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PubMed2006

Effect of the amino acid alanine on glucagon secretion in non-diabetic and type 1 diabetic subjects during hyperinsulinaemic euglycaemia, hypoglycaemia and post-hypoglycaemic hyperglycaemia.

AIMS/HYPOTHESIS: The aim of our study was to establish whether the well-known defective or absent secretion of glucagon in type 1 diabetes in response to hypoglycaemia is selective or includes lack of responses to other stimuli, such as amino acids. MATERIALS AND METHODS: Responses of glucagon to hypoglycaemia were measured in eight patients with type 1 diabetes and six non-diabetic subjects during hyperinsulinaemic (insulin infusion 0.5 mU kg(-1) min(-1)) and eu-, hypo- and hyperglycaemic clamp studies (sequential steps of plasma glucose 5.0, 2.9, 5.0, 10 mmol/l). Subjects were studied on three randomised occasions with infusion of low- or high-dose alanine, or saline. RESULTS: With saline, glucagon increased in hypoglycaemia in non-diabetic subjects but not in diabetic subjects. Glucagon increased further with low-dose (181 +/- 16 ng l(-1) min(-1)) and high-dose alanine (238 +/- 20 ng l(-1) min(-1)) in non-diabetic subjects, but only with high-dose alanine in diabetic subjects (area under curve 112 +/- 5 ng l(-1) min(-1)). The alanine-induced glucagon increase in diabetic subjects paralleled the spontaneous glucagon response to hypoglycaemia in non-diabetic subjects not receiving alanine. The greater responses of glucagon to hypoglycaemia with alanine infusion were offset by recovery of eu- or hyperglycaemia. CONCLUSIONS/INTERPRETATION: In type 1 diabetes, the usually deficient responses of glucagon to hypoglycaemia may improve after increasing the concentration of plasma amino acids. Amino acid-enhanced secretion of glucagon in response to hypoglycaemia remains under physiological control since it is regulated primarily by the ambient plasma glucose concentration. These findings might be relevant to improving counter-regulatory defences against insulin-induced hypoglycaemia in type 1 diabetes.

Adolescent↗

PubMed1996

Stimulation of adipose tissue lipolysis following insulin-induced hypoglycaemia: evidence of increased beta-adrenoceptor-mediated lipolytic response in IDDM.

The adrenergic regulation of adipose tissue lipolysis in response to insulin-induced hypoglycaemia (intravenous infusion of soluble insulin 0.10 IU.kg body weight-1.h-1 until the arterial plasma glucose fell below 2.8 mmol/l) was investigated directly in vivo in 11 insulin-dependent diabetic (IDDM) patients and 12 control subjects, using microdialysis of the extracellular space of abdominal subcutaneous adipose tissue. The tissue glycerol level (lipolysis index) and the escape of ethanol from the perfusion medium (blood flow index) were continuously monitored. During insulin infusion the arterial glucose level was reduced in parallel and the hypoglycaemic nadir was almost identical in the two groups (diabetic patients 2.2 +/- 0.1 and control subjects 2.3 +/- 0.1 mmol/l). While the maximum response of plasma epinephrine to hypoglycaemia was 30% lower in diabetic patients than in the control subjects (p < 0.05), the glycerol levels in adipose tissue and in plasma, as well as in serum non-esterified fatty acids, increased twice as much in the former as in the latter group following hypoglycaemia (p < 0.01). Addition of the beta-adrenoceptor blocker propranolol (10(4) mol/l) to the tissue perfusate almost completely prevented the hypoglycaemia-induced increase in the adipose tissue glycerol level in both groups, whereas in situ perfusion with 10(-4) mol/l of the alpha-adrenoceptor blocker phentolamine resulted in an additional increase in the tissue glycerol levels; during alpha-blockade, the glycerol response to hypoglycaemia remained enhanced by threefold in the diabetic patients (p < 0.01). In both groups local adipose tissue blood flow increased transiently in a similar way after hypoglycaemia; the increase being inhibited by in situ beta-adrenoceptor blockade. We conclude that both alpha- and beta-adrenergic mechanisms regulate adipose tissue lipolysis in response to hypoglycaemia. In IDDM, lipolysis is markedly enhanced following hypoglycaemia, despite a reduced catecholamine secretory response, because of increased beta-adrenoceptor action in adipose tissue.

