PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “hypoglycaemia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

Symptoms of hypoglycaemia in people with diabetes.

The symptoms of hypoglycaemia are fundamental to the early detection and treatment of this side-effect of insulin and oral hypoglycaemic therapy in people with diabetes. The physiology of normal responses to hypoglycaemia is described and the importance of symptoms of hypoglycaemia is discussed in relation to the treatment of diabetes. The symptoms of hypoglycaemia are described in detail. The classification of symptoms is considered and the usefulness of autonomic and neuroglycopenic symptoms for detecting hypoglycaemia is discussed. The many external and internal factors involved in the perception of symptoms are reviewed, and symptoms of hypoglycaemia experienced by people with Type 2 diabetes are addressed. Age-specific differences in the symptoms of hypoglycaemia have been identified, and are important for clinical and research practice, particularly with respect to the development of acquired hypoglycaemia syndromes in people with Type 1 diabetes that can result in impaired awareness of hypoglycaemia. In addition, the routine assessment of hypoglycaemia symptoms in the diabetic clinic is emphasized as an important part of the regular review of people with diabetes who are treated with insulin.

Aged↗

Causes, management and morbidity of acute hypoglycaemia in adults requiring hospital admission.

In the community, acute hypoglycaemia is commonly caused by therapies for diabetes mellitus or the excessive consumption of alcohol. Although most episodes do not require admission to hospital, little information is available on the causes and outcome of those that do. We retrospectively surveyed adult patients admitted to a large urban teaching hospital with acute hypoglycaemia in a 12-month period, identifying 56 admissions of 51 patients. Forty-one had diabetes mellitus, 33 (80%) of whom were receiving treatment with insulin. The others had hypoglycaemia induced by excessive consumption of alcohol or by deliberate self-poisoning with insulin. A history of psychiatric illness and/or chronic alcoholism was common. Neurological manifestations of hypoglycaemia were the principal reason for admission, observed on 50 occasions (89%), and 11 events (20%) had precipitated convulsions. Although many patients (59%) had received treatment for hypoglycaemia before admission, hypoglycaemia recurred in 16% of patients in hospital. Four patients (7%) died following admission, but in only one case was this the direct result of hypoglycaemia. However, within 15 months of the index hypoglycaemia event, a further six patients (11%) had died, mostly of causes unrelated to hypoglycaemia. Patients who require hospital admission for treatment of hypoglycaemia have a high incidence of neurological manifestations, a high rate of mental illness and other medical disorders, and may represent a high-risk subgroup with a poor long-term prognosis.

Acute Disease↗

The relationship between symptomatic and biochemical hypoglycaemia in insulin-dependent diabetic patients.

The relationship between symptomatic (subjective feelings) and biochemical (blood glucose concentration less than 3 mmol l-1) hypoglycaemia was studied in 66 randomly selected insulin-dependent diabetic out-patients under normal conditions of daily life with conventional insulin injection regimens. The patients (a) collected 7-point diurnal blood glucose profiles at home on three consecutive days and then once weekly for 3 weeks, (b) indicated whether they felt hypoglycaemic at sampling times, and (c) collected extra samples if they felt hypoglycaemic at any time during the study period. The weekly frequencies of symptomatic and biochemical hypoglycaemia were 0.99 and 1.75 per patient, respectively. Biochemical hypoglycaemia was present in 29% of the symptomatic episodes, and symptomatic hypoglycaemia accompanied 16% of the biochemical episodes. Symptomatic hypoglycaemia was experienced at a median blood glucose concentration of 3.4 mmol l-1 (range 1.4-14.9 mmol l-1). Fifty per cent of both symptomatic and biochemical episodes occurred before lunch, while the remainder were evenly distributed throughout the day. The occurrence of biochemical hypoglycaemia, but not of symptomatic hypoglycaemia, was inversely correlated with HbA1c and median blood glucose concentration. Thus symptomatic hypoglycaemia is an unreliable indicator of biochemical hypoglycaemia and of the degree of glycaemic control. Blood glucose measurements are a prerequisite for the diagnosis of hypoglycaemia.

Adult↗

Hypoglycaemia and cognitive function.

