colonoids compared to HS.ConclusionsAbnormal mucus layer in UC is due to long term changes in epithelial cells that lead to abnormal mucus secretion as well as effects of the inflammatory environment to reduce the number of GC. This continued defect in GC mucus secretion may be involved in UC recurrence.

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