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PubMed2004

Evaluating risk factors associated with severe hypoglycaemia in epidemiology studies-what method should we use?

AIMS: To determine the most appropriate regression models to use when assessing risk factors for severe hypoglycaemia and to investigate the impact of model misspecification and its clinical implications. METHODS: A total of 1229 children with Type 1 diabetes (mean age 11.7 years sd 4.1), of which 605 (49.2%) were males, were studied. Prospective assessment of severe hypoglycaemia (an event leading to loss of consciousness or seizure) was made over the 9-year period, 1992-2001. Patients were seen every 3 months and episodes of hypoglycaemia along with clinical data were recorded. Over 70% of children never experienced a severe hypoglycaemic event. Data were analysed using the Poisson regression, negative binomial, zero-inflated Poisson (ZIP) and zero-inflated negative binomial (ZINB) models. The over-dispersion and likelihood ratio statistics were calculated and the analytical methods compared. RESULTS: The Poisson regression model did not fit the data well. The negative binomial and the zero inflated Poisson and negative binomial models fitted the data better than Poisson. CONCLUSIONS: The commonly used Poisson regression models to analyse hypoglycaemia epidemiology may lead to biased parameter estimates and incorrect determination of risk factors for hypoglycaemia. We recommend the use of the negative binomial or zero inflated models to examine any risk factors associated with severe hypoglycaemia. Careful consideration must be given to the interpretation of hypoglycaemia surveys and their analysis.

Age Factors↗

PubMed2005

Frequency and predictors of hypoglycaemia in Type 1 and insulin-treated Type 2 diabetes: a population-based study.

AIMS: To ascertain the frequency and identify predictors of self-reported hypoglycaemia in Type 1 and insulin-treated Type 2 diabetes. METHODS: A random sample of 267 people with insulin-treated diabetes were recruited from a population-based diabetes register in Tayside, Scotland. Each subject prospectively recorded the number of mild and severe hypoglycaemic episodes experienced over a 1-month period. Ordinal logistic regression was performed to identify potential predictors of hypoglycaemia. RESULTS: Five hundred and seventy-two hypoglycaemic events were reported by 155 patients. The participants with Type 1 diabetes had a total of 336 hypoglycaemic events with a rate of 42.89 events per patient per year. Of these, nine were severe hypoglycaemic events, with a rate of 1.15 events per patient per year. Participants with insulin-treated Type 2 diabetes experienced a total of 236 hypoglycaemic events with a rate of 16.37 events per patient per year. Of these, five were severe hypoglycaemic events, which would be equivalent to 0.35 events per patient per year. Predictors of hypoglycaemia in Type 1 diabetes were a history of previous hypoglycaemia (P = 0.006) and co-prescribing of any oral drug (P = 0.048). In patients with insulin-treated Type 2 diabetes, a history of previous hypoglycaemia (P < 0.0001) and duration of insulin treatment (P = 0.014) were significant predictors. CONCLUSION: The incidence of self-reported severe hypoglycaemia in insulin-treated Type 2 diabetes is lower than in Type 1 diabetes but does occur more often than previously reported and with sufficient frequency to cause significant morbidity. Duration of insulin treatment is a key predictor of hypoglycaemia in insulin-treated Type 2 diabetes.

Adolescent↗

PubMed2006

Attentional functioning is impaired during acute hypoglycaemia in people with Type 1 diabetes.

AIMS: To examine the effects of acute insulin-induced hypoglycaemia on different aspects of attention and on general non-verbal reasoning in people with Type 1 diabetes. METHODS: A hyperinsulinaemic glucose clamp was used to maintain euglycaemia (4.5 mmol/l) or induce hypoglycaemia (2.6 mmol/l) on separate occasions in 16 adults with Type 1 diabetes each of whom were studied on two occasions in a counterbalanced order. During each study condition, the subjects completed parallel tests of cognitive function assessed by the Test of Everyday Attention and the Raven's Progressive Matrices. RESULTS: Hypoglycaemia caused a significant deterioration in tests sensitive to visual and auditory selective attention. During hypoglycaemia, attentional flexibility deteriorated and speed of information processing was delayed. Sustained attention and intelligence scores were preserved during hypoglycaemia. CONCLUSIONS: In people with Type 1 diabetes, hypoglycaemia causes a significant deterioration in attentional abilities, while non-verbal reasoning is preserved. It is likely therefore that many complex cognitive tasks which involve attention will be impaired during moderate hypoglycaemia during everyday life.

