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Hypoglycemia
Kinds of Hypoglycemia Selected AbstractsESTIMATING GLOMERULAR FILTRATION RATE MIGHT HELP TO AVOID HYPOGLYCEMIAJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 9 2006Andrea Corsonello MD No abstract is available for this article. [source] ORIGINAL ARTICLE: Many patients with Type 1 diabetes estimate their prandial insulin need inappropriatelyJOURNAL OF DIABETES, Issue 3 2010Aila J. AHOLA Abstract Background:, Many factors contribute to the need for prandial insulin in Type 1 diabetes. However, patients' success in achieving normal postprandial glucose concentration is understudied. The aim of the present study was to determine how often patients with Type 1 diabetes achieve normal postprandial glucose concentrations and to evaluate factors associated with postprandial hypo- and hyperglycemia. Methods:, Data on food intake, physical activity, insulin administration, and blood glucose concentration were collected using a self-administered questionnaire from 331 patients with Type 1 diabetes (43% men; mean age 49 ± 12 years; mean diabetes duration 32 ± 13 years). Of these, 179 provided data on blood glucose concentrations measured 110,150 min postprandially. One such meal per patient was randomized for analyses. Results:, Hypoglycemia (<4.0 mmol/L), normoglycemia (4.0,7.9 mmol/L), and hyperglycemia (,8.0 mmol/L) were observed after 23%, 36%, and 41% of meals, respectively. The three postprandial glycemia groups did not differ with respect to the meal composition or the timing of the postprandial blood glucose measurement. In women, postprandial hyperglycemia was associated with shorter diabetes duration and higher preprandial blood glucose concentration, whereas postprandial hypoglycemia was associated with higher physical activity. No single factor explained the postprandial glycemic state in men. Conclusions:, A total of 64% of patients estimated their prandial insulin need inappropriately, suggesting that estimation of the optimal prandial insulin dose is not easy, even after a long duration of diabetes. [source] Delay in blood glucose monitoring during an insulin infusion protocol is associated with increased risk of hypoglycemia in intensive care units,JOURNAL OF HOSPITAL MEDICINE, Issue 6 2009Rajesh Garg MD Abstract BACKGROUND: Hypoglycemia during insulin infusion therapy is a major problem. We investigated whether a delay in blood glucose (BG) monitoring during an insulin infusion protocol (IIP) in the intensive care unit (ICU) is associated with hypoglycemia. METHODS: Data were collected for 50 consecutive patients treated with Brigham and Women's Hospital's IIP. Point-of-care BG values were obtained from the bedside paper flow sheets and the exact times of individual measurements were ascertained from an internet-based glucose meter download program. Data were carefully studied for protocol time violations, defined as a delay of >10 minutes after the recommended time for BG measurement. RESULTS: A total of 2309 BG values were evaluated for time violation. A total of 1474 (63.9%) measurements had been obtained at the recommended time or earlier; 835 (36.1%) measurements had been obtained >10 minutes after the recommended time for measurement. There were a significantly higher proportion of BG values <80 mg/dL following the time violation as compared to no time violation (17.8% versus 11.6%; P < 0.001). CONCLUSION: We conclude that the risk of hypoglycemia during insulin infusion therapy is higher after a delay in BG measurement. Journal of Hospital Medicine 2009;4:E5,E7. © 2009 Society of Hospital Medicine. [source] Neurochemical changes in the developing rat hippocampus during prolonged hypoglycemiaJOURNAL OF NEUROCHEMISTRY, Issue 3 2010Raghavendra Rao J. Neurochem. (2010) 114, 728,738. Abstract Hypoglycemia is common during development and is associated with the risk of neurodevelopmental deficits in human infants. The effects of hypoglycemia on the developing hippocampus are poorly understood. The sequential changes in energy substrates, amino acids and phosphocreatine were measured from the hippocampus during 180 min of insulin-induced hypoglycemia (blood glucose < 2.5 mmol/L) in 14-day-old rats using in vivo1H NMR spectroscopy. Hypoglycemia resulted in neuroglycopenia (brain glucose < 0.5 ,mol/g). However, the phosphocreatine/creatine (PCr/Cr) ratio was maintained in the physiological range until approximately 150 min of hypoglycemia, indicating that energy supply was sufficient to meet the energy demands. Lactate concentration decreased soon after the onset of neuroglycopenia. Beyond 60 min, glutamine and glutamate became the major energy substrates. A precipitous decrease in the PCr/Cr ratio, indicative of impending energy failure occurred only after significant depletion of these amino acids. Once glutamate and glutamine were significantly exhausted, aspartate became the final energy source. N -acetylaspartate concentration remained unaltered, suggesting preservation of neuronal/mitochondrial integrity during hypoglycemia. Correction of hypoglycemia normalized the PCr/Cr ratio and partially restored the amino acids to pre-hypoglycemia levels. Compensatory neurochemical changes maintain energy homeostasis during prolonged hypoglycemia in the developing hippocampus. [source] Assessment for Hypoglycemia in Newborns During Transition: A Retrospective StudyJOURNAL OF OBSTETRIC, GYNECOLOGIC & NEONATAL NURSING, Issue 2010Newborn Care No abstract