Adipose Tissue↗

PubMed1998

Substitution of night-time continuous subcutaneous insulin infusion therapy for bedtime NPH insulin in a multiple injection regimen improves counterregulatory hormonal responses and warning symptoms of hypoglycaemia in IDDM.

In patients with insulin-dependent diabetes mellitus (IDDM) good glycaemic control confers an enhanced risk of hypoglycaemia. Nocturnal hypoglycaemia occurs frequently and contributes to the syndrome of hypoglycaemia unawareness. In order to avoid nocturnal hypoglycaemia we substituted night-time continuous subcutaneous insulin infusion (CSII) therapy in 14 patients with well-controlled IDDM using a multiple injection regimen for the more variable bedtime NPH insulin. During a stepwise hypoglycaemic clamp we studied the effect of this regimen on counterregulatory hormonal responses, warning symptoms and cognitive function. In addition, we investigated the incidence of daytime hypoglycaemia and the acceptability of night-time CSII treatment. CSII was associated with a lower frequency of hypoglycaemia (mean+/-SEM): 16.1+/-3.1 vs 23.6+/-3.3) episodes during the last 6 weeks of treatment, p=0.03 (CSII vs NPH)) with maintenance of good glycaemic control (HbA1c 7.2+/-0.2 vs 7.1+/-0.2 %, p=0.2). Hypoglycaemic thresholds for the growth hormone response and for autonomic symptoms were lower for CSII treatment than for NPH treatment. Of 14 patients 6 decided to continue with the nocturnal CSII treatment. In conclusion, nocturnal CSII improves warning symptoms and counterregulatory hormonal responses to hypoglycaemia and is an acceptable treatment strategy for patients suffering from hypoglycaemia unawareness, as demonstrated in this acute feasibility study.

Adult↗

PubMed1997

Alteration in brain glucose metabolism induced by hypoglycaemia in man.

Glucose is the usual fuel of brain tissue. As hypoglycaemia develops, a level of glycaemia is reached where glucose transport from the circulation is no longer sufficient to meet metabolic demands, and the brain signals for peripheral counter-regulatory responses and symptoms of hypoglycaemia ensue. The glycaemic threshold for these events can be shifted to lower glucose concentrations following a single episode of hypoglycaemia, and compensating central nervous system adaptations have been postulated in man. In nondiabetic subjects, rates of brain glucose uptake are initially impaired at a systemic glucose concentration of 3.6 mmol/l; whereas after 56 h of intermittent hypoglycaemia (3.0 mmol/l) brain uptake is preserved at normal rates even at 2.5 mmol/l. Increments in counter-regulatory hormones and symptoms are also triggered at lower glucose concentrations following recurrent hypoglycaemia. In 24 patients with insulin-dependent diabetes stratified into three equal groups by HbA1c value, those in the lowest third of HbA1c range had rates of brain glucose uptake at 3.0 mmol/l that were equivalent to rates measured at 5.3 mmol/l. Patients in the other HbA1c groups had rates of brain glucose uptake during hypoglycaemia that were reduced by 30% relative to normoglycaemia-comparable to reductions seen in non-diabetic subjects. Thus, alterations in glucose uptake occur in the brain in order to maintain normal brain metabolism following experimental and clinical hypoglycaemia. Because of this enhanced glucose uptake, the brain has no need to signal for counter-regulatory responses and hypoglycaemia unawareness occurs.

