In order to evaluate hypothalamic-pituitary-adrenal activity in diabetic patients in relation to neuroautonomic balance, we studied 50 consecutive hospitalized T2D patients (22F, 28M) without symptoms of neuropathy or hypercortisolism. We measured: morning, midnight and post-dexamethasone suppression cortisol (F8, F24 and F-Dex respectively) 24-hours urinary free cortisol (UFC), morning ACTH, systolic and diastolic blood pressure levels (SBP, DBP) and performed deep-breathing (DB), lying-to-standing (LS) and postural hypotension (PH) tests. Patients were subdivided according to the presence of parasympathetic (Group A, n=11), sympathetic (Group B, n=11), para- and sympathetic (Group C, n=9) dysfunction or the absence of autonomic failure (Group D, n=15). Age (whole group 58.2±9.3 yrs), BMI (whole group 30.3±4.9 kg/m2) and glycated haemoglobin (HbA1C, whole group 10.3±2.2%) were comparable among the 4 groups.
HPA activity was significantly increased in Group A compared to Group D (UFC 48.6±21.4 vs 21.6±9.8 μg/24 h, P<0.0001; ACTH 27.0±8.6 vs 15.7±5.7 pg/dl, P<0.01; F8 20.4±4.5 vs 13.6±3.8 μg/dl, P<0.05; F-Dex 1.2±0.4 vs 0.8±0.6 μg/dl, P<0.05, respectively) and Group B (UFC 26.3±11.0 μg/24 h, P<0.0001; ACTH 19.9±8.0 pg/dl, P<0.05). SBP and DBP were significantly increased in Group A compared to Group D (SBP 136.4±16.8 vs 120.7±12.9 mmHg, P<0.01 and DBP 81.0±7.7 vs 74.0±6.1 mmHg, P<0.05 respectively) and Group B (SBP 123.3±14.6, P<0.05; DBP 75.5±7.2, P<0.05).
Values of DB and LS tests resulted to be correlated to UFC (r=−0.39, P=0.006; r=−0.46, P=0.009), SBP (r=−0.32, P=0.025; r=−0.30, P=0.04) and DBP (r=−0.28, P=0.046; r=−0.32, P=0.025). Multivariate linear regression analysis showed that UFC levels were significantly associated with parasympathetic neuronal dysfunction as reflected by LS test (β=−0.44, P=0.003) after adjusting for BMI, HbA1C and disease duration. Asymptomatic diabetic autonomic unbalance is associated to increased activity of HPA axis and blood pressure levels, related to the degree of the neuronal dysfunction.
01 - 05 Apr 2006
European Society of Endocrinology