Acute hypoglycaemia impairs cerebral function, and available data indicate that cognitive performance becomes impaired at a blood glucose level of 2.6-3.0 mmol/l in healthy subjects. Methodological problems limit comparisons between studies, but in general complex tasks are more sensitive to hypoglycaemia than simple tasks, and some cognitive abilities are completely abolished. The onset of hypoglycaemic cognitive dysfunction is immediate, but recovery may be considerably delayed. There is persuasive evidence of adaptation to hypoglycaemia, partly due to increased brain glucose uptake capacity, although other mechanisms may exist. Patients who are exposed to chronic or recurrent hypoglycaemia become remarkably tolerant to the state, but this is insufficient to prevent severe hypoglycaemia with neuroglycopenic decompensation, probably because symptomatic and counterregulatory responses adapt even more. During experimental hypoglycaemia, administration of non-glucose cerebral fuels preserves cognitive function. However, little progress has been made as yet towards protecting cognitive function during hypoglycaemia in clinical practice. The chronic effects of recurrent hypoglycaemia remain contentious. There are numerous case reports of hypoglycaemic brain damage and of cognitive deterioration attributed to repeated severe hypoglycaemia. The major prospective studies, including the Diabetes Control and Complications Trial, did not report cognitive declines in intensively treated patients, but had unrepresentative study populations and may have been too short to detect such effects. Structural and functional brain changes are not only associated with recurrent severe hypoglycaemia, but also with hyperglycaemia and early disease onset and may in part be due to hyperglycaemic microvascular disease. Children may be more prone to acute metabolic insults, and there is evidence of developmental disadvantage associated with hypoglycaemic episodes.

Acute Disease↗

Influence of alcohol on cognitive performance during mild hypoglycaemia; implications for Type 1 diabetes.

AIMS: Alcohol and hypoglycaemia independently affect cognitive function. This may be relevant for insulin-treated diabetic patients who drive motor vehicles. The aim of this study was to examine the effect of mild hypoglycaemia (2.8 mmol/l) with modest alcohol intoxication (levels below UK driving limits) on intellectual performance in patients with Type 1 diabetes. METHODS: A hyperinsulinaemic glucose clamp (60 mU/m2) was used to study 17 subjects [age 35 +/- 8 years, HbA1c 8.1 +/- 1.4% (mean +/- sd)] on four occasions: (A) euglycaemia (4.5 mmol/l) with placebo, (B) euglycaemia with alcohol, (C) hypoglycaemia (2.8 mmol/l) with placebo, and (D) hypoglycaemia with alcohol. Cognitive performance was assessed using four-choice reaction time (4CRT, primary outcome), measurements of general intellectual skills [trail making B (TMB) and digit symbol substitution (DSST)], and visual information processing [visual change detection (VCD)]. A test related to driving performance (hazard perception) was also used. RESULTS: In experiments B and D the average blood alcohol level was 43 mg/dl. This was associated with deterioration in 4CRT [+ 35 ms [95% confidence interval (CI) 20, 50]] and TMB, whereas hypoglycaemia without alcohol increased 4CRT only [+ 39 ms (95% CI 5, 73)]. However, when alcohol was combined with hypoglycaemia, there was marked deterioration in all the cognitive function tests [4CRT 74 ms (95% CI 35, 113), TMB, DSST and VCD]. Hazard perception was not affected. The effect of alcohol was no different in euglycaemia than in hypoglycaemia, i.e. there was no interaction. Whereas hypoglycaemia did not reduce the likelihood that the subjects would drive, alcohol did. CONCLUSIONS: The cumulative effect of alcohol and hypoglycaemia on cognitive function together has implications for driving in patients with Type 1 diabetes. Both independently impair cognitive function and together the effects are additive. Patients with Type 1 diabetes should be educated about hypoglycaemia and driving and should avoid alcohol completely if planning to drive.

Adult↗

Hypoglycaemia in children with type 1 diabetes mellitus.

