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Inflammatory bowel disease (IBD) is a chronic lifelong condition and is related to poor quality of life (QoL). The aim of this study was to evaluate the QoL of Asian pediatric patients with IBD and to determine the clinical factors that can influence QoL. Children and adolescents aged 9 to 18 years diagnosed with IBD were enrolled from 7 hospitals. The patients completed the IMPACT-III questionnaire, and clinical data were collected. The results of the questionnaire and the correlation with clinical data were analyzed. A total of 208 patients (Crohn disease: n = 166; ulcerative colitis: n = 42) were enrolled. There was no definite QoL difference according to the Paris classification. Female sex (-5.92 ± 2.97, P= 0.0347) and active disease status (-10.79 ± 3.11, P= 0.0006) were significantly associated with poor QoL. Extreme body weight zscore and older age at diagnosis were also associated with worse QoL. Various clinical factors may affect the QoL in patients with IBD, but determining the overall QoL of patients using only these clinical factors is difficult. Therefore, regular direct measurements of QoL are necessary to better understand patients with IBD.

The aim of the study was to compare the virologic response to adefovir (ADV) add-on therapy with switching to entecavir (ETV) monotherapy in children and adolescents with chronic hepatitis B (CHB) who have developed lamivudine (LAM) resistance during LAM treatment.

The aim of the study was to compare the virologic response to adefovir (ADV) add-on therapy with switching to entecavir (ETV) monotherapy in children and adolescents with chronic hepatitis B (CHB) who have developed lamivudine (LAM) resistance during LAM treatment. Twenty-seven consecutive patients with CHB who had developed LAM resistance during LAM treatment were included. Of these 27 patients, 8 patients were treated with the addition of ADV to ongoing LAM and 8 patients were treated by switching to ETV monotherapy and each of these 16 patients were compared with the 11 patients who were treated by switching to ADV alone, as a historical control. Therapeutic responses to treatment were evaluated at 12, 24, 36, and 48 weeks from the initiation of therapy by measuring the decrement of hepatitis B virus (HBV)-DNA titers. The therapeutic period for HBV-DNA titer decrement (>2 log10IU/mL) was significantly shorter in both the LAM+ADV group and the ETV group than in the ADV group (P=0.008); however, there was no significant difference between the LAM+ADV group and the ETV group. The rate of virologic response, defined as decrement in HBV-DNA titer to undetectable levels at 24 weeks, was significantly higher in both the LAM+ADV group and the ETV group than in the ADV group (P=0.029). Both the LAM+ADV combination therapy and ETV monotherapy exhibited significantly more effective virologic responses compared to the ADV monotherapy in children and adolescents with LAM-resistant CHB, although there was no significant difference between the LAM+ADV group and the ETV group.

To assess and compare the long-term therapeutic response to lamivudine compared with interferon-α (IFN-α) in children with chronic hepatitis B.

To assess and compare the long‐term therapeutic response to lamivudine compared with interferon‐α (IFN‐α) in children with chronic hepatitis B. A total of 40 children (27 male; age, 1.3–18 y, mean, 7.7 y) with chronic hepatitis B who received lamivudine for at least 12 months were followed for a mean period of 39 (24–76) months. Their treatment efficacy was historically compared with that of 19 children (14 male; age, 2.1–17 y; mean, 10 y) who had been treated with IFN‐α and were followed for a mean period of 39 (24–104) months. Therapeutic responses were compared at 2 y after the initiation of either of the treatment methods. Two years after the initiation of treatment, the results for children treated with lamivudine versus IFN‐α were as follows: hepatitis B e antigen (HBeAg) seroconversion occurred in 26 (65%) of the 40 children versus 7 (37%) of the 19 children, P< 0.05. In the lamivudine‐treated group, the results for children treated before the age of 7 versus age >7 were as follows: HBeAg seroconversion occurred in 17 (89%) of the 19 children versus 9 (43%) of the 21 children, P< 0.01, and loss of hepatitis B surface antigen (HBsAg) occurred in 8 (42%) versus 0%, P< 0.001. Long‐term treatment of lamivudine led to significant improvement in the seroconversion rate of HBeAg in children with chronic hepatitis B compared with IFN‐α therapy. Furthermore, in preschool‐age children, it led to significant improvement in the seroconversion rate of HBeAg and HBsAg compared with school‐age children.

