Search

AIM To investigate factors associated with the healing of endoscopic submucosal dissection (ESD)-induced ulcers. METHODS We enrolled 132 patients with gastric tumors scheduled for ESD. Following ESD, patients were treated with daily lansoprazole 30 mg or vonoprazan 20 mg. Ulcer size was endoscopically measured on the day after ESD and at 4 and 8 wk. The gastric mucosa was endoscopically graded according to the Kyoto gastritis scoring system. We assessed the number of patients with and without a 90% reduction in ulcer area at 4 wk post-ESD and scar formation at 8 wk, and looked for risk factors for slower healing. RESULTS The mean size of gastric tumors and post-ESD ulcers was 17.4 ± 12.1 mm and 32.9 ± 13.0 mm. The mean reduction rates in ulcer area were 90.4% ± 0.8% at 4 wk and 99.8% ± 0.1% at 8 wk. The reduction rate was associated with the Kyoto grade of gastric atrophy at 4 wk (A0: 97.9% ± 0.6%, A1: 93.4% ± 4.1%, and A2: 89.7% ± 1.0%, respectively). In multivariate analysis, the factor predicting 90% reduction at 4 wk was gastric atrophy (Odds ratio: 5.678, 95%CI: 1.190-27.085, P = 0.029). CONCLUSION The healing speed of post-ESD ulcers was associated with the degree of gastric mucosal atrophy, and Helicobacter pylori eradication therapy is required to perform at younger age.

Cap polyposis is a rare intestinal disorder. Characteristic endoscopic findings are multiple inflammatory polypoid lesions covered by caps of fibrous purulent exudate. Although a specific treatment has not been established, some studies have suggested that eradication therapy for Helicobacter pylori (H. pylori) is effective. We report a case of a 20-year-old man with cap polyposis presenting with hematochezia. Colonoscopy showed the erythematous polyps with white caps from the sigmoid colon to rectum. Histopathological findings revealed elongated, tortuous, branched crypts lined by hyperplastic epithelium with a mild degree of fibromusculosis in the lamina propria. Although H. pylori eradication was instituted, there was no improvement over six months. We then performed en bloc excision of the polyps by endoscopic submucosal dissection (ESD), which resulted in complete resolution of symptoms. ESD may be a treatment option for cap polyposis refractory to conservative treatments. We review the literature concerning treatment for cap polyposis and clinical outcomes.

Objective The Kyoto gastritis classification categorizes the endoscopic characteristics of Helicobacter pylori (H. pylori) infection-associated gastritis and identifies patterns associated with a high risk of gastric cancer. We investigated its efficacy, comparing scores in patients with H. pylori-associated gastritis and with gastric cancer. Methods A total of 1,200 patients with H. pylori-positive gastritis alone (n=932), early-stage H. pylori-positive gastric cancer (n=189), and successfully treated H. pylori-negative cancer (n=79) were endoscopically graded according to the Kyoto gastritis classification for atrophy, intestinal metaplasia, fold hypertrophy, nodularity, and diffuse redness. Results The prevalence of O-II/O-III-type atrophy according to the Kimura-Takemoto classification in early-stage H. pylori-positive gastric cancer and successfully treated H. pylori-negative cancer groups was 45.1%, which was significantly higher than in subjects with gastritis alone (12.7%, p

