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Results for “hypoglycaemia”

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PubMed1990

Neurophysiological changes during insulin-induced hypoglycaemia and in the recovery period following glucose infusion in type 1 (insulin-dependent) diabetes mellitus and in normal man.

Hypoglycaemia (median venous blood glucose 1.8 mmol/l; range 1.6-2.3) was induced by an intravenous infusion of regular insulin in eight patients with Type 1 (insulin-dependent) diabetes mellitus (age 28.0 +/- 7.4 years; mean +/- SD, duration 15.5 +/- 5.1 years) and in 12 age-matched healthy male control subjects. Multi-channel frequency analysis of electroencephalogram (electrophysiologic brain mapping) and recording of P300 and somatosensory evoked potentials were performed before, during and immediately after the hypoglycaemic period. The hypoglycaemia produced a significant increase in low frequency electroencephalographic activity in both groups, most pronounced over anterior regions of the brain. The electroencephalographic activity was normalised immediately after the hypoglycaemic period. The patients with diabetes showed somewhat longer P300 latencies during the initial normoglycaemic examination. Hypoglycaemia caused a marked reduction of the P300 amplitude in both groups of subjects and the amplitude was not restored immediately after normalisation of blood glucose levels. The somatosensory cortical responses were not affected by hypoglycaemia. We conclude that hypoglycaemia results in impairment in cerebral function, as measured by neurophysiological techniques, which is not immediately normalised when blood glucose is restored to normal.

Adult↗

PubMed1991

Basal and insulin stimulated substrate metabolism in tumour induced hypoglycaemia; evidence for increased muscle glucose uptake.

While it has very recently been reported that tumour induced hypoglycaemia is characterised by elevated production of insulin-like growth factor 2, the tissues responsible for induction of hypoglycaemia are largely unknown. We have investigated a patient with a large retroperitoneal mass and spontaneous hypoglycaemia. When compared to a reference population the patient displayed: (1) An increased glucose disposal rate and a five-fold elevation of forearm glucose uptake. (2) A decreased endogenous glucose production rate. (3) Decreased circulating levels of lipid intermediates. (4) Increased glucose oxidation and decreased lipid oxidation. (5) Low circulating levels of insulin-like growth factor 2 and insulin-like growth factor-binding protein-3 and normal levels of insulin-like growth factor 1. (6) Normal insulin sensitivity (euglycaemic glucose clamp). Blood concentrations of insulin, C-peptide, proinsulin, glucagon, growth hormone and catecholamines were within normal range, but the growth hormone response to hypoglycaemia was blunted. The data suggest that the mechanisms behind tumour induced hypoglycaemia are of systemic nature and that the tissue most prominently affected is striated muscle.

Blood Glucose↗

PubMed1994

Thermoregulatory responses to hyperinsulinaemic hypoglycaemia and euglycaemia in IDDM.

In healthy subjects hypoglycaemia causes a fall in body temperature through increased sweating and limb blood flow, and despite increased metabolic heat production. We studied thermoregulatory responses to hyperinsulinaemic (100 mU.m-2.min-1) (a) hypoglycaemia (2.5 mmol/l) and (b) euglycaemia (4.5 mmol/l) in insulin-dependent diabetic men of short (< 5 years) and long (> 15 years) diabetes duration. Plasma noradrenaline (p < 0.0001), metabolic rate (p < 0.005), heart rate (p < 0.0001) and skin blood flow (p < 0.05) increased during hypoglycaemia and euglycaemia with a greater rise in noradrenaline during the former (p < 0.05). Plasma adrenaline (p < 0.005), forearm blood flow (p < 0.05) and systolic blood pressure (p < 0.02) increased and diastolic blood pressure decreased (p < 0.005) during hypoglycaemia, with greater changes in adrenaline (p < 0.05) and diastolic blood pressure in patients of short diabetes duration. Only two patients (diabetes duration < 2 years) sweated appropriately, while body temperature changed minimally in the two groups of patients. In summary, thermoregulatory responses to hypoglycaemia are impaired in IDDM due to attenuated sweating and adrenomedullary responses.

Adult↗

PubMed2005

Methodology for hypoglycaemia detection based on the processing, analysis and classification of the electroencephalogram.