Aims:Minimal change disease (MCD) is the most common primary nephrotic syndrome in children. Some suggested that interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) are involved in the pathogenesis of MCD. This study was done to see changes of plasma and urinary IL-8, TNF-α, and their effects on determination of permeability of glomerular basement membrane (BM) contributed by heparan sulfate proteoglycan (HSPG). Methods:Study patients consisted of 19 biopsy-proven MCD children aged 2–15 years old. Both plasma, urinary IL-8 and TNF-α were measured. Employing the Millicell system, IL-8 and TNF-α were screened for the permeability factors. We examined whether IL-8 and TNF-α regulated BM HSPG gene expression and HS synthesis in the glomerular epithelial cells (GECs). Results:Urinary IL-8 during relapse was significantly increased when compared with that of during remission or controls (13,996 ± 2,811 vs. 2,941 ± 373, 5,331 ± 640 ng/mg·cr) (p < 0.05). Urinary TNF-α during relapse was also significantly increased (364.4 ± 51.2 vs. 155.3 ± 20.8, 36.0 ± 4.5 ng/mg·cr) (p < 0.05). Plasma IL-8 during relapse was significantly increased compared to that during remission(1.19 ± 0.62 vs. 0.51 ± 0.42 ng/ml) (p < 0.05). However, the negative results were obtained in the permeability assay using the Millicell system. No difference was seen in BM HSPG gene expression and HS synthesis in the GECs. Conclusion:Therefore, it seems that both IL-8 and TNF-α may not play a disease-specific role in the pathogenesis of MCD.

Recombinant FVIIa (Novoseven®) was initially developed for the treatment of bleeding in patient with congenital hemophilia with antibodies against factors VIII and IX and FVII deficiency. The mechanism of action is to induce hemostasis at the site of injury both by forming complexes with exposed tissue factor and by directly activating factor X upon the surface of an activated platelet. More recently it has begun to use gradually in the management of bleeding patient without congenital coagulation defect. We report the successful use of recombinant factor VIIa in a pediatric patient who has intractable gastrointestinal bleeding despite of conventional medical therapy. Case: The patient is a 13-year-old female and her body weight is only 10 kg, with a prior history of cerebral palsy and epilepsy. Recently she presented a recurrent massive hematemesis and melena probably due to stress ulcer for 8 days. She had no personal or family history of a suggestive bleeding disorder. The patient had a normal platelet count and coagulation screening test. Her hospital course was complicated by recurrent gastrointestinal hemorrhage but an endoscopic intervention was not permitted due to her poor condition. Despite of conventional medication with omeprazole and sucralfate over 20 days, she suffered from recurrent hematemesis and melena. In the gastrointestinal bleeding scan with 99mTc-labeled RBCs, small intestinal hemorrhage was found. The following day, the patient was given three doses of Novoseven® at 100 μg/kg, as bolus doses with 2 hour interval, which resulted in resolution of hematemesis and melena after last dose administration. Although she had mild whole body rash after third dose administration, it was subsided soon after medication of antihistamine and steroid. No evidence of hemorrhage was documented at a follow-up gastrointestinal bleeding scan that was taken after 4 days later of treatment. The patient made a full recovery and no further treatment was required. Conclusion: We suggest that low dose of recombinant FVIIa (Novoseven®) were effective in treatment of pediatric intractable gastrointestinal hemorrhage.

Recombinant FVIIa (Novoseven®) was initially developed for the treatment of bleeding in patient with congenital hemophilia with antibodies against factors VIII and IX and FVII deficiency. The mechanism of action is to induce hemostasis at the site of injury both by forming complexes with exposed tissue factor and by directly activating factor X upon the surface of an activated platelet. More recently it has begun to use gradually in the management of bleeding patient without congenital coagulation defect. We report the successful use of recombinant factor VIIa in a pediatric patient who has intractable gastrointestinal bleeding despite of conventional medical therapy.