Katsuhito Arai

Fecal calprotectin is a clinically relevant biomarker of mucosal healing in patients with quiescent ulcerative colitis.

Calprotectin is an abundant protein in neutrophils, which infiltrate the mucosa during inflammation. Fecal calprotectin (FC) level has shown correlation with disease activity in ulcerative colitis (UC) patients. Additionally, FC level is expected to indicate mucosal healing (MH). This study was to see the significance of FC for predicting MH in patients with quiescent UC.

Prokinetics Influence the Pharmacokinetics of Rabeprazole

Background: Proton pump inhibitors (PPIs) are unstable at a low PH. Accelerated transfer of PPIs to the upper small intestine may influence the pharmacokinetics of PPIs. Aim: To see if concomitant use of mosapride citrate with rabeprazole sodium influences the pharmacokinetics of the PPI. Methods: Two-way crossover pharmacokinetic studies were conducted in 9 healthy subjects. 20 mg of rabeprazole was given orally and plasma was obtained before and 1, 2, 3, 4, 5, 6 and 8 h after the dosing. Two weeks later, 5 mg of mosapride was given concomitantly with rabeprazole and plasma was collected as above. The plasma concentrations of rabeprazole were determined by high-performance liquid chromatography. The maximum plasma concentrations (Cmax) and the area under the time-plasma concentration curve (AUC) of rabeprazole, and the time to maximum plasma concentration (tmax) were compared in the presence or absence of mosapride. Results: Concomitant use of mosapride resulted in significant increases of mean Cmax and mean AUC with ratios of 1.57 and 1.47, respectively. The median tmax changed from 4 to 3 h, although the change was not significant. Conclusions: Mosapride significantly influenced pharmacokinetics of rabeprazole. Co-administration of mosapride could have some favorable effect in PPIs-based therapy.

A case of Degos disease: demonstration of C5b-9-mediated vascular injury

Abstract A 68-year-old Japanese male presented with atrophic erythematous white lesions with peripheral dark reddish rims on his back. Multiple ulcers were detected from his stomach to his large intestine using endoscopy. Although the patient was given high doses of a steroid, aspirin, dipyridamole, and intravenous immunoglobulin therapy, he died of gastrointestinal hemorrhage, perforation and septic shock. An autopsy examination revealed pauci-inflammatory thrombotic microangiopathy with endothelial cell injury, fibrous occlusive arteriopathy, and vascular C5b-9 deposition in the wall of the gastrointestinal tract from the esophagus to the large intestine as well as in the dermis of the skin.

Elevation of carcinoembryonic antigen coinciding with disease activity of ulcerative colitis.

We report on three cases of ulcerative colitis who presented with increased levels of serum carcinoembryonic antigen (CEA) during the active stage. All cases were pancolitis with a moderate to severe disease course. After remission induction with medical therapies, serum CEA levels decreased to the normal reference range. Immunohistochemical analyses demonstrated the existence of CEA not only along with the apical surface of the colonic epithelia but also at the cytosol of the inflamed epithelia where goblet cells were depleted during the active stage. We speculate that CEA was up-regulated by inflammatory response particularly in the process of epithelial regeneration.