18 research outputs found

    Acute Onset Collagenous Colitis with Unique Endoscopic Findings

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    We experienced a rare case of 72-year-old woman with acute onset collagenous colitis (CC) induced by lansoprazole. The patient developed acute abdominal pain, watery diarrhea, and melena that are quite rare in usual CC. We could find the characteristic colonoscopic findings such as active long liner ulcers in the patient. We also observed the healing courses of these unique findings. Our case indicates two important points of view. (1) CC sometimes develops with acute onset symptoms which resemble those of ischemic colitis. (2) Colonoscopy would be useful and necessary to distinguish acute onset CC and ischemic colitis

    Collection of patient-generated health data with a mobile application and transfer to hospital information system via QR codes

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    Background and Objective: The collection of patient-generated health data (PGHD) is important for understanding a patient's daily status for efficient treatment. Mobile applications are effective for continuously collecting patient data, and it is desirable to promptly integrate such data into electronic medical records. However, most hospital information systems have limited connections with external mobile applications. Therefore, in this study, we developed a simple system that can collect data from patients with inflammatory bowel disease (IBD) and transfer the data to electronic medical records without a direct connection to a hospital information system. Methods: We developed patient-facing mobile applications and physician-facing user-defined form templates for the hospital information system. The PGHD were transferred via QR codes using a two-way linkage. The persistence rates were measured and analyzed to clarify the factors affecting the continuous usage of the application. Results: A mobile application connected to a hospital information system was implemented and used in on-site operations. Among patients with IBD using this application, 84.6%–91.7% continued to use it over six months and 72.2%–84.5% continued for over one year. Particularly, patients who used the application during the first two visits tended to be significantly frequent users. Conclusions: We developed a mobile application connected to a hospital information system using a QR code, which is a simple way to continuously collect data from patients and enables physicians to use the data efficiently for patient-centered medical care

    Validity of Diagnostic Algorithms for Inflammatory Bowel Disease in Japanese Hospital Claims Data

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    Inflammatory bowel disease (IBD) diagnoses are increasing in Japan. Some patients have symptoms that are difficult to control, and further research on IBD is needed. Claims databases, which have a large sample size, can be useful for IBD research. However, it is unclear whether the International Classification of Diseases, Tenth Revision (ICD-10) codes alone can correctly identify IBD. We aimed to develop algorithms to identify IBD in claims databases. We used claims data from the Department of Gastroenterology, Tohoku University Hospital from 1 January 2016 to 31 December 2020. We developed 11 algorithms by combining the ICD-10 code, prescription drug, and workup information. We had access to the database which contains all the information for Crohn’s disease and ulcerative colitis patients who visited our department, and we used it as the gold standard. We calculated sensitivity, specificity, positive predictive value (PPV), and negative predictive value for each algorithm. We enrolled 19,384 patients, and among them, 1012 IBD patients were identified in the gold standard database. Among 11 algorithms, Algorithm 4 (ICD-10 code and ≥1 prescription drugs) showed a strong performance (PPV, 94.8%; sensitivity, 75.6%). The combination of an ICD-10 code and prescription drugs may be useful for identifying IBD among claims data

    Allele-specific DNA methylation of disease susceptibility genes in Japanese patients with inflammatory bowel disease.

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    BACKGROUND:Inflammatory bowel disease (IBD) has an unknown etiology; however, accumulating evidence suggests that IBD is a multifactorial disease influenced by a combination of genetic and environmental factors. The influence of genetic variants on DNA methylation in cis and cis effects on expression have been demonstrated. We hypothesized that IBD susceptibility single-nucleotide polymorphisms (SNPs) regulate susceptibility gene expressions in cis by regulating DNA methylation around SNPs. For this, we determined cis-regulated allele-specific DNA methylation (ASM) around IBD susceptibility genes in CD4+ effector/memory T cells (Tem) in lamina propria mononuclear cells (LPMCs) in patients with IBD and examined the association between the ASM SNP genotype and neighboring susceptibility gene expressions. METHODS:CD4+ effector/memory T cells (Tem) were isolated from LPMCs in 15 Japanese IBD patients (ten Crohn's disease [CD] and five ulcerative colitis [UC] patients). ASM analysis was performed by methylation-sensitive SNP array analysis. We defined ASM as a changing average relative allele score ([Formula: see text]) >0.1 after digestion by methylation-sensitive restriction enzymes. Among SNPs showing [Formula: see text] >0.1, we extracted the probes located on tag-SNPs of 200 IBD susceptibility loci and around IBD susceptibility genes as candidate ASM SNPs. To validate ASM, bisulfite-pyrosequencing was performed. Transcriptome analysis was examined in 11 IBD patients (seven CD and four UC patients). The relation between rs36221701 genotype and neighboring gene expressions were analyzed. RESULTS:We extracted six candidate ASM SNPs around IBD susceptibility genes. The top of [Formula: see text] (0.23) was rs1130368 located on HLA-DQB1. ASM around rs36221701 ([Formula: see text] = 0.14) located near SMAD3 was validated using bisulfite pyrosequencing. The SMAD3 expression was significantly associated with the rs36221701 genotype (p = 0.016). CONCLUSIONS:We confirmed the existence of cis-regulated ASM around IBD susceptibility genes and the association between ASM SNP (rs36221701) genotype and SMAD3 expression, a susceptibility gene for IBD. These results give us supporting evidence that DNA methylation mediates genetic effects on disease susceptibility

    Allele-specific bisulfite pyrosequencing.

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    <p>To analyze the allele-specific DNA methylation, we individually measured the DNA methylation of each allele and compared methylation between the two alleles. Thus, the allele-specific polymerase chain reaction (PCR) was performed and the methylation levels of each of the two alleles, given allele-specific amplicons, were measured separately using pyrosequencing. The allele-specific PCR primers were designed such that each primer of 3′ end was a pair of base of heterozygous SNP. (a) The reference sequence of rs36221701 before and after bisulfite conversion. Rs36221701 contained two CpG sites denoted as CpG1 and CpG2 in 5′ to 3′ direction. By bisulfite conversion, unmethylated C is converted to U (U is converted to T by PCR). Rs362210701 (C/T) is converted to (T/T); it was impossible to distinguish the converted T and original T. Thus, we were unable to detect the origin of the allele for this SNP by PCR primers. (b) Allele-specific PCR. We designed PCR primer for rs13239907 (A/G), which is located 297 bp downstream of rs36221701 and was in complete linkage disequilibrium with rs36221701 (A→C, G→T: r<sup>2</sup> = 1.0) in JPT data from 1,000 genome project. The forward primer was common to both alleles; reverse primers were designed such that each primer of 3′ end was a pair of bases of genotypes (A or G: complementary strand). (c) Allele-specific pyrosequencing. The two given allele-specific amplicons were separately analyzed using pyrosequencing. Sequence primer 1 targeted rs13239907 and was used to check the accuracy of allele-specific PCR, whereas sequence primer 2 targeted CpG1 and CpG2 was used to analyze the ratio of methylation around rs36221701. (d) Primer details. The 3′ end of PCR primer R was a pair of base of heterozygous SNP. 5′ end of PCR primer R was biotinylated.</p
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