Hypoglycaemia (blood glucose level below 3.8 mmol l(-1)) is the most common complication in the treatment of diabetes with insulin and can cause a number of problems. Previous works have shown that hypoglycaemia causes changes in the electroencephalogram (EEG) signal. In this investigation, portable apparatus was developed to record the EEG, and a methodology was implemented, using digital signal processing and artificial neural networks (ANNs), to detect hypoglycaemia. Sixteen EEG recordings were made on eight subjects with diabetes (five male, three female), aged 35 +/- 13.5 years (mean +/- SD), during the day, over periods of 5.7 +/- 2 min. Ten of these recordings (in seven subjects) included periods of normoglycaemia and spontaneous hypoglycaemia. The result of the off-line ANN classification for each of these ten recordings was an overall accuracy rate of 71.3%, sensitivity of 71.1% and specificity of 71.5%. In the classification using four recordings from a single subject, the accuracy was 80.6%, with a sensitivity of 77.8% and a specificity of 83.9%. In the classification using recordings from five different subjects to train the ANN, the obtained accuracy rate was 49.2%, with a sensitivity of 76% and a specificity of 32.5%. The result of the classification in real time, for one subject, was an accuracy rate of 85.2%, with a sensitivity of 60% and a specificity of 100%. In conclusion, the methodology proposed and implemented justifies further studies with the objective of constructing a hypoglycaemia detector system based on the processing and classification of the EEG.

Adult↗

PubMed2002

Are hypoglycaemia and other adverse effects similar among sulphonylureas?

This review provides an updated overview of the adverse effects of sulphonylureas and identifies factors associated with variation in adverse effect rates among sulphonylureas published by different studies. A search of Medline, Embase, Current Contents and Cochrane Library was conducted to identify all papers related to sulphonylureas and adverse effects published from 1950-2001. The reference lists of all relevant papers were also searched for additional articles. The frequency of sulphonylurea-induced hypoglycaemia varied from 1.8-59%. Severe hypoglycaemia due to sulphonylurea use has been reported from 1.9-3.5%. Variation in hypoglycaemia rates may be due to differences in definitions, methods to detect and to collect information, patient characteristics, patient knowledge of the condition, threshold for symptoms, and activity level during hypoglycaemia. Other adverse effects associated with sulphonylurea use include bodyweight gain, gastrointestinal distress, disulphiram-like syndrome, dermatological reactions, haematological changes, ocular problems, and the syndrome of inappropriate secretion of antidiuretic hormone. Bodyweight gain has been reported to vary from 1.7-4.8 kg, according to the United Kingdom Prospective Diabetes Study (UKPDS-33). Controversy exists regarding cardiovascular adverse effects, but the consensus is to exercise caution in the use of these drugs as first-line therapy for patients with diabetes mellitus and coronary artery disease. The benefits of sulphonylurea treatment should be weighed against the risks associated with them. More work in this area is needed to homogenise the definition of hypoglycaemia, to get consensus on the methods for detection and data collection, as well as to further patient and physician education.

Aged↗

PubMed2002

Prediction of severe hypoglycaemia by angiotensin-converting enzyme activity and genotype in type 1 diabetes.

AIMS/HYPOTHESIS: We have previously shown a strong relationship between high angiotensin-converting enzyme (ACE) activity, presence of the deletion (D) allele of the ACEgene and recall of severe hypoglycaemic events in patients with Type 1 diabetes. This study was carried out to assess this relationship prospectively. METHODS: We followed 171 adult outpatients with Type 1 diabetes in a one-year observational study with the recording of severe hypoglycaemia. Participants were characterised by serum ACE activity and ACE genotype and not treated with ACE inhibitors or angiotensin II receptor antagonists. RESULTS: There was a positive relationship between serum ACE activity and rate of severe hypoglycaemia with a 2.7 times higher rate in the fourth quartile of ACE activity compared to the first quartile (p=0.0007). A similar relationship was observed for the subset of episodes with coma (2.9 times higher rate in fourth quartile compared to first quartile; p=0.048). The impact of serum ACE activity was most pronounced in C-peptide negative subjects (4.2 times higher rate in fourth quartile compared to first quartile; p=0.003), and in this subgroup carriers of the D allele of the ACEgene had higher rates of severe hypoglycaemia compared to the group homozygous for the insertion (I) allele. In a multiple regression analysis high serum ACE activity and impaired awareness of hypoglycaemia were identified as the only significant predictors of severe hypoglycemia. CONCLUSION: High ACE activity and the presence of the D allele of the ACE gene predict a high rate of severe hypoglycaemia in Type 1 diabetes.

