Does obesity or hyperuricemia influence lithogenic risk profile in children with urolithiasis?

BACKGROUND: There are indications that obesity and hyperuricemia may influence the formation and composition of urinary stones. The aim of our study was to determine the effect of obesity and hyperuricemia on the urinary lithogenic risk profile in a large cohort of pediatric patients. METHODS: The study population comprised 478 children with urolithiasis and 517 healthy children (reference group). We studied the effects of obesity on the lithogenic profile by dividing the patients with urolithiasis into two groups based on body mass index Z-score (patients who were overweight/obese vs. those with normal weight for age) and comparing the two groups. To study the effect of hyperuricemia on the lithogenic profile, we divided the patients with urolithiasis into two groups based on the presence or not of hyperuricemia (110 patients with urolithiasis accompanied by hyperuricemia vs. 368 patients with urolithiasis and normal serum uric acid levels) and compared the groups. RESULTS: Among the children and adolescents with urolithiasis and hyperuricemia, there was a significantly lower excretion of crystallization inhibitors (citrates, magnesium). We also found significantly negative correlations between serum uric acid levels and the urine citrate/creatinine ratio (citrate/cr.; r = -0.30, p < 0.01), as well as the magnesium/cr. ratio (Mg/cr.; r = -0.33, p < 0.01). There was no statistically significant differences in the urinary excretion of oxalates, citrates, calcium, phosphorus, magnesium and uric acid between children with urolithiasis who were either overweight or obese and children with urolithiasis who had a normal body weight. CONCLUSIONS: In our pediatric patient cohort, hyperuricemia was associated with a decrease in the excretion of crystallization inhibitors in the urine, but the clinical relevance of this observation needs to be confirmed in future studies. Obesity and overweight had no direct influence on the lithogenic risk profile in the urinary stone formers in our study, but there was an indication that higher serum uric acid may be associated with impairment in renal function, which in turn could influence the excretion of lithogenic parameters.

Cerebrospinal fluid oxidative stress during chemotherapy of acute lymphoblastic leukemia in children.

In this study the authors addressed the question whether neurotoxicity due to the chemotherapy of acute lymphoblastic leukemia (ALL) is associated with cerebrospinal fluid (CSF) oxidative stress. Examination of 38 ALL patients revealed significant increases in 8-isoprostane concentration and important decreases in total antioxidative capacity of CSF during therapy. The mean 8-isoprostane level at diagnosis was 9.05 +/- 1.62 pg/mL, and no correlations with initial leukocytosis, organomegaly, and lactate dehydrogenase levels were noted. 8-Isoprostane concentrations were increased on the 59th day of treatment (mean level: 24.85 +/- 7.59 pg/mL [P < .01]) and remained elevated at 4 points of the consolidation phase (17.28 +/- 2.16 pg/mL [P < .05]; 22.72 +/- 6.04 pg/mL [P < .05]; 24.92 +/- 6.31 pg/mL [P < .01]; 32.32 +/- 7.94 pg/mL [P < .01]) as compared to their level at diagnosis. The mean total antioxidative capacity at diagnosis was 203.08 +/- 6.17 mumol/L and was remarkably decreased on the 59th day of treatment (189.76 +/- 1.9 mumol/L [P < .05]) and at one point of the consolidation phase (188.29 +/- 3.46 mumol/L [P < .05]) as compared to the level at diagnosis. This study indicates that neurotoxicity of standard ALL treatment may be related to oxidative stress.

[Sleep disorders in childhood and adolescence, with special reference to allergic diseases]. / Zaburzenia snu w wieku dziecieco-mlodziezowym, ze szczególnym uwzglednieniem chorób alergicznych.

