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Recurrent Hypoglycaemia (recurrent + hypoglycaemia)
Selected AbstractsContinuous glucose monitoring in patients with insulinomaCLINICAL ENDOCRINOLOGY, Issue 6 2008Alia Munir Summary Background, Insulinomas are rare neuroendocrine tumours that are usually small and may take time to localize. They cause recurrent life-threatening spontaneous hypoglycaemia. Recurrent hypoglycaemia causes loss of hypoglycaemia awareness, putting the patient at further risk, but this has rarely been described in insulinoma. We describe the utility of continuous glucose monitoring (CGM) in patients with insulinoma. Patients and methods, Three patients, aged 72 years (patient 1), 37 years (patient 2) and 24 years (patient 3), with suspected insulinoma attended our investigation unit, in a university teaching hospital. Biochemical diagnosis was confirmed by elevated plasma insulin and C-peptide during biochemical hypoglycaemia [plasma glucose < 2·2 mM (40 mg/dl)]. Surgery confirmed histology in all. CGM was used to monitor frequency and time of hypoglycaemia during diagnosis and medical treatment, and after definitive surgical treatment. Results, All patients had evidence of hypoglycaemia unawareness. At diagnosis in patients 1,3, CGM revealed 6·1%, 21·9% and 71·0% of time spent in moderate hypoglycaemia (plasma glucose 2·2,3·0 mM), and 1·4%, 11·4% and 48·1% of time in severe hypoglycaemia (plasma glucose < 2·2 mM), respectively. On diazoxide this reduced to 0·6%, 5·4% and 5·7% time in moderate hypoglycaemia, and no severe hypoglycaemia in patients 1 and 3, and 0·5% in patient 2. Octreotide therapy in patients 2 and 3 resulted in 5·8% and 0% of time in moderate hypoglycaemia, respectively, and no severe hypoglycaemia. After surgical excision CGM confirmed cure in all. Conclusions, CGM in insulinoma is useful in detecting hypoglycaemia, and hypoglycaemia unawareness, monitoring response to medical therapy and for confirming cure postoperatively, and is useful in the management of this uncommon but dangerous condition. [source] The mechanisms that underlie glucose sensing during hypoglycaemia in diabetesDIABETIC MEDICINE, Issue 5 2008R. McCrimmon Abstract Hypoglycaemia is a frequent and greatly feared side-effect of insulin therapy, and a major obstacle to achieving near-normal glucose control. This review will focus on the more recent developments in our understanding of the mechanisms that underlie the sensing of hypoglycaemia in both non-diabetic and diabetic individuals, and how this mechanism becomes impaired over time. The research focus of my own laboratory and many others is directed by three principal questions. Where does the body sense a falling glucose? How does the body detect a falling glucose? And why does this mechanism fail in Type 1 diabetes? Hypoglycaemia is sensed by specialized neurons found in the brain and periphery, and of these the ventromedial hypothalamus appears to play a major role. Neurons that react to fluctuations in glucose use mechanisms very similar to those that operate in pancreatic B- and A-cells, in particular in their use of glucokinase and the KATP channel as key steps through which the metabolic signal is translated into altered neuronal firing rates. During hypoglycaemia, glucose-inhibited (GI) neurons may be regulated by the activity of AMP-activated protein kinase. This sensing mechanism is disturbed by recurrent hypoglycaemia, such that counter-regulatory defence responses are triggered at a lower glucose level. Why this should occur is not yet known, but it may involve increased metabolism or fuel delivery to glucose-sensing neurons or alterations in the mechanisms that regulate the stress response. [source] Short-term nocturnal hypoglycaemia increases morning food intake in healthy humansDIABETIC MEDICINE, Issue 2 2008S. M. Schmid Abstract Aims Hypoglycaemia during wakefulness increases hunger and food intake. Patients with Type 1 diabetes mellitus are at high risk of recurrent hypoglycaemia and weight gain. Given the background of frequent hypoglycaemic episodes during night-time sleep in diabetic patients, we investigated morning food intake after nocturnal hypoglycaemia. Methods We tested 16 healthy normal-weight subjects (eight women) on three nights. A linear fall in plasma glucose to a nadir of 2.2 mmol/l within 60 min was induced by insulin infusion immediately after sleep onset (,early hypo') or after about 3.5 h of sleep (,late hypo'). On a control night, no hypoglycaemia was induced. Spontaneous food intake at a breakfast buffet was registered on the subsequent morning. Results Compared with the control condition (700 ± 93 kcal), subjects ate more after ,late hypo' (867 ± 108 kcal; P = 0.041), but not after ,early hypo' (852 ± 111 kcal; P = 0.130). Analyses of macronutrient fractions revealed that in comparison with the control condition, subjects ate significantly more carbohydrates after both ,late hypo' (277 ± 25 kcal vs. 206 ± 23 kcal, P < 0.001) and ,early hypo' (245 ± 23 kcal, P = 0.048), with this effect being more pronounced after late than early nocturnal hypoglycaemia (P = 0.026). Conclusions In healthy subjects, nocturnal hypoglycaemia during sleep stimulates spontaneous food intake the following morning, with carbohydrate intake being especially affected. Effects were more pronounced after ,late hypo', suggesting the influence of temporal dynamics. Although healthy non-diabetic subjects were studied, similar mechanisms may contribute to the frequently observed body weight gain in insulin-treated diabetic patients. [source] In-patient management of diabetes mellitus and patient satisfactionDIABETIC MEDICINE, Issue 5 2002A. Bhattacharyya Abstract Aims To devise a system for assessing in-patient glycaemic control and care satisfaction in