Brain↗

PubMed2004

Severe hypoglycaemia, metabolic control and diabetes management in children with type 1 diabetes in the decade after the Diabetes Control and Complications Trial -- a large-scale multicentre study.

UNLABELLED: Hypoglycaemia is frequently the limiting factor in achieving optimal glycaemic control. Therefore, insulin therapy, the incidence of hypoglycaemia, and glycaemic control were investigated in 6309 unselected children with type 1 diabetes in a large-scale multicentre study. Using standardised computer-based documentation, the incidence of severe hypoglycaemia, HbA1( c) levels, insulin regimen, diabetes duration, and the number of patients attending a treatment centre were investigated for the age groups 0-<5 years ( n =782), 5-<7 years ( n =1053), and 7-<9 years ( n =4474). The average HbA1( c) level was 7.6% (no significant difference between age groups). Young children had more severe hypoglycaemic events (31.2/100 patient years) as compared to older children (19.7; 21.7/100 patient years, P <0.05) independent of the treatment regimen. Our data suggest that diabetes centres treating less than 50 patients per year have a higher incidence of hypoglycaemia in 0-<5-year-old children (43.0/100 patient years) as compared to larger centres (24.1/100 patient years; P <0.0001). Significant predictors of hypoglycaemia were younger age ( P <0.0001), longer diabetes duration ( P <0.0001), higher insulin dose/kg per day ( P <0.0001), injection regimen ( P <0.0005), and centre experience ( P <0.05). CONCLUSION: Despite modern treatment, young children have an elevated risk for developing severe hypoglycaemia compared to older children, especially when treated at smaller diabetes centres. The therapeutic goal of carefully regulating metabolic control without developing hypoglycaemia has still not been achieved. Further advances in diabetic treatment may result from giving more attention to hypoglycaemia in young children.

Age Factors↗

PubMed1994

Protection by lactate of cerebral function during hypoglycaemia.

Severe hypoglycaemia with brain dysfunction limits intensified therapy in patients with insulin-dependent diabetes mellitus, despite evidence that such therapy reduces the risk of chronic complications of the disease. We have investigated the effect of infusing lactate (a potential non-glucose fuel for brain metabolism) on protective, symptomatic neurohumoral responses and on brain function during hypoglycaemia in seven healthy men. Elevation of lactate (within a physiological range) substantially diminished catecholamines, growth hormone, cortisol, and symptomatic responses to hypoglycaemia and lowered the glucose level at which these responses began. Glucagon responses were unaffected. Lactate was also associated with a significant lowering of the glucose level at which brain function deteriorated, suggesting that brain function was protected during the hypoglycaemia. The defect in counter-regulation is similar to that seen in hypoglycaemia-prone diabetic patients. Initiation of the protective responses to hypoglycaemia (except glucagon) can be delayed by supporting metabolism with an alternative metabolic fuel. Cerebral cortical dysfunction of severe hypoglycaemia is also delayed. Our demonstration that higher brain function can be protected during hypoglycaemia may have therapeutic potential.

Adult↗

PubMed1998

Sustained elevation of cerebral blood flow after hypoglycaemia in normal man.

