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Purpose: We aimed to examine the possible association role of vitamin D and vitamin D receptor (VDR) single nucleotide polymorphisms (SNPs) in type 1 diabetes mellitus (T1DM) development, glycemic control and complications among a cohort of Egyptian children. Subjects and methods: A prospective case-control study has been conducted on 50 Egyptian children with T1DM who were comparable with 50 controls. Vitamin D and HbA1c were measured. VDR-SNPs [ Apa I (rs7975232), Taq I (rs731236) and Bsm I (rs1544410)] detection was done by polymerase chain reaction through restriction fragment length polymorphism (PCR-RFLP) technique. Vitamin D supplements were given to the included T1DM children with low vitamin D and reassessments of both HbA1c% and 25(OH)D serum levels were performed in those children three months later. Results: Eighty percent of the included diabetic patients have poor glycemic control. Vitamin D was deficient in 68% and insufficient in 16% of diabetic patients. Significant improvements in both vitamin D and glycemic status among T1DM children, who have low vitamin D and received vitamin D supplementations. There were significantly negative correlations between serum levels of vitamin D with both HbA1c % (r= –0.358, P ˂0.05) and daily insulin dose (r=−0.473, P ˂0.05). Compared with controls, T1DM children presented more commonly with Apa I a allele (OR: 2.87; 95%CI: 1.39–5.91, P ˂0.05) and Bsm I b allele (OR: 4.38; 95%CI: 2.30–8.33, P ˂0.05). Taq I t allele wasn’t significantly differing among patients and controls ( P ˃0.05). Aa+aa and Bb+bb genotypes were significantly higher among T1DM vs the controls (OR: 3.08;, 95%CI: 1.33–7.15, P ˂0.05 and OR: 9.33; 95%CI: 3.61–24.17, P ˂0.05respectively). Conclusion: Apa I and Bsm I were associated with risk of T1DM development among Egyptian children. Low vitamin D status was frequently occurring among T1DM with significant improvement in the glycemic control of such children when adding vitamin D supplements to the standard insulin therapy.

BackgroundThe exact pathogenesis of autism is still unknown. Both thyroid hormones and 25(OH)D are important for brain development, in addition to CD5; all have immunomodulatory actions by which their dysregulation may have a potential role in autism pathogenesis.ObjectivesThe objectives of this study were to assess the thyroid profile, serum 25(OH)D levels and CD5 expression levels among autistic patients and to find out the correlations between the measured biomarkers with each other on one side and with the disease severity on the other side.Patients and methodsThis cross-sectional case–control study has been conducted on 60 children with autism and 40 controls, recruited from Qena Governorate, Upper Egypt. Childhood Autism Rating Scale (CARS) score was used to assess the included patients. Biochemical assays of thyroid function in the form of free triiodothyronine (FT3), free tetraiodothyronine (FT4), thyroid-stimulating hormone (TSH) and 25(OH)D were done using commercially available enzyme-linked immunosorbent assay (ELISA) kits, while CD5 expression levels were measured using flow cytometry (FCM) analysis for all the included patients and controls.ResultsThe overall measurement results show significant higher mean serum TSH levels, mean CD5 expression levels with significant lower mean serum 25(OH)D levels among autistic children when compared with the control group (p<0.05 for all). Significant negative correlations between CD5 with FT3, FT4 and 25(OH)D were observed. CARS score showed significant negative correlations with both FT3 and 25(OH)D, while it was positively correlated with CD5 in a significant manner (p<0.05 for all).ConclusionElevated CD5 expression and decreased 25(OH)D stores could play a potential role in the pathogenesis of autism via their immune-modulator actions. High TSH serum levels among autistic children, although within the physiological range, reflect the presence of thyroid dysfunction among such children, which needs further assessment.

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Background There is a scarce research study on recurrent pneumonia in children, particularly in the developing world. This study aimed to analyse the clinical characteristics, risk factors and underlying causes of recurrent pneumonia in children. Methods It was a case‐control study involved 87 children with ≥2 episodes of radiographically confirmed pneumonia in a single year or ≥3 episodes at any time with a radiographic clearing of densities between attacks. Controls were 87 age and gender‐matched children who had never suffered pneumonia. Demographic and clinical characteristics of patients and controls were compared and evaluated for the detection of possible underlying conditions that may be the incriminated risk factor of pneumonia recurrence. Results During one‐year study, 763 patients were admitted with pneumonia and 87 (11.4%) of them met the definition of recurrent pneumonia. There were 48 (55.2%) males and 39 (44.8%) females. The mean age at diagnosis of recurrent pneumonia was 7.15 ± 1.72 years. Prematurity, small birth weight and presence of respiratory distress at birth were significantly different between patients and controls. Aspiration, congenital heart disease, gastroesophageal reflux, oro‐motor incoordination, wheezing and asthma were significant risk factors for recurrent pneumonia. Conclusion Our study showed that 11.40% of children with pneumonia had recurrent form and that most of them had an underlying illness. The most common detected risk factors for recurrent pneumonia were rural residence, low socioeconomic standard, over‐crowding, prematurity and presence of respiratory distress at birth. Aspiration, congenital heart diseases, wheezing and asthma were found to be the main underlying illnesses associated with pneumonia recurrences.