Acute Disease↗

PubMed1993

Neither moderate hypoxia nor mild hypoglycaemia alone causes any significant increase in cerebral [Ca2+]i: only a combination of the two insults has this effect. A 31P and 19F NMR study.

(1) The energy state and free intracellular calcium concentration ([Ca2+]i) of superfused cortical slices were measured in moderate hypoxia (approximately 65 microM O2), in mild hypoglycaemia (0.5 mM glucose), and in combinations of the two insults using 19F and 31P NMR spectroscopy. (2) Neither hypoxia nor hypoglycaemia alone caused any significant change in [Ca2+]i. Hypoxia caused a 40% fall in phosphocreatine (PCr) content but not in ATP level, and hypoglycaemia produced a slight fall in both (as expected from previous studies). These changes in the energy state recovered on return to control conditions. (3) A combined sequential insult (hypoxia, followed by hypoxia plus hypoglycaemia) produced a 100% increase in [Ca2+]i and a decrease in PCr level to approximately 25% of control. The reverse combined sequential insult (hypoglycaemia, followed by hypoglycaemia plus hypoxia) had the same effect. On return to control conditions there was some decrease in [Ca2+]i and a small increase in PCr content, but neither recovered to control levels. (4) Exposure of the tissue to the combined simultaneous insult (hypoxia plus hypoglycaemia) immediately after the control spectra had been recorded resulted in a fivefold increase in [Ca2+]i and a similar decrease in PCr level to 20-25% of control. There was little if any change of [Ca2+]i or PCr level on return to control conditions. (5) These results are discussed in terms of metabolic adaptation of some but not all of the cortical cells to the single type of insult, which renders the tissues less vulnerable to the combined insult.

Adenosine Triphosphate↗

PubMed2006

Induction of transcription factor CEBP homology protein mediates hypoglycaemia-induced necrotic cell death in human neuroblastoma cells.

Oxygen and glucose deprivation are direct consequences of tissue ischaemia. We explored the interaction of hypoxia and hypoglycaemia on cell survival and gene expression in the absence of glutamatergic signalling using human SH-SY5Y neuroblastoma cells as a model. In agreement with previous investigations in non-neural cells, prolonged hypoxia (0.5% O(2)) failed to induce significant cell death in this system. In contrast, exposure to hypoglycaemia induced significant necrotic cell death (> 80% after 72 h). Interestingly, hypoglycaemia-induced cell death was completely abrogated by simultaneous exposure to hypoxia, suggesting strong cytoprotective effects of hypoxia. Subsequent microarray analysis of the underlying transcriptional responses revealed that the transcription factor CEBP homology protein (CHOP) was strongly induced by hypoglycaemia, and suppressed by simultaneous hypoxia. RNA interference against CHOP significantly protected cells from glucose deprivation-induced cell death. Hypoxia-induced vascular endothelial growth factor (VEGF) activation also protected cells against hypoglycaemia-induced cell death, but VEGF failed to modify hypoglycaemia-induced CHOP induction. Our data suggest that hypoglycaemia-induced necrotic cell death of neuroblastoma cells is an active process mediated via the induction of the transcription factor CHOP, and that hypoxia counteracts this cell death via at least two distinct mechanisms: repression of CHOP and induction of VEGF.

Apoptosis↗

PubMed1984

Induction of hypoglycaemia and accumulation of 5-hydroxytryptamine in the liver after the injection of mitogenic substances into mice.

Various mitogenic substances (concanavalin A, pokeweed mitogen, polyI : polyC and a phorbol diester), as well as lipopolysaccharides (LPS or endotoxins), produced hypoglycaemia after being injected into mice. However, non-mitogenic immuno-stimulants (zymosan, carrageenan, an adjuvant peptide and interferon) did not induce hypoglycaemia. All of the mitogenic substances also induced an increase in 5-hydroxytryptamine (5-HT) in liver, but the non-mitogenic substances did not have this effect. The time course of the development of hypoglycaemia was similar to that of the increase in liver 5-HT. The dose-dependence of the hypoglycaemia induced by LPS was similar to that of the increase in liver 5-HT. In C3H/HeJ mice, the macrophages and/or lymphocytes of the mice are known to be less responsive to LPS, and both the LPS-induced hypoglycaemia and increase in 5-HT were less in these mice than in control mice (C3H/He and ddI mice). These results suggest that macrophages and/or lymphocytes may participate in the induction of hypoglycaemia and the increase in 5-HT induced by mitogenic substances and LPS. A possible correlation between hypoglycaemia and the increase in hepatic 5-HT is discussed, although the relationship is not substantiated.

