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5-Aminosalicylic acid aggravates colitis mimicking exacerbation of ulcerative colitis
( Jun Miyoshi ),( Katsuyoshi Matsuoka ),( Atsushi Yoshida ),( Makoto Naganuma ),( Tadakazu Hisamatsu ),( Tomoharu Yajima ),( Nagamu Inoue ),( Susumu Okamoto ),( Yasushi Iwao ),( Haruhiko Ogata ),( Fum 대한장연구학회 2018 Intestinal Research Vol.16 No.4
Ulcerative colitis (UC) is one of the major clinical phenotypes of inflammatory bowel diseases. Although 5-aminosalicylic acid (5-ASA) is widely used for UC and its efficacy and safety have been demonstrated, a few patients paradoxically develop a severe exacerbation of colitis by 5-ASA administration. It is crucial to know clinical features including endoscopic findings in this condition for making a correct diagnosis and a prompt decision to withdraw the medication. Here, we report case series with UC exacerbated by 5-ASA. Medical records of 8 UC patients experiencing an exacerbation of colitis after induction of 5-ASA that was improved by the withdrawal of 5-ASA but also re-aggravated by dose increase or re-administration of 5-ASA were reviewed. The patients were newly diagnosed with UC, started 5-ASA and developed an exacerbation in approximately 2 to 3 weeks. They did not appear to have systemic allergic reactions. Seven of the 8 patients had a high fever. Three of 5 patients who undertook total colonoscopy showed right-side-dominant colitis. These findings suggest clinical characteristics in this condition. Further assessment of clinical and endoscopic features in more cases is necessary for establishing diagnostic criteria and understanding underlying mechanisms in those cases where 5-ASA aggravates the colitis. (Intest Res 2018;16:635-640)
Jun Miyoshi,Hiromu Morikubo,Hiromi Yonezawa,Hideaki Mori,Tadakazu Hisamatsu 대한장연구학회 2023 Intestinal Research Vol.21 No.2
Intestinal ultrasound (IUS) is a promising modality for the management of inflammatory bowel disease (IBD) and has the potential to particularly contribute in monitoring disease activity, an advantage crucial for optimizing the therapeutic strategy. While many IBD physicians appreciate and are interested in the use of IUS for IBD, currently only a limited number of facilities can employ this examination in daily clinical practice. A lack of guidance is one of the major barriers to introducing this procedure. Standardized protocols and assessment criteria are needed such that IUS for IBD can be considered a feasible, reliable examination in clinical practice, and multicenter clinical studies can be conducted for further clinical evidence of the application of IUS in IBD for best patient care. In this article, we provide an overview of how to start IUS for IBD and introduce basic procedures. Furthermore, IUS images from our practice are provided as a color atlas for understanding sonographic findings and scoring systems. We anticipate this “first aid” article will be helpful to promote IUS for IBD in daily practice.
Lee, Ji-Seon,Park, Jeong-Rak,Kwon, Ok-Seon,Lee, Tae-Hee,Nakano, Ichiro,Miyoshi, Hiroyuki,Chun, Kwang-Hoon,Park, Myung-Jin,Lee, Hong Jun,Kim, Seung U.,Cha, Hyuk-Jin Oxford University Press 2015 Neuro-oncology Vol.17 No.1
<P><B>Background</B></P><P>Cancer stemness, observed in several types of glioma stem cells (GSCs), has been demonstrated to be an important barrier for efficient cancer therapy. We have previously reported that cancerous neural stem cells (F3.Ras.CNSCs), derived from immortalized human neural stem cells by a single oncogenic stimulation, form glial tumors in vivo.</P><P><B>Method</B></P><P>We searched for a commonly expressed stress modulator in both F3.Ras.CNSCs and GSCs and identified silent mating type information regulation 2, homolog (SIRT1) as a key factor in maintaining cancer stemness.</P><P><B>Result</B></P><P>We demonstrate that the expression of SIRT1, expressed in “cancer cells with neural stemness,” is critical not only for the maintenance of stem cells, but also for oncogenic transformation. Interestingly, SIRT1 is essential for the survival and tumorigenicity of F3.Ras.CNSCs and GSCs but not for the U87 glioma cell line.</P><P><B>Conclusion</B></P><P>These results indicate that expression of SIRT1 in cancer cells with neural stemness plays an important role in suppressing p53-dependent tumor surveillance, the abrogation of which may be responsible not only for inducing oncogenic transformation but also for retaining the neural cancer stemness of the cells, suggesting that SIRT1 may be a putative therapeutic target in GSCs.</P>