Correction to: Short-Term Symptomatic Relief in Gastroesophageal Reflux Disease: A Comparative Study of Esomeprazole and Vonoprazan.

The original version of the article unfortunately contained percentage errors in second and third paragraphs of GerdQ Score section. Below is the corrected version.

Short-Term Symptomatic Relief in Gastroesophageal Reflux Disease: A Comparative Study of Esomeprazole and Vonoprazan.

BACKGROUND AND AIM: Proton pump inhibitors and vonoprazan (a potassium-competitive acid blocker) are recommended as first-line treatments for gastroesophageal reflux disease (GERD). However, few reports have investigated the onset of action of these agents for GERD symptom relief. The present study compared the symptom relief of esomeprazole with that of vonoprazan via monitoring self-reported GERD symptoms after treatment initiation. METHODS: This was a prospective, multicenter, randomized, open-label, parallel group, comparative clinical study between esomeprazole (20 mg/day) and vonoprazan (20 mg/day) administered for 4 weeks to patients with GERD symptoms. Patients who had scores ≥ 8 on the Gastroesophageal Reflux Disease Questionnaire (GerdQ) were defined as having GERD and enrolled in this study. Sixty patients were randomly assigned to either the esomeprazole group (n = 30) or the vonoprazan group (n = 30). Treatment response rates in each drug group were evaluated according to the GerdQ. The Frequency Scale for the Symptoms of GERD (FSSG) scores from the 1st day after treatment initiation and the Global Overall Symptom (GOS) scale scores during treatment were also evaluated. RESULTS: At 4 weeks, the treatment response rates for symptom relief according to the GerdQ were 88.0% in the esomeprazole group and 81.8% in the vonoprazan group. The GOS scales, which reflect the impact of GERD symptoms, were similar for both groups. The FSSG scores decreased from the 1st to the 14th day in both groups. CONCLUSIONS: There were no substantial differences in the symptom relief between the two groups at any time point in this short-term study.

Proportion of flat- and depressed-type and laterally spreading tumor among advanced colorectal neoplasia.

BACKGROUND & AIMS: Flat- and depressed-type neoplasias along with laterally spreading tumors (LSTs) have been reported in colorectal neoplasias. We estimated the prevalence of flat and depressed types and LSTs along with their proportion among advanced neoplasias in a large average-risk population undergoing screening colonoscopy. METHODS: This was a cross-sectional study performed at a single, general community institution, with subjects who were 40 to 79 years old, asymptomatic, and who had undergone their first colonoscopy for screening between 2003 and 2009 (n = 4910). Among the neoplasias detected, advanced neoplasias were morphologically classified as the polypoid type, flat and depressed type, or LST. We determined the prevalence and proportion for each type among the advanced neoplasias, with morphologies defined according to the Japanese endoscopic classification. RESULTS: Advanced neoplasias were detected in 7.9% of men, 4.7% of women, and 6.1% of overall subjects. The polypoid type, the flat and depressed types, and the LSTs accounted for 75.3%, 7.5%, and 17.2% of advanced neoplasia, respectively. There was a high proportion of T1 cancers among the depressed types (40%). Approximately 80% of LSTs were located on the right side of the colon and more than 30% of LSTs showed high-grade dysplasia or T1 cancer. CONCLUSIONS: Most advanced neoplasias detected were of the polypoid type. LSTs accounted for a considerable proportion among advanced neoplasia and tended to be located on the right side of the colon. The influences of any LSTs need to be taken into consideration for preventing colorectal cancer.

Lack of sphingosine 1-phosphate-degrading enzymes in erythrocytes.

Platelets are known to store a large amount of the bioactive lipid molecule sphingosine 1-phosphate (S1P) and to release it into the plasma in a stimuli-dependent manner. Erythrocytes can also release S1P, independently from any stimuli. We measured the S1P and sphingosine (Sph) levels in erythrocytes by HPLC and found that the contribution of erythrocyte S1P to whole blood S1P levels is actually higher than that of platelets. In vitro assays demonstrated that erythrocytes possess much weaker Sph kinase activity compared to platelets but lack the S1P-degrading activities of either S1P lyase or S1P phosphohydrolase. This combination may enable erythrocytes to maintain a high S1P content relative to Sph. The absence of both S1P-degrading enzymes has not been reported for other cell types. Thus, erythrocytes may be specialized cells for storing and supplying plasma S1P.

Isolation of RNA aptamers against human Toll-like receptor 3 ectodomain.

Toll-like receptor 3 (TLR3) detects double-stranded RNA (dsRNA) known as a universal viral molecular pattern and activates the antiviral immune response. While TLR3 preferentially recognizes polyriboinosine-polyribocytidylic acid (poly (I:C)), a sequence-specific dsRNA has not yet been shown to activate TLR3. To determine whether TLR3 preferentially recognizes some specific sequence that acts on the signaling pathway of TLR3, in vitro selection against human TLR3 ectodomain (TLR3 ECD) was performed. After seventh selection cycle, two major classes, Family-I and -II, were emerged from 64 clones with binding constants of about 3 nM. Although these aptamers bound to TLR3 ECD with high affinity in vitro, they did not have agonist and antagonist effects on TLR3 signaling in TLR3-transfected HEK293 cells. Further analyses of the structure/function relationship of these aptamers will be carried out by mutagenesis, RNase mapping and competition assay using poly (I:C).

Pharmacokinetic changes of irinotecan by intestinal alkalinization in an advanced colorectal cancer patient.

The prevention of irinotecan (CPT-11)-induced diarrhea, a well-known adverse reaction to the drug, by treatment with intestinal alkalinization has been carried out in patients with colorectal cancer in Japan. Under acidic conditions, CPT-11 and its active metabolite, SN-38, exists preferably as the lactone form, whereas both exist as the carboxylate form under basic conditions. It has been suggested that the lactone forms of both CPT-11 and SN-38 are diffused passively across the intestinal mucosal membranes, whereas the carboxylate forms are actively transported. The intestinal uptake rate of both forms appears to be pH sensitive under physiological conditions, but it remains unclear whether intestinal alkalinization treatment affects the pharmacokinetics of CPT-11 and SN-38. This study was designed to evaluate the pharmacokinetics of CPT-11 and SN-38 in a colorectal cancer patient with or without alkalinization treatment. We found that intestinal alkalinization significantly decreased the plasma levels of CPT-11 and SN-38. In particular, the AUC of SN-38 was markedly decreased to 56 from 107 ng.h/mL. Intestinal alkalinization was effective in preventing CPT-11-induced diarrhea, but this treatment changed the pharmacokinetics of CPT-11 and SN-38 in the body.