Hypoglycaemia is a frequent acute complication of IDDM and is usually defined as a blood glucose level below 3.0 mmol/l. Hypoglycaemia stimulates several neuroendocrine responses, such as secretion of glucagon, adrenaline, growth hormone and cortisol, which are generally increased during this phenomenon. The true prevalence of hypoglycaemia is not known. Studies of the epidemiology of severe hypoglycaemia give prevalences ranging from 2.7 to 85.7 episodes per 100 patients per year. The major risk factor for severe hypoglycaemia is hypoglycaemia unawareness, which occurs particularly in patients with type 1 diabetes of long duration and in those with a history of frequent episodes of hypoglycaemia. The first step in the management of hypoglycaemia is to check blood glucose and to treat hypoglycaemia on the basis of symptoms. Hypoglycaemia requires urgent treatment with a fast-acting carbohydrate or, if severe, with parenteral glucagon or intravenous glucose. Prevention measures should be instituted to prevent subsequent episodes, particularly in younger children with hypoglycaemic seizures or when seizures are recurrent.

Adolescent↗

Multivariate models of health-related utility and the fear of hypoglycaemia in people with diabetes.

AIM: The aim was to statistically model the degree of fear of hypoglycaemia experienced by people with diabetes, and then model the resulting change in health-related utility associated with differing severity and frequency of hypoglycaemia. METHODS: The study used pooled data from two previous postal surveys among subjects with confirmed diabetes conducted in Cardiff, UK (n = 1305 responses). The fear of hypoglycaemia was characterised using the Hypoglycaemia Fear Survey (HFS [eight question worry sub-scale only]), and health-related utility using the EQ5D(index). The data were then analysed using univariate and multivariate analysis. RESULTS: Following detailed preliminary analysis, a two-stage approach was used since fear was important when estimating the EQ5D(index). Fear was then modelled as a function of the severity and frequency of hypoglycaemia while controlling for other factors such as diabetes-related complications. Each severe hypoglycaemic event resulted in a change of 5.881 units on the HFS. One or more symptomatic hypoglycaemic events over the same period results in a corresponding change of 1.773 units on the HFS. A 1 unit increase on the HFS results in a 0.008 unit decrease on the EQ5D(index). CONCLUSION: While controlling for other factors, the fear of hypoglycaemia was an important determinant of health-related utility. The magnitude of fear of hypoglycaemia was associated with the severity and frequency of hypoglycaemia. Hypoglycaemia was associated with a considerable decrement in health-related utility as a function of increased fear. Measures should be taken to minimise the severity and frequency of hypoglycaemia.

Adult↗

Drug-induced severe hypoglycaemia in Type 2 diabetic patients aged 80 years or older.

Our knowledge about the risk of hypoglycaemia associated with diabetes treatment is derived from studies that often exclude elderly people. Aim of this study was to determine the incidence and risk factors for developing severe hypoglycaemia among persons aged 80 yr or older, with Type 2 diabetes mellitus (T2DM). During a 2-yr period, all episodes of severe hypoglycaemia occurred in T2DM patients aged 80 yr or older were identified. Hypoglycaemia was defined as a symptomatic event requiring treatment with i.v. glucose and confirmed by a blood glucose determination of less than 50 mg/dl. A detailed history and blood laboratory profile were obtained for each patient. During the period of the survey a total of 124 diabetic subjects aged 80 yr or older were hospitalised and severe hypoglycaemia was reported in 31 patients (25%). This group of patients had a marked comorbidity and was found to have HbA1c values of 5.1% indicating that their diabetes was well controlled. Of these hypoglycaemic episodes, 23 (74%) occurred in patients taking glibenclamide. Diabetes therapy was prescribed by general practitioners in 24 of these patients. Seventeen subjects concomitantly received drugs that potentiated hypoglycaemia. Only 10 patients performed regular blood glucose self-monitoring. In conclusion, severe hypoglycaemia is a serious and not uncommon problem among elderly patients with T2DM; it is more frequent in patients undergoing aggressive diabetes management and in users of a long-acting sulphonylurea (eg, glibenclamide). A normal HbA1c level in this age group appears to be a powerful indicator of the risk of severe hypoglycaemia and should alert clinicians to change therapy. Finally, each patient's risk for hypoglycaemia should be considered and therapy should be individualised accordingly; in our opinion, a great number of episodes of serious hypoglycaemia may be prevented by teaching the principles of blood glucose monitoring and involving general practitioners in outpatient management of diabetes mellitus in the elderly.

Aged↗

Hypoglycaemia unawareness.