During hypoglycaemia, counter-regulatory hormones are released, cognitive function is impaired and cerebral blood flow is increased. In the immediate period after normalisation of blood glucose only counter-regulatory hormones seem to be normalised. The aim of this study was to follow the changes in cerebral blood flow during a prolonged recovery period following moderate hypoglycaemia in normal man. In 15 healthy men, hypoglycaemia was induced by an intravenous infusion of insulin (2.5 mU/kg per min) to a blood glucose of 2.2 +/- 0.3 mmol/l (mean +/- S.D.) and was kept at this level for 66 +/- 11 min. The cerebral blood flow was measured by a single photon emission computed tomography camera (SPECT) recording the clearance of intravenously administered xenon-133. Measurements were performed before, at the beginning and at the end of the hypoglycaemic period, as well as 23 +/- 5, 51 +/- 7 and 97 +/- 7 min after normalisation of the blood glucose. The basal cerebral blood flow was 50.2 +/- 5.2 ml/100 g per min, increased to 55.6 +/- 4.9 ml/100 g per min (P < 0.001) during hypoglycaemia, and remained at this level at all measurements after normalisation of blood glucose. There was no relation between the rate of fall in blood glucose or level of hypoglycaemia and increment in cerebral blood flow or the actual blood flow during hypoglycaemia. The values of plasma adrenaline, serum ACTH, serum cortisol and symptom scores increased significantly during hypoglycaemia. The adrenaline level was back to the basal level at the first measurement after normalisation of blood glucose, while the ACTH level was normalised at the subsequent measurement and the cortisol level at the last measurement. In conclusion, the results show that despite normalisation of counter-regulatory hormones and hypoglycaemic symptoms, the cerebral blood flow remains elevated for at least 97 +/- 7 min following 66 +/- 11 min of moderate hypoglycaemia, indicating that additional factors which are not coupled to the cerebral metabolism influence this vasculatory response.

Adrenocorticotropic Hormone↗

PubMed1983

The physiological effects of insulin-induced hypoglycaemia in man: responses at differing levels of blood glucose.

The aim of this study was to describe hormonal, cardiovascular and thermoregulatory responses to insulin-induced hypoglycaemia of differing levels of severity. Five normal male volunteers were rendered hypoglycaemic at intervals of 1 week by intravenous infusions of 3, 4 or 6 units of insulin/h, or by intravenous injection of 0.15 unit/kg body weight. Plasma glucose reached nadir values of 2.08 +/- 0.10, 1.82 +/- 0.21, 1.24 +/- 0.08 and 0.92 +/- 0.06 mmol/l (means +/- SEM) in the four experiments. Non-esterified fatty acid levels fell equally in all experiments but recovery was more rapid with severe hypoglycaemia. In contrast the rate of recovery of plasma glucose was slower with deeper hypoglycaemia and this appeared unrelated to the counter-regulatory response. Plasma glucagon, adrenaline and prolactin levels increased in proportion to the severity of hypoglycaemia, but peak concentrations of cortisol, growth hormone (somatotropin) and noradrenaline did not vary, suggesting that moderate hypoglycaemia had elicited maximal responses. When the areas under the curves were calculated, the cortisol responses were greater for the 6 units infusion and bolus injection than for the other infusions, and the growth hormone responses were similar for all three infusions but significantly greater with the bolus injection. Increases in heart rate and systolic blood pressure were related to the severity of hypoglycaemia, but changes in diastolic blood pressure and peripheral vascular resistance (assessed from calf and from hand blood flow) were not. Central temperature fell by 0.13 +/- 0.06 degrees C, 0.30 +/- 0.10 degrees C, 0.65 +/- 0.14 degrees C and 1.15 +/- 0.30 degrees C (means +/- SEM) in the four experiments, and the fall in skin temperature had a similar gradation. Many physiological responses to hypoglycaemia are not 'all-or-none', but vary according to the intensity of stimulus; some are already maximal at mild degrees of hypoglycaemia. Other changes are more complex, reflecting an interplay between opposing endocrine and neural responses.

Adult↗

PubMed1985

Changes in plasma volume, in transcapillary escape rate of albumin and in subcutaneous blood flow during hypoglycaemia in man.

Hypoglycaemia was induced by insulin injected intravenously (0.15 i.u./kg body weight) in seven healthy young males. Plasma volume was measured before and during hypoglycaemia by intravenous injection of 125I before hypoglycaemia and of 131I during hypoglycaemia. Plasma volume decreased and transcapillary escape rate increased significantly during hypoglycaemia. Skin temperature and local subcutaneous adipose tissue blood flow were measured in four different regions. Both tended to decrease during hypoglycaemia and decreased significantly 2 h after hypoglycaemia. There was no correlation between changes in the two measurements, suggesting that there is no simple relationship between subcutaneous blood flow and skin temperature during hypoglycaemia.

