We thank Mueller et al. (1) for their interest in our article (2), in which we demonstrated that type 1 diabetic patients present low fecal pancreatic elastase-1 (PE-1) and that PE-1 correlates with C-peptide, HbA1c (A1C), and diabetes duration. In 16 type 1 diabetic patients, they found that PE-1 concentrations were low compared with control subjects but did not correlate with A1C and diabetes duration.
Furthermore, Mueller et al. observed that patients on drugs interfering with the angiotensin system show a further reduction of PE-1. Since we did not mention treatment with these drugs in our report, we now provide this information. Eight of our 37 type 1 diabetic patients were on ACE inhibitors. PE-1 was lower in patients on ACE inhibitors (135.2 ± 25.9 vs. 297.9 ± 35.3 μg/g stools, P = 0.0211), confirming the observation of Mueller et al. Also, in patients not on ACE inhibitors, PE-1 correlated with A1C (r = −0.490, P = 0.007), diabetes duration (r = −0.400, P = 0.0325), and C-peptide (r = 0.540, P = 0.0028).
Thus, we confirm in this subgroup the correlation between A1C and PE-1 already described in our whole series (2). On the other hand, it is interesting to observe that in the series of Mueller et al., 4 of the 5 patients with A1C >8% presented PE-1 <200 μg/g stools compared with 5 of the 11 patients with A1C <8% (i.e., 80 vs. 45%), suggesting that blood glucose control also influenced, in some way, PE-1 in their patients. But why did patients on ACE inhibitors show low PE-1 values? Mueller et al. suggest a role for the inhibition of the local angiotensin-generating system, which has been described in pancreas (3). This hypothesis is intriguing. It should not be forgotten, however, that ACE inhibitors are prescribed to cure hypertension and/or microalbuminuria, which depend at least in part on diabetes duration and glycemic control, which influence PE-1 per se. When our 8 patients on ACE inhibitors were compared with the other 29, they presented a longer diabetes duration (15.8 ± 3.2 vs. 8.9 ± 1.3 years, P = 0.0388) and a trend to higher A1C (8.9 ± 0.53 vs. 7.9 ± 0.26%, P = 0.07) and lower C-peptide (0.08 ± 0.023 vs. 0.36 ± 0.089 ng/ml, P = 0.46). Their lower PE-1 values, therefore, could also be attributed to these factors and not only to a putative inhibitory effect of ACE inhibitors on exocrine pancreas function. In conclusion, we provide further evidence that in our series, PE-1 correlates with A1C. Furthermore, we confirm that type 1 diabetic patients on ACE inhibitors show lower PE-1 concentrations and thank Mueller et al. for their interest in our work and for the intriguing suggestion concerning the relationship between PE-1 and ACE inhibition.
