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PubMed2004

Cortisol and growth hormone responses to spontaneous hypoglycaemia in infants and children.

AIMS: To evaluate responses of cortisol and growth hormone (GH) to spontaneous hypoglycaemia in infants and children. METHODS: Retrospective review of laboratory and clinical data in paediatric patients investigated for suspected hypoglycaemia over a five year period. Thirty patients (16 aged <3 months) had hypoglycaemia confirmed by laboratory analysis (glucose <2.5 mmol/l) and were compared with 26 patients (11 aged <3 months) with glucose > or =2.5 mmol/l. RESULTS: The commonest causes of hypoglycaemia were transient hyperinsulinism in infants <3 months and intercurrent infection in those >6 months of age. In both hypo- and non-hypoglycaemic patients, cortisol was positively (r(s) +0.66 and +0.68) and GH inversely (r(s) -0.65 and -0.75) correlated with age. Hypo- and non-hypoglycaemic infants <3 months had median cortisol concentrations of 205 and 116 nmol/l respectively compared with 1370 and 736 nmol/l in hypo- and non-hypoglycaemic children >6 months. Conversely, median GH was 46.5 and 51.2 mU/l in hypo- and non-hypoglycaemic infants compared with 14.3 and 12.1 mU/l in older hypo- and non-hypoglycaemic patients. Older non-hypoglycaemic patients with glucose levels below the glycaemic thresholds established for cortisol and GH secretion in adults had higher cortisol and GH concentrations than patients whose glucose levels exceeded these thresholds. CONCLUSIONS: Cortisol and GH responses to spontaneous hypoglycaemia in children are highly age dependent. Young infants mount a poor cortisol response compared with older infants and children. Children older than 6 months may have glycaemic thresholds for cortisol and GH similar to those established for adults.

Blood Glucose↗

PubMed1975

Neontal hypoglycaemia in infants of insulin-dependent diabetic mothers.

Neonatal hypoglycaemia (blood glucose smaller than 20 mg/100 ml) occurred in the first 6 hours of life in 25 of 34 infants born to diabetic mothers receiving insulin. Despite severe hypoglycaemia (blood glucose smaller than 10 mg/100 ml) in 17, clinical features of hypoglycaemia were absent in all but 2. Hypoglycaemia was not related either to the level of plasma insulin in cord blood, determined as nonextracted immunoreactive insulin, or to the degree of control of maternal blood glucose during pregnancy. The frequent occurrence of severe neonatal hypoglycaemia in the infants born to diabetic mothers receiving insulin appears to be due rather to failure to maintain basal glucose homoeostasis after birth than to hyperinsulinism.

Adult↗

PubMed2003

Prevention of severe hypoglycaemia in type I diabetes: a randomised controlled population study.

AIMS: To investigate use of targeted self study material in type I diabetes patient education regarding dissemination, perceived patient benefit, and prevention of severe hypoglycaemia. METHODS: In a randomised 1:1:1 controlled study, 332 patients with type I diabetes (aged 2.6-18.9 years) were studied; 313 completed clinical follow up, 261 completed endpoint questionnaire. The intervention group received videotapes and a brochure designed to review skills for self control and treatment, aimed at preventing severe hypoglycaemia. Two control groups received a videotape and brochure with general diabetes information, or traditional treatment only, respectively. RESULTS: Yearly incidence of severe hypoglycaemia decreased from 42% to 27% in the intervention group, but not in controls. HbA1c remained unchanged. Levels of use ranged from 1 to 20 times (median 2); 40-49% had shown the materials to friends, relatives, school staff, sports coaches, etc (there was little difference between intervention and control groups). Higher benefit and learning levels resulted from the intervention material, especially in patients with severe hypoglycaemia. CONCLUSIONS: Mass distributed pedagogical devices such as high quality video programmes and brochures may contribute to the prevention of severe hypoglycaemia. Such self study materials can reach high dissemination levels and constitute a cost effective complement to regular visits to a diabetes team and to other types of education. The findings may have implications for other topics, other ages, and other diagnosis groups.