Adjuvants, Immunologic↗

PubMed2005

Neurodevelopmental outcome of hypoglycaemia in healthy, large for gestational age, term newborns.

AIMS: To evaluate the effects of transient hypoglycaemia on the first day of life in 75 healthy term large for gestational age (LGA) infants, born to non-diabetic mothers, on their neurodevelopmental outcome at the age of 4 years. METHODS: Screening for hypoglycaemia was performed 1, 3, and 5 hours after birth, and continued if blood glucose levels were low. Treatment with intravenous glucose for hypoglycaemia was started if hypoglycaemia was severe or symptomatic. Patients' development and behaviour was examined at the age of 4 years by the Denver Developmental Scale, a non-verbal intelligence test, and the Child Behaviour Check List. RESULTS: There were no significant differences between children with neonatal normoglycaemia (n = 15) and hypoglycaemia (plasma glucose <2.2 mmol/l 1 hour after birth, or <2.5 mmol/l subsequently; n = 60) in Denver developmental scale scores and child behaviour checklist scores. Although total IQ did not differ between hypoglycaemic and normoglycaemic children, one subscale (reasoning) did (mean difference 9.3, 95% CI 1.3 to 17.2). The correlation between reasoning IQ and neonatal blood glucose levels was weak and not statistically significant. When other definitions for hypoglycaemia were applied, the difference in reasoning IQ was not found. There were no differences in any of the test scores between hypoglycaemic children who had and who had not been treated with intravenous glucose. CONCLUSION: Transient mild hypoglycaemia in healthy, term LGA newborns does not appear to be harmful to psychomotor development at the age of 4 years.

Birth Weight↗

PubMed2005

Pubertal stage and hypoglycaemia counterregulation in type 1 diabetes.

AIMS: To compare physiological and autonomic responses to acute hypoglycaemia in diabetic children in pre-, mid-, and post-pubertal stages of development. METHODS: Twenty seven children (8 pre-pubertal, 7 mid-pubertal, 12 post-pubertal) with type 1 diabetes were studied. Hypoglycaemia was induced by insulin infusion until an autonomic reaction (R) was identified. Counterregulatory hormone levels were measured at baseline, R, R+15, and R+30 minutes. Haemodynamic changes and sweat production were measured. RESULTS: The mean blood glucose level at R was lower in pre-pubertal than mid-pubertal children (2.0 v 2.5 mmol/l), and was positively correlated with HbA1c. Glucagon and noradrenaline responses to hypoglycaemia were minimal in all children. A brisk increase in pancreatic polypeptide (PP) concentration only occurred in post-pubertal children. Only two children showed a sweating response to hypoglycaemia. CONCLUSIONS: The blood glucose level at which sympatho-adrenal responses to hypoglycaemia were activated was associated with glycaemic control, and varied with pubertal stage. As in adults, the glucagon response to hypoglycaemia was deficient within a few years of developing diabetes. However, sweating and secretion of PP in response to hypoglycaemia did not occur until after puberty, indicating some qualitative differences from adults.

Adolescent↗

PubMed2003

The incidence of hypoglycaemia in children with type 1 diabetes and treated asthma.

