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  • 1
    ISSN: 1432-1440
    Keywords: Type 1 diabetes ; Hypoglycemia ; Glucose counterregulation ; Insulin pumps
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We were interested in studying whether impaired hypoglycemic awareness after intensified insulin treatment with insulin pumps is associated with impaired glucose counterregulation. Glucose counterregulatory hormones were measured in 7 type I diabetic patients with altered symptoms after 6 months of continuous subcutaneous insulin infusion (CSII) (group 1) and in 9 patients with unchanged symptoms of hypoglycemia under CSII (group 2). The groups did not differ in diabetic control, duration of diabetes, or prevalence of neuropathy. Counterregulatory hormone response to an insulin-induced episode of hypoglycemia was measured before (first test) and after 6 months (second test) of CSII. Glucose nadirs and glucose recovery were similar in both groups and both tests. The mean plasma glucagon values demonstrate a lack of glucagon response in both groups and both tests. Growth hormone and cortisol increased in both groups and both tests without any difference between the groups or first and second tests. Epinephrine response was similar in both tests of group 2 (first test: 50±5 to 416±73; second test; 45±5 to 456 pg/ml), while in group 1 the response was not increased significantly in the second test [first test: 32± 6 to 346± 63; second test: 44± 7 to 575± 91 pg/ml; areas under curve (AUC) 11977 and 16345 pg×ml−1×90 min−1 (p= 0.36)]. There was a norepinephrine response in both groups and both tests, with nonsignificantly higher plasma levels during the second test [AUC in pg×ml−1×90 min−1; group 1, first test: 20954, second test: 26675 (p=0.394); group 2, first test: 20745, second test: 27089 (p=0.302)]. The results demonstrate that impaired awareness of hypoglycemic symptoms after intensified insulin therapy is not associated with impaired glucose recovery of hypoglycemia or impaired response of glucose counterregulatory hormones. Further-more, we found that the frequency of glucopenic symptoms reported by the patients during everyday life increased after CSII, while adrenergic symptoms were less frequent.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Type 1 diabetes ; Recent onset ; Glycemic control ; Nerve conduction ; Autonomic function ; Cutaneous sensation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Motor and sensory nerve conduction velocities (MNCV, SNCV), beat-to-beat variation (BBV) at rest, speed of pupillary dilation (SPD), and pupillary latency time (PLT) were measured in 32 patients aged 12–36 years after 19±2 (mean±SEM) days and again after 3, 12, and 24 months of insulin treatment. Moreover, BBV under deep respiration was determined after 12 and 24 months, and thermal discrimination thresholds (TDT) as well as pain and vibration perception thresholds (PPT, VPT) were evaluated after 24 months. Mean HbA1 levels during months 3–24 within the normal range (7.2±0.2%; mean±SEM) were observed in 20 patients (group 1), while in 12 patients (group 2) mean HbA1 of months 3–24 was elevated (10.1±0.4%). There were no significant differences between both groups with regard to the nerve function tests at baseline and after 3 months. After 12 months mean median MNCV and median, ulnar, and sural SNCV were significantly lower in group 2 than in group 1 (p〈0.05). After 24 months mean median MNCV, peroneal MNCV, median SNCV, and sural SNCV as well as both BBV tests and PLT were significantly impaired in group 2 as compared to group 1 (p〈0.05). In addition, mean malleolar VPT and PPT to heat and cold stimuli on the thenar and the foot were significantly elevated in group 2 as compared to group 1 (p〈0.05). These findings suggest that early deterioration of somatic nerve function after one year and of autonomic function after 2 years of diabetes may be prevented by effective glycemic control initiated immediately after diagnosis of the disease.
    Type of Medium: Electronic Resource
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