Hypoglycaemia is the most frequent and serious complication of insulin therapy and is three times more common in those who are intensively treated. Impaired awareness of hypoglycaemia is a major limitation to achieving tight diabetes. Asymptomatic biochemical hypoglycaemia occurs more frequently during routine blood glucose monitoring and this should alert the clinician that the individual is developing hypoglycaemic unawareness. Though the etiology of hypoglycaemic unawareness is multifactorial, possible mechanisms include chronic exposure to low blood glucose, antecedent hypoglycaemia, recurrent severe hypoglycaemia and the failure of counter-regulatory hormones. Diabetic patients with history of impaired awareness of hypoglycaemia perform poorly on cognitive function testing and this may be restored by relaxation of glycaemic control. The question of whether human insulin produces hypoglycaemia awareness has been hotly debated but this does not appear to be a major problem considering the number of patients on human insulin. The decision to use one or other of the insulins therefore rests entirely with the physician. Low blood glucose awareness training programmes can help to identify and prevent hypoglycaemia unawareness. Impaired awareness of hypoglycaemia can probably be reversed by scrupulous avoidance of hypoglycaemia.

Awareness↗

Lower incidence of severe hypoglycaemia in patients with type 2 diabetes treated with glimepiride versus glibenclamide.

BACKGROUND: Severe hypoglycaemia is a potentially life-threatening condition. The aim of the present study was to compare the frequency of severe hypoglycaemia in patients with type 2 diabetes treated with glimepiride versus glibenclamide. METHODS: This prospective, population-based, 4-year study examined the incidence of severe hypoglycaemia in a region of Germany with 200 000 inhabitants. The blood glucose of all 30 768 patients who attended the emergency department of the region's central hospital was determined to detect severe hypoglycaemia, which was defined by the requirement for intravenous glucose or glucagon injection and blood glucose value of <2.8 mmol/l. Additionally, 6631/7804 patients (85%) attended to by the emergency medical services received a blood glucose test at the emergency site. The regional prescribing frequency of both sulphonylureas was determined by an independent external institute. RESULTS: Despite glimepiride being prescribed more frequently than glibenclamide (6976 vs 6789 person-years), glimepiride induced fewer episodes of hypoglycaemia (6 vs 38 episodes); one episode occurred with a combination of the two preparations. The incidence of severe hypoglycaemia was 0.86/1000 person-years for glimepiride and 5.6/1000 person-years for glibenclamide. The characteristics of the 45 patients who presented with sulphonylurea-associated hypoglycaemia were as follows: mean age 79 years (95% CI 75.2; 82.6); glycosylated haemoglobin 5.4% (95% CI 5.1; 5.7); impaired renal function in 62%. CONCLUSIONS: In people with type 2 diabetes, glimepiride was associated with fewer episodes of severe hypoglycaemia than glibenclamide in routine clinical use. However, severe hypoglycaemia did occur with glimepiride and may be minimised if treatment targets are determined on an individual basis.

Aged↗

Prolonged but partial impairment of the hypoglycaemic physiological response following short-term hypoglycaemia in normal subjects.

Recent studies have reported reduced endocrine and symptomatic responses to hypoglycaemia 18-24 h after antecedent hypoglycaemia in both non-diabetic subjects and those with insulin-dependent diabetes mellitus. We examined these and peripheral physiological responses in eight non-diabetic subjects aged 23-35 years in the week following antecedent hypoglycaemia. Blood glucose levels were held at plateaus of 5 mmol/l and 2.5 mmol/l for 30 min during hyperinsulinaemic (60 mU x m-2x min-1) morning clamps on days 1, 3 and 8 of two study periods separated by at least 4 weeks. Measurements were made at time 0, 15 and 30 min of each plateau on each day. One the afternoon of Day 1 we also induced either euglycaemia with a blood glucose level of 5 mmol/l (control week) or hypoglycaemia of 2.9 mmol/l (hypo week) for 2 h in random order. The adrenaline response to morning hypoglycaemia (p<0.001 on all days) was attenuated on Day 3 (p<0.05) and Day 8 (p<0.05) compared to Day 1 of hypo week only. Sweating was also attenuated on Day 3 (p<0.05) and Day 8 (p<0.02) of hypo week only. Noradrenaline levels and tremor increased during hypoglycaemia on each study day (p<0.05) but did not differ between days in either week. During hypo week only, the total symptom score response to hypoglycaemia was attenuated on Day 3 (p<0.03) but not Day 8 (p=0.10). Autonomic symptoms were similarly affected. In summary, the physiological responses to hypoglycaemia are affected differentially by antecedent hypoglycaemia with sweating and adrenaline responses remaining impaired for at least adrenaline responses remaining impaired for at least 5 days.

