Foot drop in children with newly diagnosed type 1 diabetes: three case reports.

Summary: The etiology of foot drop is diverse from various diseases to mechanic injuries and includes neuropathy of the peroneal nerve. Peroneal neuropathy might also be one of the forms of diabetic neuropathy, very rarely reported as the first sign of diabetes. We describe three cases of children with newly diagnosed type 1 diabetes (TID) who developed unilateral peroneal nerve palsies and tibial nerve palsies, presenting clinically as a foot drop. In two of our cases, the symptoms of foot drop occurred shortly after starting treatment for severe diabetes ketoacidosis. In the third patient, food drop was a reason for the initial medical consultation, but eventually, TID was diagnosed. The presented cases highlight that neuropathy can be observed not only as a chronic complication of T1D, but it can also appear at the time of disease manifestation. The incorrect position of the lower limb during a keto coma may contribute to the development of neuropathy. Learning points: Neuropathy can be observed not only as a chronic complication of type 1 diabetes (T1D), but it can also appear at the time of disease manifestation. The incorrect position of the lower limb causing external pressure during a keto coma may contribute to the development of neuropathy. It is important to examine the glycemia in patients with acute peroneal neuropathy, as this kind of peripheral neuropathy can be associated with newly diagnosed T1D. Normalization of glycemia might lead to rapid neuronal recovery.

Trace elements, magnesium, and the efficacy of antioxidant systems in children with type 1 diabetes mellitus and in their siblings.

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 35th 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 (HbA1C) 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.

[Three-year observation of permanent neonatal diabetes]. / Utrwalona cukrzyca noworodków - obserwacja trzyletnia.

The aim of this paper is to present a three-year observation of four children with permanent neonatal diabetes caused by heterozygous activating mutations in both KCNJ11 gene for Kir6.2 and ABCC8 gene for SUR1 subunits (three patients after three years of clinical observation and one patient after two years of clinical observation, respectively). In three cases with Kir6.2 mutation, developmental delay was diagnosed. In all four patients the glucagon test revealed normal c-peptide secretion. During the treatment with sulfonylureas (SU), glycaemia remained within the normal range, HbA1c<7%, in our patients. In all children reduction a of SU doses was required.

Diagnostic potential of oxidative stress markers in children and adolescents with type 1 diabetes.

OBJECTIVES: To validate the diagnostic utility of oxidative stress markers in the evaluation of young type 1 diabetics, as suggested elsewhere. DESIGN: Advanced oxidation protein products (AOPP), thiobarbituric acid-reactive substances (TBARS) and total antioxidant status (TAS) were measured in sera from diabetics, their siblings and controls, with diagnostic potential evaluated by ROC analysis, and related to diabetes clinical parameters. RESULTS: In diabetics AOPP and TBARS were elevated, TAS decreased. Similar alterations were observed for AOPP and TAS in their siblings. AOPP and TAS were good indicators of diabetes. AOPP and TBARS correlated with HbA1C (independent predictor), but were poor markers of non-adequate glycemic control. The cardiovascular disease risk factors were independent predictors of TBARS concentrations. CONCLUSIONS: AOPP accumulation and TAS reduction seem to precede diabetes and might be considered as susceptibility indicators in relatives, but not as diabetes markers in general population (no diabetes specificity has been shown). Application in monitoring of metabolic control is not validated.