Background. The guidelines on selection between iron preparations, iron sulfate (IS) and iron III hydroxide polymaltose complex (HPC), for iron deficiency anemia (IDA) management in pediatrics are contradictory. Objective. The aim of the study is to compare efficacy and safety of iron (III) HPC and IS for IDA treatment in children. Materials and methods. Randomization of children (aged from 1 month to 18 years) with IDA into 2 therapeutic groups was implemented in 2019-2020. on pediatric districts of children’s city outpatient's clinic: IS dosage of 3 mg/kg/day and iron (III) HPC dosage of 5 mg/kg/day. Hemogram monitoring was performed every 14 days. The efficacy was compared according to the rate of Hb level increase, erythrocytes indices, and serum ferritin (SF) level at the recorded moment of Hb normalization. For the safety — the rate of adverse effects. Results. 65 children with IDA were included in the study and randomized into 2 groups, the median age was 2.3 years (1st; 3rd quartile = 1.1; 4.3). Hb level increase was comparable in both groups (0.34 (0.23; 0.48) g/L/day and 0.24 (0.21; 0.30) g/L/day, р = 0.891). IS is more effective than iron (III) HPC in terms of average red blood cell volume by the time of Hb normalization (83.5 (80.0; 86.7) fl against 80.7 (79.0; 82.0) fl, р = 0.006), and mean cellular hemoglobin content (28.9 (SD = 2.0) pg against 27.4 (SD = 1.8) pg, р = 0.004). The timing of SF levels normalization did not differ. Adverse effects to iron III HPC treatment occurred 5.5 times more frequently than to IS (p = 0.0001). Conclusion. The efficacy of IS and iron III HPC at standard doses is comparable. The advantage in tolerability and recovery of erythrocytic indices justifies the feasibility of using IS preparations in the first line of treatment for children with IDA.

Background. Hemostatic system pathology is topical and poorly studied issue in pediatrics. One of the main causes of coagulation pathway disorders associated with thrombotic events is abnormality in various parts of the hemostatic system. Vascular accidents are commonly caused by anticoagulation system factors deficiency. Conventionally, thrombosis is a common event in adult patients, and there is no adequate attention to disorders of primary physiological anticoagulants system in children. More often acquired anticoagulant proteins deficiency develops in presence of various pathological conditions, especially after the past infectious diseases. All these diseases (thrombophilia, trombotic events, cardiovascular pathology, nervous system diseases, genetic diseases) can occur separately and in association with each other, plus clinical picture of coagulation events may be similar. Objective. The aim of the study is to evaluate changes in the physiological anticoagulants system in children with different pathologies who have polymorphic variants in coagulation genes and who had new coronavirus infection. Methods. The study included 33 children who had severe coronavirus infection in family clusters and had severe chronic pathology potentially associated with disorders of the coagulation system (nervous system damage, hypertrophic cardiomyopathy, hereditary monogenic syndromes, hemato-mesenchymal dysplasia syndrome). All children underwent complete examination including clinical examination, laboratory, and instrumental diagnostics. Results. Preliminary study results indicate significant incidence of polymorphic variants in coagulation genes (one third of children with various diseases from the study). Some children had decreased activity of anticoagulation system glycoproteins (from 6% to 36%) that confirmed the topicality of the examination of anticoagulation system factors deficiency and the need for further dynamic follow-up, as well as revealing of trombophilia predictors in children in selected target groups. Study on revealing anticoagulation system disorders and mutations in coagulation genes will predict the risk of thrombotic disorders. Conclusion. The obtained results have confirmed the significant role of the ongoing study for comprehensive assessment of hemostatic system disorders in children. That will allow us to optimize the approach to diagnosis and personalize the management strategy for patients with different chronic pathologies and disorders of the natural anticoagulants system. The study is currently ongoing.

Various human lifestyle and environmental factors are known to influence sleep. The number of adults and children suffering from chronic sleep disorders has grown over the past decade. Lack of sleep and impaired circadian rhythms have been proven to be associated with adverse metabolic health effects. Often, such disorders are associated with gastrointestinal tract diseases, and accompanied by dysbiosis. Significant number of studies have been conducted on animal models in recent years. They have shown the correlation between the gut microbiota and brain functions. According to these results scientists have clearly demonstrated the role of gut microbiota in regulating brain function, sleep, and behavior. The number of studies with volunteers is currently limited. The bacteria forming gut microbiota have significant impact on human health by synthesizing and secreting biologically active substances such as vitamins, essential amino acids, lipids, and others. Moreover, they have an indirect effect by modulating metabolic processes and the immune system. Changes in gut microbiota diversity occur due to the lack of sleep and shifting circadian rhythms, and it can lead to changes in the structure and function of microorganisms living in the gut. This can lead to changes in the composition and number of metabolites synthesized by these microorganisms (such as short-chain fatty acids and secondary bile acids) which contributes to the development of chronic inflammation, increased body weight and endocrine changes. This article provides the literature review on issues of interaction between gut microbiota and processes occurring during sleep.

This article presents modern data on epidemiology, etiology, and clinical manifestations of mucopolysaccharidosis (MPS) type I in children. MPS develops due to deficiency of particular lysosomal enzyme which determines the disease type. The article considers in details disease's pathogenesis and classification. Evidence-based approaches to diagnosis (differential diagnosis included) are covered, moreover, special attention is paid to pathogenetic, symptomatic, and surgical treatment of MPS.