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Eosinophilic infiltration is sometimes observed histologically in ulcerative colitis (UC), but the effect of the degree of infiltration on the treatment course for UC is not completely studied. We investigated whether short-term steroid administration in UC patients refractory to maintenance therapy, with high eosinophilic infiltration in the colonic mucosa, contributed to clinical and endoscopic improvement. Ten patients with endoscopically active and pathologically high eosinophilic infiltration, based on pathological examination using endoscopic biopsy, were examined for clinical background when starting steroid treatment; clinical and endoscopic improvement before and after steroid use were assessed prospectively. The average initial steroid dosage and duration of use were 21.0 mg and 102.7 days, respectively. The mean values before and after steroid use of clinical activity index, Mayo endoscopic subscore, and UC endoscopic index of severity were 2.4 and 1.0, 1.8 and 0.7, and 3.9 and 1.1, respectively. All these scores improved significantly after steroid use (P=0.04, P

In 2012, Japan approved the use of a tag-less patency capsule (PC), which evaluates gastrointestinal patency before small-bowel capsule endoscopy (SBCE). This study aimed to evaluate the validity of our modification on the passage criteria for this PC in clinical practice. We retrospectively enrolled 326 consecutive patients who underwent PC examination before SBCE. If X-ray could not reveal the PC in the body during the judgement time (30–33 h after ingestion), we defined it as ‘estimated patency’ and performed SBCE. We employed plain computed tomography (CT) for the second judgement, as needed. The overall patency rate was 95.1%. By X-ray, 41 (12.6%) patients were judged to have ‘estimated patency’, and SBCE could be safely performed. Plain CT judgement was necessary in 32.5%. One PC case had a residual coating film associated with stenosis in a patient with Crohn’s disease (CD), and one (0.3%) SBCE case had capsule retention resulting from false CT judgement. Multivariate analysis revealed that established CD and inpatient were factors related to patency loss. In conclusion, PC is useful for examining gastrointestinal patency, keeping in mind CT misjudgement. If PC was not found in the body via X-ray, performing SBCE as ‘estimated patency’ seemed appropriate.

Cytomegalovirus (CMV) reactivation in the colon is common in patients with severe ulcerative colitis (UC). Ganciclovir (GCV) resistance conferring CMV UL97 gene mutations have been reported in recent years. However, the prevalence of UL97 gene mutations in GCV-naive CMV infection in the colon remains unknown. We investigated the prevalence of CMV UL97 gene mutations in patients with colonic CMV infection associated with or without UC. Twenty-two GCV-naive patients with colonic CMV infection, 15 with UC and 7 with other diseases, were enrolled. Frozen biopsy samples or formalin-fixed paraffin-embedded samples were used for nested polymerase chain reaction (PCR) amplification of the UL97 gene. Sanger DNA sequencing was performed. UL97 mutations were frequently detected in codons T75A (95.5%), Q126L (86.4%), and D605E (86.4%), and less frequently (

Background: Cytomegalovirus (CMV) reactivation in the colon is common in patients with severe ulcerative colitis (UC) and in immunocompromised patients, and may be associated with poor prognosis. Ganciclovir (GCV) resistance conferring CMV UL97 gene mutations have been reported in recent years. However, the prevalence of UL97 gene mutations in GCV-naive CMV colitis remains to date unknown. The present study aimed to investigate the prevalence of CMV UL97 gene mutations in Japanese patients with colonic CMV infection associated with or without UC.Methods: Twenty-two GCV-naive patients with colonic CMV infection, 15 with UC and 7 with other diseases, were enrolled. Frozen biopsy samples or formalin-fixed paraffin-embedded samples were used for nested polymerase chain reaction (PCR) amplification of the UL97 gene. Sanger DNA sequencing of the PCR products was performed.Results: UL97 mutations were frequently detected in codons T75A (95.5%), Q126L (86.4%), and D605E (86.4%), and less frequently (Conclusions: We did not detect UL97 gene mutations associated with GCV resistance in GCV-naive patients with or without UC. In contrast, T75A, Q126L, and D605E mutations may be used as genetic markers for CMV in East Asian countries.

Background: Adalimumab (ADA) trough level and anti-ADA antibody (AAA) positivity could influence mucosal healing and loss of response in patients with inflammatory bowel disease (IBD). This study aimed to clarify the correlation between ADA monitoring, including non-trough level and real-world IBD clinical outcomes.Methods: This retrospective, observational, single-center study included 19 patients with ulcerative colitis (UC) and 33 patients with Crohn’s disease (CD) treated with ADA from January 2007 to August 2018. Serum ADA and AAA levels were measured 4‒14 days after ADA administration.Results: The AAA positivity rate was 23.1% (12/52). The ADA continuity was higher in the AAA-negative group than in the AAA-positive group (P = 0.223). Receiver operating characteristic (ROC) analysis revealed that a serum AAA cut-off value of 9.2 µg/mL was associated with ADA continuity (area under the curve [AUC]: 0.767, 95% confidence interval [CI]: 0.636–0.899). The ADA level was significantly higher in the endoscopic remission group than in the non-remission group (12.4 vs. 6.4 µg/mL, P = 0.02). Based on the ROC curve analysis results of serum ADA level and endoscopic remission, the cut-off value of serum ADA level was set to 11.1 µg/mL (AUC: 0.716, 95% CI: 0.533–0.900).Conclusions: Regardless of infliximab administration history, under combined use of ADA with immunomodulators and AAA positivity, ADA continuity was significantly higher when the serum AAA level 4–14 days after ADA administration was ≥9.2 µg/mL. Furthermore, endoscopic remission can be expected with a serum ADA level of ≥11.1 µg/mL.

Background Serum pepsinogen (PG) levels correlate with the degree of gastric mucosal inflammation and atrophy, which correlate with gastric cancer risk, in patients infected with Helicobacter pylori (H. pylori). Serum PG levels change after eradication of H. pylori, but it is not known if there are corresponding changes in the gastric mucosa. We examined whether the degree of gastric atrophy correlated with PG levels measured after eradication of H. pylori. Methods We retrospectively examined the relationship between gastric atrophy and serum levels of PG I, PG II and PG I/II ratios measured after eradication of H. pylori. The degree of gastric mucosal atrophy before H. pylori eradication was scored (0, 1, 2) according to the Kyoto classification of gastritis. Results A total of 430 treated patients were enrolled. Serum levels of PG I (ρ = − 0.362 and P H. pylori eradication can be used to estimate the degree of gastric mucosal atrophy and are useful for selecting individuals with a high risk of gastric cancer after H. pylori eradication.