HMGB1 is related to disease activity in children with celiac disease.

INTRODUCTION: We aim to evaluate of the relationship between high mobility gene box-1 (HMGB1) levels and clinical, laboratory and histopathological findings at diagnosis and in remission in children with Celiac Disease (CD). MATERIAL AND METHODS: The study included 36 celiac patients at diagnosis, 36 celiac patients in remission, and 36 healthy controls. Patients with intestinal pathologies other than CD, and accompanying inflammatory and/or autoimmune diseases were excluded. Relationship between HMGB1 levels and clinical, laboratory and histopathological findings were evaluated. RESULTS: A total of 72 celiac patients [36 (18 girls, 18 boys, mean age 9.41±3.9 years) in group 1 and 36 (18 girls, 18 boys, mean age 9.91±3.36 years) in group 2] and 36 healthy controls in group 3 (19 girls, 17 boys, mean age 9.56±4 years) were included. The HMGB1 level was significantly higher in group 1 compared to group 2 and group 3 [36.63 (17.98-54.72) ng/ml vs 20.31 (16.89-29.79) ng/ml, p = 0.028 and 36.63 (17.98-54.72) ng/ml vs 20.38 (17.54-24.53) ng/ml p = 0.012, respectively]. A serum HMGB-1 level of 26.553 ng/ml was found to be a cut-off value for the CD with 61% sensitivity, 83% specificity, 78% positive predictive value, and 68% negative predictive value. Higher HMGB1 values were seen in patients with intestinal findings, anemia, anti-tissue transglutaminase IgA levels that were greater than 10 times upper limit of normal, and patients with a higher degree of atrophy as classified by Marsh-Oberhuber. CONCLUSIONS: In conclusion, it was thought that HMGB-1 might be a marker that reflects the severity of atrophy at the time of diagnosis and could be used to control dietary compliance in the follow-up. However, there is need for larger population studies in order to evaluate its value as a serological marker for the diagnosis and follow-up of CD and to find a more reliable cut-off value.

Evaluation of ketogenic diet therapy in children diagnosed with drug-resistant epilepsy: a single-center experience.

BACKGROUND: We evaluate here the effect of the ketogenic diet (KD) on children with drug-resistant epilepsy (DRE) in terms of clinical effectiveness, anthropometric measurements, and some electroencephalogram (EEG) and biochemical findings. METHODS: Included in the study were 18 children (median age 70 months, 61.1% female) who received the classical KD and modified Atkins diet (MAD) for at least one year due to DRE. The patients` demographic and laboratory data; weight, height and body mass index values; EEG and electrocardiographic findings; abdominal ultrasonography findings; and biochemical parameters were recorded at baseline and at 12 months after the initiation of the diet. A reduction of ≥50% in the number of seizures was accepted as a response to KD. RESULTS: Classic KD was chosen for 14 patients (77.8%), and MAD for four patients (22.2%). The response to KD therapy (≥50% reduction) was 55.5% (n = 10) (p = 0.008), and one patient even became seizure-free. By the 12th month of treatment, 10 patients had experienced a reduction of more than 50% in epileptiform discharges, as indicated by EEG findings. There was no difference in seizure reduction between the patients who received classical KD and MAD. A total of 11.1% of the children lost weight during KD treatment. The most common side effect was constipation (n = 10, 55.6%). At the end of one year of treatment, total cholesterol and low density lipoprotein cholesterol (LDL-C) LDL-C levels had increased dramatically, while fasting blood glucose levels had decreased significantly. CONCLUSIONS: Our study suggests that KD treatment provides good clinical efficacy in the treatment of pediatric DRE, and can significantly reduce the frequency of epileptic discharges. Also, total cholesterol and LDL-C levels increased significantly, and fasting blood glucose levels decreased significantly compared to the baseline levels.

The association of lipid metabolism and non-alcoholic fatty liver disease in children with obesity.

AIM: Obesity, insulin resistance, and hyperlipidemia have been shown as risk factors for non-alcoholic fatty liver disease. In this study, the association between lipid and lipoprotein metabolism abnormalities and the presence of non-alcoholic fatty liver disease was investigated in patients with obesity. MATERIAL AND METHODS: In this study, the clinical, laboratory and imaging findings of 357 children and adolescent patients (199 girls and 158 boys) aged 2-18 years who were diagnosed as having obesity between 2013 and 2018 were retrospectively analyzed. The clinical and laboratory features of the patients who were diagnosed as having non-alcoholic fatty liver disease using ultrasonography were compared with patients who did not have non-alcoholic fatty liver disease. All lipid and lipoprotein levels were defined as hypo-, normo- and hyperlipidemic in comparison with the reference values according to age and sex. RESULTS: The frequency of non-alcoholic fatty liver disease was 44.5% in the entire study group and was higher in males (p<0.05). The body weight, body mass index, alanine aminotransferase, glucose, insulin, non-high-density lipoprotein-cholesterol, and HOMA-IR scores were found to be higher in the patients with non-alcoholic fatty liver disease, whereas the high-density lipoprotein-cholesterol level was lower (p<0.05). There was no difference in the frequency of non-alcoholic fatty liver disease among the patients with low, normal, and high total cholesterol, triglyceride and low-density lipoprotein-cholesterol levels (p>0.05). The frequency of lipid metabolism disorder (hypolipidemia and/or hyperlipidemia) was found as 77.5% in all patients. CONCLUSION: Non-alcoholic liver disease and lipid metabolism disorders are common in children and adolescents with obesity. The frequency of non-alcoholic fatty liver disease in hypolipidemic, normolipidemic, and hyperlipidemic patients was not different. This finding indicated that the increase in the amount of body fatty tissue and insulin resistance were more important risk factors in the development of non-alcoholic fatty liver disease.