Adult↗

Rate of hypoglycaemia and insulin dosage in children during the initial therapy of type 1 diabetes mellitus.

UNLABELLED: Hypoglycaemia is a major side-effect of insulin treatment. It is known that young children with type 1 diabetes mellitus (T1DM) show a higher risk of hypoglycaemia than older children. This study was performed to analyse the incidence of hypoglycaemia within the first 14 days (day 1-day 14) of insulin treatment in children at the onset of T1DM and to evaluate the influence of age and insulin dosage. The Paediatric Quality Initiative (DPV), including data from 121 centres in Germany and Austria, provided anonymous data of 1,680 patients (age 0.7-18.8 years; 799 girls) at the onset of T1DM. Hypoglycaemia was defined as a blood glucose level (BG) <2.8 mmol/l (50 mg/dl). The hypoglycaemia rate rose continuously from day 2 (4.8%) to day 5 (11.2%) and then remained stable between 8.7%-11.2% until day 14. The hypoglycaemia rate was higher in younger than in older children (P <0.0001). Multiple regression analysis revealed an influence of age (P <0.0001), insulin dosage (P = 0.0034), and route of initial treatment (P = 0.0052) on the hypoglycaemia rate. From day 2 to day 14, the insulin dosage itself was higher in females than in males (P = 0.0147), in patients with high HbA1c (P = 0.0001), high BG (P <0.0001), or low pH (P <0.0001). There was no influence of age on the insulin dosage. CONCLUSION: During the first 14 days after onset of type 1 diabetes mellitus, young children, intravenous-treated patients and patients receiving a high insulin dosage are at particular risk of developing hypoglycaemia. In order to avoid hypoglycaemia, blood glucose should be measured frequently and the insulin dosage should be carefully adjusted. Low blood glucose levels should be treated promptly.

Adolescent↗

Prevention and treatment of hypoglycaemia unawareness in type 1 diabetes mellitus.

Unawareness of hypoglycaemia (reduced ability/failure to recognize hypoglycaemia symptoms at the physiological threshold of 3.0 mmol/l) occurs frequently in type 1 diabetes mellitus, and patients are then at risk for severe hypoglycaemia. Unawareness of hypoglycaemia is the result of earlier frequent episodes of hypoglycaemia (iatrogenic). Likewise, a history of hypoglycaemia induces unawareness, while meticulous prevention of hypoglycaemia can reverse hypoglycaemia unawareness. Therefore, it is essential that insulin therapy regimens for type 1 diabetes mellitus be designed not only to maintain near-normoglycaemia, but also to minimize hypoglycaemia. Such a goal is feasible as long as (1) a rational plan of insulin therapy is adopted, including appropriate use of the short-acting insulin analogue lispro, (2) blood glucose is properly monitored, (3) blood glucose targets are individualized, and (4) education programs are widely implemented.

Awareness↗

Hypoglycaemia after pancreas transplantation: usefulness of a continuous glucose monitoring system.

BACKGROUND: After pancreas transplantation (PTx) some patients report occasional symptoms of hypoglycaemia and at times, serious hypoglycaemia. Continuous blood glucose monitoring (CBGM) allows determination of the daily glucose profile and detection of unrecognized hypoglycaemia. The aims of our study were to determine the incidence of hypoglycaemia in PTx and evaluate whether the use of CBGM helps to detect unrecognized nocturnal hypoglycaemia. PATIENTS AND METHODS: We studied 12 patients (six males) with normal functioning PTx and kidney transplantation for more than 3 yr, with systemic drainage of endocrine secretion and stable immunosuppression. A 24-h CBGM using a microdialysis technique (GlucoDay, A. Menarini Diagnostics, Florence, Italy) was performed in all the patients. RESULTS: Three patients had asymptomatic recorded glucose levels below 3.3 nmol/L during the nocturnal period (01:00-07:00 hours) with the glucose levels during these episodes being 2.6, 2.5 and 2.5 nmol/L, and the duration of nocturnal hypoglycaemia being 27, 62 and 93 min, respectively, rising spontaneously without intervention. Patients with hypoglycaemia presented lower glycosylated haemoglobin levels when compared with those not presenting hypoglycaemic episodes, although basal glucose and insulin levels and insulin antibody titres were similar. In one of the three patients presenting hypoglycaemia CBGM was re-evaluated after including an extra snack at bedtime, with subsequent normalization of the blood glucose profile being observed. CONCLUSION: Unrecognized nocturnal hypoglycaemia is relatively frequent in patients with PTx and 24-h CBMG may be useful to detect these episodes.

