Masumi Okuda

Helicobacter pylori infection in children with chronic idiopathic thrombocytopenic purpura.

Abstract Background : Recently a high prevalence of Helicobacter pylori infection has been reported in adult patients with chronic idiopathic thrombocytopenic purpura (cITP). Furthermore, after H. pylori eradication therapy in such patients, their platelet counts have been observed to increase, suggesting that H. pylori may be a causative agent of adult cITP. However, there have been only a few reports of children with cITP. The purpose of the present paper was to examine the association between H. pylori infection and cITP in Japanese children.

Serodiagnosis of Helicobacter pylori infection is not accurate for children aged below 10

Background : In order to investigate the immune response to Helicobacter pylori in childhood, we compared anti‐H. pylori IgG and IgA antibodies with H. pylori antigen in the stool and examined the clinical usefulness of the anti‐H. pylori IgG and IgA antibodies.

Breast-feeding prevents Helicobacter pylori infection in early childhood

gastric and duodenal ulcers and has been recognized as a class I carcinogen.1 Recent epidemiological evidences suggest that acquisition of H. pylori infection occur in infancy.2–4 Some studies indicate that lactoferrin,5 sialyllactose, oligosaccharides6 and secretary IgA antibody7 that occur naturally in human milk, prevent H. pylori infection in animal models. However, there is little evidence for breastfeeding preventing H. pylori infection.7 In order to study the effectiveness of breast-feeding for H. pylori infection in terms of epidemiology, we investigated the rate of H. pylori infection and the duration of breast-feeding periods in Japanese children.

Helicobacter pylori Colonization in the First 3 Years of Life in Japanese Children

Background:  Acquisition of Helicobacter pylori infection occurs in early childhood, but the exact time of the acquisition and dynamics of infection are not clear. The aim of this study was to estimate the time of acquisition of H. pylori colonization in infants.

Macrophage Activation Syndrome in Children with Systemic-Onset Juvenile Chronic Arthritis

Macrophage activation syndrome (MAS) is a life-threatening complication in children with rheumatic diseases, particularly systemic-onset juvenile chronic arthritis (SOJCA). Because of the potential fatality of this condition, prompt recognition and immediate therapeutic intervention are important. This study assessed the clinical features of nine MAS events in five children with SOJCA. Nonremitting fever and decreased platelet and white blood cell counts led to a diagnosis of MAS. The urinary β2-microglobulin (β2MG) level was a sensitive indicator of MAS. Serum levels of β2MG and soluble interleukin-2 receptor were also elevated. These biologic markers reflecting hyperactivated cellular immunity are useful indicators of MAS. Four children treated with cyclosporin A (CSP) achieved rapid and complete recovery, but one patient without CSP died due to rapidly progressive respiratory failure. All children treated with CSP responded quickly, and fever abated within 36 h of initiation of treatment. CSP should be added to first-line therapy of MAS.

Polymerase Chain Reaction–Restriction Fragment Length Polymorphism Analysis of Clarithromycin‐Resistant Helicobacter pylori Infection in Children Using Stool Sample

Background.  To analyze clarithromycin‐resistant Helicobacter pylori infection in children, we developed a method of polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP) analysis using stool samples.

A New Infant Case of Nakajo-Nishimura Syndrome with a Genetic Mutation in the Immunoproteasome Subunit: An Overlapping Entity with JMP and CANDLE Syndrome Related to PSMB8 Mutations

Nakajo-Nishimura syndrome (NNS) is a very rare hereditary autoinflammatory disorder that generally has its onset in infancy with pernio-like rashes and gradually develops into partial lipodystrophy. A distinct homozygous PSMB8 mutation encoding an immunoproteasome subunit has recently been identified as its genetic cause. Here, we report a new case of a patient with NNS who developed exudative erythemas on his face and extremities at 2 months of age, along with high fever, elevated serum hepatic aminotransferase levels and hepatosplenomegaly. Massive infiltration of inflammatory cells was observed histologically in the dermis and subcutis without apparent leukocytoclastic vasculitis. These symptoms improved with oral corticosteroids but recurred periodically, and a thin angular face with long clubbed fingers gradually developed. Identification of the PSMB8 mutation finalized the diagnosis of NNS at 5 years of age. Understanding a variety of clinicopathological features at the developmental stages is necessary to make an early diagnosis of NNS.

A Strain-Specific Antigen in Japanese Helicobacter pylori Recognized in Sera of Japanese Children

ABSTRACT An enzyme immuno assay (EIA) test based on Japanese strain-derived high-molecular-weight cell-associated proteins (JHM-CAP) was evaluated by comparing with a previously developed EIA test based on a U.S. strain-derived high-molecular-weight cell-associated proteins (HM-CAP). Serum samples of 131 Japanese asymptomatic children (mean age, 5.5 years; range, 0 to 21 years) were tested that include 43 positive and 88 negative children as judged by Helicobacter pylori stool antigen test (HpSA test). Both tests showed comparable and reliable specificities, but the sensitivity of JHM-CAP EIA, at 93.0%, was much higher than that of HM-CAP EIA, at 67.4%. More false-negative results of HM-CAP were obtained in children under 10 years of age. Immunoblot analysis revealed that the JHM-CAP but not the HM-CAP preparation had a 100-kDa antigen recognized by JHM-CAP positive sera. It was concluded that JHM-CAP EIA is highly accurate for the serodiagnosis of H. pylori infection in Japanese young children and that the high sensitivity of JHM-CAP EIA in contrast to HM-CAP EIA is due to the presence of a 100-kDa antigen in Japanese strains that may be recognized by the host immune system at an early stage of infection.