diabetic patients admitted to hospital for reasons other than their diabetes. Methods Consecutive January to March 2001 case-notes were reviewed. Admissions with acute metabolic complications, acute myocardial infarction and pregestational or gestational diabetes were excluded. Glycaemic control, frequency of blood monitoring and management of hyperglycaemia were recorded. The diabetes treatment satisfaction questionnaire was used to assess preadmission satisfaction with care. Post-admission a 12-stem questionnaire was used to assess satisfaction with in-patient diabetes management. Results Hypoglycaemia was common. Although none developed a hyperglycaemic emergency, high blood glucose was prevalent and, frequently, persistent hyperglycaemia or recurrent hypoglycaemia was not acted on appropriately. The overall score for in-patient satisfaction with treatment was fair (4.1 ± 1.8 on a six-point scale; 6 = very satisfied and 1 = very dissatisfied). Scores were higher among patients on surgical wards than on medical wards (P = 0.008), but satisfaction did not vary when patients were stratified according to sex, age and mode of treatment. Conclusion Current systems are not achieving satisfactory in-patient glycaemic control and there is poor satisfaction with medical in-patient diabetes care. Following changes intended to produce improvements, this assessment system can be used recurrently to monitor in-patient care and satisfaction. [source] Use of therapeutic responses to glucose replacement to predict glucose patterns in diabetic patients presenting with severe hypoglycaemiaINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 8 2009Y.-Y. Lin Summary Objective:, The purpose of this study was to determine whether initial serum glucose levels, therapeutic responses to intravenous glucose replacement and changes in serum glucose levels over time could predict serum glucose patterns. Methods:, The patients enrolled in this retrospective chart review had been previously diagnosed with diabetes mellitus and were later hospitalised for severe hypoglycaemia (SH). They were all admitted to the emergency department (ED) during a 4-year period between January 2003 and December 2006. Comparison of the therapeutic responses to glucose replacement according to the serum glucose patterns [categorised into recurrent hypoglycaemia (RH), overshoot hyperglycaemia (OH) and favourable groups] during the first 48 h was performed. Results:, Compared with the favourable group, therapeutic responses to glucose replacement were significantly lower in the RH group and higher in the OH group; the changes in serum glucose levels over time were also significantly lower in the RH group and higher in the OH group. Conclusion:, Therapeutic responses to glucose replacement and changes in serum glucose levels over time can differentiate diabetic patients with RH and OH from those with favourable glucose patterns during the first 48 h after presentation in the ED with SH. We believe that a ,response-to-treatment' based strategy is useful in determining the ED disposition of diabetic patients presenting with SH. [source] Glucagon is absorbed from the rectum but does not hasten recovery from hypoglycaemia in patients with type 1 diabetesBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 1 2008David R. Parker WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT , Patients with type 1 diabetes experience recurrent hypoglycaemia and have abnormal glucose counter regulatory responses with a failure to secrete glucagon. It is unknown if rectal glucagon is absorbed and what effect this may have on counter regulation from hypoglycaemia. WHAT THIS STUDY ADDS , A rectal suppository of glucagon results in a rise in plasma glucagon with metabolic effects in normal subjects. Similarly rectal glucagon results in a rise in plasma glucagon in patients with type 1 diabetes, but 1 mg does not improve recovery rates from experimental hypoglycaemia when compared with placebo. , Larger doses of glucagon per rectum may provide pharmacological circulating concentrations with resulting therapeutic benefit during recovery from hypoglycaemia and deserves further study. AIMS A failure to secrete glucagon during hypoglycaemia is near universal in patients with type 1 diabetes 5 years after disease onset and may contribute to delayed counter-regulation during hypoglycaemia. Rectal glucagon delivery may assist glucose recovery following insulin-induced hypoglycaemia in such patients and has not been previously studied. METHODS Six male patients (age 21,38 years) with type 1 diabetes (median duration 10 years) without microvascular complications, were studied supine after an overnight fast on two separate occasions at least 14 days apart. After omission of their usual morning insulin and 45 min rest, hypoglycaemia was induced by an intravenous insulin infusion which was terminated when capillary glucose concentration reached 2.5 mmol l,1. Subjects were randomized to insert a rectal suppository containing 100 mg indomethacin alone (placebo) or 100 mg indomethacin plus 1 mg glucagon at the hypoglycaemic reaction. Serial measurements were made for 120 min. RESULTS In the two groups, mean (SD) plasma glucose concentrations fell to a similar nadir of 1.8 (0.7) mmol l,1 (placebo) and 2.1 (1.2) mmol l,1 (glucagon). Peak plasma glucagon following hypoglycaemia was higher in the glucagon group; 176 (32) ng l,1vs. 99 (22) ng l,1 after placebo (P = 0.006). However, the glucose recovery rate over 120 min after hypoglycaemia did not differ significantly. CONCLUSIONS Our results provide evidence for the absorption of glucagon from the rectum. They also indicate that 1 mg does not constitute a useful mode of therapy to hasten recovery from hypoglycaemia in patients with type 1 diabetes. [source] | ||||||||||