UNLABELLED: Allergic diseases have a significant impact on the quality of life. The aim of the study was to compare sleep parameters of allergic and non-allergic children. MATERIAL AND METHODS: Pediatric Sleep Questionnaire was used to asses sleep quality in 202 participants in a 3-year prospective study: in 122 hospitalized (mean age 7.9 +/- 4.7) (F/M 75/47) due to allergic (n = 70) or non-allergic disease (n = 52), and in 80 healthy children (mean age 6.3 +/- 5.0) (F/M 36/44). Of 70 allergic participants, 26 had atopic dermatitis (SCORAD > or = 20); 25 were with bronchial asthma (GINA' criteria) and 19 with IgE-dependent food allergy confirmed by oral food challenge. Of 52 non-allergic patients, 31 children had gastro-esophageal reflux disease and 21 children had recurrent respiratory infection. RESULTS: The group of patients needed significantly more time to fall asleep than controls (17.9 +/- 13.7 vs 12.8 +/- 8.5 min; p < 0.004). Children with food allergy and atopic dermatitis had greatest problems with falling asleep (21.4 +/- 13.8 vs 12.8 +/- 8.5 min; p < 0.006) and 20.4 +/- 14.9 vs 12.8 +/- 8.5 min; p < 0.024). The number of nights of sound sleep without waking up was lower in the study group than in controls (3.5 +/- 2.6 vs 5.0 +/- 2.7; p < 0.0002). Atopic dermatitis and food allergy were found to predispose to sleep disruption most. Snoring history was revealed in 43.4% of patients and in 6.4% of controls (p < 0.0001), being significantly more common in children with bronchial asthma and recurrent respiratory tract infections. Allergic disease was a risk factor for snoring (OR--2.94; 95%CI--1.72-5.05; p < 0.001). As many as 91% of parents did not inform doctors about poor sleep of their children. CONCLUSIONS: 1. Allergic diseases are accompanied by different sleep disorders included dyssomnias and parasomnias, e.g. bedtime resistance, disrupted sleep or sleep-disordered breathing. 2. Physicians should pay particular attention to sleep quality in children with allergic diseases irrespective of which body system is affected i.e. the skin (atopic dermatitis), the respiratory tract (bronchial asthma) or the alimentary system (food allergy).

Negative correlation between cerebrospinal fluid tau protein and cognitive functioning in children with acute lymphoblastic leukemia.

The aim of the study was to assess whether cerebrospinal fluid tau protein is associated with cognitive changes in children with acute lymphoblastic leukemia (ALL). Examination of 38 ALL patients revealed a statistically significant increase in tau protein on treatment day 59 and at two points during consolidation phase. Cognitive functioning was examined in 19 patients at an average of 3.7 years after diagnosis. The level of tau at the initiation of maintenance therapy was negatively correlated with verbal abilities measured on an intellectual scale. The study suggests that standard ALL treatment may cause a decline in cognitive functioning.

Level of tau protein in children treated for acute lymphoblastic leukemia.

Long-term neuropsychological complications such as attention and concentration disturbances, poor school performance, hyperexcitability, and even leukoencephalopathy have been described in children after chemotherapy for acute lymphoblastic leukemia. Elevation of the cerebrospinal fluid level of tau protein, associated with neuronal axons, is a neurodegenerative marker. The aim of the study was to assess the level of cerebrospinal fluid tau protein in children with acute lymphoblastic leukemia. The study included 26 patients with acute lymphoblastic leukemia and 19 patients with clinical symptoms of cerebrospinal meningitis (reference group). Tau protein levels were determined by enzyme-linked immunosorbent assay. Cerebrospinal fluid total protein level was not elevated in any of the samples. The examination was performed at diagnosis, after induction treatment, during consolidation, and after reinduction, i.e. before maintenance therapy. Neither age nor sex had an effect on tau protein levels in both groups. The mean tau protein value at diagnosis was 244.84 +/- 98.96 pg/mL in the study group (norm 300 pg/mL) and produced no correlation with initial leukocytosis, lactate dehydrogenase activity, or organomegaly at this point. Dynamic analysis revealed a statistically significant increase in tau protein after induction treatment (431.25 +/- 232.50) as compared with its level at diagnosis (244.84 +/- 98.96, P < 0.008) and later during treatment. The levels of tau protein at various points of treatment did not differ statistically significantly between the groups, except for the values obtained after termination of remission induction. The observed metabolic changes in tau protein, which is a known marker of neuronal damage, indicate that some patients are at a greater risk of central nervous system disorders. This finding requires further studies, also in reference to other central nervous system proteins, and confirms the necessity of long-term follow-up of leukemia patients.