Helicobacter pylori infection in childhood

than half of gastric ulcers are not related to H. pylori infection. In younger children, peptic ulcers are usually caused by toxic agents such as corticosteroids and NSAIDs or after stress such as burns, head injury, and systemic illness. In older children and adolescents, however, the clinical presentation and natural history of peptic ulcers are similar to those observed in adults.10 In developed countries, the rate of H. pylori infection has fallen dramatically during recent decades.11 The low incidence of H. pylori infection in peptic ulcer diseases may reflect the low prevalence of H. pylori infection. In the United States, the attributable risk of H. pylori in peptic ulcers has gradually decreased. In Caucasians, in whom the infection rate is 20%–30%, only 52% of those with duodenal ulcer and 53% of those with gastric ulcer, respectively, had H. pylori infection.12 In Japan, however, about 97% of duodenal ulcers and 95% of gastric ulcers are positive for H. pylori infection,13,14 and thus the attributable risk of H. pylori infection in peptic ulcers is still high.15 A severe gastric inflammation in children with H. pylori infection is associated with antral nodularity and positive CagA serology, and the lack of both findings in children reflects low-grade or no gastritis.16 The high incidence of nodular gastritis in children reported by Kato et al.9 in this issue of Journal of Gastroenterology is possibly related to the high prevalence of CagApositive strains of H. pylori in Japan.17 Association of H. pylori infection with clinical symptoms such as abdominal pain, nausea/vomiting, hematemesis, tarry stool, and anemia has also been studied by Kato et al.,9 and only anemia was found to be significantly associated with H. pylori infection. A wide variety of dermatologic,18 neurologic,19 and hematologic manifestations20, 21 have recently been reported in adults, and some of the manifestations including iron deficiency anemia are diminished after eradication of H. pylori. Studies on elucidation of the mechanism of such Helicobacter pylori infection is one of the most common bacterial infections, and it is recognized as a major etiology for the development of gastritis or peptic ulcer disease in both adults and children. There is evidence that the acquisition of H. pylori occurs in early childhood, probably within the first 2 years of life.1 In school-age children, however, infection may be relatively stable and the risk of reinfection is low.2 In a prospective study of asymptomatic Turkish children aged 1–4 years living in Germany, it has been shown that H. pylori colonization was a temporary phenomenon in early life.3 The H. pylori infection often remains asymptomatic in children, with low grades of gastric inflammation4 or even normal histology of gastric mucosa.5,6 The nodules were described as giving the antrum a cobblestone appearance. Nodularity in the antral mucosa appears to be associated with H. pylori gastritis as well as duodenal ulcer,7 but detailed analysis has been difficult because the prevalence of peptic ulcer disease associated with H. pylori in children is generally low in developed countries in particular. In Canada, these conditions accounted for roughly 1 in 2500 pediatric hospital admissions.8 Kato et al. performed a multicenter study and analyzed a large number of children in Japan with gastritis and duodenal and gastric ulcers on the prevalence of H. pylori.9 The evaluation revealed that the prevalence of H. pylori infection was 98.5% in nodular gastritis, 83.0% in duodenal ulcer, and 44.2% in gastric ulcer. Thus, nodular gastritis is the most common feature of H. pylori infection, followed by duodenal ulcer, in Japanese children. Duodenal ulcer is much more common than gastric ulcers in H. pylori-infected children. In this study of Japanese children, the prevalence in gastric ulcers is less than 50% of duodenal ulcers, indicating that more

JAID/JSC Guidelines for Infection Treatment 2015−Intestinal infections

The Japanese Association for Infectious Disease/Japanese Society of Chemotherapy, The JAID/JSC Guide to Clinical Management of Infectious Disease/Guideline-preparing Committee, Intestinal Infections Working Group (WG), Kenji Ohnishi a, , Yusuke Ainoda a, b, , Akifumi Imamura c, , Sentaro Iwabuchi d, , Masumi Okuda e, , Takashi Nakano f, 2 a Tokyo Metropolitan Health and Medical Corporation Ebara Hospital, Tokyo, Japan b Department of Infectious Diseases, Tokyo Womens Medical University, Japan c Department of Infectious Diseases, Tokyo Metropolitan Komagome Hospital, Tokyo, Japan d Department of Infectious Diseases, Tokyo Metropolitan Bokutoh General Hospital, Tokyo, Japan e Department of Pediatrics, Sasayama Medical Center, Hyogo College of Medicine, Sasayama, Hyogo, Japan f Department of Pediatrics, Kawasaki Medical School, Okayama, Japan