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D B Dunger

Publications and source records attributed to D B Dunger.

At least 55 records · Page 3Linked to original sources

Polycystic ovaries and eating disorders: Are they related?

A cross-sectional observational study was used to investigate the reported association between polycystic ovarian syndrome and bulimia nervosa in a group of young, post-menarcheal women in the normal population. Volunteers aged 18-25 years were recruited from two universities and two general practice surgeries in Oxford. A total of 230 women completed an interviewer-based eating disorder examination, which was used to diagnose bulimia nervosa and its variants, and to assess eating behaviour. Transabdominal ultrasound was used to diagnose the presence or absence of polycystic ovaries. Symptoms of polycystic ovarian syndrome were assessed using menstrual history, anthropometric measurements, clinical observation of acne and hirsutism, and biochemical analysis of a fasting blood sample. A total of 30% of all participants described episodes of overeating and 4% had used extreme methods of weight control. Two women were diagnosed with bulimia nervosa, and five women with binge-eating disorder; however, these diagnoses were not associated with polycystic ovaries. Scores for dieting and overall eating disorder symptoms in the polycystic ovary groups were not significantly higher than those for women with normal ovaries, and therefore the suggestion that polycystic ovaries predispose towards the development of eating disorders is not supported by this study.

Adolescent↗

Short stature in Noonan syndrome: response to growth hormone therapy.

BACKGROUND: Growth hormone (GH) has been used to promote growth in both the short and long term in a number of dysmorphic syndromes, including Turner syndrome. As this condition shares many clinical features with Noonan syndrome, it would seem logical to treat the latter group with GH. AIMS: To assess the short and long term response to GH therapy in patients with Noonan syndrome. METHODS: Analysis of patients with Noonan syndrome in the Pharmacia & Upjohn International Growth Study (this post-marketing database contains data on the majority of patients currently treated with GH in the UK). A questionnaire was also sent to participating clinicians. RESULTS: Data on 66 patients (54 males) were available for study. At the start of GH therapy children were short, compared with both normal and Noonan children. During the first year of GH therapy height velocity increased from a mean of 4.9 to 7.2 cm per year. For patients treated long term with GH, mean height SDS increased from -2.9 pretreatment to -2.6 after one year and -2.3 after five years. Of the 10 patients at near final height, only one had a height above the 3rd centile for normal adults and above the mean for untreated Noonan patients. The mean increment in final height was 3.1 cm (range -1.1 to 6.5 cm). CONCLUSIONS: GH therapy in patients with Noonan syndrome will improve height velocity in the short term. Longer-term therapy results in a waning of effect; initial indications are that final height is not improved substantially in most patients.

Adolescent↗

The risk and outcome of cerebral oedema developing during diabetic ketoacidosis.

BACKGROUND: Cerebral oedema is a major cause of morbidity and mortality in children with insulin dependent diabetes. AIMS: To determine the risk and outcome of cerebral oedema complicating diabetic ketoacidosis (DKA). METHODS: All cases of cerebral oedema in England, Scotland, and Wales were reported through the British Paediatric Surveillance Unit between October 1995 and September 1998. All episodes of DKA were reported by 225 paediatricians identified as involved in the care of children with diabetes through a separate reporting system between March 1996 and February 1998. Further information about presentation, management, and outcome was requested about the cases of cerebral oedema. The risk of cerebral oedema was investigated in relation to age, sex, seasonality, and whether diabetes was newly or previously diagnosed. RESULTS: A total of 34 cases of cerebral oedema and 2940 episodes of DKA were identified. The calculated risk of developing cerebral oedema was 6.8 per 1000 episodes of DKA. This was higher in new (11.9 per 1000 episodes) as opposed to established (3.8 per 1000) diabetes. There was no sex or age difference. Cerebral oedema was associated with a significant mortality (24%) and morbidity (35% of survivors). CONCLUSIONS: This first large population based study of cerebral oedema complicating DKA has produced risk estimates which are more reliable and less susceptible to bias than those from previous studies. Our study indicates that cerebral oedema remains an important complication of DKA during childhood and is associated with significant morbidity and mortality. Little is known of the aetiology of cerebral oedema in this condition and we are currently undertaking a case control study to address this issue.

