Yon Ho Choe

Randomized Placebo‐Controlled Trial of Helicobacter pylori Eradication for Iron‐Deficiency Anemia in Preadolescent Children and Adolescents

Background. A few cases relating H. pylori infection to iron‐deficiency anemia have been described recently. We investigated the role of H. pylori infection in iron‐deficiency anemia in preadolescent children and adolescents.

Helicobacter pylori infection with iron deficiency anaemia and subnormal growth at puberty

The purpose of this study was to determine whetherHelicobacter pylori infection can contribute to growth deficit, especially in pubescent children who need large amounts of iron for growth. A structured questionnaire was sent to the parents of 532 healthy children aged 10 to 15 years (mean 12.9) to obtain demographic information on the parents and the environment. Of the 532 questionnaires sent out, 375 (70.5%; 170 girls and 205 boys) were returned. After collecting blood samples from participants, haemoglobin, serum iron, total iron binding capacity, serum ferritin, and serum IgG antibodies to H pylori were measured. The effects of risk factors such as H pylori infection, iron deficiency anaemia, sex, socioeconomic status, type of house, and crowding index on growth were analysed using multiple regression analysis. Of 63 H pyloripositive children, 18 (28.6%) were below the 25th centile values for height, compared with 63 of 312 (20.2%) H pylori negative children. The prevalence rate ofH pylori infection was 15.5% (53 of 343) in children without iron deficiency anaemia and 31.3% (10 of 32) in those affected. The relative risk of short stature was 2.2 (95% confidence interval (CI), 1.0 to 4.8) for iron deficiency anaemia, and 1.4 (95% CI, 0.8 to 2.4) for H pylori infection. The mean height was significantly lower in the group having bothH pylori infection and iron deficiency anaemia. Therefore, H pylori infection accompanied by iron deficiency anaemia, rather thanH pylori infection per se, might delay pubertal growth.

Effect of Helicobacter pylori eradication on sideropenic refractory anaemia in adolescent girls with Helicobacter pylori infection

We investigated the effect of Helicobacter pylori eradication on sideropenic refractory anaemia in adolescent girls with H. pylori‐associated antral gastritis without evidence of haemorrhage or clinical symptoms other than sideropenic anaemia. We conducted an open therapeutic trial in 21 adolescent girls aged 15–17 y with sideropenic refractory anaemia, which was defined as iron‐deficiency anaemia refractory to oral iron therapy for 3 mo. All subjects underwent gastroduodenal endoscopy. Thirteen patients with confirmed H. pylori infection were given a 2‐wk course of triple therapy and 6 wk of oral ferrous sulfate. We compared the mean levels of haemoglobin and serum ferritin among the “initial sample” (the time when the sampling was done before treatment with oral iron),“before eradication” (the time prior to triple therapy for eradication after subjects had been given oral iron for 3 mo) and “after eradication” (the time when the follow‐up endoscopy was performed) data in 11 subjects in whom H. pylori infection was eradicated. Haemoglobin levels (g/dl) were 8.6 ±1.9, 8.6 ±1.4 and 11.3 ±2.3, respectively. Serum ferritin levels (p.g/l) were 4.6 ± 2.4, 4.2 ± 2.3 and 17.5 ± 6.7, respectively. After eradication of H. pylori, mean levels of haemoglobin (p = 0.0002) and serum ferritin (p = 0.0002) showed a prominent increase between “before eradication” and “after eradication”. In conclusion, adolescent girls with sideropenic refractory anaemia should be evaluated for H. pylori infection. If H. pylori infection is coexistent, its eradication along with iron supplementation could correct the anaemia.

Hepatocyte transplantation for glycogen storage disease type Ib.