AIMS: To investigate whether treatment of coexisting asthma has any effect on the incidence of hypoglycaemia and on glycaemic control in children with type 1 diabetes. METHODS: An observational study of children attending the paediatric diabetes clinics of five hospitals in the North Trent Region. Information on the frequency of hypoglycaemia in the preceding three months, treatment for asthma, and the individual's latest HbA1c, was recorded when they attended for review. RESULTS: Data were collected on 226 children, of whom 27 (12%) had treated asthma. Only 11/27 children with asthma were taking their prescribed inhaled steroids. All used beta agonists at least once a week. There was a reduction of 20% in the incidence of hypoglycaemia in the diabetic children with treated asthma. Of the children with diabetes and treated asthma, 52% reported an episode of hypoglycaemia in the previous three months compared to 72% of those with only diabetes. There was no difference in the proportion of children experiencing nocturnal or severe hypoglycaemia. Although not significant, those with asthma and diabetes also had better overall control (HbA1c 8.8%) compared to those with diabetes alone (HbA1c 9.3%). CONCLUSIONS: Diabetic children with treated asthma have significantly fewer episodes of hypoglycaemia and better glycaemic control compared to children with diabetes alone. This observation needs further investigation but raises an interesting question. Do the drugs used to treat asthma, in particular beta agonists, have the therapeutic potential to reduce hypoglycaemia and facilitate an improvement in glycaemic control?

Administration, Inhalation↗

PubMed2003

Best practice No 173: clinical and laboratory investigation of adult spontaneous hypoglycaemia.

Adult spontaneous hypoglycaemia is not a diagnosis per se but a manifestation of a disease. Although rare, it is important to identify spontaneous hypoglycaemia and its causes because treatment may be preventative or curative. Hypoglycaemia can occur as an epiphenomenon in many serious diseases. It is sufficient to recognise the disease's association with hypoglycaemia and then take appropriate action to prevent the recurrence of hypoglycaemia. In investigating apparently healthy individuals, common pitfalls to avoid are: failure to recognise subacute neuroglycopenia clinically; failure to document hypoglycaemia adequately during symptoms; failure to measure pancreatic hormones, counter-regulatory hormones, and ketones in hypoglycaemic samples; failure to recognise pre-analytical and analytical limitations of laboratory assays; and failure to abandon obsolete and inappropriate investigations. Providing these caveats are met, appropriate laboratory and radiological investigations will almost always uncover the cause of spontaneous hypoglycaemia.

Acute Disease↗

PubMed2000

Evaluation of patients admitted with hypoglycaemia to a teaching hospital in Central Anatolia.

Hypoglycaemia is one of the most common endocrine emergencies in practice. We analysed retrospectively the incidence and causes of hypoglycaemia in patients admitted to Erciyes University Medical School in Turkey between January 1991 and June 1998 because of hypoglycaemia. Charts were reviewed according to multiple variables including age, sex, blood glucose levels, renal and liver functions, diagnoses, symptoms, drugs, complications, sequelae, and survival status. During this period, 13 500 patients were hospitalised and hypoglycaemia was reported in 126 (0.9%) patients. The most common causes were diabetic treatments in 54 cases (42%), endocrine deficiencies in 25 cases (20%), and malignancy in 15 cases (12%), respectively. The leading endocrine deficiency was panhypopituitarism. Sheehan's syndrome was the most common cause of panhypopituitarism (44%). No underlying cause was diagnosed in seven cases. Nine patients died (7%) and neurological sequelae were observed in one patient with diabetes mellitus. We conclude that hypoglycaemia accounts for about 1% of hospital admissions. Although the hypoglycaemia could be attributed to hypoglycaemic agents in the treatment of diabetes mellitus in the majority of cases, Sheehan's syndrome was also found to be an important cause of hypoglycaemia in our hospital.

Adolescent↗

PubMed1996

Studies in hypoglycaemia in children with insulin-dependent diabetes mellitus.

Hypoglycaemia is the most important acute side effect of insulin therapy for diabetes in children. In general, children have more vigorous counterregulatory hormone responses to hypoglycaemia than adults. Children with diabetes may lose their glucagon responses to a falling blood glucose but persistence of brisk catecholamine, cortisol and growth hormone responses, coupled with the insulin resistance natural to puberty, may contribute to unstable diabetes control. Despite this, there is some evidence that younger children may not experience or at least express autonomic symptoms to the same degree as do adults. Furthermore, recurrent hypoglycaemia may induce defects in the counterregulatory responses and increase the risk of severe hypoglycaemia. Avoidance of moderate hypoglycaemia in clinical management may restore normal warning. There is research evidence to suggest that the human brain may be able to use non-glucose fuels to support its metabolism and function during hypoglycaemia but this is not yet translatable into clinical practice and care to avoid hypoglycaemia in daily life remains the patients' best protection.

