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PubMed1996

Is autonomic neuropathy a risk factor for severe hypoglycaemia? The EURODIAB IDDM Complications Study.

The hypothesis that diabetic patients with autonomic neuropathy are at increased risk of severe hypoglycaemia was examined in an epidemiological study of over 3000 IDDM patients in Europe (EURODIAB IDDM Complications Study). Autonomic function was assessed by two standard cardiovascular tests: change in heart rate and systolic blood pressure on standing. Severe hypoglycaemia was defined as an attack serious enough to require the help of another person. Compared to patients (68%) reporting no attacks in the last year, those reporting one or more attacks were older (34.0 +/- 10.7 vs 32.1 +/- 9.9 years, mean +/- SD, p < 0.0001), had had diabetes for a longer period (16.6 +/- 9.5 vs 13.8 +/- 9.1 years, p < 0.0001), had better glycaemic control (HbA1c 6.4 +/- 1.8 vs 6.9 +/- 1.9%, p < 0.0001) and were more likely (p = 0.002) to have abnormal responses to both autonomic tests (13.0 vs 7.7%). A single abnormal autonomic response was not associated with an increased risk of severe hypoglycaemia. The odds ratio for severe hypoglycaemia in people with abnormal responses to both autonomic tests, compared to those with normal responses, was 1.7 (95% confidence interval 1.3, 2.2) after controlling for age, duration of diabetes, glycaemic control and study centre. In conclusion, a combined autonomic deficit in heart rate and blood pressure responses to standing is associated with only a modest increase in the risk of severe spontaneous hypoglycaemia. Although the increase in risk is not large, severe hypoglycaemia was a frequently reported event in this study. IDDM patients with deficient autonomic responses who strive for tight glycaemic control may therefore be at particular risk of severe hypoglycaemia.

Adult↗

PubMed2005

Ketotic hypoglycaemia in children with diazoxide responsive hyperinsulinism of infancy.

UNLABELLED: Hyperinsulinism of infancy (HI) is a cause of persistent and recurrent hypoglycaemia in infancy and childhood, which if untreated can cause significant brain damage and mental retardation. The biochemical hallmark of hyperinsulinism is hypofattyacidaemic, hypoketotic hyperinsulinaemic hypoglycaemia. Diazoxide is the first line medical treatment for persistent HI. Diazoxide is an agonist of the pancreatic beta-cell KATP channel and inhibits insulin secretion. Children who develop recurrent hypoglycaemia while on therapy with diazoxide are thought to be unresponsive to this medication or non compliant with medical therapy. We report a novel observation of "ketotic" hypoglycaemia in two children on diazoxide therapy for persistent HI. Detailed assessment of the intermediary metabolites and hormones at the time of the hypoglycaemia showed appropriate insulin suppression with appropriate increases in the serum levels of non-esterified fatty acids and ketone bodies as well as an intact counter-regulatory hormone response. The precise mechanism of the hypoglycaemia is unclear. CONCLUSION: These cases illustrate that recurrent hypoglycaemia while on diazoxide therapy may be due to other mechanisms and does not imply diazoxide unresponsiveness or non-compliance.

Congenital Hyperinsulinism↗

PubMed1998

Anti-insulin antibodies may cause hypoglycaemia following pancreas transplantation.

Some pancreas transplantation (PTX) recipients experience hypoglycaemia after transplant. We studied the incidence and pattern of hypoglycaemic symptoms following PTX and later studied the glucose and pancreatic hormone response to Sustacal in patients with and without hypoglycaemia following PTX. In a survey of 54 PTX recipients who were 2 to 33 months post-transplant, 29 reported symptoms of hypoglycaemia at any time following their transplant. Of 12 patients who tried to document their blood glucose during any episode, 5 had a blood glucose less than 3.3 mmol/l, and another 5 documented a blood glucose from between 3.33 and 3.88 mmol/l. The patients reporting symptoms were less likely to be insulin resistant with longer time post-PTX, lower body mass index (BMI), and on lower doses of prednisone. Later, 12 patients with established, repeated episodes of hypoglycaemia following PTX were case-matched to PTX recipients without hypoglycaemic symptoms. Fasting glucose, free and total immunoreactive insulin (IRI), C-peptide, proinsulin and glucagon were measured following a 4 h Sustacal challenge. The hypoglycaemic group was further divided into those whose glucose rose after Sustacal (Hypo-High) and those whose blood glucose did not rise from baseline concentration (Hypo-Flat). The Hypo-High subgroup had a lower fasting free/total IRI ratio in addition to a greater increase in blood glucose after Sustacal compared with either Hypo-Flat or non-hypoglycaemic transplant recipients. The low free/total insulin ratio and hyperglycaemic response to Sustacal are consistent with the presence of anti-insulin antibodies, an established cause of hypoglycaemia. In summary, documented hypoglycaemia, while uncommon, may occur and be significant following PTX. Anti-insulin antibodies may be one of the many factors contributing to hypoglycaemia in this population.

