Etiology of diarrheal disease among children under 5 years in Egypt: a high incidence of human bocavirus.

BACKGROUND: Human bocavirus (HBoV) is globally distributed and associated with respiratory and enteric infections. Limited data are available about the incidence of HBoV in Egyptian children. We aimed to investigate the association of HBoV genotypes in children with diarrheal disease and also to determine the possibility of HBoV co-infections with other human enteric pathogens. METHODS: A total of 102 stool samples were collected from children under five years old with diarrhea. Samples were analyzed for the presence of HBoV by real-time PCR. HBoV positive samples were tested for adenovirus (AdV), rotavirus (RoV), parasitic helminths, and enteric protozoa. RESULTS: HBoV was detected in 58% of examined cases. HBoV-3 was the most prevalent genotype observed (44%; 45 of 102), followed by HBoV-2/4 (33%; 34 of 102) and HBoV-1 (30%; 31 of 102). Although the incidence of HBoV was higher in males (66.6%; 34 of 51) than females (49%; 25 of 51), the analysis showed no significant difference for HBoV between genders. The average HBoV concentrations were 5.3 × 104 GC/g in males and 1.03 × 105 GC/g in females. Among the HBoV-positive samples, the single infection of HBoV was 52.5% (31/59), while the co-infections with multiple viruses were found in 1.7% (1/59) for HBoV and AdV, 33.9% (20/59) for HBoV and RoV, and 11.9% (7/59) for HBoV, and RoV and AdV. No co-infection with parasitic helminths or enteric protozoa was found. CONCLUSIONS: The single infection of HBoV in some children suffering from acute gastroenteritis indicated that HBoV could be the main etiologic agent of the disease. The study highlights the high incidence of HBoVs genotypes with remarkable multiple co-infections in the pre-school children in Egypt.

Association of ficolin-2 (FCN2) functional polymorphisms and protein levels with rheumatic fever and rheumatic heart disease: relationship with cardiac function.

INTRODUCTION: A role for ficolin (FCN) 2 gene polymorphisms in the pathogenesis of recurrent severe streptococcal infections and rheumatic carditis has been suggested. The aim of the study was to evaluate a possible relationship between single nucleotide polymorphisms located at positions -602 and -4 of the FCN2 gene and FCN2 serum levels and risk of development of rheumatic fever (RF) and rheumatic heart disease (RHD). MATERIAL AND METHODS: Seventy-seven Caucasian Egyptian patients with RF were recruited with a control group of 43 healthy subjects. DNA was extracted for analysis of the FCN2 gene at positions -602 and -4 and serum protein level was measured by ELISA. RESULTS: FCN2 AA genotype at the -4 position was more frequently observed in RF and RHD patients, as compared to healthy subjects (p = 0.005 and p = 0.013, respectively); furthermore, the A allele was identified as a possible risk factor for the development of RF (p = 0.023, OR = 1.852, 95% CI: 1.085-3.159). The haplotype -602/-4 G/A, which was associated with low median levels of L-ficolin, was observed more frequently in the RF group when compared to the healthy subjects (74/162, 48.1% vs. 29/420, 33.7%, OR = 1.834, 95% CI: 1.034-3.252, p = 0.038). Low serum ficolin-2 level was associated with ESV and EDV increases. FCN 2 level was significantly lower with AA genotypes than GG+AG genotypes of the -4 position (56.68 ±17.90 vs. 66.05 ±18.79, p = 0.008). CONCLUSIONS: Polymorphisms linked to low levels of L-ficolin may render an individual at risk of recurrent and/or severe streptococcal infection. The -4 AA genotype and -602/-4 G/A haplotype are possible risk factors for the development of carditis.

Serum cystatin C, urinary neutrophil gelatinase-associated lipocalin and N-acetyl-beta-D-glucosaminidase in juvenile and adult patients with systemic lupus erythematosus: Correlation with clinical manifestations, disease activity and damage.

Lupus nephritis (LN) is a potentially devastating outcome of systemic lupus erythematosus (SLE). It is important to identify reliable, non-invasive methods to assess the kidneys in patients with SLE. The aim of the study was to measure the level of novel markers of renal involvement in these patients and assess their correlation with disease activity and damage. Sixtyone patients with SLE (33 adults and 28 juvenile) were included in the study. Fifty-two ageand sex-matched healthy individuals served as controls. Full history taking, thorough clinical examination and laboratory investigations were performed and disease activity and damage were assessed for all patients. Renal bio-markers including serum cystatin C, urinary neutrophil gelatinase-associated lipocalin (UNGAL) and N-acetyl-beta-D-glucosaminidase (UNAG) were assessed in patients and controls. There was a significant increase in serum cystatin C, UNGAL and UNAG levels in the adult SLE patients compared with controls (P = 0.000, P = 0.013 and P = 0.018, respectively); serum cystatin C and UNGAL levels were higher in the juvenile patients compared with controls (P = 0.038 and P = 0.000, respectively). Serum cystatin C significantly correlated with the damage index, renal biopsy class and negatively with the serum albumin; UNGAL correlated with albuminuria and the level of nephritis and UNAG negatively correlated with serum albumin level. Our study suggests that serum cystatin C, UNGAL and UNAG are important markers of LN and both cystatin C and UNAG would help in predicting the renal biopsy class.

Nesfatin-1 in childhood and adolescent obesity and its association with food intake, body composition and insulin resistance.