Adult↗

PubMed2005

Interstitial fluid glucose dynamics during insulin-induced hypoglycaemia.

AIMS/HYPOTHESIS: Glucose sensors often measure s.c. interstitial fluid (ISF) glucose rather than blood or plasma glucose. Putative differences between plasma and ISF glucose include a protracted delay during the recovery from hypoglycaemia and an increased gradient during hyperinsulinaemia. These have often been investigated using sensor systems that have delays due to signal smoothing, or require long equilibration times. The aim of the present study was to define these relationships during hypoglycaemia in a well-equilibrated system with no smoothing. METHODS: Hypoglycaemia was induced by i.v. insulin infusion (360 pmol.m(-2).min(-1)) in ten non-diabetic subjects. Glucose was sequentially clamped at approximately 5, 4.2 and 3.1 mmol/l and allowed to return to normoglycaemia. Subjects wore two s.c. glucose sensors (Medtronic MiniMed, Northridge, CA, USA) that had been inserted for more than 12 h. A two-compartment model was used to quantify the delay and gradient. RESULTS: The delay during the fall in plasma glucose was not different from the delay during recovery (8.3+/-0.67 vs 6.3+/-1.1 min; p=0.27) and no differences were observed in the ratio of sensor current to plasma glucose at basal insulin (2.7+/-0.25 nA.mmol(-1).l) compared with any of the hyperinsulinaemic clamp phases (2.8+/-0.18, 2.7+/-0.021, 2.9+/-0.21; p=NS). The ratio was significantly elevated following recovery to normoglycaemia (3.1+/-0.2 nA.mmol(-1).l; p<0.001). CONCLUSIONS/INTERPRETATION: The elevated ratio suggests that the plasma to ISF glucose gradient was decreased following hypoglycaemia, possibly due to increased skin blood flow. Recovery from hypoglycaemia is not accompanied by a protracted delay and insulin does not increase the plasma to s.c. ISF glucose gradient.

Adult↗

PubMed1998

Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia.

The plasma concentrations of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1) are abnormally high after oral glucose in partially gastrectomised subjects with reactive hypoglycaemia, suggesting a causal relationship. Because of the glucose-dependency of its effects, it is impossible to induce hypoglycaemia in normal subjects in the basal state by exogenous GLP-1, regardless of dose. To further assess the role of the incretin hormones in reactive hypoglycaemia, we reproduced the glucose and hormone profiles of the patients with reactive hypoglycaemia in 8 healthy volunteers in 4 separate protocols: 1) i.v. infusion of glucose (25 g) alone, 2) glucose together with i.v. GLP-1 infusion, and 3) and 4) glucose together with i.v. infusion of the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), at two different infusion rates. The plasma glucose, GLP-1 and GIP concentrations (low dose) obtained were comparable with those of the patients. With GLP-1, infusion of a total of 33.4 +/- 1.3 g glucose was required to obtain plasma glucose concentrations similar to those obtained by glucose infusion alone; with low GIP, 28.0 +/- 1.2 g and with high GIP 38.4 +/- 3.5 g. Insulin concentrations increased 10-fold with GLP-1 compared with i.v. glucose alone, but less with high and low GIP. In contrast, C-peptide concentrations were similar after GLP-1 and high GIP. After termination of i.v. glucose the lowest glucose concentrations were 4.5 (3.7-4.9) (median, range) for glucose alone; 2.4 (1.9-2.8) mmol/l with GLP-1; 3.7 (2.6-4.0) with low GIP and 3.3 (2.1-4.2) with high GIP. Thus, the exaggerated GLP-1 response to nutrients in patients with accelerated gastric emptying could be responsible for their high incidence of postprandial reactive hypoglycaemia.

Adult↗

PubMed1997

Frequency and correlates of severe hypoglycaemia in children and adolescents with diabetes mellitus.