Glycogen storage disease type I (GSD-I) is a group of autosomal recessive disorders with an incidence of 1 in 100,000. The two major subtypes are GSD-Ia, caused by a deficiency of glucose-6-phosphatase (G6Pase), and GSD-Ib, caused by a deficiency of glucose-6-phosphate transporter (G6PT). We report that a substantial improvement was achieved following several infusions of hepatocytes in a patient with GSD-Ib. Hepatocytes were isolated from the unused cadaveric whole livers of two donors. At the first transplantation, approximately 2 × 109 cells (2% of the estimated recipients total hepatocytes) were infused. Seven days later 1 × 109 (1% of liver mass) cryopreserved hepatocytes from the same donor were infused, and an additional 3 × 109 (3% of liver mass) cells from the second donor were infused 1 month after the second transplantation. After the hepatocyte transplantation, the patient showed no hypoglycemic symptoms despite the discontinuation of cornstarch meals. Liver biopsies on posttransplantation days 20 and 250 showed a normal level of glucose-6-phosphatase activity in presolubilization assay that was very low before transplantation. This was the first and successful clinical hepatocyte transplantation in Korea. In this study, hepatocyte transplantation allowed a normal diet in a patient with GSD-Ib, with substantial improvement in their quality of life. Hepatocyte transplantation might be an alternative to liver transplantation and dietary therapy in GSD-Ib.

Lactoferrin sequestration and its contribution to iron‐deficiency anemia in Helicobacter pylori‐infected gastric mucosa

Background and Aim:  It is known that lactoferrin serves as a source of iron for Helicobacter pylori in gastric mucosa. The present study was undertaken to investigate the relationship between lactoferrin and H. pylori infection coexistent with iron‐deficiency anemia by determining the lactoferrin levels in gastric biopsy specimens, and by locating the major sites of lactoferrin expression, according to the presence or absence of iron‐deficiency anemia.

A Possible Relation of the Helicobacter pylori pfr Gene to Iron Deficiency Anemia

H. pylori infection is thought to contribute to iron‐deficiency anemia, especially during puberty. The ferritin protein Pfr of H. pylori is homologous to eukaryotic and prokaryotic ferritins. The purpose of this study was to analyze the H. pylori pfr status in gastric biopsy specimens according to clinical data, including antral gastritis with or without iron‐deficiency anemia.

Infliximab therapy in children with Crohn’s disease: a one‐year evaluation of efficacy comparing ‘top‐down’ and ‘step‐up’ strategies

Background:  The aim of this study was to evaluate the efficacy of ‘top‐down’ regimens for the treatment of paediatric Crohn’s disease (CD) and to compare it with the effects of ‘step‐up’ treatment.

The development of eosinophilic colitis after liver transplantation in children

Abstract:  Tacrolimus‐based immunosuppression in pediatric liver transplant recipients is known to be associated with EGID. Our goal was to determine the incidence, risk factors, and characteristics of EGID in our pediatric liver transplantation program. This study was a retrospective analysis of 38 pediatric liver transplant recipients. Rectal mucosal biopsy was performed to evaluate for gastrointestinal PTLD and eosinophilic colitis. There were 14 patients (37%) who were diagnosed with eosinophilic colitis. The mean age at transplantation was 10.8 ± 1.8 months. Those with eosinophilic colitis had a higher incidence of peripheral eosinophilia (p = 0.003) during the first two months following transplantation and had a higher EBV infection rate. Symptoms, such as diarrhea, hematochezia, and abdominal pain, became apparent after an average of three months; diagnoses were made at 6.9 ± 2.0 months after transplantation. There were eight patients (57%) with elevated food‐specific IgE levels. With food restriction treatment, the symptoms of patients improved. EGID should be considered when clinical symptoms are present, because symptoms of this disorder are similar to those of gastrointestinal PTLD. It should also be considered when peripheral eosinophila is detected or when EBV seroconversion develops during the first two months following transplantation.

Polymorphism of the Helicobacter pylori feoB Gene in Korea: a Possible Relation with Iron‐Deficiency Anemia?

Background.  Helicobacter pylori is a causative agent of gastritis, and H. pylori infection is thought to be correlated with iron‐deficiency anemia (IDA) at puberty. The H. pylori feoB gene product, a high‐affinity ferrous iron transporter, plays a central role in iron acquisition and virulence. This study was undertaken to analyze H. pylori feoB status according to clinical data, including antral gastritis with or without IDA.

The Expression of Iron‐repressible Outer Membrane Proteins in Helicobacter pylori and Its Association with Iron Deficiency Anemia

Background: Helicobacter pylori infection is known to be a cause of iron deficiency anemia (IDA) that is unresponsive to iron supplements. H. pylori bind iron to a specific receptor by iron‐repressible outer membrane proteins (IROMPs) under conditions of restricted iron.