Adolescent↗

PubMed1981

Failure to induce reactive hypoglycaemia by drinking a starch-based alcohol beverage (sorghum beer).

Alcohol is a well-recognised cause of fasting hypoglycaemia but may also provoked reactive hypoglycaemia when drunk together with a carbohydratee mixer. In this study the ability of sorghum beer (an 'in-built' alcohol-starch beverage widely enjoyed in Southern Africa) to induce reactive hypoglycaemia was compared with "gin and tonic' in eight non-obese health African men. After an overnight fast, each subject drank, in random sequence on their different occasions, 2 litres of sorghum beer (carbohydrat content approximately 5% and alcohol concentration 2.24 g/dl-2.8% v/v), the same volume of a control solution providing a similar carbohydrate load, or a gin and standard tonic water mixture. No evidence of reactive hypoglycaemia was apparent during the 5 hours after the beginning of the sorghum beer tolerance tests, despite a mean peak blood alcohol level reaching 80 mg/dl. both the peak and total plasma insulin responses were significantly reduced (p less than or equal to 0.05) when compared to the brisk responses elicited by the carbohydrate solution alone and the gin and tonic drinks, with consequent hypoglycaemia. These data suggest that African home-brews are not potent causes of reactive hypoglycaemia, although they may be implicated in the development of ethanol-induced hypoglycaemia in the fasting state.

Adult↗

PubMed1993

Adrenaline and noradrenaline responses during insulin-induced hypoglycaemia in man: should the hormone levels be measured in arterialized venous blood?

To compare arterial, arterialized venous and venous measurements of plasma catecholamines during hypoglycaemia, six healthy men were studied by an iv infusion of insulin (1034 pmol.kg-1.h-1). Arterial blood glucose was clamped at the baseline level for the first 30 min and then reduced to 3.2 and to 2.5 mmol/l for 20 min subsequently. At each stage, arterial, arterialized venous and venous blood samples were simultaneously taken for analyses of plasma catecholamines. Plasma glucagon significantly declined during hyperinsulinaemic euglycaemia and then increased during hypoglycaemia. Plasma adrenaline and noradrenaline increased significantly during hypoglycaemia. During euglycaemia and mild hypoglycaemia, arterial adrenaline tended to be higher and arterial noradrenaline lower as compared with the corresponding arterialized and venous values. During marked hypoglycaemia, the arterial catecholamines were significantly higher than that of the two venous samples (p < 0.05). There was a significant correlation between the arterial and the arterialized as well as venous catecholamine values (p < 0.005). We conclude that, during euglycaemia and mild hypoglycaemia, the arterialized adrenaline values are closer to the arterial levels whereas the arterialized noradrenaline concentrations are similar to those measured in venous blood. However, during marked hypoglycaemia, both the arterialized adrenaline and noradrenaline are 20-30% lower than the arterial values, being close to the venous levels.

Analysis of Variance↗

PubMed1989

Plasma volume substitution does not inhibit plasma noradrenaline and muscle nerve sympathetic responses to insulin-induced hypoglycaemia in healthy humans.

Microelectrode recordings of muscle nerve sympathetic activity and measurements of venous plasma noradrenaline have indicated increased sympathetic outflow during acute hypoglycaemia. Plasma volume reduction during hypoglycaemia, as evidenced by increasing peripheral venous haematocrit might underly the sympathetic activation. To study the effect of prevention of plasma volume reduction during hypoglycaemia, saline containing albumin was infused intravenously in healthy adult volunteers during hypoglycaemia. Hypoglycaemia was induced by an intravenous injection of soluble insulin in a dose of 0.15 IU/kg body weight. Peripheral venous plasma noradrenaline concentrations were identical in experiments without and with plasma volume substitution. Muscle nerve sympathetic activity increased to the same extent during hypoglycaemia with and without plasma volume substitution. It is concluded that increased plasma noradrenaline concentrations and enhanced muscle nerve sympathetic activity during insulin-induced hypoglycaemia in man are not consequences of plasma volume reduction.

Adult↗

PubMed2001

Influence of hypoglycaemia, with or without caffeine ingestion, on visual sensation and performance.