Adult↗

Hypoglycaemia induced by exogenous insulin--'human' and animal insulin compared.

AIMS: A systematic review of the literature was carried out to examine whether published evidence suggests a difference in the frequency and awareness of hypoglycaemia induced by 'human' and animal insulin. METHODS: The review identified randomized controlled trials and studies of other designs including observational comparisons, case series and case reports in which the use of 'human' insulin was compared to animal insulin in people with diabetes. These were identified from bibliographic databases and hand-searches of key journals. The main outcome measures were frequency, severity, awareness and symptoms of insulin induced hypoglycaemia. RESULTS: Fifty-two randomized controlled trials, 37 of double-blind design, were identified which included one or more of the relevant outcome measures. Of these, 21 specifically investigated hypoglycaemic frequency and awareness as primary outcomes (six in people with previously reported reduced hypoglycaemic awareness). The remainder of the identified trials reported hypoglycaemic outcomes as a secondary or incidental outcome during comparative investigations of efficacy or immunogenicity. Seven of the double-blind studies reported differences in frequency of hypoglycaemia or awareness of symptoms, although none of the studies which selected subjects on the basis of previously reported impaired awareness demonstrated significant differences between insulin species. Four of the unblinded trials reported differences in hypoglycaemia. This reached statistical significance in two of the studies. A further 56 studies of other designs and case reports were considered. In addition to the 10 case reports describing individuals with impaired hypoglycaemic awareness, nine studies reported differences in the incidence and manifestation of hypoglycaemia during 'human' insulin treatment. Notably, none of the four population time trend studies found any relationship between the increasing use of 'human' insulin and hospital admission for hypoglycaemia or unexplained death among those with diabetes. The largest case series could find no support for the hypothesis that an influence of treatment with 'human' insulin on hypoglycaemia had contributed to any of the 50 deaths investigated. When all types of studies considered are ranked in order of rigour (according to the accepted 'hierarchy of evidence'), it is the least rigorous which lend most support to the notion that treatment with 'human' insulin has an effect on the frequency, severity or symptoms of hypoglycaemia. CONCLUSIONS: Evidence does not support the contention that treatment with 'human' insulin per se affects the frequency, severity or symptoms of hypoglycaemia. However, a number of studies, mainly those of less rigorous design, describe an effect when people are transferred from animal insulin to 'human' insulin. It is not possible to state how common this is or whether the phenomenon is specific to 'human' insulin or an effect resulting from stricter glycaemic control (perhaps compounded, in some cases, by neurological complications in long-standing diabetes). This remaining uncertainty makes it essential that insulin from animal sources continues to be available so that clinicians and patients may retain this choice of treatment.

Animals↗

Risk of hypoglycaemia with oral antidiabetic agents in patients with Type 2 diabetes.

In patients with Type 2 diabetes, the appropriate intensity of glucose control is determined by age, life expectancy, and the presence of concomitant disease. Geriatric patients are especially susceptible to hypoglycaemia and therefore particular care should be taken in this group characterized by polypharmacy, renal or hepatic dysfunction, cardiovascular multimorbidity and malnutrition. As hypoglycaemia is a significant cause of morbidity and mortality, treatment regimens for diabetes should minimize the occurrence of hypoglycaemic episodes and be tailored to the patient's individual needs. The pharmacological options for treating Type 2 diabetes have increased considerably and the risk of hypoglycaemia of the currently available drugs varies considerably. Metformin, thiazolidinediones, and acarbose, oral antidiabetic drugs that decrease insulin resistance or postprandial glucose absorption, are associated with a low risk of hypoglycaemia. These drugs can also be used effectively in various combination regimens; however, by improving insulin sensitivity, combinations of metformin and thiolidinediones with sulphonylureas or meglitinides may considerably increase the risk of hypoglycaemia. On account of its complex pharmacoprofile glibenclamide is a problematic substance carrying a high risk of hypoglycaemia. There are limited preliminary data indicating that, under routine conditions, glimepiride may be associated with a lower risk of hypoglycaemia than glibenclamide and is no more likely to cause hypoglycaemia than other shorter-acting agents such as gliclazide and glipizide. Nateglinide and repaglinide as short-acting insulin secretagogues may be associated with a reduced risk of hypoglycaemia compared with glibenclamide, in particular when dosed flexibly. Repaglinide might be beneficial in individuals with renal impairment.

