Background: Though effective treatment programs for severely malnourished children are available, mortality rate among children with acute malnutrition continue to rise and little is known about its long-term outcomes and potential predictors of its in-hospital and post-discharge mortality. The aim of this study was to assess the survival status and predictors for mortality in severely malnourished children admitted to Minia University Maternity and Children Hospital. Methods: A retrospective cohort study which included 135 children under 5 years of age who were admitted to the nutrition rehabilitation ward with severe acute malnutrition (SAM) during the period from January to December 2018. Data were collected from the inpatient's hospital records and the children's parents/guardians were interviewed using a detailed structured questionnaire that inquired about demographic and socioeconomic variables. The logistic and Cox regressions were used to assess the factors associated with the SAM's mortality. Results: A total of 135 children were enrolled into the study. Death rate during hospitalization was 9.6%. The survival rate at the end of the fourth week of admission was 82.4%. There were 6.7% post-discharge deaths among 104 alive discharged children which occurred within 8 weeks after discharge. The adjusted HRs (95% CIs) for total SAM deaths were 1.57 (1.10-2.99) in children < 12 vs ≥ 12 months old; 4.79 (2.23-6.10) in those with WAZ < −3SD, 2.99 (1.16-4.66) in those with edema at admission and 3.44 (1.07-9.86) in children with complications. The respective ORs (95%CIs) for in-hospital SAM deaths in the same groups of children were 2.64 (1.22-6.43), 8.10 (2.16-11.67), 3.04 (1.70-6.06) and 3.71 (1.59-6.78). The main predictor for the SAM's post-discharge mortality was illiteracy of mothers; the adjusted HR (95%CI) was 7.10 (1.58-31.93; p = 0.01). Conclusions: Age, WAZ, edema and complications at admission were predictors for both in-hospital and total SAM mortality, while mother's education contributed to the early post-discharge mortality. The identification of predictors for mortality is an important preliminary step for interventions aiming to reduce morbidity and mortality.

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PA and MAA have numerous nonspecific presentations, potentially leading to delayed diagnosis or misdiagnosis. In this paper, we present the clinical and biochemical characteristics of MMA and PA patients at initial presentation. Results. This is a retrospective review of 20 patients with PA ( n = 10 ) and MMA ( n = 10 ). The most observed symptoms were vomiting (85%) and refusing feeding (70%). Ammonia was 108.75 ± 9.3  μmol/l, showing a negative correlation with pH and bicarbonate and positive correlation with lactate and anion gap. Peak ammonia did not correlate with age of onset ( r = 0.11 and p = 0.64 ) or age at diagnosis ( r = 0.39 and p = 0.089 ), nor did pH ( r = 0.01 , p = 0.96 ; r = − 0.25 , p = 0.28 ) or bicarbonate ( r = 0.07 , p = 0.76 ; r = − 0.22 , p = 0.34 ). There was no correlation between ammonia and C3 : C2 ( r = 0.1 and p = 0.96 ) or C3 ( r = 0.23 and p = 0.32 ). The glycine was 386 ± 167.1  μmol/l, and it was higher in PA ( p = 0.003 ). There was a positive correlation between glycine and both pH ( r = 0.56 and p = 0.01 ) and HCO3 ( r = 0.49 and p = 0.026 ). There was no correlation between glycine and ammonia ( r = − 0.435 and p = 0.055 ) or lactate ( r = 0.32 and p = 0.160 ). Conclusion. Clinical presentation of PA and MMA is nonspecific, though vomiting and refusing feeding are potential markers of decompensation. Blood gas, lactate, and ammonia levels are also good predictors of decompensation, though increasing levels of glycine may not indicate metabolic instability.

Background Preptin is a 34-residue pancreatic hormone that stimulates osteoblast proliferation and reduces osteoblast apoptosis. Research aims To measure levels of serum Preptin in rachitic children and in breastmilk of their mothers and to compare with levels in healthy non-rachitic children. Methods Thirty children with rickets and another 30 non-rachitic age and sex matched controls were subjected to detailed history, physical examination including anthropometric measurements, assessment of signs of rickets and laboratory measurement of serum vitamin D, calcium, phosphorus, alkaline phosphatase and Preptin. Mothers’ breast milk Preptin were also measured. Results Significantly lower serum Preptin ( p < 0.001) in rachitic children with a significant negative correlation between serum Preptin and alkaline phosphatase ( P < 0.0001). Lower breastmilk Preptin levels in mothers of rachitic children ( P < 0.001) with a negative correlation between breastmilk Preptin and both maternal weight and BMI( P < 0.01& P < 0.02). Mothers’ milk Preptin is positively correlated with serum Preptin and calcium in non-rachitic children(P < 0.001&0.04), but negatively correlated with their mothers’ age ( P < 0.01). Conclusion Preptin may play a role in the etiology of rickets in children. Further studies are recommended to evaluate Preptin role in treatment of rickets in children.

Objective: Zinc, copper and selenium are essential for normal development and function of the central nervous system. This study aimed at assessment of serum levels of zinc, copper and selenium in children with severe acute malnutrition (SAM) with & without cerebral palsy both before and after nutritional rehabilitation. Methods: A prospective case control study involved 2 groups (Group I); included160 children with SAM of both sex, aged 6e59 months, this group was subdivided into 2equal subgroups; subgroup A: SAM without cerebral palsy, subgroup B: SAM with cerebral palsy. Group II (control group) included 96 apparently healthy children matching age and sex with the first group. Both groups were subjected to a detailed history including nutritional history. Anthropometric measurements were recorded and laboratory assessment for serum levels of (copper, zinc, & selenium) before and after nutritional rehabilitation were performed for all children. Results: Group I (A&B) showed a significant decrease in anthropometric measurements, serum zinc, serum selenium but normal copper level before nutritional rehabilitation in comparison to