Adolescent↗

PubMed1988

Glycaemic threshold for changes in electroencephalograms during hypoglycaemia in patients with insulin dependent diabetes.

The relation between blood glucose concentration, the symptoms and signs of hypoglycaemia, and electroencephalographic changes in diabetic patients is not known. The effect of hypoglycaemia on brain function was studied in 13 patients with insulin dependent diabetes. During a gradual fall in blood glucose concentration induced by a bolus injection of insulin followed by an intravenous infusion of insulin, during 60 minutes of biochemical hypoglycaemia, and after restoration of normoglycaemia with intravenous glucose electroencephalograms were evaluated continuously by period-amplitude analysis; blood samples were taken every 10 minutes throughout. No changes were seen in electroencephalograms when the blood glucose concentration was above 3 mmol/l. At a median blood glucose concentration of 2.0 (95% confidence interval 1.7 to 2.3) mmol/l alpha activity decreased abruptly in the electroencephalograms concomitant with an increase in theta activity, reflecting neuronal dysfunction in the cortex. When the blood glucose concentration was further lowered changes were observed in the electroencephalograms indicating that deeper brain structures were affected. A normal electroencephalogram was re-established at a blood glucose concentration of 2.0 (1.8 to 2.1) mmol/l. There was no significant correlation between the blood glucose concentration at the onset of changes in the electroencephalograms and age, duration of diabetes, insulin dose, haemoglobin A1c concentration, initial blood glucose concentration, rate of fall in blood glucose concentration, and appearance of symptoms and signs of hypoglycaemia. Changes in electroencephalograms during hypoglycaemia appear and disappear at such a narrow range of blood glucose concentrations that the term threshold blood glucose concentration for the onset of such changes seems justified.

Adult↗

PubMed1997

A comparison of glucagon and glucose in prehospital hypoglycaemia.

OBJECTIVE: To compare intramuscular glucagon with intravenous glucose in the prehospital management of hypoglycaemia in adults. METHODS: In the first part of the trial all UK ambulance services were asked how their personnel treat prehospital episodes of hypoglycaemia. In the second part, two protocols for treating prehospital hypoglycaemia were studied. In phase 1, intramuscular glucagon 1 mg was used. In phase 2, intravenous glucose 25 g was used; if intravenous access was not possible, intramuscular glucagon was given. RESULTS: 33 out of 43 respondent ambulance services (76.7%) only use glucagon for prehospital hypoglycaemia; the remaining services use glucose and glucagon. In the second part of the study the median duration from diagnosis to full orientation (Glasgow coma score 15) was 28 minutes (95% confidence interval 18 to 49 minutes) in phase 1 and 11 minutes (95% confidence interval 8 to 19 minutes) in phase 2. This difference is statistically significant (P < 0.005). On-scene times were not significantly different. CONCLUSIONS: Intravenous glucose is the treatment of choice in prehospital hypoglycaemia but glucagon should also be available for intramuscular use when intravenous access is not possible.

Adult↗

PubMed1996

Comparison of two cotside methods for the detection of hypoglycaemia among neonates in Nepal.

AIMS: To compare two cotside methods of blood glucose measurement (HemoCue and Reflolux II) against a standard laboratory method for the detection of neonatal hypoglycaemia in a developing country maternity hospital where hypoglycaemia is common. METHODS: 94 newborn infants and 75 of their mothers had blood glucose assessed on the same venous sample using three different methods in the Special Care Baby Unit and postnatal wards, Prasuti Griha Maternity Hospital, Kathmandu, Nepal: HemoCue and Reflolux II at the cotside; Roche Ultimate glucose oxidase method (GOM) in the laboratory. RESULTS: The mean (SD) values for blood glucose in newborn infants were GOM 2.5 (1.1) mmol/l; Reflolux II 2.1 (0.9); and HemoCue 4.2 (1.2). For mothers the values were GOM 5.3 (1.2) mmol/l; Reflolux II 3.6 (1.2); and HemoCue 5.6 (1.0). Bland-Altman plots showed that Reflolux II consistently underreads GOM blood glucose in neonates by 0.5 mmol/l (SD 0.7) and that HemoCue overreads glucose by 1.7 mmol/l (SD 0.8). For the detection of hypoglycaemia (< 2.0 mmol/l), Reflolux II achieved a sensitivity of 83%, a specificity of 62%, and a likelihood ratio of 2.2. HemoCue produced a sensitivity of 0% and a specificity of 100% using measured values. If 2.0 mmol were subtracted from all Hemocue values this rose to 81% and 68% and a likelihood ratio of 2.5. CONCLUSION: Although more accurate than Reflolux II for the measurement of blood glucose in mothers, HemoCue overreads glucose concentrations in neonates and is therefore potentially dangerous as a screening method for neonatal hypoglycaemia. Reflolux II is useful as a screening method for high risk infants (low birthweight, post-term) and could achieve a post-test probability of detecting hypoglycaemia in a high risk setting like Nepal of 50-60%.

