An impaired pancreatic polypeptide response (PP) after hypoglycemia has been described in type I diabetic patients with overt autonomic neuropathy. Some authors have suggested that PP release might be useful as sensitive indicator of autonomic neuropathy. The meal test is safer and simpler than the insulin infusion test as PP stimulus. The aim of this study was to compare PP response to insulin infusion and protein meal test and to correlate these responses to the presence of measurable neuropathic disturbances. We thus studied 13 IDDM children and adolescents and 6 normal children. In diabetics the PP response to both tests was not different from that of the control subjects, but PP response to insulin infusion was inversely correlated to the duration of illness and was significantly lower in subjects with pathological heart rate response when compared to the control group. PP responses to the two stimuli were not correlated. We suggest that reduced PP response to hypoglycemia is an early sign of autonomic neuropathy as well as impairment of beat-to-beat variation when impaired PP response to meal test is still not evident.

Adolescent↗

PubMedDate not supplied

Peripheral nerve abnormalities in newly-diagnosed diabetic children.

The prevalence of clinical and subclinical peripheral neuropathy was evaluated in 51 unselected children at the time of onset of type I diabetes. Twenty-eight patients were followed for one year in order to establish the influence of metabolic control on peripheral nerve function. Twenty-two % of the diabetic children showed nerve conduction abnormalities at the onset and 11.7% had clinical features of peripheral neuropathy. After one year of disease, these figures had changed to 14.3% and 7.1%. Five of 7 children with altered electrophysiological tests in the baseline assessment had had normalization of all parameters one year later. No correlations between insulin requirement and nerve conduction were found. The M value was significantly correlated only with median sensory conduction velocity (p less than 0.005). Significant correlations were demonstrated between HbA1 concentration and both peroneal motor conduction velocity (p less than 0.025) and median sensory conduction velocity (p less than 0.005); these correlations were still present after one year of disease. In the first period of diabetic disease there is functional rather than structural damage of the nerves. The pathogenetic role of hyperglycemia is confirmed; however individual susceptibility to nerve dysfunction may play an important role in the nerve impairment in diabetes.

Adolescent↗

PubMedDate not supplied

Relationship between metabolic control and HDL2-cholesterol in type I diabetic patients.

The relationship of the degree of metabolic control to the serum lipoprotein pattern has been studied in 62 young insulin treated diabetic patients. Stable HbA1 and 24-h mean blood glucose, but not daily insulin dosage, were positively correlated to VLDL-TG (p less than 0.001) and negatively correlated to HDL2-C (p less than 0.05). HDL2-C was higher in patients with HbA1 less than 10% than in patients with HbA1 greater than 10%. In 13 patients, in whom an improvement of metabolic control was achieved, a significant increase of HDL2-C was recorded after three months. Our data are consistent with the view that in insulin-treated patients, good metabolic control is associated with low VLDL-TG and high HDL2-C levels.

Adolescent↗

PubMedDate not supplied

Short-term subcutaneous insulin infusion in diabetic children. Comparison with three daily insulin injections.

Sixteen insulin-dependent diabetic children and adolescents were studied on intensified insulin treatment (3II) and during continuous subcutaneous insulin infusion (CSII). Mean blood glucose, M-value and 24-h glycosuria were similar in both types of treatment. Symptomatic hypoglycemia occurred more often in patients on 3II than CSII. With 3II we observed blood glucose peaks early in the morning confirming that better overnight control can be achieved by CSII.

Adolescent↗

PubMedDate not supplied

Evaluation of central nervous conduction by visual evoked potentials in insulin-dependent diabetic children. Metabolic and clinical correlations.

Peripheral neuropathy is a well-known complication of diabetes, but few data are available on central lesions. Visual evoked potentials (VEPs) seem a reliable and feasible technique for detecting a conduction delay in the central nervous system. Seventy-one insulin-dependent type 1 diabetic children (mean age 15 +/- 3 years) and 33 controls were investigated for central neuropathy. We used a pattern of reversal stimulation with television display of a checker board pattern (15 min and 30 min check size). The latencies of the positive peak (P100 wave) were significantly lengthened in 17 patients (27%) but no correlation was found between VEPs and age, duration of diabetes, insulin requirement and HbA1 level. A negative correlation was found between VEPs and peripheral nervous conduction velocity. VEPs measurement seems a simple and reliable technique for detecting early alterations in CNS function in diabetics. Our data suggest that central and peripheral nervous alterations progress simultaneously.