Clinical Trials as Topic↗

Hypoglycaemia in a Nigerian paediatric emergency ward.

Hypoglycaemia is a common problem in paediatric emergency admissions. It has not received enough attention in Nigeria. It has been shown to complicate many childhood illnesses. This study aimed to determine the prevalence of hypoglycaemia in paediatric emergency admissions, describe clinical factors that commonly predispose to it and investigate its effect on outcome of management. Three-hundred and ninety-two consecutively admitted patients were studied. Two milliliters of blood was obtained from each patient for plasma glucose determination. Hypoglycaemia was defined as plasma glucose <2.5 mmol/l (<45 mg/dl). Out of these 392, twenty-five (25) of them were hypoglycaemic giving a prevalence of hypoglycaemia to be 6.4 per cent in our emergency ward. Hypoglycaemia was found to be associated commonly with severe malaria, septicaemia, pneumonia, and protein energy malnutrition. Interval of last meal and unconsciousness were the only two significant associated factors to hypoglycaemia. However, the likelihood of hypoglycaemia is increased with night admissions and prolonged duration of illness before admissions. Presence of hypoglycaemia at admission was also found to be significantly associated with death and dying within 24 hours of admission. The prevalence of hypoglycaemia was found to be 6.4 per cent. It was found to complicate many childhood illnesses and it is associated with a higher mortality. It should be suspected in all very ill children, particularly when they are unconscious and have not eaten for over 12 hours.

Child↗

Cerebral glutamate metabolism during hypoglycaemia in healthy and type 1 diabetic humans.

BACKGROUND: The mechanisms responsible for the progressive failure of hypoglycaemia counterregulation in long-standing type 1 diabetes are poorly understood. Increased brain glucose uptake during hypoglycaemia or alterations of brain energy metabolism could effect glucose sensing by the brain and thus contribute to hypoglycaemia-associated autonomic failure. MATERIALS AND METHODS: Type 1 diabetic patients (T1DM) and healthy volunteers (CON) were studied before, during and after a hypoglycaemic (50 mg dL(-1)) hyperinsulinaemic (1.5 mU kg(-1) min(-1)) clamp test. The (1)H magnetic resonance spectroscopy of the occipital lobe of the brain was performed employing the STEAM localization technique. The water signal was suppressed by the modified SWAMP method. All spectra were acquired on a 3 Tesla scanner (80 cm MEDSPEC-DBX, Bruker Medical, Ettlingen, Germany) using a 10-cm diameter surface coil. RESULTS: During hypoglycaemia, T1DM showed blunted endocrine counterregulation. At baseline the brain tissue glucose : creatine ratio was lower in CON than in T1DM (CON 0.13 +/- 0.05 vs. T1DM 0.19 0.11; P < 0.01). During hypoglycaemia glucose : creatine ratios decreased in both groups (CON 0.07 +/- 0.08, P < 0.05; T1DM 0.03 +/- 0.03, P < 0.001). A significant drop in the glutamate : creatine ratio could only be found in CON during hypoglycaemia (CON 1.36 +/- 0.08 vs. 1.26 +/- 0.11; P < 0.01; T1DM 1.32 +/- 0.13 vs. 1.28 +/- 0.15; P = NS). The ratios of glutamine, N-acetylaspartate, choline and myo-inositol : creatine were not different between both groups and did not change throughout the experiment. CONCLUSIONS: Only in CON does moderate hypoglycaemia reduce intracerebral glutamate concentrations, possibly owing to a slower substrate flux through the tricarboxylic acid cycle in neurones. The maintenance of normal energy metabolism in T1DM during hypoglycaemia might effect glucose sensing in the brain and contribute to hypoglycaemia-associated autonomic failure.

Adult↗