Adult↗

PubMed2000

Neonatal hypoglycaemia and withdrawal symptoms after exposure in utero to valproate.

AIMS: To define, in a prospective study, the risk of hypoglycaemia-defined as blood glucose concentration < 1.8 mmol/l-in term infants exposed in utero to valproate and to describe the withdrawal symptoms. METHODS: Twenty epileptic women were treated with valproate only during pregnancy and two were treated with valproate and carbamazepine. In the first trimester, the daily median dose of valproate was 1.0 g (range 0.3-4.2) and in the third trimester 1.2 g (range 0.3-4.8). RESULTS: Thirteen of the 22 infants became hypoglycaemic. One infant had eight episodes of hypoglycaemia, one had three episodes, two had two episodes, and nine had one episode each. The lowest blood glucose concentration was 1.0 mmol/l. All episodes were asymptomatic. The maternal mean plasma concentration of total valproate during the third trimester correlated negatively with blood glucose concentration one hour after delivery (p < 0.0003) and with the development of hypoglycaemia (p < 0.0001). There was no evidence for hyperinsulinaemia as the cause of hypoglycaemia. Ten infants developed withdrawal symptoms, which correlated positively with the mean dose of valproate in the third trimester and the concentration of the free fraction of valproate in maternal plasma at delivery (p < 0.02). CONCLUSIONS: Infants exposed to valproate in utero had a significantly elevated risk of hypoglycaemia, and withdrawal symptoms were often observed.

Anticonvulsants↗

PubMed1969

Insulin response to carbohydrate ingestion after gastric surgery with special reference to hypoglycaemia.

Factors responsible for spontaneous hypoglycaemia were investigated in 23 gastrectomy patients and two patients with vagotomy and pyloroplasty. Plasma insulin and capillary blood glucose levels were followed after giving 175 ml of 50% glucose orally. In gastrectomy patients a significant correlation was found between the height of the peak blood glucose and insulin levels for the same individual. Patients with high peak glucose and insulin levels were significantly more likely to develop hypoglycaemia later in the test. These findings are compatible with the suggestion that the major factor predisposing to hypoglycaemia is a faster than average rate of emptying of the gastric remnant, but this does not explain all the results. In two cases, hypoglycaemia followed an abnormally large insulin response to oral glucose. The results of insulin injection tests in 14 patients do not exclude the further possibility that in some cases hypoglycaemia is due to excessive insulin sensitivity.

Adult↗

PubMed1979

An insulinoma presenting with reactive hypoglycaemia.

A 57-year-old woman presented with symptoms which were cured by the removal of an insulinoma. The case was atypical in that symptomatic hypoglycaemia occurred only after meals or glucose administration but never during fasting, and thus if plasma insulin activity had not been measured an incorrect diagnosis of reactive hypoglycaemia might have been made on the basis of symptoms and oral glucose-tolerance test. Reactive hypoglycaemia resulted from an increased rate of glucose assimilation and possibly also from a decreased rate of gluconeogenesis due to the immense insulin secretion provoked by glucose or food. The findings suggest that a diagnosis of hypoglycaemia should not be made until the possibility of an insulinoma has been excluded by measurement of plasma insulin activity during a period of hypoglycaemia.