Adult↗

PubMed1997

Reports of hypoglycaemia associated with the use of ACE inhibitors and other drugs: a case/non-case study in the French pharmacovigilance system database.

AIMS: To test the existence of an association between reports of hypoglycaemia and angiotensin converting enzyme inhibitors, in a spontaneous reports database. METHODS: The French Pharmacovigilance database was examined for an association between adverse drug reaction reports mentioning hypoglycaemia, and angiotensin converting enzyme inhibitors (ACEI) using the case/non-case methodology, with reports of hypoglycaemia as cases and all other reports as comparators. The association between ACEI or other chosen drugs and hypoglycaemia was also tested in the subgroups of patients taking or not antidiabetic agents (ADA). RESULTS: 428 of 93,338 reports mentioned hypoglycaemia (202/2227 with ADA (OR 40, 95% CI 33-48)). 46/5717 reports mentioned ACEI (OR 1.8 (1.25-2.54)). Other study drugs associated with hypoglycaemia were cibenzoline (OR 80 (57-112)), disopyramide (OR 32 (22-46)), nifedipine (OR 2.16 (1.32-3.51)), diltiazem (OR 1.76 (1.01-3.06)) nitrates (nitroglycerin, molsidomine) (OR 1.91 (1.16-3.16)) and frusemide (OR 1.89 (1.31-1.76)), but not nicardipine, amlodipine, felodipine or nitrendipine, diazepam, atenolol or combination thiazide diuretics. However, ACEI and other drugs were associated with ADA, so that in the subgroups of patients taking or not ADA, the association of ACEI with hypoglycaemia disappeared (OR 0.9 (0.5-1.4) and 1.2 (0.7-2.2), respectively). The same was found for other drugs except cibenzoline. CONCLUSION: The association between reporting of hypoglycaemia and ACE inhibitors was related to concomitant use of antidiabetic agents. This was true also for other drugs used in arterial disease or renal failure, such as calcium channel blockers, nitrates, and frusemide.

Adverse Drug Reaction Reporting Systems↗

PubMed1998

Hypoglycaemia leads to an increased QT interval in normal men.

Hypoglycaemia is presumed to be the cause of death in about 3% of insulin-treated diabetic patients. Some of these patients suffer from hypoglycaemic brain damage, but the majority have no evident brain damage and are supposed to have died from other causes such as a cardiac arrhythmia. The putative mechanism is a hypoglycaemia-induced prolongation of the QT interval which increases the risk of malignant ventricular tachycardia. The aim of the present study was to examine the electrocardiogram during and after hypoglycaemia in healthy men. To that end, hypoglycaemia was induced by an intravenous infusion of insulin (2.5 mU kg-1 min-1) in 10 healthy men to reach a venous blood glucose level of 2.1 +/- 0.3 mmol l-1 for 65 +/- 9 min. Before hypoglycaemia, after 20 and 50 min of hypoglycaemia and 20 and 45 min after normalization of the blood glucose, the QT interval was measured by a ruler and corrected for the heart rate. Results are given as mean +/- SD and comparisons were made with an ANOVA, except for symptom scores and plasma adrenaline where non-parametric tests were used. When this indicated significance, further analysis was performed with a two-tailed t-test. During hypoglycaemia the corrected QT interval increased from 380 +/- 20 ms1/2 to 440 +/- 30 ms1/2 (P < 0.001), and the amplitude of the T wave decreased (P = 0.002). The serum potassium level decreased from 4.3 +/- 0.3 mmol l-1 to 3.5 +/- 0.2 mmol l-1 (P < 0.001) and the plasma adrenaline concentration increased from 0.20 +/- 0.04 nmol l-1 to 2.46 +/- 2.58 nmol l-1 (P < 0.01). The results of this study confirm that a prolongation of the QT interval occurs during hypoglycaemia, but the significance of this finding still has to be proven.

