CD may be associated with H. pylori gastritis, but it does not affect the clinical presentation of the disease, except for abdominal distension; CD is associated with mild duodenal lesions. A gluten-free diet improves the symptoms in all patients independently of the presence of H. pylori gastritis. Gastric metaplasia increases in the presence of H. pylori gastritis. Further prospective studies are needed to examine the clinical and histopathological outcomes of gastric metaplasia associated with H. pylori gastritis in CD patients.

The aim of the study was to assess early and long-term incidence of venous complications, in both deceased donation (DD) and living-related (LR) liver transplantation (LT) in a pediatric population. Seventy-five liver transplants performed in 69 (39 boys, 30 girls) children at Ege University Hospital between 1997 and 2004 were prospectively monitored and reviewed. Age, sex, primary diagnosis, graft type, vascular complications and their management were evaluated. All patients received Doppler ultrasonographic examination both during operation and daily for the first three postoperative days and when necessary thereafter. The complications were classified as early and late presented. Thirty-three grafts (47.8%) were from DD and 36 (52.2%) were from LR donors. Recipients of DD were older than LR donors (mean age 10.5 +/- 5.1 and 5.0 +/- 0.7, respectively) (p < 0.05). Vascular complication occurrence was not statistically different between DDLT and LRLT recipients (p = 0.2), and between infants and children (p = 0.9). Overall, stenosis was more common than thrombosis. We observed hepatic artery (HA) thrombosis, in five of 75 (6.7%) transplants within 30 days post-transplant. Portal vein (PV) thrombosis and hepatic vein (HV) thrombosis were detected in six and one patients (8.7% and 1.3%), respectively. Six PV stenosis were identified (8.7%), while HA and HV-VC (vena cava) stenosis occurred in one and six patients (1.4% and 8.7%), respectively. All PV stenosis (6/33, 18.2%) and one PV aneurysm occurred in DDLT recipients while HV-VC stenosis were detected almost equally in LRLT and DDLT recipients (4/36 vs. 2/33). Except one, all PV stenosis were detected as a late complication and no intervention were needed. Stenosis of HV-VC was more common in girls (5/30 vs. 1/39) (p < 0.05) and the incidence was not different in DDLT and LRLT recipients (p = 0.8). In conclusion, overall incidences of thrombosis and stenosis formation after orthotopic liver transplantation (OLT) were 17.4% and 18.8%, respectively in our center. We suggest that in the cases with HA thrombosis manifested intra-operatively or within the early postoperative period, graft salvage was successful. Thrombosis of HA causes significant mortality. Thrombosis of PV was among the causes of mortality and morbidity. Stenosis of HV-VC could be managed by angioplasty and endovascular stenting with no significant effect to mortality.

In this study, we analyze the demographic features, clinical and histopathological findings in patients who underwent liver transplantation for progressive familial intrahepatic cholestasis. We also analyze outcome and impact of liver transplantation on growth and bone mineral content. Most of the patients were presented with jaundice mainly beginning within the first six months. At the time of initial admission; eight patients had short stature (height SD score<2), and four patients had weight SD score<2. Liver transplantation were performed at the age of 43.2+/-27 months (range 9 to 96 months), 6.5+/-3.5 months later after the first admission. Infection, surgical complications and osmotic diarrhea associated with severe metabolic acidosis were noted in 41.4%, 16.6% and 33.3%, respectively. One patient developed posttransplant lymphoproliferative disorder. Overall; 1 year graft and patient survival was 69.2% and 75%, respectively. At the end of the 1st year only 2 patients had height SD score<2. Linear regression of height gain against increase in total body BMD measured at the time of transplantation and 1 year after liver transplantation gave a coefficient r=0.588 (p=0.074). No correlation was found between the height gain and age and PELD score at time of transplantation, and no difference was noted between the sexes and donor type. Liver transplantation is effective treatment modality with good outcome and little morbidity, and increases the growth acceleration in patients with PFIC associated with cirrhosis.

Prolonged QTc interval (>440 ms) is a common abnormality in adult patients with CLD and has been reported to predict patient survival. In this study, 88 children who underwent evaluation for LT, including a 12-lead electrocardiogram and echocardiogram included to determine the frequency of QTc prolongation and related factors in children with CLD and the effect of LT on these factors. Sixty-nine healthy, age- and sex-matched children served as controls. QTc interval was prolonged in 40 CLD patients (45.4%). It was found to be related to PELD score and presence of portal hypertension. Mean QTc was higher in patients who died prior to LT than in the survivors without LT. Mortality risk was increased 3.66-fold in patients with prolonged QTc (p = 0.001, 95% CI: 2-7.2). Cox regression analysis showed that only PELD score was an independent predictor of survival (p = 0.001, beta = -0.41, 95% CI: 5.58-1.82). Five of 48 transplanted children died within three months post-transplant; QTc was not related to post-transplant survival (p = 0.27). QTc normalized in 63.8% patients after LT. After LT, LAD, LVEF, and LVPWT decreased. In conclusion, QTc prolongation is common in children with CLD and associated with high mortality. It may be useful for assessment of the severity of CLD and for the timing for transplantation.

Hepatopulmonary syndrome (HPS) is characterized as a triad: liver disease, intrapulmonary vascular dilatation and arterial hypoxemia. HPS is reported to be present in 4% to 32% of adult patients with end-stage liver disease and in 9%-20% of children. The pathogenesis of HPS has not been clearly identified. Portal hypertension causes impairment in the perfusion of the bowel and increases the enteral translocation of Gram (-) bacteria and endotoxins. This stimulates the release of vasoactive mediators, such as tumor necrosis factor-alpha, heme oxygenase-derived carbon monoxide and nitric oxide. Genetic alterations have not been associated with this syndrome yet; however, cytokines and chemokines have been suggested to play a role. Recently, it was reported that cumulated monocytes lead to the activation of vascular endothelial growth factor-dependent signaling pathways and pulmonary angiogenesis, which plays an important role in HPS pathogenesis. At present, the most effective and only radical treatment is a liver transplant (LT). Cirrhotic patients who are on the waiting list for an LT have a shorter survival period if they develop HPS. Therefore, it is suggested that all cirrhotic cases should be followed closely for HPS and they should have priority in the waiting list.