SUMMARY OBJECTIVE: The objective of this study is to determine the Turkish validity and reliability of COVERS. METHODS: This study was conducted on 41 newborns as methodological design. The scales, such as newborn information form, COVERS, preterm infant pain profile (PIPP), and neonatal infant pain scale (NIPS), were used in the study. Validity (e.g., language, content concurrent, and construct) and internal consistency and inter-rater reliability of the scale were conducted. RESULTS: It was found that COVERS showed a high correlation with PIPP and NIPS, and the item-total correlation of COVERS was above 0.30 during and after heel lance procedure. The Cronbach’s α values were 0.77 and 0.83 during and after heel lance procedure, respectively. The kappa values of the items of COVERS were between 0.38 and 0.78 during heel lance procedure. CONCLUSIONS: It was concluded in this study that there was a moderate correlation in intraclass correlation coefficients for scores of COVERS during both diaper change and heel lance procedures. It has been concluded that the scale is valid and reliable in 27-week-old and older newborns.

Objective. To determine the frequency of the MEFV gene mutations in pediatric patients diagnosed with HSP and to assess the effect of the MEFV gene mutations on their prognosis. Material and Methods. Ccross-sectional study; pediatric patients between 2-11 years diagnosed with HSP were included. These cases were investigated for 6 MEFV gene mutations (M694V, M680I, A744S, R202Q, K695R, E148Q). Results. Eighty cases were included in the study of which 55% were male (n= 44). The mean age was 6.44 ± 2.52 years. Disease recurrence occurred in 9 patients, invagination in 5 patients and convulsion in 1 patient during follow-up. Approximately half of the patients received steroids. The MEFV gene mutations was not detected in 44 (55%) of the patients. There was a heterozygous mutation in 19 (22%). E148Q was found in 8 patients, M694V in 5 patients, A744S in 4 patients, and the R202Q heterozygous mutation in 2 patients. The M608I homozygous mutation was detected in 1 patient and the M694V homozygous mutation in 1 patient. The compound heterozygous MEFV gene mutations was found in 15 patients. The presence of the MEFV gene mutations was not correlated with the frequency of renal and gastrointestinal involvement and prognosis, the development of complications and the use of steroids. Conclusion. The presence of the MEFV gene mutations does not correlate with the clinical course and complication in Turkish pediatric patients with HSP.

Objetivo. Determinar la frecuencia de mutaciones del gen MEFV en niños con diagnóstico de púrpura de Schonlein-Henoch y evaluar el efecto que tienen en el pronóstico. Materiales y métodos. Estudio transversal que incluyeron pacientes pediátricos de entre 2 y 11 años, con diagnóstico de púrpura de Schonlein-Henoch. Se estudiaron para detectar 6 mutaciones en el gen MEFV (M694V, M680I, A744S, R202Q, K695R y E148Q). Resultados. Se incluyeron ochenta pacientes, de los cuales el 55% eran de sexo masculino (n= 44). La media de edad fue 6,44 ± 2,52 años. Durante el seguimiento, 9 pacientes presentaron recurrencia de la enfermedad, 5 sufrieron invaginación intestinal y 1 paciente tuvo convulsiones. Aproximadamente la mitad de los pacientes recibió corticoides. En 44 pacientes (55%) no se detectaron mutaciones en el gen MEFV. En 19 pacientes (22%) hubo una mutación heterocigota. Se encontró E148Q en 8 pacientes, M694V en 5 pacientes, A744S en 4 pacientes y la mutación heterocigota R202Q en 2 pacientes. En 1 paciente se detectó la mutación heterocigota M608I y en otro paciente se encontró la mutación homocigota M694V. En 15 pacientes se encontraron mutaciones heterocigotas compuestas en el gen MEFV. Las mutaciones en el gen MEFV no se correlacionaban con la frecuencia de compromiso renal y gastrointestinal ni con el pronóstico, desarrollo de complicaciones y uso de corticoides. Conclusiones. Las mutaciones en el gen MEFV no se correlacionan con la evolución clínica ni con las complicaciones en pacientes pediátricos con púrpura de Schonlein-Henoch en Turquía.

