Funda Ozgenc

Treatment of Helicobacter pylori gastritis improves dyspeptic symptoms in Turkish children.

Background In adults, the treatment of Helicobacter pylori infection is only recommended for patients with active gastric or duodenal ulcers. It is not known whether similar guidelines can be applied to children because the prevalence of peptic ulcer disease in childhood is estimated to be much lower than in adults. The purpose of this study was to determine whether treatment of H. pylori gastritis would improve symptoms of dyspepsia in children. Methods Sixteen patients (5 boys, 11 girls) aged 14 ± 1.2 years who had symptoms of dyspepsia were evaluated using upper gastrointestinal endoscopy with biopsies to establish the diagnosis of H. pylori gastritis. They were treated for 2 weeks with clarithromycin, amoxicillin, and a proton pump inhibitor. Dyspepsia symptoms were evaluated by a questionnaire before and after treatment of the infection. The effect of H. pylori treatment on the total symptom score was analyzed with use of the Student t test. Values are presented as mean ± SEM. Results All patients had antral nodularity and chronic active gastritis with spiral-shaped organisms but no evidence of peptic ulcer disease. Mean total symptom score decreased significantly at 2 to 4 weeks after treatment (12.6 ± 0.9 vs. 2.1 ± 0.5 P < 0.001), and it remained low (2.9 ± 0.7) at follow-up 9.7 ± 1.4 months (range, 2–24 months later). Conclusion These results suggest that the treatment of H. pylori gastritis can improve dyspeptic symptoms in children.

Our Experience with Fulminant Hepatic Failure in Turkish Children: Etiology and Outcome

Fulminant hepatic failure is a rare and devastating event during childhood. The etiology of liver failure is reported to change according to age and geographical location. We aimed to investigate, retrospectively, causes and outcome of fulminant hepatic failure in Turkish children. Thirty-four children with fulminant hepatic failure were analysed by means of etiology and outcome. Etiological factor, clinical presentation, encephalopathy stage and biochemical parameters were correlated with outcome. Acute viral hepatitis was detected in 12 cases (35.2 per cent) and hepatitis A was the most commonly detected cause among cases with fulminant hepatic failure (n = 9, 26.4 per cent). Hepatitis B and non A-E infection were diagnosed in two (5.8 per cent) and one (2.9 per cent) cases, respectively. Wilsons disease was defined in four patients (12.5 per cent). Budd-Chiari syndrome (2.9 per cent), autoimmune hepatitis (2.9 per cent) and mushroom poisoning (2.9 per cent) were other detected causes of fulminant hepatic failure in this group. No viral, metabolic, toxic or anatomic reason could be detected in the remaining 15 (44.1 per cent) patients and they were evaluated as cryptogenic. Mortality was 67.6 per cent (23 cases). Encephalopathy grade, total and indirect bilirubin levels were found to be significantly higher in patients who died (p = 0.004, p = 0.03, p = 0.04). Seven patients could have been transplanted (two cadavaric, five living related) and the mortality of this group was 28.5 per cent (n = 2). It was concluded that fulminant hepatitis A virus (HAV) infection is the most common detectable cause of fulminant hepatic failure in Turkish children.

Current therapeutic approaches in childhood chronic hepatitis B infection: A multicenter study

Background and Aim:  The aim of the present study was to compare the therapeutic efficacy of three different regimens in childhood chronic hepatitis B (CHB) infection.

Therapeutic vaccination in the immunotolerant phase of children with chronic hepatitis B infection

Aim. Hepatitis B virus (HBV) infection is a major global health concern and is the most common cause of chronic liver disease worldwide. Our aim was to investigate the efficacy of specific HBV vaccination as active immunotherapy in treating chronic hepatitis B (CHB) infection during the immunotolerant phase of children with normal aminotransferase values and high viral load. Materials and methods. Seventy-four patients never vaccinated before were randomly and prospectively recruited into two groups. Group 1 included 43 patients vaccinated with three standard injections of the GenHevac B vaccine at 30-day intervals. Group 2 contained 31 patients who did not receive any medication or vaccination (control group). Postvaccination serologic and virologic evaluation was performed 6 months after the first injection and at the end of the 12th month. Response to therapy was defined as loss of HBV DNA in serum and hepatitis B e antigen (HBeAg) seroconversion (loss of HBeAg), development of hepatitis B e antibody (anti-HBe). Results. The mean baseline alanine aminotransferase (ALT) value in Group 1 was 33.0 ± 9.6 IU/l, 34.6 ± 13.9 IU/l at 6 months after first injection and 34.3 ± 17.1 IU/l at end of 12 months (P > 0.05). In Group 1 the HBV DNA load at the start of immunization was 3571 ± 1292 pg/ml; this value was 3220 ± 1217 pg/ml at the 6th month and 2931 ± 1292 pg/ml at the 12th month (P > 0.05). In Group 2 the mean ALT values at the beginning of therapy and at the 6th and 12th months were 32.6 ± 7.8, 32.3 ± 8.0 and 30.3 ± 7.3 IU/l, respectively (P > 0.05), and the mean viral load HBV DNA values were 3909 ± 1378, 3546 ± 869 and 3106 ± 718 pg/ml, respectively (P > 0.05). There was no statistically significant difference between Group 1 and Group 2 at the end of the 6th and 12th months in the mean ALT values and mean viral load of HBV DNA (P > 0.05). Except for one patient in each group, hepatitis B surface antigen and HBeAg clearance or hepatitis B surface antibody and anti-HBe seroconversion were not observed during follow-up (P > 0.05). Conclusion. In this multicentered study comparison of vaccinated and unvaccinated groups of immunotolerant children with CHB infection showed no difference in the clearance of HBV DNA or seroconversion from HBeAg to anti-HBe. Different immunization protocols should be considered for future investigations in the immunotolerant phase of children with CHB infection.