Background Enterovirus D68 (EV-D68) is a re-emerging, high-morbidity pathogen that causes severe respiratory infection and acute flaccid myelitis in children. EV-D68 is phylogenetically divided into 4 major groups—clade A through D—and each clade has subclades defined by genetic variant. Outbreaks of all strains have been reported in more than 10 countries. However, no study has compared the viral genomic characteristics of EV-D68 in contemporaneous outbreaks in different countries. Methods An outbreak of EV-D68 in children younger than 15 years occurred in Niigata, Japan, from October through November 2018. The patients were admitted to hospital with respiratory distress and wheezing episodes. RNA extracted from nasopharyngeal samples was tested by EV-D68-specific PCR. Clade was determined by semi-nested PCR analysis of the VP1 region, and the phylogenetic tree of the VP1 sequence was constructed. To clarify viral genomic characteristics, we compared the clade to those of outbreaks occurring during 2014–2018 in other countries. Results EV-D68 testing of 47 patients yielded positive results for 22 (47%) (median age 4.6 years; IQR, 2.9–6.7), and 15 (69%) had a past medical history of allergic disease. No patient developed acute flaccid myelitis. The VP1 sequences from all isolates belonged to clade B3, the same clade detected during the 2015 outbreak in Japan (figure). Interestingly, EV-D68 outbreaks were reported in France and Italy (clades D1/B3 and D1, respectively) during this period. Although the EV-D68 clades responsible for outbreaks in 2014 differed by region, clade B3 is now the dominant clade and has caused concurrent EV-D68 outbreaks in children since 2015 (table). Conclusion In 2018, an EV-D68 clade B3 outbreak occurred among children in Niigata, Japan. This clade is now dominant and periodically circulates around the world. Because EV-D68 can cause simultaneous outbreaks worldwide and is associated with high morbidity, detailed real-time epidemiological surveillance of EV-D68 is warranted. Disclosures All authors: No reported disclosures.

Persons with untreated atrophic thyroiditis develop a permanent height deficit. Adequate thyroxine replacement therapy can improve growth and the probability of attaining normal adult height. However, height deficit is related to duration of thyroxine deficiency, regardless of the adequacy of thyroxine replacement therapy after diagnosis.1 Several studies reported that use of adjunctive therapy with growth hormone (GH) and gonadotropin-releasing hormone agonist (GnRHa) to improve the final height of patients.2-5 The rationale for this therapy is to prolong the growth period by inhibiting pubertal progression and delaying epiphyseal fusion,6 although GH deficiency in atrophic thyroiditis patients usually improves after L-thyroxine treatment. We report a case of autoimmune atrophic thyroiditis in a boy who presented with GH deficiency even after his enlarged pituitary gland had decreased in size. Combined treatment with GH, GnRHa, and L-thyroxine was successful in allowing the patient to attain normal adult height.

Background Antisense peptide nucleic acids (PNAs) are synthetic polymers that mimic DNA/RNA and inhibit bacterial gene expression in a sequence-specific manner. Methods To assess activity against non-typeable Haemophilus influenzae (NTHi), we designed six PNA-peptides that target acpP, encoding an acyl carrier protein. MICs and minimum biofilm eradication concentrations (MBECs) were determined. Resistant strains were selected by serial passages on media with a sub-MIC concentration of acpP-PNA. Results The MICs of six acpP-PNA-peptides were 2.9-11 mg/L (0.63-2.5 μmol/L) for 20 clinical isolates, indicating susceptibility of planktonic NTHi. By contrast, MBECs were up to 179 mg/L (40 μmol/L). Compared with one original PNA-peptide (acpP-PNA1-3'N), an optimized PNA-peptide (acpP-PNA14-5'L) differs in PNA sequence and has a 5' membrane-penetrating peptide with a linker between the PNA and peptide. The optimized PNA-peptide had an MBEC ranging from 11 to 23 mg/L (2.5-5 μmol/L), indicating susceptibility. A resistant strain that was selected by the original acpP-PNA1-3'N had an SNP that introduced a stop codon in NTHI0044, which is predicted to encode an ATP-binding protein of a conserved ABC transporter. Deletion of NTHI0044 caused resistance to the original acpP-PNA1-3'N, but showed no effect on susceptibility to the optimized acpP-PNA14-5'L. The WT strain remained susceptible to the optimized PNA-peptide after 30 serial passages on media containing the optimized PNA-peptide. Conclusions A PNA-peptide that targets acpP, has a 5' membrane-penetrating peptide and has a linker shows excellent activity against planktonic and biofilm NTHi and is associated with a low risk for induction of resistance.