is available for this article. [source] Hypoglycemia and its effect on the brainJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2008DACVECC, Natara L. Loose DVM First page of article [source] Field Safety and Efficacy of Protamine Zinc Recombinant Human Insulin for Treatment of Diabetes Mellitus in CatsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2009R.W. Nelson Background: This study describes the efficacy of a new protamine zinc recombinant human insulin (PZIR) preparation for treating diabetic cats. Objective: To evaluate effects of PZIR on control of glycemia in cats with newly diagnosed or poorly controlled diabetes mellitus. Animals: One hundred and thirty-three diabetic cats 120 newly diagnosed and 13 previously treated. Methods: Prospective, uncontrolled clinical trial. Cats were treated with PZIR twice daily for 45 days. Control of glycemia was assessed on days 7, 14, 30, and 45 by evaluation of change in water consumption, frequency of urination, appetite, and body weight, serum fructosamine concentration, and blood glucose concentrations determined 1, 3, 5, 7, and 9 hours after administration of PZIR. Adjustments in dosage of PZIR were made as needed to control glycemia. Results: PZIR administration resulted in a significant decrease in 9-hour mean blood glucose (199 ± 114 versus 417 ± 83 mg/dL, X± SD, P < .001) and serum fructosamine (375 ± 117 versus 505 ± 96 ,mol/L, P < .001) concentration and a significant increase in mean body weight (5.9 ± 1.4 versus 5.4 ± 1.5 kg, P= .017) in 133 diabetic cats at day 45 compared with day 0, respectively. By day 45, polyuria and polydipsia had improved in 79% (105 of 133), 89% (118 of 133) had a good body condition, and 9-hour mean blood glucose concentration, serum fructosamine concentration, or both had improved in 84% (112 of 133) of the cats compared with day 0. Hypoglycemia (<80 mg/dL) was identified in 151 of 678, 9-hour serial blood glucose determinations and in 85 of 133 diabetic cats. Hypoglycemia causing clinical signs was confirmed in 2 diabetic cats. Conclusions and Clinical Relevance: PZIR is effective for controlling glycemia in diabetic cats and can be used as an initial treatment or as an alternative treatment in diabetic cats that do not respond to treatment with other insulin preparations. [source] Hypoglycemia and Tumor Lysis Syndrome Associated with Peritoneal Mesothelioma in a HorseJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2006Alison M. LaCarrubba First page of article [source] Balancing Risk and Benefit with Oral Hypoglycemic DrugsMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 3 2009Ole-Petter R. Hamnvik MB Abstract Clinicians are faced with an expansive array of treatment choices when caring for patients with type 2 diabetes. Because patient compliance may be affected when media sensationalism about controversial findings is misunderstood, we sought to clarify the recent controversy surrounding the cardiovascular and bone-health risks of thiazolidinediones, the risk of lactic acidosis with metformin, and the risk of hypoglycemia with oral therapies. The side effect profile of thiazolidinediones includes fluid retention, heart failure; and an increased risk of fracture. A recent controversial meta-analysis suggested that rosiglitazone increases the risk of myocardial infarction, which is possibly related to thiazolidinedione-induced lipid changes, weight gain, congestive heart failure, and anemia. Metformin is restricted to patients with normal renal function because of concerns that metformin may cause lactic acidosis. However, few cases of metformin-associated lactic acidosis have been reported, and most have occurred in patients with other reasons for developing lactic acidosis, such as sepsis or renal failure. Although the use of metformin continues to increase, observational studies have not been able to demonstrate an increased incidence of lactic acidosis in metformin-treated patients, even when it is used in populations with relative contraindications. Some oral hypoglycemic medications can cause hypoglycemia. Hypoglycemia is especially common in older patients, alcoholics, and patients with liver or renal disease. Patients on sulfonylureas and meglitinides have the highest incidence of hypoglycemia because of their pharmacological action of increasing insulin secretion. Of the sulfonylureas, glyburide presents the highest risk of hypoglycemia. Combination therapies, especially those regimens containing a sulfonylurea, increase the risk of hypoglycemia. Mt Sinai J Med 76:234,243, 2009. © 2009 Mount Sinai School of Medicine [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] Hypoglycemia induced changes in cell death and cell proliferation in the organogenesis stage embryonic mouse heartBIRTH DEFECTS RESEARCH, Issue 3 2004Gautam S. Ghatnekar Abstract BACKGROUND Hypoglycemia is a side effect of diabetes therapy and causes abnormal heart development. Embryonic heart cells are largely resistant to teratogen-induced apoptosis. METHODS Hypoglycemia was tested for effects on cell death and cell proliferation in embryonic heart cells by exposing mouse embryos on embryonic day (E) 9.5 (plug = E0.5) to hypoglycemia (30,50 mg/dl glucose) in vivo or in vitro for 24 hr. Long-term effects of in vivo exposure on conceptus viability were evaluated at E18.5. Cell death was evaluated on E10.5 by: 1) two TUNEL assays in sectioned embryos to demonstrate DNA fragmentation; 2) confocal microscopy in whole embryos stained