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PubMed1999

Cognitive function and mood after profound nocturnal hypoglycaemia in prepubertal children with conventional insulin treatment for diabetes.

OBJECTIVES: To examine the frequency of nocturnal hypoglycaemia, and the effects on cognitive function and mood, in children with insulin dependent diabetes mellitus (IDDM). DESIGN: Two overnight glucose profiles, in the home environment, and assessments of cognitive function and mood the following day. Twenty nine prepubertal patients with IDDM (median age, 9.4 years; range, 5.3-12.9) and 15 healthy controls (single overnight profile), median age 9.5 (range, 5.6-12.1) years were studied. RESULTS: Asymptomatic hypoglycaemia (glucose < 3.5 mmol/l) was observed in 13 of 29 patients studied on night 1: four of these and seven others were hypoglycaemic on night 2. The median glucose nadir was 1.9 (range, 1.1-3.3) mmol/l and the median duration of hypoglycaemia was 270 (range, 30-630) minutes. Hypoglycaemia was related to insulin dose, but not glycosylated haemoglobin (HbA1c) values, and was partially predicted by a midnight glucose of < 7.2 mmol/l. Cognitive performance was not altered after hypoglycaemia but a lowering of mood was observed. CONCLUSIONS: Young children on conventional insulin regimens are at high risk for profound, asymptomatic nocturnal hypoglycaemia, which is difficult to predict. There was no short term effect on cognitive function but mood change was detected.

Body Mass Index↗

PubMed2005

Low levels of dehydroepiandrosterone sulphate in plasma, and reduced sympathoadrenal response to hypoglycaemia in premenopausal women with rheumatoid arthritis.

OBJECTIVES: To evaluate the function of the hypothalamic-pituitary-adrenal axis and sympathoadrenal system in premenopausal women with rheumatoid arthritis (RA). METHODS: Insulin-induced hypoglycaemia (0.1 IU/kg) was produced in 15 glucocorticoid-naive patients with long term RA with low disease activity and in 14 healthy women matched for age and body mass index. Concentrations of glucose, adrenocorticotropic hormone (ACTH), cortisol, Delta4-androstenedione (ASD), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), 17alpha-hydroxyprogesterone (17OHP), epinephrine (EPI), norepinephrine (NE), interleukin 6 (IL6), and tumour necrosis factor alpha (TNFalpha) were analysed in plasma. RESULTS: Patients had comparable responses of glucose, cortisol, ACTH, ASD, and 17OHP to hypoglycaemia, without any signs of hypothalamic insufficiency. Patients had lower basal DHEAS than controls (3.03 (0.37) micromol/l v 5.1 (0.9) micromol/l, respectively; p<0.05); borderline lower basal DHEA levels (p = 0.067); while the response of DHEA to hypoglycaemia was comparable to that of controls. Patients with RA had lower EPI (p = 0.005) and NE (p<0.001) responses to hypoglycaemia. TNFalpha and IL6 were higher (p<0.05) in patients with RA (TNFalpha 8 (2.8) pg/ml in RA v 1.1 (0.5) pg/ml in controls and IL6 15.1 (6.7) pg/ml v 1.4 (0.7) pg/ml). CONCLUSIONS: Lower basal DHEAS levels, without concomitant differences or changes in DHEA, ASD, 17OHP, and cortisol responses to hypoglycaemia in patients with RA, indicate an isolated decrease in adrenal androgen production. Significantly lower responses of EPI and NE to hypoglycaemia may suggest sympathoadrenal hyporeactivity in patients with RA.

Adrenocorticotropic Hormone↗

PubMed1988

Adverse neurodevelopmental outcome of moderate neonatal hypoglycaemia.