Adenoma, Islet Cell↗

PubMed1987

Nocturnal convulsions and insulin-induced hypoglycaemia in diabetic patients.

Convulsions may occur as a consequence of insulin-induced hypoglycaemia. We report three patients with insulin-dependent diabetes, who presented with generalized tonic-clonic seizures associated with nocturnal hypoglycaemia. None of the patients had experienced hypoglycaemia during waking hours and the convulsions were mistakenly diagnosed as idiopathic epilepsy. Recognition of the possible hypoglycaemia aetiology of these convulsions permitted appropriate alteration of the insulin regimens with no recurrence of convulsions. In one case, the seizure was associated with bilateral fractures of the neck of the humerus. Unrecognized hypoglycaemia should be considered as a possible cause of convulsions in insulin-dependent diabetic patients.

Adult↗

PubMed2005

Severe hyperinsulinaemic hypoglycaemia in a baby born to a mother taking oral ritodrine therapy for preterm labour.

Hyperinsulinism of infancy is a major cause of persistent hypoglycaemia in the newborn period. Transient mild self-limiting hyperinsulinaemia and hypoglycaemia have been described in neonates born to mothers taking ritodrine therapy for premature labour. Ritodrine crosses the placental barrier and enters the fetal circulation readily but the mechanism of how it causes hyperinsulinaemia and hypoglycaemia is unclear. We report the case of severe prolonged hyperinsulinaemic hypoglycamia in a neonate born to a mother taking ritodrine therapy from 16 weeks' gestation for preterm labour. The hyperinsulinaemic hypoglycaemia was managed with oral nifedipine as diazoxide was contraindicated due to fluid overload. Possible mechanisms of ritodrine-induced hypoglycaemia and insulin secretion are discussed.

Adult↗

PubMed1992

Cognitive and psychomotor function during severe insulin-induced hypoglycaemia in insulin-dependent diabetic patients.

Cognitive and psychomotor function, hormonal counterregulation and symptom awareness during severe insulin-induced hypoglycaemia were evaluated in 10 insulin-dependent diabetic patients. The glucose-clamp technique (Biostator) was applied to achieve a stable hypoglycaemic (39 +/- 2 mg/dl) plateau. A battery of 7 neuropsychological tests and a standardized questionnaire assessing hypoglycaemia symptoms were administered during euglycaemia and hypoglycaemia. There was a significant increase in counterregulatory hormone response (cortisol, growth hormone, p less than 0.05). Every patient experienced symptoms during severe hypoglycaemia. Four patients, however, were not aware of this threatening metabolic state. There was a significant performance decrement in all but two neuropsychological tests (Aiming Center I, Aiming Center II, Line Tracing Errors, Reaction Time, p less than 0.01; Digit Symbol, p less than 0.05). Performance of simple motor tasks as well as cognitive tasks requiring complex discrimination deteriorated similarly. Furthermore, the patients' general well-being (subjective condition) worsened considerably. In conclusion, a significant impairment of neuropsychological functions emerged during severe hypoglycaemia in insulin-dependent diabetes mellitus, even in the face of adequate hormonal counterregulation, and did not always coincide with an appropriate patient awareness of the actual metabolic state.

Adult↗

PubMed1984

Insulin hypoglycaemia test guided by a glucose controlled insulin infusion system.