Hepatocellular carcinoma in children and effect of living-donor liver transplantation on outcome

Abstract:  Hepatocellular carcinoma (HCC) is primarily observed in the older children and in most cases it develops in association with liver cirrhosis. Liver transplantation offers a good chance for long‐term cure. To evaluate the outcome of children with HCC and the impact of living‐donor orthotopic liver transplantation (OLT) on survival a retrospective review of radiographic, laboratory, pathologic, and therapeutic data in 13 children (six female and seven male) with chronic liver disease accompanied with HCC were studied. The patients were divided into two groups according to therapeutic modality: transplanted and non‐transplanted patients. Kaplan–Meier survival curves in various therapeutic groups were plotted. The mean age of patients was 6.4 ± 4.8 yr. Pediatric end‐stage liver disease score was adapted to model for end‐stage liver disease score for HCC and ranged between 1–44 and 18–44, respectively. The underlying liver diseases were tyrosinemia type 1 (n = 6), chronic hepatitis B infection (n equals;6), glycogen storage disease type 1 (n = 1). Alfa‐feto protein levels were elevated in all patients except one. Median number of tumor nodules was three (1–10), median maximal diameter of tumor nodules was 3.4 cm (0.5–8). Eleven patients were eligible for OLT whereas two patients were not eligible. Seven of the 11 patients considered for transplantation underwent living‐donor OLT. Remaining four patients died while waiting on cadaveric transplant list. Overall 1 and 4‐yr survival rates for all patients were 53.3 and 26.6%, respectively, and were found significantly higher in transplanted children than non‐transplanted children (72%, 72% vs. 33% and 16.6%). No patient had tumor recurrence at median of 36‐month follow‐up after OLT. OLT is a life‐saving procedure for children with chronic liver disease accompanying with HCC. Living‐donor OLT avoids the risk of tumor progression and transplant ineligibility in these children.

Inflammatory myofibroblastic tumor of small bowel wall in childhood: Report of a case and a review of the literature

Benign intestinal tumors are rare in children, however we describe an inflammatory myofibroblastic tumor (IMT) of the jejunum in a 2‐year‐old girl who presented with an intestinal obstruction. During laparotomy, an annular mass around the jejunum was resected, from which a histological diagnosis of IMT was made. A review of the literature for this rare entity emphasizes the importance of histological confirmation of its benign nature. Because of the risk of local recurrence, IMT cases should have a long‐term follow up.

Positive association of macrophage migration inhibitory factor gene-173G/C polymorphism with biliary atresia.

Background: Macrophage migration inhibitory factor (MIF) is a pleiotrophic lymphocyte and macrophage cytokine; it is likely to play an important role in innate immunity. Its expression was increased in several inflammatory diseases, and MIF gene polymorphisms have an effect on disease outcome and response to glucocorticoid treatment. Aim: To investigate the role of the 173G/C polymorphism of the MIF gene for susceptibility to biliary atresia (BA). Method: Between February 2002 and November 2004, 18 patients (mean age 1 ± 0.4 years) diagnosed as having BA were studied. After informed consent, blood was collected, and DNA was obtained. MIF 173C/G polymorphism was detected using the polymerase chain reaction-restriction fragment length polymorphism based method. BA patients were compared with a group of chronic liver disease patients (CLD) (n = 36) and a group of unrelated healthy controls (n = 103). Results: MIF-173C allele frequency was significantly higher than both the CLD and healthy control groups (P = 0.03, odds ratio [OR] 4.4, 95% confidence interval [CI] 1.3-15.1; P = 0.000, OR 4.1, 95% CI 2.3-7.6, respectively). Univariate analysis showed that MIF-173G/C polymorphism was significantly associated with BA (for GC genotype, OR = 6, 95 % CI 2.8-11.5, P = 0.000). There was no significant correlation between pediatric end stage liver disease score and MIF genotypes both in BA and CLD groups. Conclusion: Our results suggest that the -173C allele of the MIF gene might be associated with the susceptibility to BA.