with Lysotracker; 3) flow cytometry in dispersed heart cells stained for TUNEL and myosin heavy chain (MHC) to quantify and characterize cell type susceptibility; and 4) immunohistochemistry (IHC) and Western analysis in sectioned embryos to evaluate potential involvement of caspase-3 active subunit and p53. Effects on cell proliferation were evaluated by IHC and Western analysis of proliferating cell nuclear antigen (PCNA). RESULTS In vivo hypoglycemic exposure on E9.5 reduced viability in conceptuses examined on E18.5. Hearts examined on E10.5 demonstrated increased TUNEL and Lysotracker staining. In hearts of embryos exposed to hypoglycemia, flow cytometry demonstrated increased TUNEL-positive cells and cells dual-labeled for TUNEL and MHC. Protein expression of caspase-3 active subunit and p53 was increased and PCNA was markedly reduced in hearts of embryos exposed to hypoglycemia. CONCLUSIONS Hypoglycemia reduces embryonic viability, induces significant cell death, and reduces cell proliferation in the E9.5 mouse heart, and these processes may involve active caspase-3 and p53. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source] Liver glycogen metabolism during short-term insulin-induced hypoglycemia in fed ratsCELL BIOCHEMISTRY AND FUNCTION, Issue 7 2008Simoni Obici Abstract The activities of glycogen phosphorylase and synthase during infusions of glucagon, isoproterenol, or cyanide in isolated liver of fed rats submitted to short-term insulin-induced hypoglycemia (IIH) was investigated. A condition of hyperinsulinemia/hypoglycemia was obtained with an intraperitoneal injection of regular insulin (1.0,U,kg,1). The control group received ip saline. The experiments were carried out 60,min after insulin (IIH group) or saline (COG group) injection. The rats were anesthetized and after laparotomy, blood was collected from the vena cava for glucose and insulin measurements. The liver was then infused with glucagon (1,nM), isoproterenol (2,µM), or cyanide (0.5,mM) during 20,min and a sample of the organ was collected for determination of the activities of glycogen phosphorylase and synthase 5,min after starting and 10,min after stopping the infusions. The infusions of cyanide, glucagons, and isoproterenol did not change the activities of glycogen synthase and glycogen phosphorylase. However, glycogen catabolism was decreased during the infusions of glucagon and isoproterenol in IIH rats, being more intense with isoproterenol (p,<,0.05), than glucagon. It was concluded that short-term IIH promoted changes in the liver responsiveness of glycogen degradation induced by glucagon and isoproterenol without a change in the activities of glycogen phosphorylase and synthase. Copyright © 2008 John Wiley & Sons, Ltd. [source] Models of white matter injury: Comparison of infectious, hypoxic-ischemic, and excitotoxic insultsDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 1 2002Henrik Hagberg Abstract White matter damage (WMD) in preterm neonates is strongly associated with adverse outcome. The etiology of white matter injury is not known but clinical data suggest that ischemia-reperfusion and/or infection-inflammation are important factors. Furthermore, antenatal infection seems to be an important risk factor for brain injury in term infants. In order to explore the pathophysiological mechanisms of WMD and to better understand how infectious agents may affect the vulnerability of the immature brain to injury, numerous novel animal models have been developed over the past decade. WMD can be induced by antenatal or postnatal administration of microbes (E. coli or Gardnerella vaginalis), virus (border disease virus) or bacterial products (lipopolysaccharide, LPS). Alternatively, various hypoperfusion paradigms or administration of excitatory amino acid receptor agonists (excitotoxicity models) can be used. Irrespective of which insult is utilized, the maturational age of the CNS and choice of species seem critical. Generally, lesions with similarity to human WMD, with respect to distribution and morphological characteristics, are easier to induce in gyrencephalic species (rabbits, dogs, cats and sheep) than in rodents. Recently, however, models have been developed in rats (PND 1,7), using either bilateral carotid occlusion or combined hypoxia-ischemia, that produce predominantly white matter lesions. LPS is the infectious agent most often used to produce WMD in immature dogs, cats, or fetal sheep. The mechanism whereby LPS induces brain injury is not completely understood but involves activation of toll-like receptor 4 on immune cells with initiation of a generalized inflammatory response resulting in systemic hypoglycemia, perturbation of coagulation, cerebral hypoperfusion, and activation of inflammatory cells in the CNS. LPS and umbilical cord occlusion both produce WMD with quite similar distribution in 65% gestational sheep. The morphological appearance is different, however, with a more pronounced infiltration of inflammatory cells into the brain and focal microglia/macrophage ("inflammatory WMD") in response to LPS compared to hypoperfusion evoking a more diffuse microglial response usually devoid of cellular infiltrates ("ischemic WMD"). Furthermore, low doses of LPS that by themselves have no adverse effects in 7-day-old rats (maturation corresponding to the near term human fetus), dramatically increase brain injury to a subsequent hypoxic-ischemic challenge, implicating that bacterial products can sensitize the