Adolescent↗

PubMedDate not supplied

Effect of insulin treatment on osteocalcin levels in diabetic children and adolescents.

To investigate bone mineral metabolism in insulin-dependent diabetes mellitus, serum osteocalcin, a marker of bone formation, was measured in 31 diabetic children at onset of disease and 15 days after metabolic improvement by insulin therapy. As a control group for osteocalcin levels we studied 31 healthy sex- and age-matched children. Mean values of serum osteocalcin at onset of diabetes were significantly lower than in control group (p < 0.001), but we did not find any difference after 15 days of insulin therapy. Osteocalcin and parathyroid hormone concentrations were significantly greater after 15 days of insulin treatment than at onset of disease (p < 0.001 and p < 0.01, respectively). The osteocalcin levels were negatively correlated both with fructosamine and with glycosylated hemoglobin (p < 0.01 and p < 0.001, respectively), and positively correlated with the degree of metabolic acidosis at onset (p < 0.05). Therefore we postulate that during glycometabolic imbalance there is a decrease in bone turnover that could be one of the etiological factors of diabetic osteopenia.

Child↗

PubMedDate not supplied

Cardiovascular and hormonal responses to cold pressor test in insulin-dependent diabetic adolescents with microalbuminuria.

Cardiovascular responses to cold pressor test and associated changes in blood concentrations of renin, aldosterone, and catecholamines were measured in 11 type I diabetic patients with microalbuminuria; 11 type I diabetic patients with normoalbuminuria matched for age, duration of diabetes, metabolic control; and in nine normal control subjects. Heart rate, renin, aldosterone, and catecholamines concentrations in diabetic patients and controls at baseline were similar, but higher mean blood pressure was evident in microalbuminuric than normoalbuminuric patients (p < 0.01) and controls (p < 0.05). Heart rate and mean blood pressure during cold pressor test in control subjects and type I diabetic patients increased significantly but similarly, regardless of the presence of microalbuminuria. Catecholamines, but not renin-aldosterone release, was associated to blood pressure modifications during the test. Peak values of mean blood pressure induced by cold test were positively correlated to baseline values in control subjects (r = 0.658, p < 0.05) and normoalbuminuric (r = 0.725, p < 0.01), but not microalbuminuric diabetics. These data suggest that the higher blood-pressure values at rest observed in microalbuminuric than normoalbuminuric diabetics are not associated with a higher cardiovascular response to cold hypertensive stimulus.

Adolescent↗

PubMedDate not supplied

Further evidence of cholinergic impairment of the neuroendocrine control of the GH secretion in Down's syndrome.

There are data indicating that cholinergic activity is precociously impaired in Down's syndrome (DS). On the other hand, acetylcholine as well as arginine (ARG) play a major stimulatory role in the neural control of growth hormone (GH) secretion in humans, likely acting via the inhibition of hypothalamic somatostatin release. The aim of the present study was to verify the effects of pyridostigmine (PD, 120 mg p.o.), a cholinesterase inhibitor, and ARG (0.5 g/kg i.v.) on the growth hormone-releasing hormone (GHRH) (1 microgram/kg i.v.)-induced GH rise in 15 adult patients with DS (M/F: 8/7; age 26.5 +/- 2.2 years; body mass index, BMI: 25.7 +/- 1.0 kg/m2) in which the potentiating effect of PD on GH secretion has been reported to be reduced. The results in DS were compared to those in 15 normal subjects (NS) (M/F: 8/7; age: 30.0 +/- 1.3 years; BMI: 21.4 +/- 0.4 kg/m2). Basal GH and insulin growth factor I (IGF-1) levels in DS (1.8 +/- 0.7 and 206.5 +/- 21.0 micrograms/l) were similar to those in NS (1.4 +/- 0.3 and 179.4 +/- 11.0 micrograms/l). The GH response to GHRH alone in DS (526.5 +/- 120.1 micrograms/l/h) was lower (p < 0.05) than that recorded in NS (895.4 +/- 153.7 micrograms/l/h). The GHRH-induced GH rise was potentiated by PD both in DS (1,138 +/- 184.2 micrograms/l/h; p < 0.02 vs. GHRH alone) and in NS (2,213.8 +/- 212.8 micrograms/l/h; p < 0.005 vs. GHRH alone); however, as the percent potentiating effect of PD was similar in both groups (215 and 247%, respectively) the GH response to GHRH + PD in DS was lower (p < 0.005) than that in NS. The GHRH-induced GH rise was also potentiated by ARG in both DS (2,243 +/- 362.4 micrograms/h; p < 0.001 vs. GHRH alone) and NS (2,764.3 +/- 325.7 micrograms/l/h; p < 0.005 vs. GHRH alone). As the percent potentiating effect of ARG in DS was more marked than in NS (425 vs. 308%, respectively), the GH response to GHRH + ARG became similar in both groups. No sex-related difference was found in the GH response to various stimuli both in DS and NS. In conclusion, these data demonstrate that the potentiating effect of PD but not that of ARG is impaired in adults with DS in whom a reduced somatotrope responsiveness to GHRH is present. These findings indicate that in DS the pituitary GH releasable pool is fully preserved while an impairment of the tuberoinfundibular cholinergic pathways could lead to somatostatinergic hyperactivity and low somatotrope responsiveness to GHRH.

