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Hypoglycemic Episodes (hypoglycemic + episode)
Selected Abstracts,Dead-in-bed' syndrome , a diabetes nightmarePEDIATRIC DIABETES, Issue 5 2008Dror Koltin Abstract:, We report in this study the death in bed of a 14-yr-old girl with type 1 diabetes and a review of the existing literature on this topic. Diagnosed at 5 yr of age, the patient followed a relatively benign disease course. Hemoglobin A1c was 6.6,8.4%, and there were no hospital admissions apart from the one at diagnosis. Hypoglycemic episodes were not excessive or severe. At age 14 yr, the patient was found dead in bed after having been well the night before. No apparent explanation could be provided. The ,dead-in-bed' syndrome accounts for 5,6% of mortality cases in patients with type 1 diabetes, amounting to two to six cases per 10 000 patient years. Theories attempting to explain the mechanism for this syndrome include hypoglycemia or cardiac autonomic dysfunction. This case emphasizes several problems faced by clinicians: the risk for sudden death in youth with diabetes, which may compromise good glycemic control, the question of early detection of autonomic dysfunction, and the need to understand this phenomenon better and search for preventive measures. [source] Differential effects of low glucose concentrations on seizures and epileptiform activity in vivo and in vitroEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2006Anne Kirchner Abstract In vivo, severe hypoglycemia is frequently associated with seizures. The hippocampus is a structure prone to develop seizures and seizure-induced damage. Patients with repeated hypoglycemic episodes have frequent memory problems, suggesting impaired hippocampal function. Here we studied the effects of moderate hypoglycemia on primarily generalized flurothyl-induced seizures in vivo and, using EEG recordings, we determined involvement of the hippocampus in hypoglycemic seizures. Moderate systemic hypoglycemia had proconvulsant effects on flurothyl-induced clonic (forebrain) seizures. During hypoglycemic seizures, seizure discharges were recorded in the hippocampus. Thus, we continued the studies in combined entorhinal cortex,hippocampus slices in vitro. However, in vitro, decreases in extracellular glucose from baseline 10 mm to 2 or 1 mm did not induce any epileptiform discharges. In fact, low glucose (2 and 1 mm) attenuated preexisting low-Mg2+ -induced epileptiform activity in the entorhinal cortex and hippocampal CA1 region. Osmolarity compensation in low-glucose solution using mannitol impaired slice recovery. Additionally, using paired-pulse stimuli we determined that there was no impairment of GABAA inhibition in the dentate gyrus during glucopenia. The data strongly indicate that, although forebrain susceptibility to seizures is increased during moderate in vivo hypoglycemia and the hippocampus is involved during hypoglycemic seizures, glucose depletion in vitro contributes to an arrest of epileptiform activity in the system of the entorhinal cortex,hippocampus network and there is no impairment of net GABAA inhibition during glucopenia. [source] Biphasic insulin aspart vs. human insulin in adolescents with type 1 diabetes on multiple daily insulin injectionsPEDIATRIC DIABETES, Issue 1 2006Henrik Mortensen Abstract:, The aim was to compare clinical efficacy and safety of two treatment regimens: biphasic insulin aspart (BIAsp) injected at all three meals plus neutral protamine Hagedorn (NPH) insulin at bedtime vs. a human insulin regimen, premixed human insulin at breakfast and soluble insulin at lunch and dinner and NPH at bedtime. A total of 167 adolescents (80 males and 87 females) with type 1 diabetes was included in the trial (multinational, randomized, open-label, and parallel group). Each subject received either of two treatment regimens for a 4-month period. BIAsp was injected immediately before main meals, human insulin products 30 min before meals, and NPH at night. Glycemic control was monitored by eight-point evaluations (after 6 and 16 wks) and hemoglobin A1c (HbA1c) (after 2, 6, and 16 wks). Safety evaluations included adverse events and incidence of hypoglycemic episodes. HbA1c (mean ± SD) after 4 months on BIAsp (9.39 ± 0.14) was not significantly different from that with human insulin (9.30 ± 0.15). The average postprandial glucose