Adult↗

PubMed1996

Visual information processing during controlled hypoglycaemia in humans.

A general impairment of cognitive performance occurs during acute insulin-induced hypoglycaemia, but little objective evidence is available for disruption of more specific cognitive processes. The effect of controlled hypoglycaemia on the early stages of visual information processing and contrast sensitivity was examined in a homogeneous group of 20 nondiabetic human subjects. Hypoglycaemia caused a significant disruption in general cognitive performance as assessed by a digit symbol task (P < 0.001) and the trail making B task (P < 0.05). Hypoglycaemia also produced a highly significant deterioration in performance on all of the visual information processing tasks, namely inspection time (IT) (P = 0.01), visual change detection (VCD) (P < 0.005) and visual movement detection (VMD) (P < 0.005). A significant deterioration in contrast sensitivity was observed during hypoglycaemia (P < 0.005). In contrast, no significant effect of hypoglycaemia was demonstrated on standard clinical measures of visual acuity or stereoscopic vision. Thus, although hypoglycaemia caused no detectable deterioration in visual acuity as measured by Snellen-type tests, a marked deterioration occurred in the speed of visual information processing and in contrast sensitivity. As many decisions are made under conditions of limited perceptual time and low visual contrast (e.g. when driving), the disruptive effect of moderate insulin-induced hypoglycaemia on visual perception will have important practical implications in diabetic humans exposed to this metabolic stress. The present results are congruent with other evidence which shows that the early stages of visual information processing are susceptible to deterioration by general cerebral insults.

Adult↗

PubMed1998

Hypoglycaemia on and after admission in Kenyan children with severe malaria.

We investigated the pathophysiology of hypoglycaemia in severe malaria in African children, especially the potential importance of glycerol as a substrate for gluconeogenesis, and whether substrate limitation contributes to hypoglycaemia in severe disease. Of 171 children with moderate or severe malaria, 16% were hypoglycaemic on admission, while at least 9% of children with severe malaria treated with quinine and a concurrent 4% dextrose infusion had a definite episode of hypoglycaemia after admission. Blood levels of gluconeogenic precursors are as high (alanine and lactate) or higher (glycerol) in those with either hypoglycaemia on or after admission as they are in children never having an episode of hypoglycaemia. Among children with severe malaria, however, those having a definite episode of hypoglycaemia at some stage are more acidotic and have greater evidence of renal impairment than those who are never hypoglycaemic (mean base excess -14.4 vs. -7.2, p < 0.001, mean creatinine 97 vs. 64, p < 0.001 and mean urea 8.1 vs. 5.8, p = 0.03, respectively). These data do not support a role for reduced gluconeogenic substrate supply in the pathogenesis of hypoglycaemia in severe childhood malaria, but do support the hypothesis that gluconeogenesis is impaired. Commonly-used bedside blood glucose monitoring devices may overestimate blood glucose measurements in the normal range, and paradoxically may also seriously overestimate the frequency of hypoglycaemia.

Chi-Square Distribution↗

PubMed2005

Preserved inhibitory effect of recurrent hypoglycaemia on the male gonadotrophic axis.