Full-field visual evoked potentials and visual information processing were measured in 16 normal, healthy subjects during a hyperinsulinaemic clamp. A randomized cross-over design was used across three conditions: hypoglycaemia and caffeine; hypoglycaemia and placebo; and euglycaemia and caffeine. The latency of the P100 component of the pattern-reversal visual evoked potential increased significantly from rest to hypoglycaemia, but no effect of caffeine was found. Subjects were subsequently divided into two median groups based on the increase in P100 latency in the placebo condition (Group 1, +0.5 ms; Group 2, +5.6 ms). In the absence of caffeine, an inverse correlation between the increase in P100 latency from rest and a deterioration in visual movement detection was found for Group 2, but not for Group 1. Caffeine ingestion resulted in a further increase in P100 latency, from rest to hypoglycaemia, for subjects in Group 2. Hypoglycaemia in the absence of caffeine produces changes in visual sensation from rest to hypoglycaemia. In those subjects most sensitive to the effects of hypoglycaemia (Group 2), the increase in P100 latency was associated with poorer performance in tests of visual information processing. Caffeine ingestion produced further increases in P100 latency in these subjects.

Adult↗

PubMed2001

Hypoglycaemia and cognitive function in diabetes.

The human brain is almost totally dependent on a continuous supply of glucose, deprivation of which rapidly causes malfunction. In the brain there are regional differences in the susceptibility to neuroglycopenia with the cerebral cortex being most sensitive while deeper structures are more resistant. A fall in blood glucose provokes a hierarchy of responses including secretion of counter-regulatory hormones and development of warning symptoms which alert the individual to treat the hypoglycaemia. Symptoms are generated when blood glucose falls to specific threshold concentrations, although these are dynamic and can be modified by various factors. Symptoms can be classified as autonomic and neuroglycopenic, with the latter being related to altered cognitive functioning. Acute hypoglycaemia produces electroencephalographic (EEG) changes as well as neurophysiological abnormalities including increased latency and/or reduced amplitude of sensory evoked potentials. At blood glucose below 3 mmol/l cognitive functioning becomes impaired but the degree of dysfunction differs in various domains and a battery of psychometric tests are required to assess impairment of cognitive function during hypoglycaemia. Complex, attention-demanding and speed-dependent responses are most impaired with accuracy often preserved at the expense of speed. Cognitive function does not recover fully until 40-90 min after blood glucose is restored to normal. Hypoglycaemia also provokes changes in mood, increases anxiety and may induce depression and fear of further hypoglycaemia, which can modify behaviour and influence quality of glycaemic control. Recurrent severe hypoglycaemia may have long-term sequelae in the form of cumulative cognitive impairment and impaired awareness of hypoglycaemia.

Acute Disease↗

PubMed2001

Driving mishaps and hypoglycaemia: risk and prevention.

Driving is a complex, multi-task activity that can be affected by cognitive impairment resulting from episodes of severe hypoglycaemia. Intensive insulin therapy increases the likelihood of severe hypoglycaemia but there have been few studies examining effects on driving skills. A survey carried out recently indicated that patients with type 1 diabetes had twice the incidence of driving accidents than their non-diabetic spouses or patients with type 2 diabetes. The motor accidents were associated with more frequent low blood glucose while driving and less frequent self-monitoring. In driving simulation tests it was found that driving has an intrinsic metabolic demand that can contribute to hypoglycaemia. Driving performance began to deteriorate at around 3.6 mmol/l but drivers frequently did not recognise and failed to treat the hypoglycaemia. Those who did self-treat had more driving relevant symptoms and less neuroglycopenia quantified by EEG alpha-theta differences. Patients should be recommended not to begin driving if blood glucose is below 4.5 mmol/l and should not continue to drive if they suspect that blood glucose has fallen below 4 mmol/l while driving. If hypoglycaemia is suspected patients should immediately pull off the road, measure blood glucose if possible, treat themselves as necessary and not resume driving until glucose and cognitive-motor function return to normal. The problems of driving and hypoglycaemia should be discussed with patients with diabetes and behavioural interventions instigated. To this end, Blood Glucose Awareness Training (BGAT) and Hypoglycaemia Anticipation, Awareness and Treatment Training (HAATT) have been developed and shown to markedly reduce incidence of driving mishaps.

Accidents, Traffic↗