UNLABELLED: Frequency and correlates of severe hypoglycaemia have been retrospectively analysed in a cohort of diabetic children and adolescents with median (range) age 14.5 (3.2-25.5) years followed from the onset of the disease by the same diabetic clinic. During the years 1992-1994, 53 of the 187 patients reported 74 hypoglycaemic episodes: the average frequency of hypoglycaemia during the 3 years surveyed was 14.9 episodes/ 100 patients per year. Frequency of hypoglycaemia decreased significantly with age (chi 2 = 24.1; P < 0.0001) and was independent of duration of diabetes. Glycosylated haemoglobin and insulin dose were similar in patients with and without hypoglycaemia, matched for age and duration of diabetes. One out of two hypoglycaemic episodes occurred during sleep and no explanation was available for 50% of episodes. CONCLUSION: In this study severe hypoglycaemia was more frequent in young children than in adolescents and was independent of metabolic control and insulin dose.

Adolescent↗

PubMed2005

Dominantly inherited hyperinsulinaemic hypoglycaemia.

Congenital hyperinsulinism (HI), the most important cause of hypoglycaemia in early infancy, is a heterogeneous disease with two types of histological lesions, focal and diffuse, with major consequences in terms of surgical approaches. In contrast to focal islet-cell hyperplasia, always sporadic to our knowledge, diffuse hyperinsulinism is a heterogeneous disorder involving several genes, various mechanisms of pathogenic mutations and different transmissions: (i) channelopathy involving the genes encoding the sulphonylurea receptor (SUR1) or the inward-rectifying potassium channel (Kir6.2) in recessively inherited HI or more rarely dominantly inherited HI; (ii) metabolic disorders implicating the short-chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) enzyme inrecessively inherited HI, the glucokinase gene (GK), the glutamate dehydrogenase gene (GLUD1) when hyperammonemia is associated, dominant exercise-induced HI with still-unknown mechanism, and more recently the human insulin receptor gene in dominantly inherited hyperinsulinism. Thus, dominant HI disorders always correspond to diffuse HI, where most hypoglycaemia occur in infancy, and are sensitive to medical treatment. Channel causes could be due to dominant negative mutation with one abnormality in channels composed of four Kir6.2 subunits and four SUR1 subunits, leading to a complete destruction of the channel structure or function, or due to haploinsufficiency with only one functional allele, leading to 50% of functional protein, which is not sufficient to obtain enough opened channels to maintain the membrane depolarized. Metabolic causes are due to a gain of function of enzyme activity (deregulated enzymes), except for physical exercise-induced hyperinsulinaemic hypoglycaemia, of still-unknown cause. Congenital hyperinsulinism (HI) is the most important cause of hypoglycaemia in early infancy (Aynsley-Green et al 2000; Cornblath et al 1990; Pagliara et al 1973; Thomas et al 1977). The inappropriate oversecretion of insulin is responsible for profound hypoglycaemia that requires aggressive treatment to prevent severe and irreversible brain damage (Volpe 1995). HI is a heterogeneous disease associated with several genes, various mechanisms of pathogenic mutations and different transmissions (Dunne et al 2004).

Exercise↗

PubMed2004

Comparative analysis of conventional and an adaptive computer-based hypoglycaemia education programs.

Adaptive interactive computer-based education programs which can be personalized to patients' needs and skills might be more suitable for patients' training as compared to conventional ones. We tested whether there are differences between an adaptive and a conventional version of a computer-based hypoglycaemia education program concerning successful training and user friendliness. One hundred and twenty randomized diabetic patients were enrolled in this study. The two different programs were compared by using the following criteria: (1) the number of actions needed to get out of or prevent hypoglycaemia, (2) the need for external help, (3) the average time needed for completing one task and (4) user friendliness as determined by a questionnaire. Patients using the adaptive computer-based hypoglycaemia education program needed less actions to get out of or prevent hypoglycaemia, less external help and less time to finish tasks. Furthermore, the user friendliness of the adaptive computer program received a significantly better rating by the patients. The adaptive computer-based hypoglycaemia education program shows significantly better results as compared to a conventional one. Therefore, using adaptive computer-based programs might be helpful for education of patients.

Attitude to Computers↗

PubMed1999

Anger state during acute insulin-induced hypoglycaemia.

