ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P946 | DOI: 10.1530/endoabs.63.P946

Screening of abnormal glucose metabolism in cystic fibrosis could there be a place for DPP-4 inhibitors in early stages?

Begoña Pla Peris1, Clara Marijuan Sánchez1, Nerea Aguirre Moreno1, Iñigo Hernando Alday1, Sara Jiménez Blanco1, Miguel Sampedro Nuñez1, Rosa Girón Moreno2, Monica Marazuela Azpiroz1 & Alfonso Arranz Martin1

1Division of Endocrinology and Nutrition, Hospital Universitario de la Princesa, Madrid, Spain; 2Division of Pulmonary and Respiratory diseases, Hospital Universitario de La Princesa, Madrid, Spain.

Introduction: Abnormal glucose metabolism (AGM) is the most common extra-pulmonary comorbidity in people with cystic fibrosis (CF) and has a high negative impact on the underlying disease. Elevated postprandial glucose level is usually the first manifestation, which is traditionally detected by 75-gram oral glucose tolerance test (OGTT). The aim of this study was to evaluate glycemic pattern during continuous glucose monitoring (CGM) in patients with impaired glucose metabolism previously detected by OGTT. Compare both methods and examine the short-term response to DPP-4 inhibitor (DPP-4i).

Methods: We included CF adult patients with consecutively abnormal glucose metabolism by OGTT in our clinic in stable clinical situation and with informed consent. We used CGM (DexcomG4Platinum) during 2 weeks, with DPP-4i administration during the second week. We compared both screening methods and CGM glucose response to treatment.

Results: We evaluated 13 patients (seven males, aged 25 [22–38] years). Mean CF progression time was 23.2±9.5 years. Eight cases met criteria for cystic fibrosis related diabetes (CFRD) by OGTT, four for impaired glucose tolerance (IGT) and 1 for indeterminate glycemia (INDET). Mean fasting plasma glucose was 94.4±10.6 mg/dl. We observed glucose >200 mg/dl by CGM in four patients without CFRD initial diagnosis (corresponding in most cases to breakfast and dinner time intervals). In two patients diagnosed with CFRD by OGTT, CGM glucose > 200 mg/dl was not identified. No significant correlation between CF progression time and dysglycemia was found. We observed a strong positive correlation (r=0.8) between mean CGM glucose and glucose >200 mg/dl by CGM (P=0.001). After use of DPP-4i a decrease in mean CGM glucose and in variability was noted (113.9–106.5 mg/dl and 14.2–10.5 mg/dl, respectively), P<0.02. % of glycemias within 131–240 mg/dl CGM range improved from 24±14% without use of DPP-4i, to 16±9% with use of DPP-4i (P=0.001). A non-significant decrease in CGM glucose >200 mg/dl without and with use of DPP-4i was found. We observed a strong negative correlation (r=0.7) both for CF progression time and HOMA ß (P<0.05) and for HOMA ß and dysglycemia, this last one non-significant.

Conclusion: Use of CGM provides additional information to traditional methods of detecting AGM in adult patients with CF. DPP-4i may be a useful therapeutic alternative in early stages of dysglycemia. The role of this treatment in the overall improvement of AGM in adult patients with CF should be confirmed with clinical studies.