Adolescent↗

Elevated leptin levels are associated with excess gains in fat mass in girls, but not boys, with type 1 diabetes: longitudinal study during adolescence.

Adolescents, in particular girls, with type 1 diabetes may gain excessive weight during puberty. We present the results of a longitudinal study aimed to determine the roles of leptin and insulin in changes in body composition in subjects with type 1 diabetes and controls. Forty-six children (23 boys) with type 1 diabetes and 40 controls (20 boys) were followed from 8-17 yr of age. Height, weight, and sc skinfolds were assessed every 6 months, and a blood sample taken for leptin determination. Throughout the age range, body mass index (mean +/- SEM) was greater by 1.45 +/- 0.69 kg/m(2) in girls and 1.46 +/- 0.55 kg/m(2) in boys with type 1 diabetes compared with control values. In girls with type 1 diabetes, this reflected greater percent body fat (3.2 +/- 1.0%; P = 0.002), whereas in boys it related to differences in fat-free mass. Both boys and girls with type 1 diabetes had higher leptin levels adjusted for percent body fat than controls; in the girls this was related to insulin dose (regression coefficient B = 0.006 +/- 0.003; P = 0.04) and greater gains in fat mass. Hyperinsulinemia and raised leptin levels are associated with gains in fat mass throughout puberty in girls, but not boys, with type 1 diabetes.

Adipose Tissue↗

Growth hormone therapy and growth in children with Noonan's syndrome: results of 3 years' follow-up.

Growth data from the first 3 yr of a multicenter study examining the efficacy and safety of recombinant human GH [rhGH; 4 IU (1.3 mg)/m(2).day, sc] in children with Noonan's syndrome (NS) are reported for 23 subjects. Sixteen male and seven female patients (age, 9.3 +/- 2.6 yr at onset of GH therapy, mean +/- SD; range, 4.8-13.7) were each assessed at 1, 2, and 3 yr after starting treatment. Comparisons were made with a group of eight subjects (six males and two females, age, 9.0 +/- 4.1 yr; range, 4.1-14.8) with NS, not treated with rhGH, measured over the same period. All treated subjects underwent annual cardiac assessment. Height SD score increased from -2.7 +/- 0.4 at the start of GH therapy to -1.9 +/- 0.9 3 yr later (P < 0.001, two-tailed t test). This corresponded to an increase in height from 116.1 +/- 13.2 to 137.3 +/- 14.0 cm. Height velocity increased from 4.4 +/- 1.7 cm/yr in the year before treatment to 8.4 +/- 1.7 (P < 0.001), 6.2 +/- 1.7 (P < 0.001), and 5.8 +/- 1.8 (P = 0.01, two-tailed t test compared with baseline) during the first, second, and third years of GH treatment, respectively. Height acceleration was not significant during the second or third years when pubertal subjects were excluded. The comparison group showed an increase in height from 116.0 +/- 19.8 to 131.9 +/- 21.1 cm over the 3 yr (height SD score, -2.7 +/- 0.6 to -2.4 +/- 0.7, P = 0.3). None of the 23 children developed hypertrophic cardiomyopathy during GH treatment. The increase in growth rate in NS resulting from 1 yr of GH therapy seems to be maintained during the second year, although height velocity shows a less significant increase over pretherapy values. Possible abnormal anabolic effects of rhGH on myocardial thickness were not confirmed, and no treated patient developed features of hypertrophic cardiomyopathy.

Adolescent↗

Hypoglycemia and resistance to ketoacidosis in a subject without functional insulin receptors.