immature CNS. Contrary to this finding, other bacterial agents like lipoteichoic acid were recently shown to induce tolerance of the immature brain suggesting that the innate immune system may respond differently to various ligands, which needs to be further explored. MRDD Research Reviews 2002;8:30,38. © 2002 Wiley-Liss, Inc. [source] A reduction in severe hypoglycaemia in type 1 diabetes in a randomized crossover study of continuous intraperitoneal compared with subcutaneous insulin infusionDIABETES OBESITY & METABOLISM, Issue 11 2009A. Liebl Aim: Continuous intraperitoneal insulin infusion (CIPII) with the DiaPort system using regular insulin was compared to continuous subcutaneous insulin infusion (CSII) using insulin Lispro, to investigate the frequency of hypoglycemia, blood glucose control, quality of life, and safety. Methods: In this open, randomized, controlled, cross-over, multinational, 12-month study, 60 type 1 diabetic patients with frequent hypoglycemia and/or HbA1c > 7.0% with CSII were randomized to CIPII or CSII. The aim was to obtain the best possible blood glucose while avoiding hypoglycemia. Results: The frequency of any hypoglycemia was similar (CIPII 118.2 (SD 82.6) events / patient year, CSII 115.8 (SD 75.7) p = 0.910). The incidence of severe hypoglycemia with CSII was more than twice the one with CIPII (CIPII 34.8 events / 100 patient years, CSII 86.1, p = 0.013). HbA1c, mean blood glucose, and glucose fluctuations were not statistically different. Treatment-related severe complications occurred mainly during CIPII: port infections (0.47 events / patient year), abdominal pain (0.21 events / patient year), insulin underdelivery (0.14 events / patient year). Weight gain was greater with CSII (+ 1.5 kg vs. , 0.1 kg, p = 0.013), quality of life better with CIPII. Conclusions: In type 1 diabetes CIPII with DiaPort reduces the number of severe episodes of hypoglycemia and improves quality of life with no weight gain. Because of complications, indications for CIPII must be strictly controlled. CIPII with DiaPort is an alternative therapy when CSII is not fully successful and provides an easy method of intraperitoneal therapy. [source] The relationship of postprandial glucose to HbA1cDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S2 2004Rüdiger Landgraf Abstract The gold standard for the assessment of the overall glycemic control is the determination of HbA1c. There are, however, insufficient data to determine reliably the relative contribution of fasting and postprandial plasma glucose to HbA1c. Increasing evidence suggests that excessive excursions of postprandial glucose might be important for the development of micro- and macroangiopathic complications. With respect to the treatment options, one important question to be answered is whether premeal, postmeal or fasting plasma glucose, alone or in combination, will be necessary in adjusting the therapy to achieve optimal HbA1c levels while minimizing hypoglycemia. HbA1c is difficult to predict from fasting plasma glucose. There are indications that there is a shift in the relative contribution from postprandial glucose at good to fair HbA1c levels (<7.3% to <9.2%) to fasting plasma glucose at high HbA1c (>9.3%). There is also a better correlation of afternoon and evening plasma glucose with HbA1c than with prebreakfast and prelunch plasma glucose values. Since the definition on how to define postprandial glucose is still a matter of debate and since postprandial glucose depends on the premeal blood glucose level and, on the time of the meal, its size and composition and the therapeutic strategy, the data so far available are inconclusive and the best correlation of HbA1c is with the area under the glucose profiles. Continuous glucose monitoring under daily life conditions will be the key to definitely unravel the relationship among HbA1c and fasting, premeal, postprandial and postabsorptive plasma glucose. Copyright © 2004 John Wiley & Sons, Ltd. [source] Evidence for a vicious cycle of exercise and hypoglycemia in type 1 diabetes mellitusDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2004A. C. Ertl Abstract Exercise is a cornerstone of diabetes management as it aids in glycemic control, weight management, reducing blood pressure, and improving the quality of life of patients. Unfortunately, owing to the complexity and difficulties of regulating exogenous insulin in a physiologic manner during exercise, physical activity often results in hypoglycemia in patients with type 1 diabetes mellitus (type 1 DM). When glucose levels fall below threshold glycemic levels, neuroendocrine, autonomic nervous system (ANS), and metabolic glucose counterregulatory mechanisms are activated. These hypoglycemic counterregulatory mechanisms in type 1 DM can be blunted irreversibly by disease duration or by acute episodes of prior stress. These reduced (or absent) counterregulatory responses result in a threefold increase in severe hypoglycemia when intensive glycemic control is implemented in type 1 DM 1. Much recent work has been focused on determining the in vivo mechanisms responsible for causing the increased incidence of severe hypoglycemia in type 1 DM. Studies from several laboratories have demonstrated the role played by episodes of antecedent hypoglycemia in producing blunted glucose counterregulatory responses during subsequent exposures of hypoglycemia. Until recently, the mechanisms responsible for exercise related hypoglycemia in type 1 DM have been