There has been considerable debate over whether asymptomatic neonatal hypoglycaemia results in neurological damage. In a detailed multicentre study of 661 preterm infants hypoglycaemia was found to be common. Moderate hypoglycaemia (plasma glucose concentration less than 2.6 mmol/l) occurred in 433 of the infants and in 104 was found on three to 30 separate days. There was considerable variation among the centres, implying differences in decisions to intervene. The number of days on which moderate hypoglycaemia occurred was strongly related to reduced mental and motor development scores at 18 months (corrected age), even after adjustment for a wide range of factors known to influence development. When hypoglycaemia was recorded on five or more separate days adjusted mental and motor developmental scores at 18 months (corrected age) were significantly reduced by 14 and 13 points respectively, and the incidence of neurodevelopmental impairment (cerebral palsy or developmental delay) was increased by a factor of 3.5 (95% confidence interval 1.3 to 9.4). These data suggest that, contrary to general belief, moderate hypoglycaemia may have serious neurodevelopmental consequences, and reappraisal of current management is urgently required.

Cerebral Palsy↗

PubMed2006

Emergency management of diabetes and hypoglycaemia.

OBJECTIVE: Hypoglycaemia is the commonest diabetic emergency and is associated with considerable morbidity and mortality. This study looked at the use of the emergency services by people with diabetes, with particular reference to hypoglycaemia. METHOD: Data were collected on all attendances related to diabetes at accident and emergency departments at two district general hospitals in Surrey, UK, over a one year period. RESULTS: Hypoglycaemia was the commonest reason for attendance at accident and emergency. The management of hypoglycaemia was variable, the most frequent method of treatment being intramuscular glucagon administered by the ambulance service. Ninety per cent of patients with hypoglycaemia were either discharged or self-discharged from the accident and emergency department, and half of these patients had no follow up arranged. CONCLUSIONS: Hypoglycaemia is the commonest diabetic emergency and current management is suboptimal. Standardised protocols and better education of healthcare professionals and patients are required.

Aged↗

PubMed1991

Spontaneous hypoglycaemia due to a pleural fibroma: role of insulin like growth factors.

A 64 year old woman with a long history of "drop attacks" and dizzy spells was found to have spontaneous hypoglycaemia. A slowly enlarging pleural mass had been present for at least five years. At thoracotomy the mass (weight 1.7 kg) was excised and the hypoglycaemia ceased. Histologically the tumour was a pleural fibroma, with no features of malignancy. Endocrine tests before surgery showed a subnormal growth hormone response to spontaneous hypoglycaemia, a reduced concentration of serum insulin like growth factor I (IGF-I), and an inappropriately high concentration of serum insulin like growth factor II (IGF-II). After resection of the tumour the growth hormone response to insulin induced hypoglycaemia and the IGF-I and IGF-II concentrations were normal. These data suggest that the hypoglycaemia was due to production of IGF-II by the tumour, causing increased glucose utilisation and an impaired growth hormone counterregulatory response to hypoglycaemia.

Female↗

PubMed2002

Hypoglycaemia and counterregulation during childhood.

Hypoglycaemia is particularly common in young children with type 1 diabetes mellitus yet the normal protective counterregulatory responses have been little studied in this age group. The studies reported have shown conflicting results, in part related to prior glycaemic control and also to the method of investigation used. Counterregulatory hormone responses during both spontaneous and experimentally induced episodes of nocturnal hypoglycaemia do appear to be blunted, which may be a function of sleep itself. Although studies of cognitive function have consistently shown defects in certain areas of neurocognitive performance, particularly in those children with early-onset diabetes or a prior history of severe hypoglycaemia, the contribution of nocturnal hypoglycaemia to the development of these impairments has not been evaluated. In young adults and adolescents, nocturnal hypoglycaemia has been linked to cardiac arrhythmia and the risk of sudden death. The development of new techniques for continuous subcutaneous glucose monitoring may allow detailed study of counterregulatory responses and symptom recognition in young children. Effective intensification of insulin therapy without an increased risk of hypoglycaemia may be possible using new insulin analogues or continued subcutaneous intravenous infusion (CSII), thus improving patient compliance and overall quality of clinical care.

Adolescent↗

PubMed1994

Diabetic death bed: post-mortem determination of hypoglycaemia.