Humans with congenital absence of the islets of Langerhans and mice rendered null for the insulin receptor rapidly develop severe hyperglycemia and ketoacidosis and, if untreated, die in the early neonatal period. In contrast, children with homozygous or compound heterozygous mutations of the insulin receptor gene, although hyperglycemic postprandially, survive for many months without developing ketoacidosis. Paradoxically, they often develop hypoglycemia. The rarity of the condition and the difficulties of undertaking metabolic studies in ill infants have limited the physiological information that might explain the clinical features. We studied a boy with Donohue's syndrome who represents a further example of the null phenotype, with two different and novel nonsense mutations in the alpha-subunit of the receptor. He survived for 8 months without developing ketoacidosis, and fasting hypoglycemia was a frequent problem. Despite the complete absence of insulin receptors, evidence for persistent insulin-like effects on fat and liver was seen; fasting plasma beta-hydroxybutyrate and nonesterified fatty acid levels were low, fell further during the early postprandial period, and failed to rise in response to hypoglycemia. The inverse relationships between plasma insulin and insulin-like growth factor-binding protein-1 levels were maintained, suggesting persistent hepatic effects of insulin. GH levels measured over a 6.5-h period were low throughout. Thus, the differences between congenital insulin deficiency vs. insulin receptor deficiency in humans may be explained by persistent insulinomimetic activity of the grossly elevated plasma insulin presumably being mediated through the type 1 insulin-like growth factor receptor. As GH plays a critical role in the regulation of ketogenesis during insulinopenia in humans, but not in rodents, this may contribute to the distinct phenotype of human vs. mouse insulin receptor knockouts.

3-Hydroxybutyric Acid↗

The role of IGF-binding proteins in mediating the effects of recombinant human IGF-I on insulin requirements in type 1 diabetes mellitus.

To determine the role of IGF-binding proteins in mediating the direct effects of recombinant human IGF-I on insulin requirements in type 1(insulin-dependent) diabetes mellitus, overnight changes in IGF-I, IGF-II, and IGF-binding protein-1, -2, and -3, collected under euglycemic conditions, were compared in nine subjects after double blind, randomized, sc administration of recombinant human IGF-I (40 microg/kg) or placebo at 1800 h. On both nights a somatostatin analog infusion (300 ng/kg x h) suppressed endogenous GH production, and three timed discrete GH pulses (total, 0.029 IU/kg x night) ensured identical GH levels. After recombinant human IGF-I administration, IGF-I levels and the IGF-I/IGF-binding protein-3 ratio increased [mean +/- SEM:IGF-I, 401 +/- 22 ng/ml; placebo, 256 +/- 20 ng/ml (P = 0.0002); IGF-I, 0.108 +/- 0.006; placebo, 0.074 +/- 0.004 (P = 0.0003), respectively], and insulin requirements decreased (IGF-I, 0.12 +/- 0.03; placebo, 0.23 +/- 0.03 U/kg x min; P = 0.008). The normal within-individual inverse relationships between insulin and IGF-binding protein-1 levels were observed (lag time 2 h: r = -0.34; P < 0.01). Yet despite reduced free insulin levels (8.5 +/- 1.5; placebo, 12.2 +/- 1.2 mU/liter; P = 0.03), IGF-binding protein-1 levels were reduced after recombinant human IGF-I administration (53.7 +/- 6.8; placebo, 82.2 +/- 11.8 ng/ml; P = 0.008). The largest reductions in free insulin levels after recombinant human IGF-I and thus putative improvement in insulin sensitivity occurred in subjects with the smallest increase in the plasma IGF-I/IGF-binding protein-3 ratio (r = 0.7; P = 0.03). Taken together, these data are consistent with the hypothesis that transcapillary movement of IGF-I (perhaps mediated by IGF-binding protein-1), out of the circulation facilitates altered insulin sensitivity. These data have important implications for risk-benefit assessment of recombinant human IGF-I therapy in type 1 diabetes mellitus.