attributed to relative or absolute increases of insulin levels or incomplete glycogen repletion after physical activity. Owing to the qualitative similarity of neuroendocrine, ANS, and metabolic responses to hypoglycemia and exercise, we have hypothesized that neuroendocrine and ANS counterregulatory dysfunction may also play an important role in the pathogenesis of exercise-related hypoglycemia in type 1 DM. Vicious cycles can be created in type 1 DM, where an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and ANS responses to a subsequent episode of either stress, thereby creating further hypoglycemia (Figure 1). This article will review the recent work that has studied the contribution of counterregulatory dysfunction to exercise-induced hypoglycemia in type 1 DM. Copyright © 2004 John Wiley & Sons, Ltd. 1. Reciprocal vicious cycles may be created in type 1 diabetes mellitus (type 1 DM), whereby an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and autonomic nervous system responses to a subsequent episode of either stress, thereby creating further hypoglycemia [source] Continuous glucose monitoring in managing diabetes in childrenDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 4 2002Phyllis W. Speiser Abstract Continuous glucose monitoring (CGM) devices have now been added to the repertoire of technological devices useful in the management of patients with diabetes. In this issue, Schiaffini and colleagues confirm and extend published data describing the benefits of CGM in diabetic children. Specifically, such monitoring enables clinicians to detect occult hypoglycemia not otherwise discernable with intermittent testing of blood glucose. Although results of monitoring are not yet available in real time, the data can be used to adjust insulin regimens to allow more effective glycemic control. This is especially important in the pediatric population for whom strict glycemic control has traditionally been limited owing to concerns about the negative effects of hypoglycemia on the developing central nervous system. Additionally, postprandial hyperglycemia can be more readily detected and controlled. CGM provides new and important informaton not necessarily provided by measurement of HbA1c, and will likely prove an indispensable adjunct to diabetes care. Finally, this procedure has potential applications in the diagnosis and management of patients with other metabolic disorders. Copyright © 2002 John Wiley & Sons, Ltd. [source] Diabetes management in the new millennium using insulin pump therapyDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2002Bruce W. Bode Abstract Current goals of therapy of type 1 and 2 diabetes are to achieve near normal glycemia, minimize the risk of severe hypoglycemia, limit excessive weight gain, improve quality of life and delay or prevent late vascular complications. As discussed in this review, insulin pump or continuous subcutaneous insulin infusion (CSII) therapy provides a treatment option that can dramatically aid in achieving all of these goals. In comparison to multiple daily injections (MDI), CSII uses only rapid-acting insulin, provides greater flexibility in timing of meals and snacks, has programmable basal rates to optimize overnight glycemic control, can reduce the risk of exercise-induced hypoglycemia, and enhances patients' ability to control their own diabetes. Most important, in adults and adolescents with type 1 diabetes, CSII has been shown to lower HbA1c levels, reduce the frequency of severe hypoglycemia and limit excessive weight gain versus MDI without increasing the risk of diabetic ketoacidosis. Similarly positive results are being seen with CSII in adults with type 2 diabetes. The effectiveness of CSII and improvements in pump technology have fueled a dramatic increase in the use of this therapy. Practical guidelines are presented for selection of patients, initiation of treatment, patient education, follow-up assessments and troubleshooting. The recent introduction of methods for continuous glucose monitoring provides a new means to optimize the basal and bolus capabilities of CSII and offers the hope of the development of a feedback-controlled artificial pancreas. Copyright © 2002 John Wiley & Sons, Ltd. [source] Status Epilepticus,Induced Neuronal Loss in Humans Without Systemic Complications or EpilepsyEPILEPSIA, Issue 8 2000Denson G. Fujikawa Summary: Purpose: To determine the regional distribution of neuronal damage caused strictly by status epilepticus (SE) without systemic complications, underlying brain pathology, or a history of preexisting epilepsy. Methods: The medical records and electroencephalograms (EEGs) of three deceased patients who developed SE in the hospital were reviewed. Their brains were formalin-fixed, and 17 brain regions were selected, embedded in paraffin, and sectioned. Alternate sections were stained with either hematoxylin and eosin and cresyl violet to determine the extent of neuronal loss and gliosis or glial fibrillary astrocytic protein to confirm the extent of astrocytic proliferation. Results: The three patients died 11 to 27 days after the onset of focal motor SE; none had hypotension, hypoxemia, hypoglycemia, or significant hyperthermia. Two patients had no prior seizures and no underlying brain pathology. The third patient, who had leptomeningeal carcinomatosis, had one seizure 2 months before the onset of SE. The duration of SE was 8.8 hours to 3 days. EEGs showed unilateral temporal lobe sharp-wave