The post-mortem biochemical determination of hypoglycaemia in the practice of forensic medicine is notoriously imprecise and attracts perennial criticisms, particularly from those who may be alien to the peculiarities of medical jurisprudence. There has been re-emphasis recently on the neuropathological pathoclisis ascribed to prolonged hypoglycaemia. Unfortunately, the value perceived is limited by pathognomonic unreliability owing to agonal multifactorial influences and rapidly fatal nocturnal hypoglycaemia. The predicament is oppressive to a consideration of preponderant evidence and an unpopular diagnosis of peri-mortem hypoglycaemia, unless audacious, may be precluded simply because the proof is difficult. This is likely to contribute to diagnostic under-estimation of enigmatic diabetic deaths. A suspected case of lethal nocturnal hypoglycaemia in a young diabetic on 'animal' insulin is presented to restore some perspective to the clinico-pathological deference for an endangered post-mortem diagnosis of hypoglycaemia inferred from minimal evidence.

Adult↗

PubMedDate not supplied

Visual function during acute hypoglycaemia.

Hypoglycaemia symptoms are of particular interest in view of the importance of hypoglycaemia unawareness. Visual symptoms arising during acute hypoglycaemia may be the result of metabolic disturbances in the visual pathways within the central nervous system or impairment of the refractive apparatus of the eye and binocular function. This study investigated the effect of hypoglycaemia upon visual acuity, binocular interaction and contrast sensitivity. Various aspects of visual function were examined in ten normal subjects before, during and after acute insulin-induced hypoglycaemia. A simultaneous study of hypoglycaemic symptoms enabled us to relate the objective findings to the symptoms as reported by the subjects. Snellen visual acuity, fusion and stereopsis were not affected by hypoglycaemia. Five subjects noted visual disturbance. Eight developed significant impairment of contrast sensitivity, which closely matched the lowered blood glucose concentration. These observations suggest that hypoglycaemic visual symptoms are due to neuroglycopenia of central visual pathways rather than changes within the refractive apparatus or abnormality of binocular function. Although these symptoms are not a constant feature of the hypoglycaemic state, subtle impairment of visual function occurs in most cases. Contrast sensitivity testing can be useful for assessment of fine changes in visual function.

Accommodation, Ocular↗

PubMed2005

Bench-to-bedside review: Antidotal treatment of sulfonylurea-induced hypoglycaemia with octreotide.

The major potential adverse effect of use of sulfonylurea agents (SUAs) is a hyperinsulinaemic state that causes hypoglycaemia. It may be observed during chronic therapeutic dosing, even with very low doses of a SUA, and especially in older patients. It may also result from accidental or intentional poisoning in both diabetic and nondiabetic patients. The traditional approach to SUA-induced hypoglycaemia includes administration of glucose, and glucagon or diazoxide in those who remain hypoglycaemic despite repeated or continuous glucose supplementation. However, these antidotal approaches are associated with several shortcomings, including further exacerbation of insulin release by glucose and glucagon, leading only to a temporary beneficial effect and later relapse into hypoglycaemia, as well as the adverse effects of both glucagon and diazoxide. Octreotide inhibits the secretion of several neuropeptides, including insulin, and has successfully been used to control life-threatening hypoglycaemia caused by insulinoma or persistent hyperinsulinaemic hypoglycaemia of infancy. Therefore, this agent should in theory also be useful to decrease glucose requirements and the number of hypoglycaemic episodes in patients with SUA-induced hypoglycaemia. This has apparently been confirmed by experimental data, one retrospective study based on chart review, and several anecdotal case reports. There is thus a need for further prospective studies, which should be adequately powered, randomized and controlled, to confirm the probable beneficial effect of octreotide in this setting.

Adult↗

PubMed1998

Hypoglycaemia during intensified insulin therapy of children and adolescents.

Good metabolic control prevents or at least postpones late vascular complications, but several studies indicate that such good metabolic control cannot be reached without simultaneous increase in the incidence of severe hypoglycaemia. We have been able to reduce late complications through multiple insulin therapy adjusted on the basis of active self control combined with active psychosocial support and education. A prospective regular registration of all hypoglycaemic incidents in about 130 diabetic children and adolescents shows that in spite of reasonably good HbA1c values (mean and median 6.9%, corresponding to 7.9% with the DCCT method), we have less incidence of severe hypoglycaemia (13-17 per 100 patient years) than reported in other recent studies (20-25 per 100 patient years). We saw no correlation between HbA1c and severe hypoglycaemia, but most hypoglycaemia was caused by mistake or reasons not related to degree of metabolic control. Our conclusion is that there is no inevitable relation-ship between low HbA1c and hypoglycaemia. Instead hypoglycaemia should be prevented parallel to and in the same way as we try to reach good metabolic control.