Adolescent↗

Blood pressure does not rise before the onset of microalbuminuria in children followed from diagnosis of type 1 diabetes. Oxford Regional Prospective Study Group.

OBJECTIVE: To examine whether a rise in blood pressure could be detected before the onset of microalbuminuria (MA) in a cohort of children followed from diagnosis of type 1 diabetes. RESEARCH DESIGN AND METHODS: The Oxford Regional Prospective Study is an incident cohort study of children with type 1 diabetes aged (mean +/- SD) 9.8 +/- 3.7 years at diagnosis. Subjects were assessed annually from diagnosis, with measurement of HbA1c, arterial blood pressure (random zero), and three urine samples for estimation of the albumin/creatinine ratio. During follow-up, 63 of 494 children developed MA at one or more annual assessments and were designated as cases for a nested case-control study. Each case was matched for sex and age at diagnosis with two normoalbuminuric control subjects. Blood pressure (BP) data were compared at corresponding years of diabetes duration. RESULTS: Cases with MA were similar to normoalbuminuric control subjects with respect to age and BMI, but they had higher mean HbA1c levels (mean difference 1.1%, P < 0.001). In the years before the onset of MA, the diastolic BP standard deviation score (SDS) was significantly higher than zero in cases (mean 0.49, P < 0.001) and in control subjects (0.50, P < 0.001). No difference could be detected between cases and control subjects before the onset of MA in either systolic or diastolic BP (mean difference systolic -1.2 mmHg [95% CI -4.7 to 2.7], mean difference diastolic 0.1 mmHg [-2.4 to 2.6]). However, within the cases, the onset of MA was associated with elevations in systolic and diastolic BP SDSs (F = 16.1, P < 0.001; and F = 18.0, P < 0.001). BMI, but not HbA1c, was associated with systolic and diastolic BP SDSs in the subjects with MA (F = 0.6, P = 0.4; and F = 12.3, P = 0.001). However, the association of BP with MA remained signifcant for systolic BP (P = 0.001) and for diastolic BP (P < 0.001) after adjusting for BMI. CONCLUSIONS: A rise in systemic BP cannot be detected before the first appearance of MA in children with type 1 diabetes. BP rises concurrently with the onset of MA and is also closely related to BMI.

Albuminuria↗

Clinical and psychological course of diabetes from adolescence to young adulthood: a longitudinal cohort study.

OBJECTIVE: To determine the clinical and psychological course of diabetes through adolescence and the relationship with glycemic control in young adulthood. RESEARCH DESIGN AND METHODS: A longitudinal cohort study of adolescents recruited from the register of the outpatient pediatric diabetes clinic. A total of 76 individuals (43 male patients, 33 female patients) aged 11-18 years completed baseline assessments, and 65 individuals (86%) were reinterviewed as young adults (20-28 years of age). Longitudinal assessments were made of glycemic control (HbA(1c)), weight gain (BMI), and development of complications. Adolescents completed self-report questionnaires to assess emotional and behavioral problems as well as self-esteem. As young adults, psychological state was assessed by the Revised Clinical Interview Schedule and the self-report Brief Symptom Inventory. RESULTS: Mean HbA(1c) levels peaked in late adolescence and were worse in female participants (average 11.1% at 18-19 years of age). The proportion of individuals who were overweight (BMI >25.0 kg/m(2)) increased during the 8-year period from 21 to 54% in female patients and from 2 to 28% in male patients. Serious diabetes-related events included death in one patient and cognitive impairment in two patients. Individuals in whom diabetic complications developed (25% of male patients and 38% of female patients) had significantly higher mean HbA(1c) levels than those without complications (difference 1.9%, 95% CI 1.1-2.7, P < 0.0001). Behavioral problems at baseline were related to higher mean HbA(1c) during the subsequent 8 years (beta = 0.15, SEM (beta) 0.04, P < 0.001, 95% CI 0.07-0.24). CONCLUSIONS: The outcome for this cohort was generally poor. Behavioral problems in adolescence seem to be important in influencing later glycemic control.