Introduction. Dyslipidemia is one of the major complications of obesity; vitamin D deficiency and insulin resistance are attending metabolic complications in dyslipidemic obese children. Objective. To determine if vitamin D deficiency and insulin resistance are risk factors for dyslipidemia in obese children. Materials and Methods. This study was conducted in the Department of Pediatrics at Bagcilar Training and Research Hospital in Istanbul, Turkey between 2014 and 2015. Obese patients whose age range was 8-14 were included in the study. The serum triglyceride, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, fasting glucose, insulin, alanine aminotransferase, vitamin D levels were measured; a liver ultrasonography was performed. Homeostatic model assessment (HOMA-IR), was used to calculate insulin resistance. Results. 108 obese children were included; 39 (36.11%) had dyslipidemia. The average fasting blood glucose (88.74 ± 7.58 vs. 95.31 ± 6.82; p= 0.0001), insulin level (14.71 ± 12.44 vs. 24.39 ± 15.02; p= 0.0001) and alanine aminotransferase level (23.45 ± 11.18 vs. 30.4 ± 18.95; p= 0.018) were significantly higher in the children with dyslipidemia. In the dyslipidemic obese children, the average hepatosteatosis rate and HOMA-IR level were higher; 28 (71.9%) had hepatosteatosis, 37 (94.87%) had insulin resistance; the vitamin D levels were <20 ng/ml in 69.3%. Vitamin D deficiency was significantly more common (p= 0.033). The multivariate regression analysis confirmed that the increase in the HOMA-IR level (p= 0.015) and the low vitamin D level (p= 0.04) were important risk factors for dyslipidemia. Conclusion. Obese children in our region exhibit low vitamin D and increased HOMA-IR levels, which are efficient risk factors of dyslipidemia.

Introducción. La dislipidemia es una de las mayores complicaciones de la obesidad; la deficiencia de vitamina D y la resistencia a la insulina son complicaciones metabólicas que se presentan en niños obesos con dislipidemia. Objetivo. Determinar si la deficiencia de vitamina D y la resistencia a la insulina son factores de riesgo de dislipidemia en niños obesos. Materiales y métodos. Este estudio se llevó a cabo en el Departamento de Pediatría del Hospital Universitario y de Investigación Bagcilar en Estambul, Turquía, entre 2014 y 2015. Se incluyeron en el estudio pacientes obesos de 8 a 14 años de edad. Se midió la concentración sérica de triglicéridos, colesterol total, colesterol de las LDL, colesterol de las HDL, glucemia en ayunas, insulina, alanina aminotransferasa y vitamina D; también se hicieron ecografías hepáticas. La resistencia a la insulina se calculó utilizando el índice de la evaluación del modelo homeostático (HOMA-IR). Resultados. Se incluyeron en el estudio 108 niños obesos, de los cuales 39 (36,11%) padecían dislipidemia. Los valores promedio de glucemia en ayunas (88,74 ± 7,58 frente a 95,31 ± 6,82; p= 0,0001), insulina (14,71 ± 12,44 frente a 24,39 ± 15,02; p= 0,0001) y alanina aminotransferasa (23,45 ± 11,18 frente a 30,4 ± 18,95; p= 0,018) fueron significativamente más altos en los niños con dislipidemia. En los niños obesos con dislipidemia, la tasa promedio de esteatosis hepática y el índice HOMA-IR fueron más altos: 28 niños (71,9%) tuvieron esteatosis hepática y 37 (94,87%), presentaron resistencia a la insulina; las concentraciones de vitamina D fueron <20 ng/ml en el 69,3% de los niños. La deficiencia de vitamina D fue notablemente más frecuente (p= 0,033). El análisis de regresión multivariante confirmó que el aumento del índice HOMA-IR (p= 0,015) y el bajo nivel de vitamina D (p= 0,04) fueron factores importantes de riesgo de dislipidemia. Conclusión. En los niños obesos de nuestra región se observanbajas concentraciones de vitamina D y aumento del índice HOMA-IR, ambos factores de riesgo significativos para la dislipidemia.