Adolescent↗

PubMed1980

Effect of beta-blockade on hormone release during hypoglycaemia in insulin-dependent diabetics.

Previous studies have shown that non-selective, but not beta 1-selective, beta-blockers prolong the duration of hypoglycaemia. In order to elucidate possible mechanisms key hormones as well as alanine levels were measured following insulin-induced hypoglycaemia in 7 insulin-dependent diabetics. The subjects were treated with placebo, propranolol (a non-selective agent) or metoprolol (a beta 1-selective drug) prior to the hypoglycaemia. Treatment with either beta-blocking agent led to higher levels of adrenaline, glucagon, cortisol and growth hormone during hypoglycaemia as compared to those reached on placebo. The adrenaline levels during placebo treatment in response to hypoglycaemia appeared less in these diabetics than that previously reported for non-diabetics. The plasma alanine levels were similar and decreased following insulin administration irrespective of type of treatment. The data show that the release of key glycogenolytic and gluconeogenic hormones is not inhibited by beta-blockers during hypoglycaemia but is instead augmented or, possibly, hormonal clearance is reduced. It is suggested that the delayed recovery in blood glucose on a non-selective beta-blocker is partly due to lack of gluconeogenic substrates such as lactate and glycerol.

Adrenergic beta-Antagonists↗

PubMed1985

The importance of plasma free insulin and counterregulatory hormones for the recovery of blood glucose following hypoglycaemia in type 1 diabetics.

After induction of hypoglycaemia in 31 Type 1 (insulin-dependent) patients, the 10 patients with the slowest recovery of blood glucose from hypoglycaemia were arbitrarily compared with the 10 patients with the fastest recovery of blood glucose. No differences were found between the two groups regarding response of glucagon to hypoglycaemia, whereas the epinephrine (2-fold), norepinephrine (2.4-fold) and cortisol responses were significantly greater in the group with the slow recovery. The plasma free insulin concentrations were higher (2-fold) in the group with slow recovery from 30 min after stop of insulin and throughout the study. This may be explained by a 3-fold greater amount of insulin binding antibodies in this group compared to the group with fast recovery from hypoglycaemia. An inverse significant correlation was demonstrated between the rates of recovery and the amounts of insulin binding antibodies in all the patients (P less than 0.02). This implicates that enhanced counterregulatory hormone responses in the group with the slow recovery from hypoglycaemia could not compensate for the hypoglycaemic effect of a concomitant higher plasma free insulin concentration. Insulin binding antibodies, acting as a depot of circulating insulin, may be a risk factor of prolonged hypoglycaemia in Type 1 diabetics.

Adolescent↗

PubMed2003

Insulin levels measured with an insulin-specific assay in patients with fasting hypoglycaemia related to endogenous hyperinsulinism.

OBJECTIVE: The finding of insulin levels above a minimum threshold at the time of symptomatic hypoglycaemia is crucial in the diagnosis of endogenous hyperinsulinism. The aim of this study was to evaluate insulin levels at the time of hypoglycaemia with an insulin-specific assay in such patients. DESIGN AND METHODS: We measured insulin levels in 15 patients with fasting hypoglycaemia related to endogenous hyperinsulinism using an insulin-specific immunoradiometric assay (IRMA) without any significant cross-reaction with intact proinsulin. RESULTS: Insulin levels were below 6 mIU/l in all the samples taken at the time of symptomatic hypoglycaemia in 6/15 patients, and in some of the samples in three patients; insulin levels were below 3 mIU/l in samples from 5 patients. C-peptide levels were above 0.6 ng/ml in all these samples. The lowest proinsulin level was 35 pmol/l. Insulin levels were measured with a less specific RIA (40% cross-reaction with proinsulin) in 8/15 patients and were above 6 mIU/l in all samples in seven patients, and all but one sample in the 8th patient. Mean concomitant C-peptide and insulinoma size were lower in those patients with insulin-IRMA levels below 6 mIU/l. CONCLUSION: Symptomatic hypoglycaemia below 0.45 g/l can result from insulin levels below 6 or even 3 mIU/l; lower insulin levels and secretion could be observed preferentially in small insulinomas. If an insulin assay devoid of any significant cross-reaction with intact proinsulin is employed, measuring C-peptide (and/or proinsulin) levels at the time of symptomatic hypoglycaemia is mandatory to make the diagnosis of endogenous hyperinsulinism.