Adolescent↗

Metabolic impact of puberty on the course of type 1 diabetes.

Puberty is characterised by important physiological and hormonal changes. In type 1 diabetes, abnormalities in the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis play a important role. Spontaneous hyper-GH secretion arises, with reduced circulating IGF-1 levels, both leading to a reduction in insulin sensitivity. From a clinical point of view, these abnormalities are linked to a deterioration glycaemic control, often more marked in females (in whom the degree of insulin resistance during puberty seems to be higher). These abnormalities in the GH/IGF-1 axis in may constitute a risk for the development of microangiopathic complications. Optimisation of insulin therapy has practical limitations and intensification of insulin therapy poses problems (weight gain, nocturnal hypoglycaemia). Several alternative therapeutic approaches have been explored to restore insulin sensitivity, either through a direct effect on the GH/IGF-1 axis, or through drugs with a direct insulin sensitivity effect, but all these approaches remain to be confirmed and the safety and acceptability of these treatments to be established on a long-term basis.

Blood Glucose↗

The potential role of insulin analogues in the treatment of children and adolescents with Type 1 diabetes mellitus.

The main therapeutic challenge in the treatment of Type 1 diabetes is maintenance of near-normoglycaemia in order to prevent long-term complications and avoid hypoglycaemia. This goal is relevant from the onset of the disease and is feasible if physiological models of insulin replacement are used and patients are educated in the strategy of intensive insulin therapy. Although the use of available insulins within a multiple injection regimen has improved, metabolic control it is still far from being optimal. The recent introduction of insulin analogues with a short- and long-acting profile seems promising in improving metabolic control and quality of care. Insulin lispro and insulin aspart, the short-acting insulin analogues offer a better post-prandial profile, while insulin glargine the new long-acting insulin analogue might provide better overnight control. In fact, the theoretical combination of an acute prandial insulin peak with a flat interprandial and overnight plasma profile would closely mimic the 24-hr insulin profile of non-diabetic individuals. This would possibly lead to lower post-prandial blood glucose excursion and better fasting blood glucose associated with minimal risk of hypoglycaemia. The possible reduction of hypoglycaemia is especially important in children as recurrent episodes might represent a potential risk for cognitive impairment. However, recent clinical research on the short-acting insulin analogues demonstrates the difficulties of translating these theoretical benefits into clinical relevant advantages. This might happen to other insulin analogues and requires further and larger studies in order to fully exploit the theoretical advantages of insulin analogues in the paediatric population. Safety issues should also be carefully monitored when introducting analogues in long-term therapy.

Adolescent↗

Association between postnatal catch-up growth and obesity in childhood: prospective cohort study.

OBJECTIVE: To identify predictors of postnatal catch-up growth from birth to two years and its relation to size and obesity at five years. DESIGN: Regional prospective cohort study. SETTING: Avon longitudinal study of pregnancy and childhood, United Kingdom. SUBJECTS: 848 full term singletons from a 10% random sample of the Avon longitudinal study of pregnancy and childhood. MAIN OUTCOME MEASURES: Maternal birth weight, prepregnancy weight, pregnancy weight gain, height, smoking, and parity, and paternal height. Weight and length of infants at birth, two years, and five years expressed as standard deviation (SD) scores from the UK reference scores for 1990. Percentage fat mass and total fat mass (estimated from skinfolds) and waist circumference at five years. RESULTS: Size at birth was representative of the national reference. Overall, 30. 7% (260 of 848) of infants showed a gain in SD score for weight greater than 0.67 SD scores between zero and two years, indicating clinically significant catch-up growth. These children had lower weight, length, and ponderal index at birth than other children, and were more often from primiparous pregnancies. They also had taller fathers than other children, and their mothers had lower birth weights and were more likely to smoke during pregnancy. Children who showed catch-up growth between zero and two years were heavier, taller, and fatter (body mass index, percentage body fat, and waist circumference) at five years than other children. CONCLUSIONS: In this contemporary well nourished cohort, catch-up growth was predicted by factors relating to intrauterine restraint of fetal growth. Children who showed catch-up growth between zero and two years were fatter and had more central fat distribution at five years than other children. Mechanisms that signal and regulate early catch-up growth in the postnatal period may influence associations between small size at birth and risks for disease in adulthood.