increment in the BIAsp group was about half the increment in the human insulin group; the difference not statistically significant. The body mass index (BMI) increased in both groups, but significantly (p = 0.005) less in the BIAsp group. However, in males on BIAsp, the BMI decreased compared with those on human insulin (p = 0.007). No significant group differences were found for the rate of hypoglycemic episodes. We concluded that the BIAsp regimen was associated with similar glycemic control and similar incidence of hypoglycemic episodes as human insulin. However, the BIAsp regimen caused a significantly smaller increase in BMI, particularly in males, compared with the human insulin regimen. [source] Characteristics of glycemic control in young children with type 1 diabetesPEDIATRIC DIABETES, Issue 4 2002Francine Ratner Kaufman Abtract: Background: The Diabetes Control and Complications Trial (DCCT) demonstrated that the rate-limiting step to the intensification of diabetes management in adolescents and adults was hypoglycemia. Young children were presumed to be at even greater risk for hypoglycemia with severe consequences, particularly if they had HbA1c levels < 8%. Subjects: A retrospective chart review was performed on 148 patients with type 1 diabetes on insulin injection therapy who were < 8 yr of age (mean age 5.7 ± 1.5, mean diabetes duration 3.0 ± 1.4 yr) followed quarterly from July 1999 to June 2001. Methods:, The subjects were divided into two groups based on their mean HbA1c values (< 8 vs. , 8%) averaged over the 2-yr time period. The following variables were analyzed comparing the two groups: age, duration of diabetes, insulin dose, severe hypoglycemic episodes, episodes of diabetic ketoacidosis (DKA), percentage of glucose levels above, within, and below the target range, and number of diabetes home-management competencies obtained. Results:, Patients with HbA1c < 8% spent more time within target range (40.0 vs. 29.5%, p = 0.0001) and less time above their target range (36.9 vs. 51.2%, p = 0.0003). There was no difference in the percentage of glucose levels below target (23.2 vs. 19.4%, p = NS), percentage of severe hypoglycemic episodes (3 vs. 7 episodes per 100 patient-yr, p = NS), or episodes of DKA (1 vs. 3 episodes per 100 patient-yr, p = NS) between the two groups. Subjects with lower HbA1c levels had acquired more home-management competencies (4.0 vs. 3.5, p = 0.01). Conclusions:, If families are competent in fundamental diabetes management, young children can achieve HbA1c levels < 8.0% without increasing the risk of hypoglycemia. [source] Electrocardiographic Alterations during Hyperinsulinemic Hypoglycemia in Healthy SubjectsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2008Tomi Laitinen M.D. Background: We evaluated the arrhythmogenic potential of hypoglycemia by studying electrocardiographic (ECG) changes in response to hyperinsulinemic hypoglycemia and associated sympathoadrenal counterregulatory responses in healthy subjects. Methods: The study population consisted of 18 subjects, aged 30,40 years. Five-minute ECG recordings and blood samplings were performed at baseline and during the euglycemic and hypoglycemic hyperinsulinemic clamp studies. PR, QT, and QTc intervals of electrocardiogram and ECG morphology were assessed from signal-averaged ECG. Results: Although cardiac beat interval remained unchanged, PR interval decreased (P < 0.01) and QTc interval (P < 0.001) increased in response to hyperinsulinemic hypoglycemia. Concomitant morphological alterations consisted of slight increases in R-wave amplitude and area (P < 0.01 for both), significant decreases in T-wave amplitude and area (P < 0.001 for both), and moderate ST depression (P < 0.001). Counterregulatory norepinephrine response correlated with amplification of the R wave (r =,0.620, P < 0.05) and epinephrine response correlated with flattening of the T wave (r =,0.508, P < 0.05). Conclusions: Hyperinsulinemic hypoglycemia with consequent sympathetic humoral activation is associated with several ECG alterations in atrioventricular conduction, ventricular depolarization, and ventricular repolarization. Such alterations in cardiac electrical function may be of importance in provoking severe arrhythmias and "dead-in-bed" syndrome in diabetic patients with unrecognized hypoglycemic episodes. [source] | ||||||||||