Background: Accurate anthropometric measurements and critical analysis of growth data allow the clinician to promptly recognize children with short stature. The aim of this study was to determine the frequency of etiological factors causing short stature among children referred to the pediatric endocrinology clinic of Assiut University Children's Hospital, the main tertiary care center in Upper Egypt. Methods: We conducted this descriptive observational study from May 2012 to December 2015, to analyze 637 children (boys 354, girls 283) with short stature. Evaluation included: detailed medical history, physical examination, laboratory tests, bone age and chromosomal analysis. Results: Endocrinological causes accounted for 26% of short stature [of them, 11.8% had growth hormone deficiency (GHD)], 63.6% had normal variants of growth [of them, 42% had familial short stature (FSS), 15.8% had constitutional growth delay (CGD) and 5.5% a combination of both]. Interestingly, celiac disease (CD) constituted 6.6% of children with short stature in our cohort. Conclusions: Although potentially treatable causes such as GHD, hypothyroidism and CD accounted for a considerable percentage of short stature in our study, the majority of short stature in children had normal variations of growth. Growth hormone treatment in children, however, should be promptly initiated with specific clinical indications. CD is a not uncommon cause of short stature.

Activating variants in the TGFbeta-1 and VEGF gene promoters are associated with post-UTI renal scar formation in children. The TGFbeta-1 509T allele predicts renal scarring independent of VUR.

B regulatory cells (Breg) refer to characteristic subsets of B cells that generally exert anti-inflammatory functions and maintain peripheral tolerance mainly through their ability to secrete interleukin-10 (IL10). Dysregulation in the function of Breg cells was reported in several autoimmune diseases. However, the relation between Breg and children with type 1 diabetes (T1D) is poorly understood. Thus, this study is aimed at determining whether Breg cells play a role in T1D in children or not, so we hypothesized that an altered phenotype of B cell subsets is associated with T1D in children. Children with T1D (n=29) and control children with normal blood glucose levels (n=14) were recruited. The percentages of different circulating IL10-producing Breg subsets, including B10, immature transitional, and plasmablasts were determined using flow cytometry analysis. Furthermore, the association between different IL10-producing B cells and patient parameters was investigated. The percentage of circulating IL10+CD24hiCD27+ (B10) and IL10+CD24hiCD38hi (immature transitional) subsets of Breg cells was significantly lower in T1D patients than in healthy controls. Moreover, these cells were also negatively correlated with fasting blood glucose and HbA1c levels. Breg cells did not correlate with autoantibody levels in the serum. These findings suggest that certain Breg subsets are numerically deficient in children with T1D. This alteration in frequency is associated with deficient islet function and glycemia. These findings suggest that Breg cells may be involved in the loss of auto-tolerance and consequent destruction of pancreatic cells and could, therefore, be a potential target for immunotherapy.

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