Insulin hypoglycaemia test (IHT) for assessment of hypothalamic-pituitary-adrenocortical (HPA) function in patients with pituitary tumours is usually performed by bolus injection of insulin, a procedure which includes the risk of overdosage and/or the need of repeated administration. This study describes that a glucose controlled insulin infusion system (GCIIS) permits to perform the IHT with standardized hypoglycaemia. Ten healthy volunteers and 10 patients with pituitary tumours were studied using the GCIIS (Biostator) on static control (Mode 1:1, BI 35, QI 10, RI 20, FI 300). Insulin administration was discontinued and the GCIIS used only for monitoring of blood glucose (BG), when BG had fallen below 40 mg/dl and initial clinical symptoms for hypoglycaemia were observed. In controls, the GCIIS guided IHT achieved a sufficient degree of hypoglycaemia (BG 27.6 +/- 2.0 mg/dl; mean +/- SEM) and physiological responses for GH (peak 49.4 +/- 6.7 ng/ml), Prl (peak 1766 +/- 614 microU/ml), ACTH (peak 76.0 +/- 8.7 pg/ml) and cortisol (peak 252 +/- 15 ng/ml). The total amount of insulin given was 0.115 +/- 0.012 U/kg. In the patients with pituitary tumours however, the required insulin dose varied markedly from 0.090 (pituitary insufficiency) to 0.340 U/kg (Cushing's syndrome). Minimum BG obtained was 32.5 +/- 1.9 mg/dl. Partial impairment of hypothalamic-pituitary function and, in particular, patients requiring exogenous cortisol supplementation during stress, could be identified. In conclusion, special advantages of the GCIIS-guided IHT are: Optimal insulin dosage with standardized hypoglycaemia due to automatic adjustment to the individual insulin sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1987

Glucoregulatory hormone response to insulin-induced hypoglycaemia following long-term calcium antagonism with felodipine in patients with essential hypertension.

The effect of 8 weeks' treatment with the dihydropyridine calcium antagonist felodipine on glucoregulatory hormone response following insulin-induced hypoglycaemia was evaluated in 7 patients with essential hypertension, WHO grade I-II. After an iv insulin injection (0.1 IU/kg), blood glucose decrement and nadir were similar before and during felodipine treatment. Basal glucagon, noradrenaline, adrenaline, GH and cortisol levels were unchanged, and the response to insulin-induced hypoglycaemia was similar before and during felodipine treatment. Basal plasma dopamine levels were similar and did not change during insulin-induced hypoglycaemia before and during felodipine treatment. Basal serum levels of TSH, T3 and T4 were unaltered following felodipine. In conclusion, long-term treatment with felodipine did not alter the hypoglycaemic effect of exogenous insulin, or the recovery from hypoglycaemia or the glucoregulatory hormone response to insulin-induced hypoglycaemia in patients with essential hypertension.

Adult↗

PubMed1997

Late post-prandial hypoglycaemia as the sole presenting feature of secreting pancreatic beta-cell adenoma in a subtotally gastrectomized patient.

In this paper we describe for the first time late post-prandial hypoglycaemia as the sole presenting feature of an insulinoma in a patient who had previously undergone subtotal gastrectomy. The symptoms of hypoglycaemia always occurred 1-3 h after meals, not in the fasting state. Because of the history of gastrectomy and because post-prandial hypoglycaemia was reproduced by an oral glucose tolerance test, the diagnosis of reactive hypoglycaemia was made. Eighteen months later a fasting test was performed: venous plasma glucose decreased from 3.8 mmol/l to 2.7 mmol/l between 14 and 20 h of fast while plasma immunoreactive insulin did not decrease and plateaued at 185 pmol/l. Plasma C-peptide (0.9 nmol/l) and proinsulin (70 pmol/l, split 64, 65) were also elevated. All islet hormones increased in response to i.v. glucose and were suppressed after diazoxide. Although pre-operative procedures were negative in localizing an insulinoma, the patient underwent an operation and an insulinoma was detected at the body level of the pancreas. Thus, insulinoma should be considered in the differential diagnosis of reactive hypoglycaemia in gastrectomized patients. Response of islet hormones to glucose and their suppression by diazoxide are evidence of a secreting insulinoma even in the absence of preoperative localization of the pancreatic adenoma.

Blood Glucose↗

PubMed1998

Dose-related effects of growth hormone on IGF-I and IGF-binding protein-3 levels in non-islet cell tumour hypoglycaemia.