Adult↗

Both insulin sensitivity and insulin clearance in children and young adults with type I (insulin-dependent) diabetes vary with growth hormone concentrations and with age.

AIMS/HYPOTHESIS: We measured insulin clearance rates in children and young adults with Type I (insulin-dependent) diabetes mellitus to establish their relation with insulin sensitivity and with factors such as growth hormone secretion and body mass index. METHODS: We studied 46 subjects mean (range) age 14.4 (9.8-24.6) years), body mass index 21.1 (15.8-29.6) Kgm2[ using an overnight (1800-0800 hours) variable rate insulin infusion euglycaemic clamp protocol (5 mmol/l). Plasma free insulin concentrations during steady-state euglycaemia were used as an index of insulin sensitivity and insulin clearance determined as a ratio of insulin infusion rate to plasma free insulin. RESULTS: During steady-state euglycaemia (0500-0730 hours), insulin sensitivity mean (SEM) plasma insulin 0.020 (0.002) mU/l[ and insulin clearance rates 19.1 (1.8) ml.kg-1.min[ varied with age non-linearly and in a reciprocal fashion to each other (cubic regression F = 4.09, p = 0.01; F = 3.55, p = 0.02, respectively). Insulin sensitivity was negatively related to BMI (r = -0.37, p = 0.011) and mean overnight growth hormone concentrations (r = -0.40, p = 0.007). Insulin clearance was only related to growth hormone concentrations (r = -0.37, p = 0.014). These relations were still evident after stepwise multiple regression analysis (potential determinants: C peptide, sex, age, puberty stage, HbA1c, duration of diabetes): insulin sensitivity r = 0.55, p < 0.001; insulin clearance r = 0.37, p < 0.02. CONCLUSIONS/INTERPRETATION: Insulin clearance rates vary with age in young subjects with Type I diabetes and are highest during mid-adolescence when insulin sensitivity is at its lowest. Both insulin sensitivity and insulin clearance are related to circulating growth hormone concentrations.

Adolescent↗

Pseudohypoparathyroidism--another monogenic obesity syndrome.

Obesity is a common feature of pseudohypoparathyroidism (PHP) type 1a, but is usually associated with short stature. We describe two children referred because of hyperphagia and excessive weight gain from early infancy. Tall stature in both children initially confounded the diagnosis of PHP, but on follow-up both children developed the typical hormonal abnormalities and Case 2 developed typical skeletal features of Albright hereditary osteodystrophy. PHP type 1a is caused by germline loss of function mutations in the alpha subunit of GS, the ubiquitously expressed G protein that couples many hormone receptors to the adenylate cyclase second messenger system. Recent evidence suggest that the hypothalamic GS protein coupled melanocortin-4 receptor (MC4R) may mediate the central effects of leptin on inhibition of satiety. Similar patterns of infancy onset hyperphagia, excessive weight gain and tall stature are seen in subjects with congenital leptin deficiency and in subjects with MC4R mutations. We suggest that the genetic mutations in GSalpha which underlie PHP type 1a may also directly result in severe obesity. This diagnosis should be considered in any child with a history of hyperphagia and early onset morbid obesity.

Child, Preschool↗

Freezing method affects the concentration and variability of urine proteins and the interpretation of data on microalbuminuria. The Oxford Regional Prospective Study Group.

