Serum ACE Predicts Severe Hypoglycemia in Children and Adolescents With Type 1 Diabetes
- 1Division of Pediatrics, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping, Sweden
- 2Division of Child and Adolescent Psychiatry, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping, Sweden
- 3Center for Medical Technology Assessment, Department of Health and Society, Linköping University, Linköping, Sweden
OBJECTIVE—To investigate whether risk of severe hypoglycemia is related to serum (S) ACE level during intensive treatment in type 1 diabetic children.
RESEARCH DESIGN AND METHODS—A cohort of 86 intensively treated type 1 diabetic patients was studied during 1999–2000. In 1999, the age range was 7–19 years (median 12.8), diabetes duration was 1.2–14.7 years (5.3), insulin dose was 0.4–1.7 units · kg−1 · 24 h−1 (1.0), and the HbA1c year mean was 4.7–10.2% (6.8). HbA1c, insulin doses, and events of severe hypoglycemia (needing assistance from another person) were prospectively registered at regular visits, scheduled quarterly. S-ACE was determined once.
RESULTS—Severe hypoglycemia was correlated to S-ACE (r = 0.22, 95% CI 0.01–0.41, P = 0.0093). The square root of severe hypoglycemia was correlated to S-ACE (r = 0.27, 95% CI 0.06–0.45, P = 0.0093). Patients with S-ACE at the median level or above (n = 44) reported a mean of 3.0 yearly events of severe hypoglycemia compared with 0.5 events in patients with S-ACE lower than the median (n = 42) (P = 0.0079). Of the patients with an S-ACE at the median level or above, 27 (61%) reported severe hypoglycemia, compared with 17 (40%) patients with an S-ACE lower than the median (P = 0.0527). Insulin dose, HbA1c, age, onset age, duration, C-peptide, and sex did not differ between these two groups. S-ACE was negatively correlated with age (r = −0.27, 95% CI −0.46 to 0.07, P = 0.0265) but not with HbA1c, duration, or blood pressure.
CONCLUSIONS—The elevated rate of severe hypoglycemia among patients with higher S-ACE suggests, among other factors, that a genetic determinant for severe hypoglycemia exists. Further evaluation is needed before the clinical usefulness of this test can be elucidated.
Address correspondence and reprint requests to Dr. S. Nordfeldt, Department of Molecular and Clinical Medicine, Division of Pediatrics, Faculty of Health Sciences, S-581 85 Linköping, Sweden. E-mail:.
Received for publication 15 May 2002 and accepted in revised form 22 October 2002.
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