This study sought to examine the effects of insulin-induced hypoglycaemia on anger state, and to describe the associations between change in the anger state and measures of anger trait and anger expression (assessed using the State-Trait Anger Expression Inventory). A hyperinsulinaemic glucose clamp was used to achieve controlled euglycaemia (5.0 mmol/L) and hypoglycaemia (2.6 mmol/L) in 18 nondiabetic subjects and 30 people with insulin-dependent diabetes mellitus (IDDM). Subjects underwent both hypoglycaemic and euglycaemic conditions, separated by 2 weeks, in a counterbalanced order. During each study condition subjects were asked to complete a questionnaire on anger state. Results at euglycaemia and hypoglycaemia were compared, and differences between the conditions were correlated with measures of anger trait and anger expression. Hypoglycaemia caused both nondiabetic and IDDM subjects to report a significant increase in feelings of anger, despite being in a nonconfrontational setting. However, there were no clear associations between an individual's change in reported anger and measures of anger trait and anger expression. No association was found between the change in anger state and the intensity of an individual's symptomatic response to hypoglycaemia.

Adult↗

PubMed1999

Long-term follow-up of insulin-dependent diabetes mellitus patients with recurrent episodes of severe hypoglycaemia.

We conducted a long-term clinical follow-up of 20 insulin-treated diabetic patients with the problem of repeated severe hypoglycaemic events, identified during 1982-1984. Furthermore, we investigated the reproducibility of a standardized insulin-infusion test among eight of these patients and 10 insulin-dependent diabetes mellitus patients without the problem of severe hypoglycaemia. At start of the follow-up, the patients were characterized, which revealed that proposed risk factors for severe hypoglycaemia were very common and that at least one predisposing factor was present in all patients. No fatal episode of hypoglycaemia occurred in this group of patients during the follow-up. Emergency visits due to hypoglycaemia decreased during the follow-up from 1.05 year(-1) in 1982-1984 to 0.42 year(-1) in 1992-1994 (P=0.024). No association to HbAlc was seen (P=0.11). A correlation with the change to multiple insulin regimen was seen with a incidence of 1.27 year(-1) before the change to 0.47 year(-1) after (P=0.003). The glucose response to an insulin-infusion test appeared reproducible among the patients with recurrent attacks of severe hypoglycaemia.

Adult↗

PubMed1980

The riddle of tumour hypoglycaemia revisited.

In summary, hypoglycaemia due to non-pancreatic tumour is relatively common among the causes of fasting hypoglycaemia in the adult. Most of the neoplasms are large, and present as masses in the mediastinum or retroperitoneal space. Although therapy is difficult, successful palliation by surgery or radiotherapy has been achieved in a number of cases. Although many theories have been advanced to explain the hypoglycaemia, the best documented mechanism is production of an insulin-like substance by the tumour. Both low molecular weight (NSILA-s) and high molecular weight (SNILP) peptides have been reported to be elevated in some cases of tumour hypoglycaemia. Further study of this class of peptides will no doubt lead to assays that may facilitate diagnosis of tumour hypoglycaemia, as well as offer new approaches to the therapy of this disease.

Amino Acid Sequence↗

PubMed1983

Ketotic hypoglycaemia.

Ketotic hypoglycaemia is the most common form of childhood hypoglycaemia. This disorder classically manifests itself between the ages of 18 months and 5 years, and generally remits spontaneously before 8 or 9 years of age. A presumptive diagnosis is made by documenting a low blood sugar in association with ketonuria, ketonaemia and typical symptoms of hypoglycaemia. The definitive diagnosis is established by demonstrating an inability to tolerate a provocative ketogenic diet, or a fast. Susceptible or affected children develop severe hypoglycaemia and ketosis on this diet within 24 hours. Plasma alanine concentrations on either a normal or ketogenic diet were significantly lower in ketotic hypoglycaemic children compared with normal children. In contrast to adults, even normal children develop hypoglycaemia and ketonaemia when calorically deprived for relatively short periods of time (32 to 36 hrs).

3-Hydroxybutyric Acid↗

PubMed1997

Cerebral metabolic rate for glucose after neonatal hypoglycaemia.