discharges in one patient and independent temporal lobe sharp-wave discharges bilaterally in the other two patients. In addition to widespread neuronal loss and reactive gliosis in the hippocampus, amygdala, dorsomedial thalamic nucleus, and Purkinje cell layer of the cerebellum, we report for the first time periamygdaloid (piriform) and entorhinal cortical damage occurring acutely after SE in humans. Conclusions: In the absence of systemic complications or preexisting epilepsy, SE produces neuronal loss in a distribution similar to that from domoic acid-induced SE in humans and from kainic acid- and pilocarpine-induced SE in rats. [source] Treatment satisfaction with insulin glargine in patients with diabetes mellitus in a university hospital clinic in SwedenEUROPEAN DIABETES NURSING, Issue 1 2009M Annersten Gershater RN, MNSc Research Nurse Abstract Background: Few studies evaluate patients' perspectives when a new drug is intro-duced to treat chronic diseases such as diabetes mellitus. The clinical role of a new insulin treatment, in terms of the relationship between higher cost and better treat-ment outcomes (as defined from the patient perspective) has been discussed. We sought to explore patient satisfaction with a new insulin treatment (insulin glargine). At its launch in 2002/3 it was purported to provide constant, peakless insulin release following once- or twice-daily administration, thus leading to fewer hypoglycaemic episodes while providing metabolic control equivalent to that achieved with NPH human basal insulin. Aims: To investigate the indications used for prescription of a new drug and its clinical effects on glycosylated haemoglobin (HbA1c) levels, perceived hypoglycaemic events and patient satisfaction. Methods: The Diabetes Treatment Satisfaction Questionnaire (Status Version, DTSQ-s), which measures satisfaction with treatment regimen, and perceived frequency of hyperglycaemia and hypoglycemia, was circulated to all living patients who had ever started treatment with insulin glargine at the Department of Endocrinology at Malmö University Hospital. Medical records of 913 patients were assessed for HbA1c levels at 0 and 12 months after starting insulin glargine therapy. Results: Completed questionnaires were returned by 615 of 960 patients (64%) who had ever started insulin glargine. The main indications for starting treatment were physicians' or nurses' initiatives, desire for fewer fluctuations and improved metabolic control. HbA1c levels fell by 0.41% for patients with type 1 diabetes and by 0.68% for those with type 2 diabetes. The mean DTSQ-s score was 28.45 for satisfaction, whereas the mean perceived hypoglycaemic/hyperglycaemic events score was 3. Conclusion: Treatment satisfaction was very high and perceived frequency of hypoglycaemia/hyperglycaemia was very low. The indications for treatment of insulin glargine are being followed in accordance with national recommendations. Copyright © 2009 FEND [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] Diabetes mellitus and geriatric syndromesGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 2 2009Atsushi Araki Diabetes mellitus is associated with an increased prevalence and incidence of geriatric syndrome: functional disabilities, depression, fall, urinary incontinence, malnutrition and cognitive impairment. Geriatric syndrome not only leads to frailty, loss of independence and low quality of life, but also becomes a major obstacle in the treatment and care of diabetic people. The risk factors or contributing factors of geriatric symptoms are micro- and macrovascular complications, age-rated comorbid disease and aging per se. Comprehensive geriatric assessment of geriatric syndrome, including basic activities of daily living, instrumental activities of daily living, gait and balance, visual acuity, the Mini-Mental State Examination, depression scores, history and risk of fall, urination and nutrition, should be performed as part of the care of elderly diabetic patients, in particular old-old patients. Because geriatric syndromes are multifactorial and share risk factors, diabetic people with any geriatric symptoms should be treated with a common concentric strategy, such as supervised exercise therapy including muscle-strengthening training, psychological support, social support for adherence, and good glycemic control with avoidance of hypoglycemia. [source] Switch to oral hypoglycemic agent therapy from insulin injection in patients with type 2 diabetesGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2008Takashi Okamoto Aim: We aimed to determine the feasibility of substituting thiazolidinedione-based therapy for insulin injection therapy in patients with type 2 diabetes. Methods: Thirty-six subjects (17 men and 19 women) aged 67.8 ± 11.3 years with an average insulin dose of 0.46 ± 0.17 U/kg bodyweight, a duration of insulin therapy of 6.1 ± 8.2 years and an average hemoglobin A1c (HbA1c) of 6.8 ± 1.3% were switched from insulin injection therapy to pioglitazone, glimepiride and voglibose combination therapy. Results: The number of subjects achieving HbA1c levels of less than 7% at 4 months was 30. The success rate of switch therapy was 83% (30/36). HbA1c was significantly reduced from 6.7 ± 1.3% to 5.9 ± 0.7% at 4 months after the switch (P < 0.01) in 32 patients who completed the planned 4-month study. No adverse effects including heart failure, liver dysfunction or severe hypoglycemia were observed. The insulin dose and the