OBJECTIVE: Hypoglycaemia-induced decreases in male LH and testosterone concentrations are possibly mediated by activation of the hypothalamus-pituitary-adrenal (HPA) axis or by an increase in PRL. As counterregulatory stress hormone release is attenuated during recurrent hypoglycaemia, we questioned whether the gonadotrophic axis and PRL adapt similarly. DESIGN: We performed two consecutive hypoglycaemic clamps on day 1 and one clamp on the following day in 15 healthy men. Blood concentrations of gonadotrophins, PRL, testosterone, ACTH and cortisol were measured during the first and the third clamp, taking place at the same time of day. RESULTS: During hypoglycaemia, serum concentrations of LH and testosterone decreased (P < 0.003 for both), PRL, ACTH and cortisol increased (P < 0.001), and FSH remained unchanged (P = 0.90). The hypoglycaemia-induced decreases in LH and testosterone concentrations were similar during the first and the last clamp (P > 0.28 for both) whereas the increase in PRL, ACTH and cortisol was markedly attenuated during the third clamp (P < 0.001). CONCLUSIONS: LH and testosterone responses do not adapt to recurrent hypoglycaemia, whereas the increase in PRL is attenuated, indicating adaptation. Considering the marked decrease in the responses of PRL and the HPA axis after antecedent hypoglycaemia, the data suggest that the hypoglycaemia-induced decreases in LH and testosterone concentrations, not adapting to recurrent hypoglycaemia, are mediated independently, probably by blood glucose itself.

Adaptation, Physiological↗

PubMed1996

Survey of the definition and screening of neonatal hypoglycaemia in Australia.

OBJECTIVE: To determine the approach to identifying neonatal hypoglycaemia and the definition of neonatal hypoglycaemia used by neonatal paediatricians in Australian Level 3 neonatal intensive care units (NICU). METHODOLOGY: A questionnaire was sent to the 101 neonatal paediatricians in the 22 Level 3 NICU in Australia asking their method of screening for, and definition of, neonatal hypoglycaemia. RESULTS: Responses were received from 70 neonatal paediatricians, including all 22 directors. A bedside glucose meter is used in 19 of 22 NICU to screen for hypoglycaemia, whilst one NICU uses a glucose analyzer and another NICU uses a visual colour comparison method. One NICU does not screen, but has blood glucose measured in a satellite laboratory. If the screening method suggests hypoglycaemia, 62 of 63 neonatal paediatricians proceed to blood glucose determination in a laboratory, mostly using plasma samples. Based on the laboratory measurement, the definition of neonatal hypoglycaemia ranged from < 1.1 to 3.0 mmol/L. CONCLUSIONS: The majority of neonatal paediatricians in Australian NICU screen for neonatal hypoglycaemia using a bedside glucose meter. There is a wide range in the definition of neonatal hypoglycaemia from < 1.1 to 3.0 mmol/L.

Australia↗

PubMed2006

Unrecognised hypoglycaemia in children and adolescents with type 1 diabetes using the continuous glucose monitoring system: prevalence and contributors.

AIM: To determine prevalence of hypoglycaemia, and contributing factors, in children with type 1 diabetes, using the Medtronic MiniMed continuous glucose monitoring system (CGMS). METHODS: Fifty-one children and adolescents with diabetes were studied with the CGMS. The studies were analysed for frequency and duration of hypoglycaemia (below 3.5 and 2.5 mmol/L). Contributing clinical factors were determined. Occurrence of nocturnal hypoglycaemia was related to bedtime and fasting home glucose recording. RESULTS: Hypoglycaemia was common, with 1 (0-4.2) (median (range)) episode per patient per 24 hours, and 0.33 (0-2) episodes per patient per night. Nocturnal episodes were longer than daytime episodes [97.5 (5-720) versus 35 (5-295) minutes for episodes below 3.5 mmol/L, P < 0.001; and 75 (10-640) versus 25 (5-200) minutes for episodes below 2.5 mmol/L, P < 0.001], and less likely to be recognised by the subject (P < 0.001 for episodes below both 3.5 and 2.5 mmol/L). Nocturnal hypoglycaemia was more common with a bedtime glucose recording <6 mmol/L, but also occurred frequently in subjects with glucose recordings >10 mmol/L. No bedtime glucose value reduced the risk of nocturnal hypoglycaemia to <10%. CONCLUSION: Hypoglycaemia, assessed using the CGMS, is common in children with type 1 diabetes and can be prolonged (although is predominantly mild). Bedtime home glucose recordings are poorly predictive of hypoglycaemia during the following night. Continuous glucose monitoring has proven very useful in management of individual patients, particularly adolescents experiencing difficulties with adherence to diabetes management.