Acetylcholine↗

PubMedDate not supplied

GH secretion in Prader-Labhard-Willi syndrome: somatotrope responsiveness to GHRH is enhanced by arginine but not by pyridostigmine.

Low somatotrope responsiveness to secretagogues has been reported in patients affected by Prader-Labhard-Willi Syndrome (PLWS). In normal subjects, GH response to GHRH is known to be greatly potentiated to the same extent by pyridostigmine (PD) or arginine (ARG) which probably act via inhibition of hypothalamic somatostatin release. To clarify somatotrope responsiveness in 7 PLWS patients, we studied GH response to GHRH alone and to GHRH combined with PD or ARG. Eight normal short children were studied as controls (NC). GH response to GHRH in PLWS was lower than in NC (AUC: 615 +/- 205 micrograms/l.h, vs 1271 +/- 333 micrograms/l.h, p < 0.02). In NC, the GHRH-induced GH rise was potentiated to the same extent by PD or ARG. In contrast, in PLWS PD failed to increase the GH response to GHRH (AUC: 615 +/- 205 micrograms/l.h vs 621 +/- 176 micrograms/l.h, n.s.) which was enhanced by ARG (AUC: 615 +/- 205 micrograms/l.h vs 1633 +/- 425 micrograms/l.h, p < 0.02). However, the GH response to GHRH + ARG in PLWS was lower than in NC. In conclusion, our results demonstrate that in PLWS the low somatotrope responsiveness to GHRH is not enhanced by cholinergic potentiation while it is increased by arginine.

Adolescent↗

PubMedDate not supplied

Multiple insulinomas of the pancreas: a patient report.

Whereas there is general agreement about the biochemical diagnosis of hyperinsulinism, the value of imaging to differentiate diffuse from focal pancreatic lesions is still a matter of debate. We describe a case of multiple adenomas of the pancreas in an eleven year-old boy. The source of hyperinsulinism was detected by pancreatic ultrasound examination and confirmed by MRI as a single adenoma of the pancreas. These radiological exams did not identify three other pancreatic adenomata. Our report outlines the difficulties in anatomically localizing the source of excessive insulin secretion in cases of hyperinsulinemic hypoglycemia.

Blood Glucose↗

PubMedDate not supplied

Prevalence and correlations of early microvascular complications in young type I diabetic patients: role of puberty.

The prevalence and correlates of the early signs of renal, retinal and neurological microvascular complications were evaluated in 317 young patients with type I diabetes mellitus. Microalbuminuria was detected in 11% of patients and appeared to be strongly and positively related to HbA1c (p < 0.01) and less significantly to duration of diabetes (p < 0.02). Retinopathy was detected in 22.7% of patients and it was associated with duration of diabetes (p < 0.001). Peripheral neuropathy was detected in 18.5% of patients and there was a strong association with HbA1c (p < 0.01) and a weaker one with duration of diabetes (p < 0.05). Microalbuminuria was not detected in prepubertal patients while a similar frequency of retinopathy and neuropathy was observed in prepubertal and postpubertal patients. These results suggest that: 1) In short-term type I diabetic patients neuropathy is the most frequent microvascular complication, but after 10 years of diabetes, retinopathy exceeds the other complications; 2) Short-term metabolic control may influence the frequency of neuropathy and microalbuminuria but not retinopathy; 3) Puberty is involved in the appearance of microalbuminuria.

Adolescent↗