Adult↗

PubMed2005

The Glu23Lys polymorphism in KCNJ11 and impaired hypoglycaemia awareness in patients with type 1 diabetes.

Impaired awareness of hypoglycaemia affects approximately 25% of all patients with type 1 diabetes (T1D). Duration of diabetes and tight glycaemic control represent the main risk factors for hypoglycaemia unawareness. However, even among patients with good glycaemic control and longstanding T1D, awareness of hypoglycaemia may be intact. Genetic factors might explain some of this remaining variability, and genes involved in central glucose sensing should represent plausible candidates. Some evidence indicates that ventromedial hypothalamus glucose-responsive neurons require the potassium inward rectifier (KIR) 6.2 subunit of the K(ATP) channel to sense glucose. Therefore, the effects of the Glu23Lys polymorphism in the KCNJ11 (KIR6.2) gene (potassium inwardly rectifying channel, subfamily J, member 11) on impaired hypoglycaemia awareness in 217 patients with T1D were studied. Hypoglycaemia awareness status was determined using standardized questionnaires. Genotyping of the Glu23Lys in a cohort of T1D subjects was done using the TaqMan allelic discrimination assay (frequency of the Lys-allele = 0.35; P = 0.57 for Hardy-Weinberg equilibrium). The study confirms that diabetes duration, C-peptide, and HbA(1c) represent risk factors for impaired hypoglycaemia awareness. However, no significant effect of the Glu23Lys polymorphism on impaired hypoglycaemia awareness was observed with or without adjustment for age, diabetes duration, C-peptide, and HbA(1c). Even though the study provides a relatively large dataset, it is possible that small differences may have been missed.

Adult↗

PubMed2004

Food cravings during acute hypoglycaemia in adults with Type 1 diabetes.

BACKGROUND: Food craving is defined as an intense desire to eat a specific foodstuff. It may be distinguished from the sensation of hunger, which is relieved by nonspecific foodstuffs. No controlled studies have examined the effects of hypoglycaemia on food cravings. Thus, the aim of this study was to examine change in cravings for eight specified food types during euglycaemia and insulin-induced hypoglycaemia. METHODS: Thirteen adults with Type 1 diabetes attended two experimental sessions where acute hypoglycaemia was induced with either insulin aspart or human soluble insulin. Food cravings were assessed, using a questionnaire, at baseline and at the onset of the autonomic reaction to hypoglycaemia ("R"). RESULTS: The mean arterialised blood glucose concentration at baseline was 6.0+/-0.3 mmol l(-1) and at R was 1.9+/-0.4 mmol l(-1) (P<.01). Fifteen percent of subjects reported having a craving for food during euglycaemia. The prevalence increased to 65% during hypoglycaemia (P<.01). Cravings for seven of the eight food types increased during hypoglycaemia, but the greatest effect sizes (>1.0 standard deviations) were observed for three food types that had a high carbohydrate content. CONCLUSIONS: In people with Type 1 diabetes, acute hypoglycaemia produces a highly reliable generalised increase in cravings for food, particularly foodstuffs with a high content of carbohydrate. The mechanisms behind this response remain to be elicited.

Adult↗

PubMed1994

Restoration of hypoglycaemia awareness in patients with long-duration insulin-dependent diabetes.