AIMS: Microalbuminuria and, to a lesser extent, renal tubular proteins are widely used in the early detection of incipient nephropathy in diabetes mellitus. Recent reports have indicated detrimental effects of storage at -20 degrees C on urine proteins. This study investigated the effects of storage on the measurement of urine proteins and discusses implications for the interpretation of data. METHODS: Two-hundred and sixty-eight specimens, collected from children with Type 1 diabetes, split into duplicate aliquots and stored at -20 degrees C and -70 degrees C, respectively, for 6-8 months, were analysed for albumin, retinol binding protein, N-acetyl glucosaminidase and creatinine, in the same assays to eliminate inter-assay variability. Two independent non-diabetic cohorts of children provided urine specimens, which were stored at -20 degrees C for one cohort and -70 degrees C for the other, to determine normal ranges for urine proteins. RESULTS: Storage at -20 degrees C led to a variable underestimation of all three urine proteins in 20% of specimens. Creatinine was unaffected. This underestimation was greater in more concentrated urine (r2 = 0.38, P < 0.001, n = 262). Consequently storage at -20 degrees C increased the variance of the albumin/ creatinine ratio more than the variance of albumin concentration. Temperature of storage affected the normal range, which was 0.1-2.1 mg/mmol at -20 degrees C compared to 0.3-3.1 mg/mmol at -70 degrees C. The prevalence of microalbuminuria (> 2SD above the geometric mean in non-diabetic specimens stored at -20 degrees C) was 27% after storage at -70 degrees C vs. 24% after -20 degrees C. The prevalence of microalbuminuria (>2SD above the geometric mean in nondiabetic specimens stored at -70 degrees C) was 21% after storage at -70 degrees C vs. 17% after -20 degrees C. CONCLUSIONS: Urine proteins are significantly but variably underestimated after storage at -20 degrees C. These effects account for increased variance and differences in the normal range, but have less effect on the detection of microalbuminuria than might be predicted.

Acetylglucosaminidase↗

Alterations in sleep physiology in young children with insulin-dependent diabetes mellitus: relationship to nocturnal hypoglycemia.

OBJECTIVES: To examine the effect of diabetes per se and nocturnal hypoglycemia on sleep in children with insulin-dependent diabetes mellitus (IDDM). DESIGN: Overnight polysomnography was performed on 3 occasions in 29 children with IDDM - twice during metabolic profiling. Sleep data were analyzed from 14 children (median [range], 8.7 [5.9 to 12.9] years) with a night of hypoglycemia and a nonhypoglycemic night. Seven children in the control group (9 [5.6 to 11.4] years) underwent 2 nights of polysomnography, once during metabolic profiling (to assess the effects of metabolic profiling), and 15 members of the control group had polysomnography only (to assess the effects of diabetes per se and to compare with the index group). RESULTS: Children with IDDM had disrupted sleep compared with the control group (short wakes, percentage of sleep time, 0.8 [0.5 to 1.9] vs 0.0 [0.0 to 0.3], median [interquartile range], IDDM vs control group, respectively, P =.001; long wakes, 1.2 [0.7 to 3. 0] vs 0.0 [0.0 to 0.0], P =.033; total number of wakes, 6 [3.5 to 11. 5] vs 1 [0 to 2], P =.002). Blood sampling disrupted sleep with increased long wakes as percentage of sleep time (0.3 [0.0 to 3.8] vs 4.3 [3.1 to 16.9], nonsampling vs sampling night, respectively, P =.003). Episodes of hypoglycemia were profound, with a glucose nadir of 2.0 [1.4 to 3.3] mmol/L (35.0 [24.5 to 57.8] mg/dL) and prolonged, 308 [30 to 630] minutes, with no effect on sleep. CONCLUSIONS: Children with diabetes had disrupted sleep compared with a control group, but there was no effect of profound nocturnal hypoglycemia on sleep quality. J Pediatr 2000;137:233-8)

Blood Glucose↗