Clinical Diabetology (ISSN 2450-7458) is published six times a year by "Via Medica sp. z o.o." sp.k.

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Aims/hypothesis. The aim of the work was to evaluate the vestibular organ condition in children and young adults suffering from Type I (insulin-dependent) diabetes mellitus. Methods. The group examined consisted of 95 children and young adults aged from 6 to 28 years with Type I diabetes diagnosed. The diabetic group was divided into subgroups according to duration of the disease, compensation of the disease, and presence and character of hypoglycaemic incidents, and presence of diabetic complications. The control group consisted of 44 healthy children and young adults aged 6 to 28 years. After collecting detailed medical history in each case an electronystagmographic test was performed using the computed two-canal electronystagmographer. Results. Within the diabetic group 6 patients complained about vertigo and balance disorders. Spontaneous nystagmus occurred in 10 cases, positional one in 21 cases. Impaired optokinesis occurred in 36 cases and impaired eye tracking test in 33 cases. In caloric tests there was partial canal paresis in 4 cases and directional preponderance in 7 cases. Conclusion/interpretation. Metabolic disturbances present in Type I diabetes cause disturbances in different parts of vestibular organ but mostly in its central part. Comparing disturbances in the vestibular organ with clinical and biochemical parameters characterising diabetes, the range of vestibular organ impairment in diabetes mellitus type 1 seems to depend mainly on the presence and character of hypoglycaemic incidents and the duration of the disease and to some extent on the compensation of diabetes. [Diabetologia (2002) 45:728-734]

Background. Magnesium (Mg), selinium (Se), zinc (Zn), manganese (Mn), and copper (cu) are involved in the mechanisms of antioxidant defense. Mn and cu, which participate in the generation of reactive oxygen species (ROS), also have pro-oxidative properties. Objectives. To evaluate the levels of Mg, Se, Zn, Mn, and cu, as well as the effectiveness of antioxidant defense mechanisms in children with Type 1Diabetes Mellitus (T1DM) and in their siblings. The preliminary findings were originally reported in 2009 at the 35 th annual conference of the International Society for Pediatric and adolescent Diabetes (ISPaD) in Ljubljana, Slovenia. Material and Methods. The study involved 87 children with T1DM, 2-19 years old, treated for T1DM for an average of 3.5 years. The sibling and control groups comprised 27 and 41 children, aged 4.5-16.5 years and 10.5-18 years respectively. The parameters named above were assessed in relation to metabolic compensation levels (Hb a1c ) and disease duration. Results. compared with the control group, T1DM children had lower plasma levels of Mg and Zn and higher levels of cu; the siblings had lower levels of Zn; T1DM children had lower copper/zinc superoxide dismutase (cuZnSOD) activity; and both T1DM children and their siblings had higher catalase (caT) activity and lower total antioxidant status (TaS) levels. Conclusions. There may be a correlation between impaired antioxidant status and Mg and Zn deficiency and increased cu levels in T1DM children. Oxidative stress in T1DM is accompanied by alterations in enzymatic activity and non-enzymatic mechanisms of antioxidant defense. The decreased TaS levels noted in T1DM patients may impair the effectiveness of non-enzymatic antioxidant systems. The increased caT activity and unimpaired selenium-dependent glutathione peroxidase (Se-GSHPx) activity point indirectly to enhanced ROS generation in T1DM children. The impaired antioxidant defense found in the siblings of T1DM patients may indicate that genetic factors play a role (Adv Clin Exp Med 2014, 23, 2, 259-268).

In summary, the switch from insulin therapy to SU treatment in PNDM related to KCNJ11 mutations was found to be an efficient and safe therapeutic method over a period of 34-month median follow-up. Although no serious side effects were associated with SU treatment, their use in Kir6.2 PNDM requires further attention, particularly in children, adolescents, and patients with advanced chronic diabetes complications.

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Mutations in SUR1 are the cause of about 15% of Kir6.2 negative permanent ND in Poland. The clinical phenotype of SUR1 diabetic mutation carriers is heterogeneous and it appears to be modified by variable sensitivity to insulin.