Background Human parechovirus type 3 (HPeV3) and enteroviruses (EVs) are the major viral pathogens causing severe diseases in neonates and young infants. Although two infections typically occur in summer, and initial clinical presentations are similar, differences in clinical and laboratory characteristics of HPeV3- and EV- infections are not well described. Methods From January 2014 to December 2016, we prospectively obtained serum and/or cerebrospinal fluid (CSF) samples from febrile neonates and young infants < 4 months suspecting sepsis and meningoencephalitis in Niigata, Japan. RNA/DNA were extracted from the samples and viral etiologies including HPeV3, EVs, and/or herpes simplex virus were tested using the real-time PCR, followed by genetic sequencing and typing. The comparison was made between HPeV3- and EVs-infected patients based on their medical records and subsequent questionnaires using appropriate statistical analyses. Results In total, we obtained 212 serum and 170 CSF samples from 222 patients. HPeV3 and EVs were detected for 56 (25%) and 43 patients (19%) (Figure), and their median ages were 29 and 24 days (P = 0.58), respectively. HPeV3-infected patients presented with higher median body temperature (38.9 °C vs 38.5 °C, P < 0.001), heart rates (184/minute vs. 161/minute, P = 0.002), peripheral coldness (72% vs. 34%, P < 0.001), skin mottling (65% vs. 23%, P < 0.001), and grunting (22% vs. 5%, P = 0.014) than EVs-infected patients. Additionally, systemic inflammatory response syndrome (SIRS) was more frequently observed in HPeV3-infected patients than in EVs-infected patients (82% vs. 58%, P = 0.009). In the laboratory data, median white blood cell count was lower in HPeV3-infected patients than those in EVs-infected patients (5,200/µL vs. 8,900/µL, P < 0.001). The pleocytosis was observed 58% of EVs-infected patients, but none of the HPeV3-infected patients (P < 0.001); however, HPeV3 RNA was frequently detected than EVs in CSF (90% vs 66%, P = 0.012). Conclusion This study showed that HPeV3-infected neonates and young infants presented more severe clinical manifestations than those infected with EVs. Significant tachycardia, poor peripheral circulation, and fulfilling SIRS criteria at the presentation may be the clues considering HPeV3 infection rather than EVs infection. Disclosures All authors: No reported disclosures.

To the Editor: Varicella-zoster virus (VZV), a human herpesvirus, is the causative agent of varicella (chickenpox) and herpes zoster (shingles). Worldwide, children are routinely vaccinated with a live attenuated varicella vaccine containing the Oka vaccine (vOka) strain of VZV, originally developed in Japan (1–3). Although the risk for secondary transmission of the vOka strain from immunocompromised vaccinees to susceptible persons is relatively high, the risk for transmission from immunocompetent vaccinees is low (1). We report secondary transmission of the vOka strain from an immunocompetent girl with a history of varicella vaccination to her healthy susceptible brother. Herpes zoster developed in a healthy 3-year-old girl 2 years after she had received the varicella vaccine (lot VZ040; Biken, Osaka, Japan). She received oral acyclovir treatment and fully recovered by day 19 after herpes zoster onset. On the same day that the girl recovered, her immunocompetent 2-year-old brother was found to have fever and a rash consisting of 10–20 papulovesicles; mild varicella was diagnosed. The boy had no known history of contact with persons infected with varicella or with persons who administered the varicella vaccine. After receiving oral acyclovir treatment, the boy recovered without systemic complications. On day 19 after the girl’s onset of herpes zoster, an enzyme immunoassay (Denka Seiken, Tokyo, Japan) confirmed the presence of VZV-specific immunoglobulin (Ig) G (titer 48.9, well above the detection limit of 2.0) but not IgM. The boy showed seroconversion of VZV-specific IgG from a titer of