Effect of micronutrients supplementation, vitamin A, zinc, folic acid and selenium in management of infants with persistent diarrhea

Persistent diarrhea is still one of the most important pediatric health problems all over the world. Aim of this work was to study the effect of micronutrient supplementation [Zinc, vitamin A, folio acid and selenium] in management of infants with persistent diarrhea. The present study included seventy-five infants suffering from persistent diarrhea. Cases were distributed randomly into five groups. Studied groups were given zinc [first group], vitamin A [Second group], folio acid [Third group], selenium [fourth group] and the fifth group was supplied with mixture of all above micronutrients Fifteen healthy infants of matched age and sex were served as normal controls. History taking, clinical examination and the following laboratory investigations were done; stool examination, stool bacterial culture, D-xylose test, serum albumin, transferrin, prealbumin, sodium and potassium and complete blood count. Cases with persistent diarrhea were followed up for 3 weeks where the laboratory investigations were done at the end of this period. Only 22.67%of studied cases were exclusively breast-fed. Recovery time was significantly shorter and weight gain was significantly higher in zinc, vit. A and micronutrients mixture groups than folic acid and selenium groups [P<0. 05]. Significant increase in hemoglobin, RBCs and serum albumin in zinc, vit A and micronutrients mixture group as compared to before treatment [P<0, 05]. Significant increase in blood D-xylose, serum prealbumin and serum transferrin in all studied groups as compared to before treatment [P<0. 05]. From the present study it could be concluded that zinc and/or vitamin A with dietetic intervention are effective in management of persistent diarrhea. While folic acid and selenium has no apparent beneficial effect in management of persistent diarrhea

Bone mineral density and biochemichal markers in children with chronic liver disease

Metabolic bone disease is known to complicate chronic liver disease. The aim of the present study was to determine bone mineral density [BMD] and bone turnover in children with chronic liver disease [CLD] and to assess the possible correlations with the severity of liver disease. Thirty hospitalized children with CLD,14 males and 16 females, aged 2-14 years and twenty age- and sex - matched healthy controls were enrolled. BMD was measured by dual energy X-ray absorptiometry at the lumber spines. Serum levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone [PTH], osteocalcin and carboxy- terminal telopeptide of type I collagen [ICTP] were measured. The severity of liver disease was assessed using Desmet's modification of Knodell's histological activity index. BMD was significantly lower in patients than in controls and osteoporosis was found in 8 [27%] of the patients. BMD was significantly correlated negatively with severity of liver disease and positively with serum osteocalcin level. No correlation was found between BMD and calcium, phosphorus? alkaline phosphatase, PTH, and ICTP serum levels. Serum osteocalcin level was significantly lower and serum ICTP was higher but not statistically significant in patients than in controls. Serum calcium, phosphorus, and PTH values in patients did not differ from those of controls. Levels of osteocalcin, but not PTH and ICTP9 were significantly correlated inversely with severity of liver disease. Ascitic patients had significantly lower BMD and serum osteocalcin values than non-ascitic patients, and also had significantly higher serum levels of ICTP than the controls. The results of this study indicate that BMD is decreased in children with CLD that is related to the severity of liver disease. The biomarkers of bone turnover reflect that decreased bone formation, rather than increased bone resorption, is the major contributor of bone loss in these patients

Tracheobronchial aspirate proinflammatory cytokines: early predictors of chronic lung disease in neonates with respiratory distress syndrome

The objectives of the present study were to investigate if early measurements of proinflammatory cytokines in tracheobronchial aspirate fluid from neonates with respiratory distress syndrome [RDS] could be used to early predict chronic lung disease [CLD]. This is in comparison with other risk factors including gestational age, birth weight, prenatal steroid, mode of delivery, duration of exposure to FiO[2] >0.21, peak inspiratory pressure [PIP] and duration of ventilatory support, air leaks, patent ductus arteriosus [PDA], and intraventricular hemorrhage [IVH]. Thirty-six preterm infants less than 34 weeks of gestation with RDS were mechanically ventilated and days 2 and 7 - measurements of concentrations of tumor necrosis factor-alpha [TNF-alpha] and the interleukins IL-1beta, IL-6, and IL-8 were made, using enzyme immunoassay techniques. Echo-Doppler and head ultrasonography studies were done for each patient. Each patient was followed-up for 28 days. Ten patients developed CLD, six patients died before the elapse of 28 days, and 20 patients experienced uncomplicated course of RDS. Infants who developed CLD had significantly increased concentrations of TNF-alpha, IL-1beta, IL-8, and IL-6 on days 2 that persist by day 7. TNF-alpha, IL-6, IL-8, and IL-1beta concentrations correlated significantly with lower gestational age, birth weight, time spent on a ventilator, duration of supplemental oxygen, maximal PIP, symptomatic PDA, and appearance of air leak. IL-6 cut-off point level of 650 pg/ml at day 2 predicts CLD with accuracy of 100%, and IL-1beta cut-off point level of 165 pg/ml at day 2 predicts CLD with accuracy of 100%. In conclusion, increased concentrations of tracheobronchial aspirate fluid proinflammatory cytokines could be the most valuable early predictor of CLD and will assist in selecting infants for early interventions including corticosteroid treatment or more selective blockage of components of inflammation

effect of valproate monotherapy on hepatic and hemostatic functions in epileptic children: value of L-carnitine supplementation

The study included 15 epileptic children without previous hepatic or hemostatic defects [10 males and 5 females] aging 2 to 14 years selected from the outpatients attending the Pediatric Neurology Clinic of the Pediatric Department of Tanta University Hospital. We excluded patients receiving other medications which affect hepatic or platelet function, fifteen healthy children of matched age and sex served as controls. History, clinical examination and the following investigations were done for all of the cases: EEG, complete blood count, total serum proteins, albumin, bilirubin, ammonia, and alanine aminotransferase [ALT]. Hemostatic studies included bleeding time [BT], clotting time [CT], prothrombin time [PT], activated partial thromhopiastin time [PTT], serum fibrinogen, protein C, von Willebrand factor antigen, platelet count and platelet aggregation. All of the hepatic and hemostatic parameters were done before, and 9 weeks after commencement of antiepileptic therapy with valproate [VPA]. Serum valproate level was measured after establishment of therapy and showed a good complience to treatment. L-carnitine was measured before and after valproate therapy then oral L-carnitine was supplemented in a dose of 100 mg/kg/day for two weeks in all of the studied cases. The studied hepatic and hemostatic function parameters mentioned above were repeated again after L-carnitine supplementation. Valproate therapy was associated with a significant decrease in serum L-carnitine with impairment of hepatic functions [manifested by a significant increase in serum bilirubin, ammonia and ALT]. Following oral administration of L-carnitine there was a significant decrease in serum bilirubin and ALT, Hemostatic disturbances were also observed after valproate therapy in the studied cases [manifested by a significant increase in BT, CT, PT and PTT, with a significant decrease in serum fibrinogen, serum protein C, platelet count and platelet aggregation], VPA therapy or L-carnitine administration did not significantly affect Von Willebrand factor. Most of the studied hemostatic parameters improved significantly in response to oral L-carnitine. None of our studied cases showed life threatening or Reye-like hepatotoxicity. We conclude that within the usual therapeutic serum levels of VPA, it could be associated with L-carnitine deficiency and hepatic synthetic dysfunction as well as decreased number and function of platelets. Most of these abnormalities could be reversed by co-administration of L-carnitine. The latter might be recommended in epileptic children on VPA therapy particularly those with abnormal liver or platelet functions and those at risk for hepatotoxicity