RESUMO
PURPOSE: The high prevalence of non-alcoholic fatty liver disease (NAFLD) in obese children with obstructive sleep apnoea (OSA) calls for early non-invasive screening. The aim of this study was to use ultrasonographic liver echogenicity and elasticity to evaluate the early stages of liver injury in obese children with OSA. METHODS: Fifty-five obese children with OSA aged 12 to 15 years were included. The control group (n = 56) consisted of healthy, non-obese children. All children underwent ultrasound examination to assess liver echogenicity using the hepatorenal index (HRI) and real-time elastography to determine the liver fibrosis index (LFI). Polysomnographic parameters, sonographic values, and clinical-biochemical assessment were statistically analysed according to OSA and its severity. Subgroup 1 was obese children with OSA and AHI < 5 and subgroup 2 was obese children with OSA and AHI ≥ 5. RESULTS: Higher average values of HRI and LFI were recorded in the group of obese paediatric patients with OSA (mean age ± SD, 14.1 ± 2.2 year; 53% male; BMI z-score, 2.6 ± 0.35) compared to the control group (1.37 ± 0.19 vs. 1.12 ± 0.07, p < 0.001 and 1.82 ± 0.31 vs. 1.02 ± 0.27, p < 0.001). A significantly higher LFI was recorded in subgroup 2 compared to subgroup 1 (2.0 ± 0.3 vs. 1.6 ± 0.2, p < 0.001) while laboratory parameters and HRI (1.4 ± 0.2 vs. 1.4 ± 0.2, p = 0.630) did not change significantly. A strong positive correlation was found between the severity of OSA and the LFI (r = 0.454; p < 0.01). CONCLUSIONS: These findings suggest that ultrasound elastography is a useful non-invasive screening test for OSA-related steatohepatitis in obese adolescents, but other clinical studies are needed to confirm this result.
RESUMO
STUDY AIMS: The study assessed the presence of sleep abnormalities in children who had recently been diagnosed with celiac disease (CD) and not started a gluten free diet (GFD). The children's polysomnographic profiles were also characterized and further compared with healthy children of the same age. METHODS: This prospective cross-sectional study involved 46 pediatric subjects (aged 1-19 years) who had recently been diagnosed with CD and not started a GFD. The control group consisted of 32 healthy children (aged 2-17 years). All children underwent anthropometric measurement, laboratory testing and standard overnight observation with in-laboratory video-PSG. The study and control group were divided into subgroups according to the subjects' median ages (8.1 years): celiac children aged less than 8.1 years (n = 23) and more than 8.1 years (n = 23), healthy children less aged than 8.1 years (n = 16) and more than 8.1 years (n = 16). RESULTS: No significant differences in the basic demographic and anthropometric parameters between the celiac and control group were observed. Significantly prolonged sleep latency (SOL) was evident in the celiac subjects (21.89 ± 20.77 min. vs. 10.99 ± 7.94 min, p = 0.02), with a probability of prolonged SOL of 4.23-fold greater (OR = 4.23; 95 % CI 1.1-16.22) than the healthy controls, especially in the subgroup of older celiac patients. No significant differences in the sleep period time (SPT), total sleep time (TST), wake during sleep (WASO), sleep efficiency (SE) and sleep stage distribution and cyclization were found. The respiratory rates during sleep indicated a significantly greater incidence of the central apnea-hypopnea index (CAHI) (0.54 ± 0.78 vs. 0.18 ± 0.24, p = 0.03) with a 3.16-fold greater probability of pathological CAHI (OR = 3.16; 95 % CI 1.02-9.77) than the control group. An increased incidence of CSA in the subgroup of younger celiac patients compared to younger healthy controls was especially evident. CONCLUSIONS: The findings of our study suggest a difference in sleep architecture and an increased incidence of CSA in children with untreated CD, but additional research is required to verify the results.