[The problem of comorbid disorders in attention deficit hyperactivity disorder in children and adolescents: clinical cases]. / Problema komorbidnykh rasstroistv pri sindrome defitsita vnimaniya s giperaktivnost'yu u detei i podrostkov i ikh korrektsiya: klinicheskie nablyudeniya.

The problem of comorbid disorders in attention deficit hyperactivity disorder (ADHD) is considered, which occur in at least 60% of patients and lead to additional difficulties in intra-family, school and social adaptation. Children and adolescents with ADHD have a wide range of neurological and somatic disorders caused by complex polygenic pathogenetic mechanisms. Among the pathologies associated with ADHD in this cohort of children, neurotic and anxiety manifestations, motor disorders: dyspraxia, discoordination, impaired gross and fine motor skills, tics, behavioral disorders, enuresis, tension cephalgia are common disorders. Treatment of ADHD should be pathogenetic, taking into account the main symptoms of ADHD and manifestations of comorbid disorders, since it is quite long. When choosing pharmacotherapy, it is preferable to use drugs with verified efficacy not only in the correction of ADHD, but also concomitant behavioral, motor and emotional disorders. Also an important aspect in the pediatric clinic is the use of drugs with a reliable safety profile.

The 1858T PTPN22 gene variant contributes to a genetic risk of type 1 diabetes in a Ukrainian population.

The 1858T variant of the protein tyrosine phosphatase gene, PTPN22, is associated with an increased risk of several autoimmune diseases. The aim of this study has been to investigate the possible association of 1858C-->T PTPN22 polymorphism and type 1 diabetes (T1D) in Caucasians from Ukraine. Overall, the distribution of 1858 PTPN22 genotypes differed significantly between the T1D patient group (n = 296) and the control group (n = 242) (P = 0.0036). When both groups were classified according to sex, the TT genotype and T allele showed a statistically significant higher frequency in T1D female patients (5.9 and 22.8%, respectively) in comparison with the female controls (0 and 11.9%) (P = 0.008 for both analyses). The patients with the TT genotype were significantly younger at the onset of T1D compared with those with genotypes TC and CC (P = 0.035 and 0.019, respectively). In our Ukrainian Caucasian cohort, we confirmed the association between T1D and the PTPN22,1858T allele.