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Background Childhood obesity proves to be an important public health issue, since it serves as a potential risk factor for multiple diseases. Food addiction could also serve as an important etiological factor. As childhood obesity plays a serious issue also in Hungary, we aimed to adapt and validate the Hungarian version of the Yale Food Addiction Scale for Children (H-YFAS-C). Methods A total of 191 children were assessed with the H-YFAS-C and the Eating Disorder Inventory (EDI). The following psychometric properties were analyzed: internal consistency, construct validity, convergent, and discriminant validity. Results A good construct validity was revealed by confirmatory factor analysis (RMSEA = 0.0528, CFI = 0.896, χ 2 value = 279.06). Question 25 proved to have no significant effect on its group and was removed from further analyses. The Kuder-Richardson 20 coefficient indicated good internal consistency (K20 = 0.82). With the use of the eight EDI subscales, a good convergent and discriminant validity could be determined. Food addiction was diagnosed in 8.9% of children. The mean symptom count was 1.7 ± 1.2 (range: 0-7). Females were more often diagnosed with food addiction than males (p = .016; OR = 3.6, 95% CI: 1.2-10.6). BMI percentiles were significantly higher in children with diagnosed food addiction (p = .003). There proved to be no correlation between age and the occurrence of food addiction. Discussion and conclusion Our results show that H-YFAS-C is a good and reliable tool for addictive-like behavior assessment.

Introduction: Hereditary spastic paraplegia is the overall term for clinically and genetically diverse disorders characterized with progressive and variable severe lower extremity spasticity. The most common causes of autosomal dominantly inherited hereditary spastic paraplegias are different mutations of the spastin gene with variable incidence in different ethnic groups, ranging between 15-40%. Mutations in the spastin gene lead to loss of spastins function, causing progressive neuronal failure, which results in axon degeneration finally., Aim: The molecular testing of spastin gene is available in the institution of the authors since January, 2014. The experience gained with the examination of the first eleven patients is described in this article., Method: After polymerase chain reaction, Sanger sequencing was performed to examine the 17 exons of the spastin gene. Multiplex ligation-dependent probe amplification was performed to detect greater rearrangements in the spastin gene. Eight of the patients were examined in the genetic counseling clinic of the authors and after detailed phenotype assessment spastin gene testing was obtained. The other three patients were referred to the laboratory from different outpatient clinics., Results: Out of the 11 examined patients, four different pathogenic mutations were found in 5 patients., Conclusions: The first Hungarian data, gained with the examination of spastin gene are presented in this article. The five patients, in whom mutations were detected, represent 45.5% of all tested patients with hereditary spastic paraplegia, which is similar to those published in the international literature. Molecular testing and subsequent detailed genotype-phenotype correlations of the Hungarian patients may serve valuable new information about the disease, which later on may influence our therapeutic possibilities and decisions.

The occurrence of multimetabolic syndrome was studied in 114 (63 boys, 51 girls) obese children. From the blood sample taken after on overnight fast blood sugar, serum insulin, and lipid levels were determined. During oral glucose tolerance test blood sugar concentrations were followed. Body mass index, body fat (on the basis of skinfold measurements), lean body mass and waist/hip ratio were calculated and blood pressure was measured 6 times in all subjects. Multimetabolic syndrome was found in 16% of boys and 19.6% of girls. No significant sex difference in the frequency of multimetabolic syndrome was found. Patients with multimetabolic syndrome could not be characterized by high waist/hip ratio any other antropometric parameter. The duration of obesity was significantly higher in subjects with multimetabolic syndrome than in those not suffering from the syndrome. This finding supports the hypothesis that the development of the multimetabolic syndrome is a process. The authors emphasize the significance of this problem and the importance of early recognition and prevention.