Evaluation of validity of Integrated Management of Childhood Illness guidelines in identifying edema of nutritional causes among Egyptian children.

OBJECTIVE: The aim of this study was to assess the validity of the Integrated Management of Childhood Illness (IMCI) algorithm to detect edematous type of malnutrition in Egyptian infants and children ranging in age from 2 months to 5 years. MATERIALS AND METHODS: This study was carried out by surveying 23 082 children aged between 2 months and 5 years visiting the pediatric outpatient clinic, Ain Shams University Hospital, over a period of 6 months. Thirty-eight patients with edema of both feet on their primary visit were enrolled in the study. Every child was assessed using the IMCI algorithm 'assess and classify' by the same physician, together with a systematic clinical evaluation with all relevant investigations. RESULTS: Twenty-two patients (57.9%) were proven to have nutritional etiology. 'Weight for age' sign had a sensitivity of 95.5%, a specificity of 56%, and a diagnostic accuracy of 78.95% in the identification of nutritional edema among all cases of bipedal edema. Combinations of IMCI symptoms 'pallor, visible severe wasting, fever, diarrhea', and 'weight for age' increased the sensitivity to 100%, but with a low specificity of 38% and a diagnostic accuracy of 73.68%. CONCLUSION AND RECOMMENDATIONS: Bipedal edema and low weight for age as part of the IMCI algorithm can identify edema because of nutritional etiology with 100% sensitivity, but with 37% specificity. Revisions need to be made to the IMCI guidelines published in 2010 by the Egyptian Ministry of Health in the light of the new WHO guidelines of 2014.

Von Willebrand Factor and Factor VIII levels in Egyptian children with newly diagnosed acute lymphoblastic leukemia in relation to peripheral blast cells and steroid therapy.

BACKGROUND: Endothelial dysfunction has been reported in children with acute lymphoblastic leukemia (ALL). The aim of this study is to assess Von Willebrand Factor antigen (VWF antigen) and Factor VIII (FVIII) in newly diagnosed ALL patients, in relation to peripheral blast (PB) cells, steroid therapy, and any prognostic potential. PROCEDURE: VWF antigen and FVIII were assessed initially (D0) and at day 8 (D8) steroid therapy for 32 newly diagnosed ALL patients with and without peripheral blood blast cells. RESULTS: At diagnosis, patients with PBs had a significantly higher levels of VWF antigen (102.7 ± 22.9% vs. 56.9 ± 8%, P<0.001) and FVIII (93.4 ± 15.9% vs. 6 62.6 ± 18.1%, P<0.001) than those without. Following steroid therapy, both factors decreased in those with PBs, whereas an increase above baseline was observed in those without PBs. Furthermore, there was a significant positive correlation between PBs and both VWF antigen (P<0.001) and FVIII levels (P=0.002). High-risk patients were comparable with standard-risk group in mean values of VWF antigen (P=0.234) and FVIII (P=0.891) at diagnosis. After 12 months from diagnosis, all patients without PB achieved and maintained complete remission. Those with initial PB reported relapse (12.5%) or death (4.2%) during follow-up. CONCLUSIONS: Markers of endothelial dysfunction namely VWF and FVIII were related to circulating blast cells and steroids therapy through lysis of lymphoblasts results in reduction of both factors, with risk of thrombosis during induction with marked disintegration of malignant cells.

Plasma adrenomedullin level in Egyptian children and adolescents with type 1 diabetes mellitus: relationship to microvascular complications.

BACKGROUND: Adrenomedullin (AM) is known to be elevated in different clinical situations including diabetes mellitus (DM), but its potential role in the pathogenesis of vascular complications in diabetic children and adolescents is to be clarified. Hence, the study aimed at assessment of plasma adrenomedullin levels in children and adolescents with type 1 DM and correlation of these levels with metabolic control and diabetic microvascular complications (MVC). METHODS: The study was performed in the Diabetes Specialized Clinic, Children's Hospital of Ain Shams University in Cairo, Egypt. It included 55 diabetic children and adolescents (mean age 13.93 +/- 3.15 years) who were subdivided into 40 with no MVC and 15 with MVC. Thirty healthy subjects, age-and sex-matched, were included as control group (mean age 12.83 +/- 2.82 years). Patients and controls were assessed for glycosylated hemoglobin (HbA1c) and plasma adrenomedullin assay using ELISA technique. RESULTS: Mean plasma AM levels were significantly increased in patients with and without MVC compared to control group, (110.6 pg/mL, 60.25 pg/mL and 39.2 pg/mL respectively) (P < 0.01) with higher levels in those with MVC (P < 0.05). Plasma AM levels were positively correlated with both duration of diabetes (rho = 0.703, P < 0.001) and glycemic control (HbA1c) (rho = 0.453, P < 0.001). CONCLUSION: Higher plasma AM levels in diabetics particularly in those with MVC & its correlation with diabetes duration and metabolic control may reflect the role of AM in diabetic vasculopathy in the pediatric age group.

Urinary excretion of n-acetyl-beta-D-glucosaminidase and retinol binding protein as alternative indicators of nephropathy in patients with type 1 diabetes mellitus.

Diabetic nephropathy (DN) is usually characterized by glomerular dysfunction, with microalbuminuria as an early indicator. Urinary excretion of smaller molecular weight proteins such as n-acetyl-beta-glucosaminidase (beta-NAG) and retinol binding protein (RBP) indicate proximal tubular dysfunction, and may identify diabetic patients at risk of developing diabetic nephropathy. In a trial to assess renal tubular function, urinary excretion of beta-NAG (by colorimetric assay) and RBP (by ELISA) were determined in 59 type 1 diabetic patients (mean age 15 +/- 3.2 yr). Of the 59 patients, 11 were microalbuminuric while 48 had normal urinary albumin excretion (UAE). Patients were compared with 40 matched healthy subjects. Diabetic patients with microalbuminuria (n = 11) had concomitant renal tubular disorder indicated by high urinary beta-NAG in all (100%) and RBP in 10 (90.9%) of them. Meanwhile, patients without microalbuminuria (n = 48) had both tubular markers excreted in urine in significantly higher amounts than controls (mean beta-NAG = 6.88 vs. 3.76 U/g Cr, p < 0.001; RBP = 386.6 vs. 151.8 microg/dL, p < 0.001). Among those patients, 29 (61%) had raised urinary beta-NAG activity, and 39 (82%) had increased loss of RBP in urine. A significant correlation was found between urinary beta-NAG and RBP in normoalbuminuric patients (r = 0.66, p < 0.001), as well as between each of the two tubular markers and HbA1c (r = 0.83, p < 0.001). At 30 and 36 months of follow-up, two out of 48 (4.2%) diabetic patients developed persistent microalbuminuria. Both had elevated baseline HbA1C, and urinary beta-NAG. In conclusion, proximal tubular dysfunction may occur independent of glomerular alteration. Whether tubular markers precede the development of microalbuminuria needs further study.