Functional and biochemical characteristics of the muscle system in children with type I diabetes

Abstract

Background. The purpose of the study was to determine possible markers of skeletal muscle damage in children with type 1 diabetes mellitus (T1DM) and their relationship with the features of disease course. Materials and methods. The observation group consisted of 98 children with type 1 diabetes mellitus: the first group included 22 people without disorders of the muscular system; the second — 42 patients with dynapenia; the third — 34 children with diabetic myopathy. Control group — 30 relatively healthy children. Assessment of the static endurance of skeletal muscles, determination of the level of creatine kinase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, periostin and cardiotrophin-1 in blood serum were performed in all patients. Results. The conducted studies demonstrate that children with diabetes, regardless of the structural and functional state of their muscular system, have signs of skeletal muscle damage, which were most expressed in diabetic myopathy and progressed with maximal deterioration of glycemic control. It was found that the highest content of alkaline phosphatase was characteristic of children from group 1, while in patients with diabetic myopathy its serum content was not statistically different from that of controls. These disorders occurred against the background of changes in alkaline phosphatase activity, the level of which was highest in children from group 1, while in patients with diabetic myopathy, its serum content was not statistically different from that of controls. At the same time, during the course of diabetic myopathy in children with T1DM, there was an increase in lactate dehydrogenase activity by 1.2 times (p < 0.01) and cardiotrophin-1 by 300 times (p < 0.01) compared to the corresponding indicator of the control group. Serum periostin level was increased in all patients with T1DM. Its maximum values were determined in group 1, whose periostin concentration exceeded control indicators by 103 times (p < 0.01). With deterioration of skeletal muscle state, there was a gradual decrease in periostin serum level, but in patients with dynapenia, it was 35.5 times higher than in the control group (p < 0.05) and 19.2 times higher in those with diabetic myopathy (p < 0.05). Conclusions. The course of type 1 diabetes in children is accompanied by skeletal muscle damage, the first clinical sign of which is a decrease in the static muscle endurance against the background of worsening disease course. Alkaline phosphatase, lactate dehydrogenase, periostin, and cardiotrophin-1 are biochemical markers of skeletal muscle damage in children with type 1 diabetes. A common feature of the changes in the specified indicators is their increase; however, each clinical condition of the skeletal muscles corresponds to its own configuration of changes in the abovementioned markers.