Adolescent↗

PubMed2004

Hypoglycaemia and driving in people with insulin-treated diabetes: adherence to recommendations for avoidance.

BACKGROUND: Hypoglycaemia impairs driving performance, so drivers with insulin-treated diabetes should try to avoid hypoglycaemia when driving, and treat it effectively if it occurs. It is not known how many insulin-treated drivers are familiar with, or adhere to, recommended safe practice. METHODS: We surveyed a representative sample of 202 current drivers with insulin-treated diabetes (115 with Type 1 diabetes), using a structured questionnaire. Data were obtained on driving history, estimated frequency of hypoglycaemia, and measures taken to avoid and treat hypoglycaemia when driving. RESULTS: The licensing authority (DVLA) and motor insurance company had been informed by almost all participants. Sixty-four participants (31.7%) had experienced hypoglycaemia while driving, and 27 (13.4%) reported that this had occurred within the preceding year. A minimum blood glucose level of 4.0 mmol/l or higher was considered necessary for driving by 151 drivers (74.8%), and 176 (87.1%) reported always keeping carbohydrate in their vehicle. However, 77 (38.1%) reported never carrying a glucose meter when driving, and 121 (59.9%) that they never test blood glucose before driving, or test only if symptomatic of hypoglycaemia. Most participants (89%) would stop driving to treat hypoglycaemia and would not resume driving immediately, although only 28 (13.9%) would wait longer than 30 min. Almost half of participants were failing to observe at least one essential aspect of safe driving. CONCLUSIONS: Compliance with statutory requirements to inform the licensing authority and motor insurer is good, and drivers' perceptions of the minimum safe blood glucose level for driving are encouraging. However, most drivers rely on symptoms to detect hypoglycaemia while driving, and seldom test blood glucose before driving. Patient education should emphasize the role of blood glucose monitoring in relation to driving, and highlight the potential deterioration in driving performance when blood glucose falls below 4.0 mmol/l.

Accidents, Traffic↗

PubMed1987

Prediction and management of nocturnal hypoglycaemia in diabetes.

Blood glucose measurements were made at 2200, 0200, and 0800 h in 102 children with diabetes during a 24 hour planned admission to hospital. Nocturnal hypoglycaemia (less than 3.0 mmol/l) occurred in 24 of 71 (34%) children on twice daily insulin and in three of 31 (10%) children on once daily insulin. Predictive value modelling showed that a blood glucose concentration of less than 7 mmol/l at 2200 h was the best predictor of nocturnal hypoglycaemia, with a sensitivity of 63%, specificity of 94%, and positive and negative predictive values of 83%. Blood glucose measurement at 0800 h had no predictive value for nocturnal hypoglycaemia. The mean (SD) glycosylated haemoglobin concentration of children on twice daily insulin who had nocturnal hypoglycaemia was 55 (8) mmol HMF/mol Hb, which was significantly less than that of children on twice daily insulin who did not have hypoglycaemia (64 (11) mmol HMF/mol Hb) or those on once daily insulin (62 (11) mmol HMF/mol Hb). A controlled trial was then performed in which 29 children with diabetes who had a blood glucose concentration at 2200 h of less than 7 mmol/l measured by Reflocheck were randomised into two groups, one of which received 10 g carbohydrate supplement and the other of which did not. Thirteen of the 14 children in the control group had hypoglycaemia at 0200 h, whereas the snack prevented hypoglycaemia in 12 of 15 in the test group. Blood glucose values in the two groups at 0800 h were similar. We conclude that bedtime glucose measurement in children on twice daily insulin is a useful predictor for nocturnal hypoglycaemia, which can be prevented by a small carbohydrate snack in those at risk.

Adolescent↗