***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND Poor growth and delayed maturation in children with sickle cell disease ( SCD ) may be due , in part , to mild zinc deficiency . OBJECTIVE The objective was to determine the effects of zinc supplementation on growth and body composition in children with SCD . DESIGN Forty-two prepubertal children ( 20 girls and 22 boys ) aged 4 - 10 y with SCD-SS were r and omly assigned to receive 10 mg elemental Zn/d in cherry syrup ( zinc group ) or cherry syrup alone ( control group ) . The 2 groups were stratified by sex and initial height status . Dietary intakes were evaluated and anthropometric , high-precision knee-height , and plasma zinc measurements were made at baseline and at 3 , 6 , and 12 mo . Body composition was determined every 6 mo with dual-energy X-ray absorptiometry , and z scores for anthropometric variables were computed from national reference data . Longitudinal-mixed-effects analysis was used to test for differences between the groups over the 12-mo observation period . RESULTS Thirty-eight children completed the study . No significant differences were observed at baseline . After 12 mo , the zinc group had significantly greater mean ( + /- SE ) increases in height ( 0.66 + /- 0.29 cm/y ) , sitting height ( 0.97 + /- 0.40 cm/y ) , knee height ( 3.8 + /- 1.2 mm/y ) , and arm circumference z scores ( 0.27 + /- 0.12 cm/y ) . Height-for-age and weight-for-age z scores decreased significantly by 0.11 + /- 0.04 and 0.13 + /- 0.05 , respectively , in the control group but did not change significantly in the zinc group . CONCLUSIONS Prepubertal children with SCD-SS may have zinc deficiency and may benefit from zinc supplementation to improve linear growth and weight gain Objective There are some reports in which a condition of zinc deficiency and its associated outcomes with a change in concentration of serum copper among the thalassemic patients has been highlighted . The aim of this prospect i ve study was to determine the serum zinc and copper levels in children with beta-thalassemia major . Methods In this cross sectional study all children under 12 years affected by beta thalassemia major ( 40 patients ) were evaluated for serum zinc and copper levels in Qazvin thalassemia center ( Qazvin , Iran ) in 2007 .  Serum measurements for zinc and copper were performed by atomic absorption spectrophotometer . Findings The mean concentrations of serum zinc and copper levels were 67.35±20.38 and 152.42±24.17 µg/dl respectively . Twenty-six ( 65 % ) of thalassemic patients had zinc concentration under 70 µg/dl ( hypozincemia ) . None of the thalassemic children had copper deficiency . No significant correlation between serum zinc level with age , weight , height , body mass index , duration of blood transfusion , desferrioxamine dose and ferritin level was observed in thalassemic patients ( P=0.3 ) . Conclusion This study revealed that hypozincemia is common in thalassemic patients , but in contrast , there is no copper deficiency . Further evaluation in this regard is recommended Objective In beta thalassemic patients , tissue damage occurs due to oxidative stress and it happens because of the accumulation of iron in the body . This study was conducted to determine the effect of zinc and vitamin E supplementation on antioxidant status in beta-thalassemic major patients . Methods This double blind r and omized clinical trial was carried out on 120 beta thalassemic patients older than 18 years . Patients were r and omly categorized in four groups . Zinc ( 50mg/day ) and vitamin E ( 400mg/day ) supplements were administered for former and latter group , respectively . In the third group both supplements were administered in similar doses . The fourth ( control ) group received no supplement . The effect of supplementations on serum zinc and vitamin E , superoxide dismutase ( SOD ) , glutathione peroxidase ( GPX ) , total antioxidant capacity ( TAC ) and body mass index ( BMI ) were measured at the beginning and the end of the study . Findings Serum zinc levels in group 1 and 3 were significantly increased ( P<0.007 and P<0.005 , respectively ) . Serum vitamin E levels in group 2 and 3 were also increased significantly ( P<0.001 ) . Mean GPX activity in group1 , 2 and 3 decreased significantly ( P<0.015 , P<0.032 and P<0.029 , respectively ) . Mean SOD activity and TAC did not show significant change after supplementation . BMI had significant increase in all treated groups ( P<0.001 ) . Conclusion Our results suggest that beta thalassemic patients have enhanced oxidative stress and administration of selective antioxidants