Nesfatin-1 is an anorexigenic peptide that controls feeding behavior and glucose homeostasis. However, there is little data that exists regarding nesfatin-1 secretion in obese children and young adolescents. The aim of this study is to investigate serum nesfatin-1 in childhood and adolescent obesity and to study potential correlations with food intake, anthropometric indices, body composition and insulin resistance. Forty obese children and adolescents and 40 healthy control subjects were studied. Anthropometric measurements were assessed, dietary food intake was evaluated based on 3-days food record and body composition indices were evaluated using bioelectrical impedance analysis. Lipid profile, fasting blood sugar, fasting insulin and HOMA-IR were measured. Fasting serum nesfatin-1 was quantitatively assayed by ELISA. Serum nesfatin-1 was significantly higher in obese group (2.49±1.96 ng/ml) than in control group (0.70±0.81 ng/ml), P=0.001. Positive correlations with serum insulin (P=0.001), HOMA-IR (P=0.000), BMI-SDS (P=0.04), body fat % (P=0.000), fat mass (P=0.000), fat free mass (P=0.03), CHO % (P=0.000), and saturated fat % (P=0.01) were found. While significant negative correlation with protein % (P=0.000) was observed. In conclusion, our results denote that nesfatin-1 might have an important role in regulation of food intake and pathogenesis of insulin resistance in obese children and young adolescents.

Serum cystatin C is a poor biomarker for diagnosing acute kidney injury in critically-ill children.

BACKGROUND: Accurate diagnosis of acute kidney injury (AKI) is problematic especially in critically-ill patients in whom renal function is in an unsteady state. AIM: Our aim was to evaluate the role of serum (S.) cystatin C as an early biomarker of AKI in critically-ill children. SUBJECTS AND METHODS: S. creatinine and S. cystatin C were measured in 32 critically-ill children who were at risk for developing AKI. AKI was defined by both: Risk,-injury,-failure,-loss, and-endstage renal disease (RIFLE) classification and glomerular filtration rate (GFR) <80 ml/min/1.73 m(2). GFR was estimated by both Schwartz formula and S. cystatin C-based equation. RESULTS: S. cystatin C was not statistically higher in AKI patients compared with non-AKI by RIFLE classification (median 1.48 mg/l vs. 1.16 mg/l, P = 0.1) while S. creatinine was significantly higher (median 0.8 mg/dl vs. 0.4 mg/dl, P = 0.001). On estimating GFR by the two equations we found, a lag between rise of S. cystatin C and creatinine denoted by lower GFR by Schwartz formula in four patients, on other hand, six patients had elevated S. cystatin C with low GFR despite normal creatinine and GFR, denoting poor concordance between the two equations and the two markers. The ability of S. creatinine in predicting AKI was superior to S. cystatin with area under the curve (AUC) 0.95 with sensitivity and specificity (100% and 84.6%, respectively) using the RIFLE classification. The same findings were found when using Schwartz formula. CONCLUSION: S. cystatin C is a poor biomarker for diagnosing AKI in critically-ill children.

Association of tumor necrosis factor-alpha gene polymorphisms with juvenile systemic lupus erythematosus nephritis in a cohort of egyptian patients.

INTRODUCTION: The production of tumor necrosis factor (TNF)-alpha has been deeply deregulated in systemic lupus erythematosus. We evaluated the association of -863C>A and -1031T>C polymorphisms of the TNF gene with susceptibility to and clinical manifestations of juvenile systemic lupus erythematosus. MATERIALS AND METHODS: This study was performed on 70 juvenile patients with systemic lupus erythematosus (mean age, 13.0 ± 4.2 years). Ninety age- and sex-matched children served as a controls. All participants were genotyped for the TNF -863C>A and -1031T>C polymorphisms by polymerase chain reaction-restriction fragment length polymorphism method. Analysis of serum TNF-alpha was done by solid-phase sandwich enzyme immunoassay. RESULTS: The mean serum TNF-alpha was significantly higher in the SLE patients compared to controls (P < .001). Regarding all participants, the mean serum TNF-alpha was significantly higher in children with -863AA genotype compared to carriers of -863C allele (P < .001). The TNF -863AA genotype frequencies were significantly higher in the patients group compared with the controls (P = .005) and were associated with increased risk for SLE development (odds ratio, 4.05; 95% confidence interval, 1.38 to 13.13; P = .005). The -863AA variant was associated with nephritis (P < .001) and Raynaud phenomenon (P = .001). CONCLUSIONS: The -863A allele of the TNF gene can be used as a genetic marker for SLE susceptibility and was associated with high TNF-alpha production, Raynaud phenomenon, and nephritis in juvenile SLE Egyptian patients.

Effect of high-flux versus low-flux dialysis membranes on parathyroid hormone.

INTRODUCTION. Hyperparathyroidism is a common finding in patients with renal insufficiency and parathyroid hormone (PTH) is considered a uremic toxin responsible for many of the abnormalities of the uremic state and bone disease. The aim of this study was to investigate the influence of permeability of low-flux versus high-flux dialysis membranes on intact PTH during hemodialysis in children. MATERIALS AND METHODS. Forty-four children aged between 4 and 13 years old on regular hemodialysis were enrolled in a prospective study. Low-flux polysulfone membranes were used for at least 6 months and then the patients were switched to use high-flux polysulfone membranes for 3 months. Serum electrolytes and intact PTH before and after dialysis were compared before and after changes in dialysis membrane. RESULTS. At the end of the 3-month use of high-flux filters, predialysis intact PTH level (49.40 ± 19.64 ng/dL) showed a highly significant decline (P < .001) compared to the predialysis intact PTH (21.67 ± 4.85 ng/dL) with low-flux membranes at the start of the study. Intact PTH level correlated negatively with serum ionized calcium and positively with serum phosphorus levels only in the predialysis samples with the use of low-flux but not high-flux filters. CONCLUSIONS. In children, high-flux dialysis membranes are more efficient in removal of intact PTH, one of the middle-sized uremic toxins, than low-flux membranes.