Hypoglycaemia without warning is a dangerous complication of insulin-dependent diabetes mellitus and it limits the use of intensified insulin therapy to reduce chronic diabetic complications. To investigate the possibility of restoring awareness; symptomatic, cognitive, and hormonal responses to controlled hypoglycaemia were studied in insulin-dependent diabetic patients with long disease duration (6 with good glycaemic control and 6 with poor control) before and after hypoglycaemia avoidance. At the start of the study, all had loss of hypoglycaemia awareness. Responses to the initial challenge were small (pooled area under curve [AUC] adrenaline 5.75 [SE 0.07] nmol/L per 260 min, pooled AUC symptom score 80 [1.3]) and only started when plasma glucose was significantly lower than the 2.8 (0.1) mmol/L at which cognitive function deteriorated. After 4.1 (1.1) months' scrupulous hypoglycaemia avoidance, hormone and symptom responses to the challenge were increased (AUC adrenaline 15.9 [0.1] nmol/L per 260 min, p = 0.01; AUC symptom score 275 [7], p < 0.001), starting at plasma glucose concentrations significantly higher than that causing cognitive dysfunction. Glycosylated haemoglobin did not deteriorate significantly. We conclude that the normal hierarchy of subjective awareness before cognitive dysfunction during hypoglycaemia can be restored by avoiding hypoglycaemia. This is independent of disease duration or initial metabolic control.

Adult↗

PubMed1995

Hypoglycaemia associated with use of inhibitors of angiotensin converting enzyme.

The use of angiotensin-converting-enzyme (ACE) inhibitors has been associated with increased insulin sensitivity in diabetic patients. Although such an effect could be beneficial in the treatment of hypertension or congestive heart failure in diabetic patients, it might also precipitate severe hypoglycaemia. To test this hypothesis we carried out a nested case-control study, using data in the Dutch PHARMO system (1986-92), among diabetic patients treated with insulin or with oral antidiabetic drugs, who were admitted to hospital with hypoglycaemia. We identified 94 patients who had been admitted with hypoglycaemia and selected 654 controls from the same cohort. With adjustment for a wide range of potential confounding factors, hypoglycaemia was significantly associated with current use of ACE inhibitors (odds ratio 2.8 [95% CI 1.4-5.7]). Both among users of insulin and among users of oral antidiabetic drugs, use of ACE inhibitors was significantly associated with an increased risk of hospital admission for hypoglycaemia (2.8 [1.2-6.4] and 4.1 [1.4-12.2], respectively). Although ACE inhibitors have several advantages over other antihypertensive drugs in diabetes, the risk of hypoglycaemia should be taken into account. Further investigation of the mechanism is needed since as many as 13.8% of all hospital admissions for hypoglycaemia might be attributable to use of ACE inhibitors.

Adult↗

PubMed2004

A new table for prevention of hypoglycaemia during physical activity in type 1 diabetic patients.

OBJECTIVE: The ability to adjust both insulin and nutrition to allow safe participation in physical activity and high performance has recently been recognized as an important management strategy in these patients. In particular, the important role played by the patient in self-monitoring blood glucose during physical activity and then using these data to improve performance and decrease hypoglycaemias is now fully accepted. The primary objective of this study is to compare different therapeutic options in exercising Type 1 diabetic patients (n=67) with or without CHO compensation and/or with or without insulin dosage reduction in order to prevent hypoglycaemias during and after exercise. METHODS: Sixty-seven type 1 diabetic patients were aggregated into four treatment categories according to four strategies to prevent hypoglycaemia episodes, with or without carbohydrate compensation and/or with or without insulin dosage reduction. The protocol included 7 different disciplines and 9 subgroups according to 3 different durations (<20 min., 20-60 min., > 60 min.) and 3 intensity degrees (<60% of Maximal Heart Rate, 60-75% and > 75%). RESULTS: Our study shows that by replacing adequately the carbohydrates during the practice of physical exercise it is possible to prevent almost all hypoglycaemia episodes, independently of the insulin dosage adjustments. Furthermore, the amount of extra-carbohydrates correlates well with the number of hypoglycaemia while the decrease in insulin dosage does not. CONCLUSION: Adequate carbohydrate replacement during and after exercise seems to be the most important measure to prevent hypoglycaemia. However, the insulin dosage adjustment does not play such an important role. A decrease from 20 to 30% seems reasonable only for a long duration exercise (> 60 min.). Finally, a new user-friendly table for prevention of hypoglycaemia is proposed for physical activity of different intensity and duration.