Adult↗

PubMed1989

Fasting for 72 h decreases the responses of counterregulatory hormones to insulin-induced hypoglycaemia in normal man.

We have evaluated the influence of fasting on the response of counterregulatory hormones to insulin-induced hypoglycaemia. Eight healthy, non-obese volunteers were studied after an overnight fast and again after a 72-h fast period. Levels of blood glucose were higher after overnight fasting (4.59 +/- 0.10 mmol/l) than after 72 h of fasting (3.38 +/- 0.12 mmol/l). Hypoglycaemia was induced by a constant insulin infusion (2.4 mU/kg/min) and clamped between 2.1 and 2.3 mmol/l of glucose by a variable glucose infusion. Hypoglycaemia evoked stimulation of glucagon release after the overnight fast but did not alter release after 72 h of fasting. The response of other counterregulatory hormones were also influenced by the longer fasting period: the normal rise in adrenaline levels during hypoglycaemia was delayed and attenuated and the normal rise in cortisol levels was absent; paradoxically, cortisol levels decreased during hypoglycaemia. Seventy-two hours of fasting, therefore, profoundly alters hormonal responses to hypoglycaemia.

Adult↗

PubMed2004

Incidence and risk factors for neonatal hypoglycaemia in Kerala, India.

OBJECTIVES: To detect the incidence and risk factors that predicted the occurrence of neonatal hypoglycaemia and to identify neonates who require mandatory blood glucose screening during the first 48 h of life. DESIGN: Hospital based prospective study in a maternity centre in south India. SETTING: Labour room, postnatal wards and newborn nursery of the Institute of Maternal and Child Health, Medical College, Kozhikode, India. PATIENTS: Six hundred and four neonates were enrolled in the study by a systematic random sampling method from 1 August to 1 November 2002. INTERVENTION/MEASUREMENT: Random blood glucose levels were estimated by the standard glucose oxidase--peroxidase method on two occasions 24 h apart, during the first 2 days of life. Nineteen clinical characteristics of the mother-baby pair were analysed statistically in relation to the occurrence of hypoglycaemia. RESULTS: The incidence of neonatal hypoglycaemia in the present study group was 41/1000 live births. Eight variables strongly and independently predicted the risk of neonatal hypoglycaemia, at least one being present in 89.1% of the hypoglycaemic neonates. They included prematurity, low birthweight, maternal diabetes mellitus, delay in initiation of breastfeeding for more than 2 h postnatally, maternal pre-eclampsia and eclampsia, birth asphyxia, cold stress or hypothermia, and maternal oligohydramnios. CONCLUSIONS: Hypoglycaemia was a common problem in apparently normal asymptomatic babies. Apart from the classic 'text book risk factors', maternal oligohydramnios and a breastfeeding delay of more than 2 h after delivery predicted the risk of neonatal hypoglycaemia in this group. Mandatory blood glucose screening in babies with any one of the above mentioned risk factors serves as an easy and cost effective measure for the prompt identification of this condition.

Blood Glucose↗

PubMed2001

Reactive hypoglycaemia due to late dumping syndrome: successful treatment with acarbose.

