DOI: https://doi.org/10.22141/2224-0551.12.6.2017.112835

Influence of pancreatic steatosis severity on the course of pediatric nonalcoholic fatty pancreas disease

Yu.M. Stepanov, O.Yu. Lukianenko, N.Yu. Zavhorodnia, N.H. Hravyrovska

Abstract


Background. Nonalcoholic fatty pancreas disease is an excessive fat infiltration of the pancreas due to obesity in the absence of secondary steatosis. Nonalcoholic liver disease is associated with progredient course; whether presence and progression of nonalcoholic fatty pancreas disease is accompanied by specific structural and laboratory findings, it still remains unclear. Objective: to establish the features of sonological and laboratory fin­dings in children with nonalcoholic fatty pancreas disease depending on steatosis degree. Materials and ­methods. We observed 93 children aged 7 to 17 years, the average age was 11.87 ± 2.82 years. Degree of pancreatic steatosis was evaluated by ultrasonography. In order to determine pancreatic fibrosis and steatosis, shear wave elastography and steatometry (quantitative estimation of the ultrasound attenuation with determination of average ultrasound attenuation coefficient (UAC)) were performed using Ultima PA Expert apparatus (Radmir, Ukraine). Liver fibrosis and steatosis were diagnosed with the usage of FibroScan 502 Touch (France) with controlled attenuation parameter (CAP) function. Depending on the presence of pancreatic steatosis, children were divided into the following groups: group 1 — 50 patients with pancreatic steatosis and obesity/overweight; this group was divided into subgroups: S1 — 20 individuals with degree 1 pancreatic steatosis, S2 — 22 children with degree 2 pancreatic steatosis, S3 — 8 subjects with degree 3 pancreatic steatosis; group 2 — 30 patients without pancreatic steatosis with obesity/overweight, group 3(control) — 13 children with normal weight. All patients and their parents had given their agreement to participate in the study. We provided blood count with determination of erythrocyte sedimentation rate (ESR), liver function test (alanin aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGTP) and test for serum amylase level. Insulin level was determined by immunoassay with calculation of Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Statistical analysis was performed using Statistica 7.0 software by one-way analysis of variance followed by post hoc analysis. Results. Children with degree 3 pancreatic steatosis compared to group 3 demonstrated higher level of ESR — by 1.86 times (p = 0.01), ALT — by 1.86 times (p = 0.006), AST — by 1.96 times (p = 0.00019), GGTP — by 2.10 times (p = 0.0001). We found that patients with pancreatic steatosis had higher level of insulin vs control group (S1 subgroup — 18.38 ± 5.07 μU/ml; S2 — 30.76 ± 3.92 μU/ml; S3 — 33.70 ± 5.37 μU/ml; group 2 — 18.70 ± 2.98 μU/ml; group 3 — 9.480 ± 5.067 μU/ml (p = 0.00262)). Also, patients with pancreatic steatosis demonstrated higher level of HOMA-IR compared to the control group (S1 — 4.04 ± 0.87; S2 — 7.11 ± 0.96; S3 — 7.99 ± 1.35; group 2 — 3.81 ± 0.73; group 3 — 1.94 ± 0.92 (p = 0.00156)). CAP level increased in patients with pancreatic steatosis (S1 subgroup — 234.50 ± 9.94 dB/m; S2 — 239.05 ± 8.99 dB/m; S3 — 245.33 ± 17.21 dB/m; group 2 — 197.87 ± 7.70 dB/m; group 3 — 172.754 ± 12.170 dB/m (p = 0.00156)). UAC had maximal level in children of S3 subgroup (S1 — 2.55 ± 0.08 dB/cm; S2 — 2.56 ± 0.09 dB/cm; S3 — 2.74 ± 0.14 dB/cm; group 2 — 2.26 ± 0.08 dB/cm; group 3 — 1.72 ± 0.15 dB/cm (p = 0.00001)). Patients with pancreatic steatosis had higher level of liver and pancreatic stiffness, but significance of difference was low (p = 0.59). Conclusions. Pediatric nonalcoholic fatty pancreas disease wаs accompanied by liver steatosis, higher level of inflammation markers and insulin resistance that increased with growth of steatosis degree.


Keywords


nonalcoholic fatty pancreas disease; nonalcoholic fatty liver disease; steatometry; elastometry; children

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