Adult↗

PubMed1985

The effect of hypoglycaemia on visual function: a clinical and electrophysiological study.

Disturbance of vision commonly accompanies hypoglycaemia. This study was designed to investigate the nature of the visual disturbance, the blood glucose threshold at which the disturbance occurred and the physiological basis. Measurements were made of the corrected visual acuity, colour vision (100 Hue test), visual evoked potentials (VEP), electroencephalography (EEG) frequency analysis and psychometry (digit recall) during stepwise induction of controlled hypoglycaemia produced by an intravenous insulin infusion. Six male volunteers and five insulin-dependent diabetic subjects were studied. During hypoglycaemia corrected visual acuity was unchanged. Colour vision was significantly impaired. Baseline VEP were normal in both groups but significantly prolonged during hypoglycaemia (mean increment 10.8 ms) and increased by greater than 5 ms in nine out of 11 subjects. Quantitative EEG analysis demonstrated slowing with a power density spectral shift from fast alpha to slow alpha, theta and delta which correlated with VEP latency and amplitude changes. The findings have clinical implications. A deterioration in colour vision is likely to impair the ability to read reagent strips by eye. VEP measurements in diabetic patients are likely to be misleading if hypoglycaemia is present; EEG changes are a sensitive index of cortical dysfunction during hypoglycaemia and provide a theoretical basis for developing a portable device to detect early hypoglycaemia.

Adult↗

PubMed1991

Physiological disturbances in hypoglycaemia: effect on subjective awareness.

Deficiencies in the release of glucagon and adrenaline during hypoglycaemia in diabetic patients are associated with a high frequency of severe hypoglycaemic episodes. These have been attributed to a resulting inability to increase hepatic glucose output acutely. A more important consequence may be reduced awareness of impending hypoglycaemia. Such hypoglycaemia unawareness is related to, but not entirely explained by, diminished sympathetic activity, perhaps due to failure to activate the sympathoadrenal system until a lower blood glucose level is achieved. The patient's subsequent failure to act appropriately would then be due to impaired cerebral function preventing the perception of sympathoadrenal activation during the more severe hypoglycaemia. Unawareness of moderate hypoglycaemia is common in diabetic patients. Autonomic neuropathy probably accounts for only a few cases of hypoglycaemia unawareness and other factors which are potentially important include duration of diabetes, glycaemic control, insulin species, and the degree and frequency of hypoglycaemia. Further research is required to discover both the pathophysiological mechanisms of, and the treatment needed to reverse or prevent, the abnormality.

Awareness↗

PubMed1997

The counterregulatory response to hypoglycaemia in women with the polycystic ovary syndrome.

