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Severe Hyperglycaemia (severe + hyperglycaemia)
Selected AbstractsHyperglycaemia and mortality of diabetic patients with candidaemiaDIABETIC MEDICINE, Issue 9 2005M. S. Bader Abstract Aims To determine whether the degree of hyperglycaemia has an impact on in-hospital mortality in diabetic patients with candidaemia. Methods A retrospective cohort study of 87 diabetic patients with candidaemia admitted between June 1995 and June 2003 was carried out at two medical centres. Patients were stratified into two groups: those with moderate hyperglycaemia (7 days post-candidaemia mean blood glucose < 13.9 mmol/l) and those with severe hyperglycaemia (7 days post-candidaemia mean blood glucose , 13.9 mmol/l). A stepwise logistic regression analysis was performed to determine whether the degree of hyperglycaemia was a significant predictor of mortality. Results During the follow-up period from admission till discharge, 34 (39.1%) patients had died. Nine (69.2%) of 13 patients with severe hyperglycaemia have died while 25 (33.8%) of 74 patients with moderate hyperglycaemia have died. Multivariate analysis identified three independent determinants of death; Apache II score , 23 [OR 8.1, 95% CI (2.6, 25.3), P = 0.0003], mean blood glucose levels 7 days post-candidaemia , 13.9 mmol/l [OR 6.8, 95% CI (1.2, 38.2), P = 0.03], and mechanical ventilation [OR 6.5, 95% CI (2.21), P = 0.03]. Conclusion Severe hyperglycaemia is an important marker of increased mortality among hospitalized diabetic patients with candidaemia. [source] Diabetes and mitochondrial bioenergetics: Alterations with ageJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 4 2003Fernanda M. Ferreira Abstract Several studies have been carried out to evaluate the alterations in mitochondrial functions of diabetic rats. However, some of the results reported are controversial, since experimental conditions, such as aging, and/or strain of animals used were different. The purpose of this study was to evaluate the metabolic changes in liver mitochondria, both in the presence of severe hyperglycaemia (STZ-treated rats) and mild hyperglycaemia (Goto-Kakizaki (GK) rats). Moreover, metabolic alterations were evaluated both at initial and at advanced states of the disease. We observed that both models of type 1 and type 2 diabetes presented alterations on respiratory chain activity. Because of continual severe hyperglycaemia, 9 weeks after the induction of diabetes, the respiratory function declined in STZ-treated rats, as observed by membrane potential and respiratory ratios (RCR, P/O, and FCCP-stimulated respiration) assessment. In contrast, GK rats of 6 months age presented increased respiratory ratios. To localize which respiratory complexes are affected by diabetes, enzymatic respiratory chain activities were evaluated. We observed that succinate dehydrogenase and cytochrome c oxidase activities were significantly augmented both in STZ-treated rats and GK rats of 6 months age. Moreover, H+ -ATPase activity was also significantly increased in STZ-treated rats with 3 weeks of diabetes and in GK rats of 6 months age as compared to controls. Therefore, these results clearly suggest that both animal models of diabetes present some metabolic adjustments in order to circumvent the deleterious effects promoted by the high glucose levels typical of the disease. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:214,222, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10081 [source] Improving the early management of blood glucose in emergency admissions with chest painPRACTICAL DIABETES INTERNATIONAL (INCORPORATING CARDIABETES), Issue 3 2001Martin K Rutter MRCP (UK) Locum Consultant Physician Abstract Hyperglycaemia is associated with a worse prognosis after myocardial infarction and good blood glucose control in the peri-infarct period has been shown to improve outcome. Our primary study was undertaken with the aims of assessing the prevalence and management of hyperglycaemia in patients admitted with acute chest pain. Ninety-three patients admitted to either Coronary Care (CCU) or Emergency Medical Admission Units (EMAU) with chest pain were studied and of these 14 (15%) had severe hyperglycaemia (>11.0,mmol/L). Blood glucose was not measured in seven (8%) patients and in only 1/14 (7%) patient were established guidelines for the management of hyperglycaemia applied. A revision of management protocol was undertaken and after 18 months we repeated the review of management of hyperglycaemia. Of 114 patients 22 (21%) had severe hyperglycaemia, blood glucose was not measured in ten (9%) and management guidelines were followed in 13 (65%). A major improvement in management of blood glucose in emergency admissions with chest pain has been demonstrated. Further staff education, discussion and review of protocol are indicated to improve and maintain performance on CCU and EMAU. Copyright © 2001 John Wiley & Sons, Ltd. [source] Multiple Mechanisms Of Early Hyperglycaemic Injury Of The Rat Intestinal MicrocirculationCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2002H Glenn Bohlen SUMMARY 1. Hyperglycaemia in the vast majority of humans with diabetes mellitus is the end result of profound insulin resistance secondary to obesity. For patients in treatment, hyperglycaemia is usually not sustained but, rather, occurs intermittently. In in vivo studies of the rat intestinal microcirculation, endothelial impairment occurs within 30 min at D -glucose concentrations , 300 mg/dL. Endothelial-dependent dilation to acetylcholine and constriction to noradrenaline is impaired. Vasodilation to exogenous nitric oxide (NO) remains normal. 2. When initiated before hyperglycaemia, suppression of oxygen radicals by both scavenging and pretreatment with cyclo-oxygenase blockade to prevent oxygen radical formation minimized endothelial impairments during hyperglycaemia. Neither treatment was effective in restoring endothelial function once it was damaged by hyperglycaemia. 3. A mechanism that may initiate the arachidonic acid, oxygen radical process is activation of specific isoforms of protein kinase C (PKC). De novo formation of diacylglycerol during hyperglycaemia activates PKC. Blockade of the ,II PKC isoform with LY-333531 prior to hyperglycaemia protected NO formation within the arteriolar wall, as judged with NO-sensitive microelectrodes. Furthermore, once suppression of endothelial dilation was present in untreated animals, PKC blockade could substantially restore endothelial-dependent dilation. 4. These results indicate that acute hyperglycaemia is far from benign and, in the rat, causes rapid endothelial impairment. Both oxygen radical scavenging and cyclo-oxygenase blockade prior to bouts of hyperglycaemia minimize endothelial impairment with limited side effects. Blockade of specific PKC isozymes protects endothelial function both as a pre- or post-treatment during moderately severe hyperglycaemia. [source] | ||||||||||