Background: Ursodeoxycholic acid (UDCA) is a safe drug used in the treatment of cholestatic liver disorders in children. The aim of this study was to investigate the synergistic effect of UDCA in combination with phototherapy in treating indirect neonatal hyperbilirubinemia. Methods: Present double-blinded, randomized clinical trial was conducted among neonates with jaundice who were under treatment with phototherapy in the neonatal ward affiliated with the Zabol University of Medical Sciences in 2017. The patients (200 neonates) were randomly divided into intervention (phototherapy+ UDCA) and control (phototherapy alone) groups. The intervention group received 15 mg/kg UDCA daily. Results: Total bilirubin levels at birth, 24, 48, and 72 hours after therapy were 16.89± 2.49, 14.28± 2.05, 11.62± 2.46, and 10.26± 1.92 mg/dl in controls and 15.79± 2.18, 12.77± 1.86, 10.08± 1.66, and 8.94± 1.38 mg/dl in intervention group respectively (P< 0.001). The ratio of neonates with total bilirubin< 10 mg/dl were 28% and 55% after 48 hours, and 64% and 90% after 72 hours of therapy initiation in phototherapy alone and phototherapy+ UDCA groups respectively (P< 0.001). The mean reduction of direct bilirubin was not significantly different between the groups. Conclusion: UDCA was effective in accelerating reduction of total bilirubin level in neonates with unconjugated hyperbilirubinemia under phototherapy but had no effect on direct bilirubin levels.

Prebiotic-supplemented and regular formula were similar to breast milk regarding prophylactic effects for diarrhoea, constipation and respiratory tract infections in the first year of life. Prebiotic-supplemented formula may be an appropriate substitution for breast milk when breast milk in unavailable.

Context: Thalassemia is a genetic disorder of hemoglobin production. Patients with thalassemia major (TM) require regular blood transfusions to keep a compatible hemoglobin level for oxygenating organs. These patients suffer from different complications such as infections, autoimmunity and alloimmunization due to transfusion. Such complications link the immune system to TM pathogenesis. In the present study, we have reviewed the latest data available on interactions of TM pathophysiologic determinants and immune system components. Evidence Acquisition: A comprehensive search was performed on PubMed, Scopous, and Web of Knowledge databases using keywords thalassemia, immune system, autoimmune, alloimmune, adaptive immunity, innate immunity, complications, and immunesenescnce. Results: It seems that persistent antigenic stimulation and oxidative stress from excessive iron are the two main pathophysiologic factors of TM impacting the immune system. Regarding innate immunity, functional activity of neutrophils, and natural killer cells (NKCs) is decreased in TM. On the other hand, higher levels of TNF-α and IL-1β, IL-6, IL-8, and C-reactive protein proinflammatory cytokines have been observed in the serum of patients. TM patients have demonstrated higher ratios of regulatory B lymphocytes (CD19+, CD38+, CD24+), helper T cells, suppressor T cells, and T regulatory (CD4+/CD25+/Foxp3+) lymphocytes. TM patients have shown significant higher levels of IgA immunoglobin respective to normal counterparts that may predispose them to diabetes and coeliac disease. Immune cells, however, rendered lower than optimal activity in TM patients, which may be due to nutritional insufficiencies. Potential relationships have been suggested between immune system and various thalassemia compilations including heart infraction, hypertension, atherosclerosis, diabetes, thyroid dysfunction, and osteoporosis. Conclusions: Immune genetic determinants may be involved in modulating the clinical picture of TM. TM patients generally represents with higher immune cell counts, likely as a result of persistent antigenic challenge from blood transfusions. However, these patients face compromised immune cell functions. The role of immunologic interactions in pathogenesis of TM needs to be further divulged in future studies.

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ContextCeliac disease (CD) is a common phenomenon in children with Type 1 diabetes (T1D). In the present review, we have discussed the pathogenesis, diagnostic biomarkers, risk factors, and prognosis of CD in the context of pediatric T1D.Evidence AcquisitionLiterature published in Web of Science, PubMed, Scopus, Google Scholar, and Cochrane Library were scrutinized up to the end of 2017. The keywords of celiac disease, Type 1 diabetes, children, and pediatric were used in different combinations.ResultsImmune cytotoxic reactions along with dampen immune regulatory functions contribute to CD in the context of pediatric T1D. Many children with simultaneous CD and T1D do not represent with the clinical signs of the enteropathy rendering a diagnostic challenge. The most common screening tests in these children are routine serological tests of CD, anti - endomysial, anti - transglutaminase, and anti - deamidated gliadin peptide antibodies. Typing for human leukocyte antigens of DQ - 2 and DQ - 8 may assist in the diagnosis of silent CD in children with T1D. The most significant shared non - HLA genetic loci of CD and T1D comprise CTLA - 4, TAGAP, IL - 18RAP, PTPN2, RGS1, SH2B3, CCR5. Interactions between these loci can be important in susceptibility to CD in T1D. Some new biomarkers have been suggested for diagnosis of CD including ischemia-modified albumin (IMA), soluble syndecan-1 (SSDC-1), regenerating gene Iα (REG-Iα), Neurotensin, and Zonulin, which can be useful for diagnosis and screening of CD in childhood T1D.ConclusionsOverall, active seropositive CD seems to be of clinical importance in T1D with significant impacts on the quality of life and predisposition to diabetes associated complications. It is important to detect CD in the context of T1D to prevent potential risks contributing to morbidities and mortalities associated with either CD or T1D.