OBJECTIVE: The pathogenetic mechanisms behind insulin resistance in polycystic ovary syndrome (PCOS) are far from fully elucidated. Aberrant counterregulatory responses to hypoglycaemia have been reported in patients with insulin resistance, and recent reports suggest that plasma glucose may be regulated at lower levels in women with PCOS. In this study we investigated the complete hormonal counterregulatory response to hypoglycaemia in women with PCOS. DESIGN: Prospective cross-sectional study. PATIENTS: Eight obese (BMI > or = 25) and 10 non-obese (BMI < 25) women with PCOS, diagnosed by means of ultrasonography and clinical signs of chronic anovulation. Eight obese and 9 non-obese controls. MEASUREMENTS: Hypoglycaemia was induced by an intravenous bolus of soluble insulin (0.15 IU/kg body weight). The counterregulatory responses of cortisol, GH, catecholamines, glucagon, chromogranin A (CGA), and neuropeptide Y (NPY) were studied together with symptoms of hypoglycaemia. RESULTS: The obese women with PCOS had a more pronounced truncal-abdominal body fat distribution (waist hip ratio, WHR) and were hyperinsulinaemic, compared with the obese controls. All the women exhibited blood glucose levels (< 2 mmol/l) well below the threshold for the hormonal counterregulatory response and for the appearance of clinical symptoms. The non-obese women with PCOS showed a greater increase in serum concentrations of GH than the lean controls. The obese women with PCOS exhibited blunted responses of noradrenaline and NPY, but similar increases of adrenaline and CGA, compared with the obese controls. They also showed a lower symptom score during hypoglycaemia. The response of noradrenaline to hypoglycaemia correlated inversely with fasting insulin levels in the women with PCOS. Among all the obese women (PCOS and controls pooled) basal levels of noradrenaline correlated inversely with the WHR. CONCLUSIONS: All the women with PCOS, independent of BMI, body fat distribution and insulin levels, showed preserved counterregulatory responses to hypoglycaemia. The reduced plasma levels of noradrenaline and the lower perception of hypoglycaemic symptoms in the obese women with PCOS could both reflect a lower activation of the sympathetic nervous system. This aberration seems related to truncal-abdominal obesity and hyperinsulinaemia. The finding of an increased response of GH in the lean women with PCOS could support previous suggestions of an altered activity of the GH/IGF-I system in these women.

Adult↗

PubMed2000

Neonatal hypoglycaemia in infants of diabetic mothers.

OBJECTIVE: To determine whether umbilical cord blood glucose correlates with subsequent hypoglycaemia after birth in infants of well-controlled diabetic mothers. METHODOLOGY: Thirty-eight term infants of well-controlled diabetic mothers were enrolled. Five mothers had pre-existing diabetes. Of the 33 gestational diabetic mothers, 16 were managed on insulin and 17 on diet. Maternal blood glucose was maintained between 4 and 8 mmol/L during labour and delivery. Infants' plasma glucose levels were measured from venous cord blood and serially, at less than 30 min, 1 h and 2 h of life by glucose hexokinase method. Blood glucose levels were further monitored by bedside Dextrostix for 24 h. RESULTS: Eighteen (47%) infants developed hypoglycaemia (blood glucose level less than 2 mmol/L) during the first 2 h of life. There was no difference in the cord blood glucose levels between infants with or without hypoglycaemia (3.7 +/- 1.1 vs 4.5 +/- 1.1 mmol/L, respectively). Infants of mothers with diabetes diagnosed prior to 28 weeks gestation were at a higher risk of developing hypoglycaemia (8 of 10 vs 10 of 28, OR 7.2, 95%CI 1.3-40.7). Hypoglycaemic infants were of significantly higher birthweight, and were more likely to be born to Caucasian mothers and by Caesarean section. Raised maternal fructosamine blood level, the need for insulin treatment or the infant's haematocrit were not different between infants with or without hypoglycaemia. CONCLUSIONS: In well-controlled diabetic mothers, the incidence of early hypoglycaemia in infants is still high, particularly in those mothers who had a longer duration of diabetes. Cord blood glucose level did not identify the infants with hypoglycaemia.

Birth Weight↗

PubMed1999

Diabetic hypoglycaemia.

Hypoglycaemia is a major factor preventing insulin-treated patients from achieving normoglycaemia. This reflects the inadequacy of current insulin treatment, which causes high insulin concentrations in the post-absorptive period. Physiological defences to hypoglycaemia include autonomic activation, which limits the fall in glucose level and causes symptoms, alerting patients to an impending episode. Many patients develop defective responses and hypoglycaemia unawareness after longstanding disease or with tight glycaemic control and are then prone to severe attacks. This may be the result of repeated hypoglycaemic episodes, which by altering cerebral glucose uptake, disturb the mechanisms that activate the central response to hypoglycaemia. Preventing further hypoglycaemia can partially reverse these defects and restore symptomatic awareness. Clinical hypoglycaemia has also been implicated in the 'dead in bed' syndrome and in chronic cognitive impairment. The problem of hypoglycaemia will eventually be solved by better insulin delivery and non-invasive glucose meters, but until then, more focused education may have a more substantial impact.

Awareness↗

PubMed2001

Short-term effects of severe hypoglycaemia in children and adolescents with type 1 diabetes. A cost-of-illness study.