OBJECTIVE: We studied the effect of neonatal hypoglycaemia on the local cerebral metabolic rate for glucose (LCMRglc). MATERIALS AND METHODS: Eight newborn infants with neonatal hypoglycaemia were studied. The LCMRglc in the whole brain, in five cerebral regions and in skeletal muscles were quantitated using positron emission tomography (PET) and 2-[18F]Fluoro-2-deoxy-D-glucose (FDG). The PET studies were performed at the age of 5.3 +/- 6.2 days during normoglycaemia. The LCMRglc of these infants were compared to the age-adjusted LCMRglc of eight infants with suspected hypoxic-ischaemic brain injury but with normal neurological development. RESULTS: After neonatal hypoglycaemia the age-adjusted LCMRglc in the whole brain was not lower than LCMRglc of the control infants (5.33 +/- 0.60 mumol/100 g/min vs. 6.71 +/- 0.60 mumol/100 g/min). Also the metabolic rate for glucose (MRglc) in the skeletal muscles was similar in hypoglycaemic and control infants (5.56 +/- 2.48 mumol/100 g/min vs. 6.99 +/- 2.41 mumol/100 g/min). CONCLUSION: MRglc in brain and in skeletal muscle seems to be normal after neonatal hypoglycaemia, although larger group of patients with more severe hypoglycaemia are needed to confirm this finding.

Animals↗

PubMed2006

Severe and protracted hypoglycaemia associated with co-trimoxazole use.

Co-trimoxazole (trimethoprim-sulfamethoxazole) is a commonly prescribed antimicrobial agent. Although it is well tolerated in most patients, serious adverse events related to its use have been described. Hypoglycaemia is a rare but potentially life-threatening complication of therapy. We describe a case of refractory hypoglycaemia complicated by seizure associated with co-trimoxazole for the treatment of Pneumocystis carinii pneumonia in a patient with AIDS. We also review 13 previously reported cases of co-trimoxazole-induced hypoglycaemia. Among this patient population, renal insufficiency was the most prevalent predisposing risk factor (93%). The mean daily dose of co-trimoxazole was 4.5 double strength (160 mg trimethoprim/800 mg sulfamethoxazole) tablets per day. Serum insulin levels were raised or inappropriately normal in 88% of cases in which they were measured, suggesting a sulfonylurea-like effect of co-trimoxazole as the mechanism of hypoglycaemia. All cases required intravenous glucose administration, and 43% experienced protracted (>12 hours) hypoglycaemia. Dosage adjustments should be made when prescribing co-trimoxazole to patients with renal dysfunction.

AIDS-Related Opportunistic Infections↗

PubMed2005

[Hypoglycaemia--diagnosis and therapy in emergencies].

Hypoglycaemia defined as blood sugar below 2.5 mmol/L, is always an important medical emergency. The primary therapy is simple and consists of iv glucose. The occurrence of hypoglycaemia is directly connected to fuel balance, determined by the availability of glucose, free fatty acids and ketone bodies. An intact fuel balance and maintenance of normal blood sugar concentration is dependent upon: (1) an adequate caloric and qualitative dietary intake; (2) afunctionally intact hepatic glucogenolytic and gluconeogenic enzyme system; (3) an adequate supply of endogenous gluconeogenic substrates (lactate, amino acids and glycerol) (4) an adequate energy supply provided by the beta-oxidation of fatty acids to synthesize glucose and ketone bodies and (5) a normal endocrine system (insulin, glucagon, catecholamines and growth hormone) for integrating and modulating these processes. Disturbances in each of these factors may lead to hypoglycaemia. Glucose, like oxygen, is of essential and fundamental importance for the brain metabolism. The major contribution of the brain to the basal metabolic rate (70% in neonates versus 20% in adults) is an important factor contributing to the frequency and severity of a hypoglycaemic syndrome in the paediatric age. If hypoglycaemia is suspected, blood should be obtained prior to treatment for serum glucose determination and an extra tube (5 ml) serum should be obtained and refrigerated for further investigations. The first voided urine has to be tested for ketones using a dipstick and also refrigerated for further investigations. Basic laboratory investigations, anamnestic informations and clinical findings allow rapid tentative diagnosis and determine the specialized investigations out of the refrigerated material. A rapid definitive diagnosis is important for the specific treatment and to avoid recurrent and prolonged hypoglycaemia.

Blood Glucose↗