Comparison of tropisetron and granisetron in the control of nausea and vomiting in children receiving combined cancer chemotherapy.

Tropisetron and granisetron are selective serotonin (5-HT 3 ) antagonists that have been proven effective in the prevention of nausea and vomiting in adults and children receiving cancer chemotherapy. This prospective, randomised study was designed to compare the efficacy of the two agents in the prevention of vomiting and nausea in children receiving highly emetogenic chemotherapy for various malignancies. A total of 51 children (mean age: 7.7 - 4.8 year) were studied in 133 chemotherapy cycles. In 66 chemotherapy cycles, the children received tropisetron as an antiemetic agent in a dose of 0.2 mg/kg/24 h intravenously and, in 67 cycles, they received granisetron 40 w g/kg/24 h intravenously before cytotoxic drug administration during the days they received chemotherapy. The response per 24 h of chemotherapy was defined as complete (no nausea and vomiting), partial (1-4 events of vomiting and/or nausea), and failure (more than 4 events o fvomiting and/or nausea). Efficacy of antiemetic therapy was evaluatedas acute (Day 1) and overall was based on the worst day during the chemotherapy. Complete control of acute vomiting was achieved in 74% of tropisetron and 88% of granisetron patients ( P = 0.04), and complete control of acute nausea in 56% and 82% respectively ( p = 0.002). Overall response by means of complete control of both vomiting and nausea during the whole therapy period was 29% of tropisetron group and 55% of granisetron group ( p = 0.007). The statistical analysis (depending on the emetogenicity of the chemotherapy cycles) showed increased efficacy of granisetron in highly (grade 3) emetogenic chemotherapy cycles ( p = 0.002), whereas there was no differencein the very highly emetogenic cycles ( p = 0.7). Also, granisetron was found to be more effective than tropisetron, especially in patients heavier than 25 kg ( p = 0.02). The adverse reactions were few and mild. There were no differences in the tolerability of the two antiemetic therapy modalities. In conclusion, granisetron was found to be more effective than tropisetron in controlling nausea and vomiting in children receiving highly emetogenic chemotherapy. This increased antiemetic efficacy of granisetron might have been related to maximal dose differences according to body weight.

Celiac disease in children with Down syndrome : Importance of follow-up and serologic screening

Background : Celiac disease, also known as gluten‐sensitive enteropathy, is a chronic inflammation disease of the small intestinal mucosa. Detection of Ig‐A antigliadin antibodies (AGA) and antiendomysial antibodies (EMA) in serum is important in the diagnosis and screening for celiac disease. Antiendomysial antibodies have greater sensitivity compared to antigliadin antibodies. It has been reported that the prevalence of celiac disease is higher in children with Down syndrome than the other autoimmune conditions. The aim of the present study was to investigate the incidence of celiac disease in children with Down syndrome, to assess the availability of Ig‐A AGA and EMA for serologic screening, and to highlight the importance of follow‐up for children with Down syndrome.

Association between anti-endomysial antibody and total intestinal villous atrophy in children with coeliac disease

BACKGROUND There is growing evidence to suggest that detection of anti-gliadin antibody (AGA) and anti-endomysial antibody (EmA) can serve as sensitive markers of the degree of histological abnormalities in patients with coeliac disease. AIM To evaluate the association between the presence of AGA and EmA and villous atrophy in intestinal biopsies of children with suspected coeliac disease. SETTINGS AND DESIGN Intestinal samples of 46 children with failure to thrive, chronic diarrhoea, malabsorption and short stature with either AGA and/or EmA positivity were evaluated, retrospectively. The diagnosis of coeliac disease was based on ESPGHAN criteria. METHODS AND MATERIAL Patients with total villous atrophy who fulfilled the ESPGHAN criteria for the diagnosis of coeliac disease were diagnosed to have coeliac disease. Nine patients without villous atrophy were taken as negative controls for this study. AGA-IgA was measured both by immunoflourescence (IF) and ELISA and EmA-IgA by IF while patients were on normal diet. Relationship between autoantibody positivity and intestinal total villous atrophy was evaluated. RESULTS Overall positivity for AGA IgA was 85% (39/46) by IF+ELISA and EmA positivity was 85% (39/46) by IF within the study group. Histological examination revealed total villous atrophy with lymphocyte infiltration and crypt hyperplasia in 37 (80%) patients. AGA IgA was positive in 14 (38%) and 31 (84%) of these children by ELISA and IF, respectively. EmA positivity was detected in 35/37 (95%) cases with atrophy and 4/9 (44%) without atrophy (p=0.002). Thirty out of 37 (81%) patients with villous atrophy had both AGA IgA (IF) and EmA positivity (p=0.186). All of the sixteen patients that had both positive AGA IgA (ELISA+IF) and EmA had total villous atrophy (p=0.037). CONCLUSION A significant association between total villous atrophy and EmA positivity has been documented in this study.