UNLABELLED: The aim of this study was to describe costs and other short-term effects of severe hypoglycaemia in children and adolescents with type 1 diabetes. The study comprised a geographic population of 129 patients <19 y of age with families prospectively registering detailed data after self-reported severe hypoglycaemia. In the period Jan.-Dec. 1998, 16 events were reported with unconsciousness and 95 events without unconsciousness but needing the assistance of another person. Of all events, 20-30% had effects requiring the assistance of people other than parents, school absence, parents' absence from work, extra transport and/or telephone calls. Patient (family) activities were cancelled after 10% (5%) of events. Increased worry for parents was reported after 8% and poor sleep after 7% of events. Hospital visits took place at 5% and hospitalizations at 3% of all events. Patients with severe hypoglycaemia indicated lower global quality of life (p=0.0114). The average socio-economic burden for events of severe hypoglycaemia was estimated at EURO 17,400 yearly per 100 type 1 diabetes patients. Average cost was estimated at EURO 239 per event of severe hypoglycaemia with unconsciousness or EURO 478 yearly per patient with unconsciousness, and EURO 63 per event of severe hypoglycaemia without unconsciousness but needing assistance from another person or EURO 307 yearly per patient in this category. These are conservative estimates and do not include unpaid time and other intangibles, possible road traffic accidents, disabling or premature deaths. CONCLUSIONS: The results suggest the potential for socio-economic savings and increased quality of life for patients and families from severe hypoglycaemia prevention programs.

Adolescent↗

PubMed1990

Beta-adrenoceptor blockade and hypoglycaemia. A randomised, double-blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

1. The effect of 1 week of treatment with propranolol LA (160 mg), atenolol (100 mg) and metoprolol CR (100 mg) on awareness of and the physiological responses to moderate hypoglycaemia were compared with placebo using a randomised, cross-over design in 12 healthy volunteers. 2. All three beta-adrenoceptor antagonists reduced resting heart rate, systolic blood pressure and heart rate responses to submaximal exercise compared with placebo. 3. Under hyperinsulinaemic (60 mu m-2 min-1) clamp conditions, at a blood glucose of 2.5 mmol l-1, atenolol prevented the rise in systolic and atenolol and metoprolol CR prevented the fall in diastolic blood pressure usually associated with hypoglycaemia. At this level of hypoglycaemia, the expected increase in heart rate was inhibited by atenolol but not metoprolol CR. Pre-treatment with propranolol LA resulted in a significant pressor response and a bradycardia during hypoglycaemia. In addition the normal increase in finger tremor was abolished by propranolol LA. 4. During hypoglycaemia all three beta-adrenoceptor blockers augmented sweating compared with placebo but hypoglycaemic symptoms, awareness and slowing of reaction time were the same with drugs and placebo. 5. The rise in plasma adrenaline and other counter-regulatory hormones during hypoglycaemia was enhanced by beta-adrenoceptor blockade. 6. We conclude that beta-adrenoceptor antagonists modify the physiological and hormonal responses to, but do not adversely affect awareness of, moderate hypoglycaemia in healthy volunteers.

Adrenergic beta-Antagonists↗

PubMed2006

Risk for severe hypoglycaemia with unawareness in GH-deficient patients during the insulin tolerance test.

OBJECTIVE: The insulin tolerance test (ITT) has been suggested as the gold standard for diagnosing GH deficiency (GHD). The ITT is, however, potentially hazardous. Glucose monitoring during the ITT varies between centres and there is surprisingly little information on the actual level of blood glucose nadir and the duration of hypoglycaemia in patients undergoing the ITT. The aim of the present study was to closely monitor the blood glucose level and to register the presence of symptoms and signs of hypoglycaemia during the ITT. DESIGN AND PATIENTS: Sixteen patients (seven women), aged 22-59 years were consecutively recruited for an ITT, and showed GHD (peak GH < 3 microg/l). RESULTS: In five (31%) of the patients unawareness of hypoglycaemia was recorded, the median nadir blood glucose level was 1.4 mmol/l (range 1.1-1.9) and the duration of blood glucose < 2.2 mmol/l was 25 min (range 20-33). The remaining 11 patients were symptomatic, and tiredness (n=6) and dizziness (n=3) were the most frequent symptoms. In these symptomatic patients the median nadir blood glucose level was 1.3 mmol/l (range 1.0-1.6) and the duration of blood glucose < 2.2 mmol/l was 25 min (range 15-30). CONCLUSIONS: In patients with GHD subjected to the ITT, symptoms of hypoglycaemia were scarce and a third showed unawareness. Close blood glucose monitoring is recommended at the ITT as low nadir blood glucose levels and long duration of hypoglycaemia may be present irrespective of symptoms of hypoglycaemia. Recommendations for intervention with intravenous glucose, at unacceptable low blood glucose levels or at prolonged hypoglycaemia, are warranted.

