Background. Posttransplant lymphoproliferative disease (PTLD) is a life-threatening condition the incidence of which in pediatric solid organ transplantation may be related to the immunosuppressive load. It has been suggested that tacrolimus, a new and potent immunosuppressor, causes an increased incidence of this syndrome. Methods. The incidence, early signs, and risk factors for lymphoproliferative disease were reviewed in a cohort of 89 pediatric liver transplant recipients treated with tacrolimus. Results. Eighteen patients (20%) developed a PTLD-16 concomitant to a primary Epstein-Barr virus (EBV) infection and 2 with previous immunity against EBV. Three additional patients had preliminary signs of PTLD concomitant to primary EBV infection, but did not develop individualized lymphoid masses. Six patients died (6.7% of all tacrolimus-treated patients). Mean tacrolimus blood level during the 3 months preceding EBV infection reached 11.8±1.8 ng/ml in PTLD patients versus 9.4±3.4 ng/ml in non-PTLD patients(0.05<P<0.1). Previous OKT3 or antithymocyte globulin treatment was also significantly associated to PTLD. There was no association with age, rejection episodes, steroid-resistant rejection, prior cytomegalovirus infection, HLA mismatch, living donor or cadaveric organ transplantation, United Network for Organ Sharing status at the time of orthotopic liver transplant, and primary or rescue tacrolimus treatment. A significant increase of total γ-globulin level occurred in PTLD patients, and mono/oligoclonal production was significantly associated to PTLD. Conclusion. In EBV-infected pediatric liver transplant recipients, use of OKT3 or antithymocyte globulin and high tacrolimus blood levels are risk factors for a significant increase in the incidence of PTLD. An increase in totalγ-globulin level and appearance of mono/oligoclonal immunoglobulin production are the major preliminary signs of the syndrome.

Leptin is an adipocyte-secreted hormone which plays a key role in energy homeostasis. Our aim was to determine the relationship between serum leptin and clinical and biochemical features in overweight children and adolescents. Overweight children and adolescents followed in this Unit with serum leptin ascertained were included. Clinical, biochemical and abdominal ultrasound data were analysed. Statistical analysis was performed byttest, χ², Pearson's correlation and linear regression. One outlier of serum leptin was excluded to perform correlation and regression. Serum leptin was determined in 357 patients. At the first visit, the mean age was 9·5 (sd3·2) years and mean BMIz-score was 1·72 (sd1·34) (girls 1·71 (sd1·16); boys 1·72 (sd1·11)). Serum leptin levels were significantly related to: sex (mean: girls 48·0 ng/ml, boys 34·4 ng/ml;P = 0·003); Tanner stage (mean: I–II 37·0 ng/ml, III–V 45·2 ng/ml;P = 0·035); systolic blood pressure (mean: normal 41·3 ng/ml, high 44·0 ng/ml;P = 0·009); BMIz-score (r0·136;P = 0·010); C-peptide (r0·17;P = 0·002); insulin (r0·34;P < 0·001); homeostasis model assessment of insulin resistance (HOMA-IR) (r0·25;P < 0·001) and aspartate aminotransferase (r− 0·12;P = 0·023). In the multivariate analysis (with leptin as the dependent variable and sex, Tanner stage, BMIz-score, systolic blood pressure, aspartate aminotransferase, C-peptide, insulin and HOMA-IR as independent variables), sex and BMI were determinant factors. The present study in overweight children and adolescents showed that being female and greater BMI were significantly and independently associated with increased serum leptin. In this large cohort other associations with leptin described in the literature can be discharged.

Objectives: Iron deficiency is the most common cause of anemia in children with inflammatory bowel disease, although the real prevalence is unknown. Intravenous iron is suggested as the first line treatment. This study aims to determine the prevalence of iron deficiency anemia in children with inflammatory bowel disease followed in a Pediatric Gastroenterology Unit of a tertiary center and to evaluate this unit's experience with intravenous iron. Materials and methods: A retrospective cohort study was designed involving children with inflammatory bowel disease followed in that unit between January 2001 and April 2016. Laboratory results were collected at the moment of diagnosis, after one-year follow-up and prior each IV iron administration performed during the study period. Anemia was defined according to World Health Organization criteria and the iron deficiency was defined using recent guidelines. Results: Were studied 69 patients 71% had CD and 29% UC. 50.7% were female. Mean patient age at diagnosis was 13.3 years (range 1--17 years). Prevalence of ID and IDA at diagnosis was 76.8% and 43.5%, respectively. After one year follow-up, those values decreased to 68.1% (p = .182) and 21.7% (p = .002), respectively. Hemoglobin significantly increased (p < .001). Intravenous iron was administered to 92.8% of patients. No adverse reactions were reported. Conclusions: Intravenous iron is the first line in the treatment of Iron deficiency anemia in Inflammatory Bowel disease and it is safe and effective. Persistent anemia and iron deficiency are common.