maximum blood glucose on the switch day were significantly lower and the age was significantly higher in the subjects who achieved HbA1c less than 7% at 4 months compared to those who did not (P < 0.05). Conclusion: Thiazolidinedione-based oral combination therapy may efficiently and safely substitute relatively high-dose insulin injection therapy in patients with type 2 diabetes. [source] Brain Apparent Water Diffusion Coefficient Magnetic Resonance Image During a Prolonged Visual AuraHEADACHE, Issue 6 2010Robert Belvķs MD (Headache 2010;50:1045-1049) Background., Reversible changes in brain magnetic resonance imaging (MRI) weighted in diffusion-weighted images (DWI) and apparent water diffusion coefficient (ADC) maps have been reported in acute stroke, epilepsy, eclampsia, and hypoglycemia, but they are contradictory regarding to migraine aura. Objective., A 41-year-old woman with known basilar migraine for 5 years consulted about a persistent visual aura (visual snow phenomenon) plus bilateral paresthesias in the extremities for 4 days. The headache was treated with success with 10 mg of wafer rizatriptan and 600 mg of ibuprophen. Methods., The neurologic and ophthalmologic examination were normal. An urgent brain MRI detected no lesions in T1, T2, fluid-attenuated inversion recovery, and DWI, but an abnormal signal appeared in the left occipital lobe in ADC and (r)ADC maps. The brain MRI angiography, carotid ultrasound study, transesophageal echocardiography, 24-hour cardiac Holter monitoring, and thrombophilia study were normal. Results., A new brain MRI 8 days after did not show any previous lesion in the same sequences. Conclusions., We present a patient with migraine and transitory abnormal signals in the ADC map of an occipital region during persistent visual aura. The clinical-radiological relationship is congruent. Some similar cases have showed these MRI signals during the aura, suggesting cytotoxic edema, without ischemic lesions in the MRI controls. Theses ADC images probably appear in complex auras. [source] Disturbed hepatic carbohydrate management during high metabolic demand in medium-chain acyl,CoA dehydrogenase (MCAD),deficient mice,HEPATOLOGY, Issue 6 2008Hilde Herrema Medium-chain acyl,coenzyme A (CoA) dehydrogenase (MCAD) catalyzes crucial steps in mitochondrial fatty acid oxidation, a process that is of key relevance for maintenance of energy homeostasis, especially during high metabolic demand. To gain insight into the metabolic consequences of MCAD deficiency under these conditions, we compared hepatic carbohydrate metabolism in vivo in wild-type and MCAD,/, mice during fasting and during a lipopolysaccharide (LPS)-induced acute phase response (APR). MCAD,/, mice did not become more hypoglycemic on fasting or during the APR than wild-type mice did. Nevertheless, microarray analyses revealed increased hepatic peroxisome proliferator-activated receptor gamma coactivator-1, (Pgc-1,) and decreased peroxisome proliferator-activated receptor alpha (Ppar ,) and pyruvate dehydrogenase kinase 4 (Pdk4) expression in MCAD,/, mice in both conditions, suggesting altered control of hepatic glucose metabolism. Quantitative flux measurements revealed that the de novo synthesis of glucose-6-phosphate (G6P) was not affected on fasting in MCAD,/, mice. During the APR, however, this flux was significantly decreased (,20%) in MCAD,/, mice compared with wild-type mice. Remarkably, newly formed G6P was preferentially directed toward glycogen in MCAD,/, mice under both conditions. Together with diminished de novo synthesis of G6P, this led to a decreased hepatic glucose output during the APR in MCAD,/, mice; de novo synthesis of G6P and hepatic glucose output were maintained in wild-type mice under both conditions. APR-associated hypoglycemia, which was observed in wild-type mice as well as MCAD,/, mice, was mainly due to enhanced peripheral glucose uptake. Conclusion: Our data demonstrate that MCAD deficiency in mice leads to specific changes in hepatic carbohydrate management on exposure to metabolic stress. This deficiency, however, does not lead to reduced de novo synthesis of G6P during fasting alone, which may be due to the existence of compensatory mechanisms or limited rate control of MCAD in murine mitochondrial fatty acid oxidation. (HEPATOLOGY 2008.) [source] Molecular spectrum of SLC22A5 (OCTN2) gene mutations detected in 143 subjects evaluated for systemic carnitine deficiency,HUMAN MUTATION, Issue 8 2010Fang-Yuan Li Abstract Systemic primary carnitine deficiency (CDSP) is caused by recessive mutations in the SLC22A5 (OCTN2) gene encoding the plasmalemmal carnitine transporter and characterized by hypoketotic hypoglycemia, and skeletal and cardiac myopathy. The entire coding regions of the OCTN2 gene were sequenced in 143 unrelated subjects suspected of having CDSP. In 70 unrelated infants evaluated because of abnormal newborn screening (NBS) results, 48 were found to have at least 1 mutation/unclassified missense variant. Twenty-eight of 33 mothers whose infants had abnormal NBS results were found to carry at least 1 mutation/unclassified missense variant, including 11 asymptomatic mothers who had 2 mutations. Therefore, sequencing of the OCTN2 gene is recommended for infants with abnormal NBS results and for their mothers. Conversely, 52 unrelated subjects were tested due to clinical indications other than abnormal NBS and only 14 of them were found to have at least one mutation/unclassified variant. Custom