Mesenchymal tumours are a well recognised cause of spontaneous hypoglycaemia. The mechanism is thought to relate to hypersecretion by tumour cells of high molecular mass insulin-like growth factor-II (pro-IGF-II), with consequent suppression of growth hormone (GH) secretion. The use of recombinant human (rh)GH has been reported to alleviate hypoglycaemia in non-islet cell tumour hypoglycaemia, and the mechanism is thought to relate to GH-mediated increments in serum levels of IGF-binding protein-3 (IGFBP-3), thereby reducing the bioavailability of IGF-II. We report the effect of increasing doses of rhGH on the clinical condition and serum IGF-I and IGFBP-3 levels in two patients with solitary pleural fibrous tumours causing severe hypoglycaemia. Hypoglycaemia was successfully alleviated in each patient although, despite using large doses of rhGH, the observed increments in IGFBP-3 were only modest. We postulate that the beneficial effects of rhGH in this situation are likely to be multifactorial and not simply related to increments in serum IGFBP-3 levels.

Aged↗

PubMed1987

Plasma Met-enkephalin and catecholamine responses to insulin-induced hypoglycaemia in greyhounds.

The involvement of endogenous opioid peptides in the stress response was investigated by measuring plasma concentrations of Met-enkephalin-like immunoreactivity (MLI), adrenaline and noradrenaline during insulin-induced hypoglycaemia in conscious greyhounds. Moreover, the molecular forms of circulating MLI were characterized using gel filtration chromatography. In the first group of animals, i.v. administration of insulin (0.3 units/kg) provoked marked hypoglycaemia (blood glucose concentrations fell from 4.4 +/- 0.1 to 1.5 +/- 0.2 mmol/l; mean +/- S.E.M.) which was associated with significant (P less than 0.001) rises in plasma MLI concentrations from a basal concentration of 45 +/- 8 to a peak of 189 +/- 39 ng/l. A within-subject study comparing five different insulin doses ranging from 0.004 to 0.3 units/kg showed dose-related effects on blood glucose with nadir concentrations of 4.1 +/- 0.6 mmol/l (after the smallest dose of insulin) and 0.8 +/- 0.1 mmol/l (after the largest dose of insulin). This was associated with dose-related rises in plasma MLI with peak concentrations of 56 +/- 17 and 558 +/- 35 ng/l, plasma adrenaline with peak concentrations of 0.45 +/- 0.06 and 15.76 +/- 1.33 nmol/l and plasma noradrenaline with peak concentrations of 0.49 +/- 0.07 and 2.27 +/- 0.45 nmol/l following the smallest and largest doses of insulin respectively. These results are the first demonstration of raised plasma MLI concentrations following hypoglycaemia. Moreover, they show that the hormonal responses vary with the degree of hypoglycaemia achieved. Together with reports by other investigators these findings might suggest opioid modulation of the responses of the sympathoadrenal system to hypoglycaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

Persistent hyperinsulinaemic hypoglycaemia of infancy: case report.

Hyperinsulinism, although rare, is the most common cause of persistent hyperinsulinaemic hypoglycaemia in infancy. Because of persistent hypoglycaemia, serious difficulties are encountered in the long term management of this condition. A male neonate, after an uncomplicated full-term pregnancy, had been admitted to another hospital with convulsions on the third post-natal day. Meningitis had been suspected at that time and treated with phenobarbital and he had been discharged from the hospital. At three-months old he was referred to our department for persistent convulsions and lethargy. His parents were of 1st degree consanguinity. His blood glucose level was found to be 24 mg/dl (1.33 mmol/L). Because of the dangerously high insulin level during hypoglycaemia (insulin/glucose > 0.3), the absence of ketonuria, and the need for a high dose of glucose infusion (> 15 mg/kg/min) to achieve normoglycaemia and a glycaemic response to glucagon despite the hypoglycaemia, a diagnosis of persistent hyperinsulinaemic hypoglycaemia of infancy was made. Since maximal doses of prednisone, glucagon, diazoxide, octreotide and high infusion of glucose were ineffective in achieving normoglycaemia, a subtotal (80%) pancreatectomy was done. Postoperatively intermittent hypoglycaemic episodes continued. These were controlled with low doses of octreotide. Histology revealed diffuse adenomatous hyperplasia (nesidoblastosis). The boy is now in the sixth post-operative month and developing normally.

Anti-Inflammatory Agents↗