Adult↗

PubMed1992

Changes in renal function during acute insulin-induced hypoglycaemia in patients with type 1 diabetes.

The effect of acute hypoglycaemia on renal function was examined in eight male patients with Type 1 diabetes who had normal urinary albumin excretion. Insulin was given as a bolus intravenous injection (0.125 U kg-1) and plasma glucose fell to a nadir of 1.6 (SE 0.2) mmol l-1, with all patients experiencing an acute autonomic reaction. Renal plasma flow fell from 674 (106) to 540 (198) ml min-1 during hypoglycaemia (p less than 0.01) and returned to 655 (181) ml min-1 (NS vs baseline). Glomerular filtration rate (GFR) declined from 143 (23) to 110 (36) ml min-1 during hypoglycaemia (p less than 0.02), rising to 150 (44) ml min-1 in the recovery period (NS vs baseline). The urinary flow rate and urinary albumin excretion rate both fell significantly in response to hypoglycaemia (10.6 (1.2) to 4.7 (1.1) ml min-1; p less than 0.002, and 46.2 (10.6) to 26.0 (10.5) micrograms min-1, respectively). Urinary dopamine excretion also declined, from 322 (37) to 211 (29) mumol min-1 (p less than 0.005) but sodium excretion was unchanged. Plasma adrenaline concentration (0.2 (0.03) to 1.7 (0.4) nmol l-1; p less than 0.01) and plasma renin activity (0.49 (0.13) to 1.08 (0.17) ng-Ang 1 l-1 h-1; p less than 0.01) increased during hypoglycaemia, but changes in plasma noradrenaline and angiotensin II levels did not attain significance. These acute changes in renal function, observed during hypoglycaemia in diabetic patients, may result from direct stimulation of the efferent sympathetic nerves to the kidney, complemented by the hormonal changes induced by hypoglycaemia.

Adult↗

PubMed1993

Frequency and symptoms of hypoglycaemia experienced by patients with type 2 diabetes treated with insulin.

This study ascertained the prevalence of severe hypoglycaemia and loss of awareness of hypoglycaemia in patients with Type 2 diabetes treated with insulin. One hundred and four sequentially selected Type 2 diabetic patients were compared with 104 patients with Type 1 diabetes who were matched for duration of insulin therapy. The patients were interviewed using a standardized questionnaire. During treatment with insulin, 18 Type 2 patients had experienced fewer than two episodes of hypoglycaemia, while 86 had experienced two or more episodes; 80 (93%) reported normal awareness, six (7%) reported partial awareness, and none had absent awareness of hypoglycaemia. All 86 Type 1 diabetic patients matched to the 86 Type 2 patients had experienced multiple episodes of hypoglycaemia; 71 (83%) had normal awareness, 14 (16%) had partial awareness and one patient (1%) reported absent awareness of hypoglycaemia. The Type 1 patients who had altered awareness of hypoglycaemia had longer duration of diabetes and insulin therapy (normal awareness: 5 (1-17) years (median (range)) vs partial awareness: 9 (3-18) years, p < 0.01). Similarly, Type 2 patients with altered awareness had longer duration of diabetes (normal awareness: 11 (2-25) years vs partial awareness: 19 (8-24) years, p < 0.02) and had received insulin for longer (normal awareness: 3 (1-18) years vs partial awareness: 12 (6-17) years, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