designed oligonucleotide array CGH analysis revealed a heterozygous ,1.6 Mb deletion encompassing the entire OCTN2 gene in one subject who was apparently homozygous for the c.680G>A (p.R227H) mutation. Thus, copy number abnormalities at the OCTN2 locus should be considered if by sequencing, an apparently homozygous mutation or only one mutant allele is identified. ©2010 Wiley-Liss, Inc. [source] Perception of hunger to insulin-induced hypoglycemia in anorexia nervosaINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 3 2001Yoshikatsu Nakai Abstract Objective We studied the effect of insulin-induced hypoglycemia on changes of hunger ratings in anorectic patients before and after cognitive-behavioral therapy. Method The subjects were 17 females with restricting anorexia nervosa at low body weight (AN-R), 6 anorectic patients whose weight was restored after cognitive-behavioral therapy (AN-T), and 11 age-matched female controls. All subjects gave hunger ratings by linear visual analog technique before and after insulin or saline injection. Results Hunger ratings increased significantly 45 min after insulin injection in control females. However, ratings paradoxically decreased after insulin injection in AN-R females. They increased slightly after insulin injection in AN-T females, but the difference was not statistically significant. One-factor analysis of variance for the peak values of hunger ratings was significant. These values in control females were significantly higher than those in AN-R and AN-T females. Discussion These results suggest that perception of hunger to insulin-induced hypoglycemia in AN patients is disturbed. © 2001 by John Wiley & Sons, Inc. Int J Eat Disord 29: 354,357, 2001. [source] Cell resilience in species life spans: a link to inflammation?AGING CELL, Issue 4 2010Caleb E. Finch Summary Species differences in life span have been attributed to cellular survival during various stressors, designated here as ,cell resilience'. In primary fibroblast cultures, cell resilience during exposure to free radicals, hypoglycemia, hyperthermia, and various toxins has shown generally consistent correlations with the species characteristic life spans of birds and mammals. However, the mechanistic links of cell resilience in fibroblast cultures to different species life spans are poorly understood. We propose that certain experimental stressors are relevant to somatic damage in vivo during inflammatory responses of innate immunity, particularly, resistance to reactive oxygen species (ROS), low glucose, and hyperthermia. According to this hypothesis, somatic cell resilience determines species differences in longevity during repeated infections and traumatic injuries in the natural environment. Infections and injury expose local fibroblasts and other cells to ROS generated by macrophages and to local temperature elevations. Systemically, acute phase immune reactions cause hypoglycemia and hyperthermia. We propose that cell resilience to somatic stressors incurred in inflammation is important in the evolution of longevity and that longer-lived species are specifically more resistant to immune-related stressors. This hypothesis further specifies Kirkwood's disposable soma theory. We suggest expanding the battery of stressors and markers used for comparative studies to additional cell types and additional parameters relevant to host defense and to their ecological specificities. [source] ORIGINAL ARTICLE: Many patients with Type 1 diabetes estimate their prandial insulin need inappropriatelyJOURNAL OF DIABETES, Issue 3 2010Aila J. AHOLA Abstract Background:, Many factors contribute to the need for prandial insulin in Type 1 diabetes. However, patients' success in achieving normal postprandial glucose concentration is understudied. The aim of the present study was to determine how often patients with Type 1 diabetes achieve normal postprandial glucose concentrations and to evaluate factors associated with postprandial hypo- and hyperglycemia. Methods:, Data on food intake, physical activity, insulin administration, and blood glucose concentration were collected using a self-administered questionnaire from 331 patients with Type 1 diabetes (43% men; mean age 49 ± 12 years; mean diabetes duration 32 ± 13 years). Of these, 179 provided data on blood glucose concentrations measured 110,150 min postprandially. One such meal per patient was randomized for analyses. Results:, Hypoglycemia (<4.0 mmol/L), normoglycemia (4.0,7.9 mmol/L), and hyperglycemia (,8.0 mmol/L) were observed after 23%, 36%, and 41% of meals, respectively. The three postprandial glycemia groups did not differ with respect to the meal composition or the timing of the postprandial blood glucose measurement. In women, postprandial hyperglycemia was associated with shorter diabetes duration and higher preprandial blood glucose concentration, whereas postprandial hypoglycemia was associated with higher physical activity. No single factor explained the postprandial glycemic state in men. Conclusions:, A total of 64% of patients estimated their prandial insulin need inappropriately, suggesting that estimation of the optimal prandial insulin dose is not easy, even after a long duration of diabetes. [source] Incidence of severe hypoglycemia with tight glycemic control: the higher the better?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009M. J. Schultz No abstract is available for this article. [source] | ||||||||||||||||||||||||||||||||||||||||||||||