may preclude oxidative damage Zinc deficiency is a common nutritional problem in adult sickle‐cell disease ( SCD ) patients . Hyperzincuria and increased requirement of zinc due to continued hemolysis in SCD are probable bases for zinc deficiency in these patients . Zinc deficiency affects adversely T‐helper1 ( TH1 ) functions and cell mediated immunity and interleukin (IL)‐2 production is decreased in zinc deficient subjects . We hypothesized that zinc supplementation will improve T‐helper1 function and decrease incidence of infections in patients with SCD . We tested this hypothesis in 32 SCD subjects who were divided in three groups ( Grs A , B , and C ) . Grs A ( n = 11 ) and B ( n = 10 ) were zinc deficient based on cellular zinc criteria and Gr C ( n = 11 ) were zinc sufficient . Gr A subjects were observed for 1 year ( baseline ) , following which they received zinc acetate ( 50 to 75 mg of elemental zinc orally daily ) for 3 years . Gr B subjects were observed for 1 year ( baseline ) , following which they received placebo for 1 year and then switched to zinc supplementation ( 50 to 75 mg of elemental zinc orally daily ) for 2 years . Gr C subjects did not receive any intervention inasmuch as they were zinc sufficient . Prolonged zinc supplementation result ed in an increase in lymphocyte and granulocyte zinc ( P = 0.0001 ) , and an increase in interleukin‐2 production ( P = 0.0001 ) , decreased incidence of documented bacteriologically positive infections ( P = 0.0026 ) , decreased number of hospitalizations and decreased number of vaso‐occlusive pain crisis ( P = 0.0001 ) . The predominant pathogens isolated were staphylococci and streptococci involving the respiratory tract and aerobic gram‐negative bacteria , particularly Escherichia coli , involving the urinary tract . Further confirmation of our observations will require prospect i ve studies of zinc supplementation in a larger number of SCD patients . Am . J. Hematol . 61:194–202 , 1999 . © 1999 Wiley‐Liss , The toxicity of oral zinc was investigated in patients hospitalized for chronic leg ulcers .  Untoward effects were monitored by reference to clinical tolerance , hematological , hepatic and renal parameters , and serum concentrations of copper and iron . The investigation was conducted by comparing two groups of patients who initially did not differ significantly with regard to ulcer area , hemoglobin , leukocytes , copper , iron and zinc .  Both groups had serum zinc concentrations in the lower normal range . One group was treated with 3 daily doses of 220 mg oral zinc sulfate and the other with placebo , and hence , untoward effects of zinc should have become manifest in the zinc-treated group . This was not the case . Therefore , oral zinc appears to be well tolerated clinical ly and does not cause hematological , renal or hepatic toxicity . In view of the increasing interest in and range of indications for zinc , particularly in conditions associated with cellular immunological hyporeactivity , this finding is a prerequisite for the institution of clinical zinc therapy Previously , we have documented primary testicular failure in adult male subjects with sickle cell anemia . We have also reported the occurrence of zinc deficiency and suggested that and rogen deficiency may be related to zinc deficiency in such patients . In this study , we present data with respect to the effect of oral zinc supplementation on serum testosterone levels in adult male patients with sickle cell anemia . An increase in serum testosterone , neutrophil zinc , and neutrophil alkaline phosphatase activity was observed in the zinc‐supplemented group in comparison with the group on placebo . Additionally , body weight increased and serum lactic dehydrogenase activity decreased in response to zinc supplementation . We conclude that and rogen deficiency in adult male subjects with sickle cell anemia is correctable with zinc supplementation and that the determination of neutrophil zinc and alkaline phosphatase activity in the neutrophils may be utilized as good indicators of body zinc status in such subjects Abstract In a controlled trial on the effect of oral zinc sulphate in the  healing of sickle-cell leg ulcers  , the healing-rate in the treatment group was three times faster than in the placebo group 
    Output:
    
According to the results , there is no evidence from r and omised controlled trials to indicate any benefit of zinc supplementation with regards to serum zinc level in patients with thalassaemia .
There is mixed evidence on the benefit of using zinc supplementation in people with sickle cell disease .