Reactive hypoglycaemia is a rare disease which occurs postprandially in everyday life involving blood glucose levels below 2.5 to 2.8 mmol/l. We report on a 66-year-old patient who developed symptomatic reactive hypoglycaemia due to late dumping syndrome 10 years after oesophagectomy with cervical anastomosis. A 75 g sucrose load revealed a plasma glucose level of 9.4 mmol/l after one hour, followed by symptomatic hypoglycaemia with a plasma glucose level of 1.8 mmol/l after three hours. Concomitantly, high concentrations of insulin (3216 pmol/l at a glucose level of 9.4 mmol/l and 335 pmol/l at a glucose level of 1.8 mmol/l) and glucagon-like peptide 1 (GLP-1) (375 pmol/l at a glucose level of 9.4 mmol/l and 85 pmol/l at a glucose level of 1.8 mmol/l) were measured. While the patient was under treatment with acarbose, another sucrose load did not provoke symptomatic hypoglycaemia (plasma glucose nadir of 4.6 mmol/l after two hours). Insulin and GLP-1 levels increased much less, to peak levels of 375 pmol/l and 75 pmol/l respectively, after one hour when plasma glucose was 6.8 mmol/l. We conclude that in patients with reactive hypoglycaemia due to gastrointestinal surgery, acarbose decreases rapid glucose absorption associated with hyperglycaemia and GLP-1 secretion, and thus diminishes excessive insulin release. Acarbose is therefore a successful treatment modality for reactive hypoglycaemia due to late dumping syndrome.

Acarbose↗

PubMed2002

Predictors of glycaemic control and hypoglycaemia in children and adolescents with type 1 diabetes from NSW and the ACT.

OBJECTIVES: To audit glycaemic control and incidence of severe hypoglycaemia in children and adolescents with type 1 diabetes in New South Wales (NSW) and the Australian Capital Territory (ACT). DESIGN: A multicentre, population-based, cross-sectional study from 1 September to 31 December, 1999. PARTICIPANTS: 1190 children and adolescents aged 1.2-15.8 years with type 1 diabetes, identified from three hospital-based paediatric diabetes units, four private city-based paediatric practices and 18 regional outreach clinics in NSW and the ACT. MAIN OUTCOME MEASURES: HbA(1c) level and incidence of severe hypoglycaemia (defined by unconsciousness or seizures). RESULTS: The response rate was 67% (1190 of a target group of 1765). The median HbA(1c) level was 8.2% (interquartile range, 7.6%-9.1%). Significant predictors of HbA1c level in a multiple regression model were duration (b = 0.05; 95% CI, 0.02-0.07) and insulin dose/kg (b = 0.46; 95% CI, 0.27-0.66). At least one episode of severe hypoglycaemia in the previous three months was reported in 6.7%, and the rate of severe hypoglycaemia was 36/100 patient-years. Significant predictors of hypoglycaemia in a Poisson regression model were younger age (P = 0.03), male sex (P = 0.04), longer diabetes duration (P = 0.02), and > 3 daily insulin injections (P = 0.02), but not HbA(1c) level. Children with diabetes had higher BMI standard deviation scores compared with population standards, and those in the highest quartile of BMI standard deviation score were younger, had shorter diabetes duration and had higher HbA(1c) level. CONCLUSIONS: Many children and adolescents with type 1 diabetes have suboptimal glycaemic control, placing them at high risk of developing microvascular complications. Those with longer diabetes duration are at increased risk of suboptimal glycaemic control and severe hypoglycaemia and should be targeted for interventional strategies.

Adolescent↗

PubMed2000

Haemorrhagic shock and encephalopathy syndrome: report of two cases with special reference to hypoglycaemia.

Haemorrhagic shock and encephalopathy syndrome (HSES) is a devastating disorder affecting infants. So far no cases have been reported in Switzerland. It is characterised by the abrupt onset of hyperpyrexia, shock, encephalopathy, diarrhoea, disseminated intravascular coagulation (DIC) and renal and hepatic failure in previously healthy infants. Severe hypoglycaemia has been repeatedly reported in association with HSES. However, the pathophysiology of the hypoglycaemia is not clear. We report on two infants (2 and 7 months old) with typical HSES, both of whom were presented with nonketotic hypoglycaemia. In the first case, plasma insulin was 23 pmol/l at the time of hypoglycaemia (0.1 mmol/l). In the second case, increased values for interleukin-6 (IL-6) (319 pg/ml) and IL-8 (1382 pg/ml) were found 24 hours after admission, whereas IL-1 and tumour necrosis factor-alpha (TNF-alpha) were not measurable. Alpha-1-antitrypsin was decreased (0.6 g/l). In hyperpyrexic, unconscious and shocked infants, HSES should be considered and hypoglycaemia should be specifically looked for. Hypoglycaemia is not caused by hyperinsulinism but may be secondary to the release of cytokines.

Brain Diseases↗