Magen-Darm- und Verdauungssystem

Abstrakt

Glucagon-Like Peptide-1 Receptor Pet/Ct in Patients with and Without Post Gastric Bypass Hypoglycemia: A Prospective, Matched Case-Control Study

Matthias Hepprich, Kwadwo Antwi, Patricia Wiesner, Claudia Cavelti-Weder, Marc Y. Donath, Emanuel R. Christ, Damian Wild

Purpose: The aim of this pilot study is to prospectively compare in vivo glucagon like peptide-1 (GLP-1) receptor expression in the duodenum and pancreas of patients with and without postprandial hypoglycemia after gastric bypass using GLP-1 receptor imaging with 68Ga-DOTA-exendin-4 PET/CT.

Methods: Five patients after Roux-Y-gastric bypass (RYGB) surgery with postprandial hypoglycemia (PGBH) and five patients after RYGB without PGBH matched for sex, age, operative procedure and postoperative interval underwent 68Ga-DOTAexendin- 4 PET/CT. Total 68Ga-DOTA-exendin-4 uptake in the duodenum and pancreas, defined as the sum of the standard uptake value (SUVsum) for each voxel in the volume of interest (VOI) was measured by two independent readers who were blinded for the clinical information. Additionally, three further patients with PGBH who received 68Ga-DOTA-exendin-4 PET/CT at our center were added to the analysis. Clinical follow up data was collected for all patients with PGBH.

Results: 68Ga-DOTA-exendin-4 PET/CT exhibited a greater range of total duodenal and pancreatic uptake (SUVsum) for matched hypoglycemic patients (2144-7802, median 3022) than for matched normoglycemic patients (5104-7507, median 7072), with no statistical significant difference of total uptake=total in vivo GLP-1 receptor expression (p=0.187). In one patient with PGBH a focal tracer uptake in the pancreatic tail was identified. Four patients with PGBH required ultimately a reversal of their gastric bypass surgery due to insufficient dietary and medical therapy of their hypoglycemic episodes.

Conclusion: 68Ga-DOTA-exendin-4 uptake appears not to be significantly different in patients with PGBH compared to matched normoglycemic patients but may reflect varying stages of the complex pathophysiology of postbariatric hypoglycemia.