ECE2021 Oral Communications Young Investigator Awards (12 abstracts)
1Ghent University Hospital, Endocrinology, Ghent, Belgium; 2Ghent University Hospital, Rehabilitation Sciences, Gent, Belgium; 3Ghent University Hospital, Gastro-Intestinal Surgery, Ghent, Belgium
Background
Precise diagnostics for postprandial reactive hypoglycaemic syndrome (PRHS) after gastric bypass surgery (GBS) are lacking. Oral glucose tolerance tests are advocated but might cause early dumping in this population and often cause hypoglycaemic values in a normal population.
Aim
To evaluate glycaemic responses during liquid and solid mixed meal tolerance tests (LMMTT and SMMTT) in a post-GBS population.
Subjects and methods
Twenty-two subjects (age 49 ± 10 years, BMI 29.8 ± 4.9 kg/m2) who were at least one year after GBS, with or without subjective complaints of PRHS, and 14 age-matched control subjects (6 normal-weight, 8 obese) participated. With a 1-week interval, all underwent a 3-hour LMMTT and SMMTT (with equal caloric and macronutrient content). Serum glucose concentration was determined using hexokinase method, insulin with immunoassays (COBAS, Roche Diagnostics). Hypoglycaemic symptoms during testing were evaluated using a 4-point Likert scale for the Edinburgh Hypoglycaemia Scale (EHS) and divided into three EHS subcategories (autonomic, neuroglycopenic, malaise symptoms).
Results
In the GBS group, mean nadir glucose levels did not differ between LMMTT and SMMTT (70 ± 16 mg/dl vs 71 ± 15 mg/dl, P > 0.05). During LMMTT, three and 10 subjects had glucose levels < 54 mg/dl and < 70 mg/dl, respectively which did not differ from the SMMTT where this was two and 10 subjects, respectively (P > 0.05). During LMMTT, markedly higher maximal glucose and insulin levels were observed than during SMMTT (glucose: 186 ± 27 mg/dl vs 156 ± 27 mg/dl, P < 0.001; insulin: 169 (107 240) mU/l vs 92 (71 146) mU/l, P = 0.002; respectively). Rates of increase and decrease were greater during LMMTT for both glucose (P < 0.001 and P = 0.001, respectively) and insulin (P = 0.001 and P = 0.006, respectively) levels. Short after ingestion (15 and 30), there were more autonomic, neuroglycopenic and malaise symptoms and at 150 and 180 there were more autonomic symptoms during LMMTT vs SMMTT (all P < 0.05). No-one from the control group developed glucose levels < 54 mg/dl during either test whereas three and one developed glycaemia < 70 mg/dl during LMMTT and SMMTT, respectively. The control group had more autonomic symptoms during LMMTT (at 120 and 150) in comparison to the post-GBS group (all, P < 0.05).
Discussion
In a post-GBS population, although a LMMTT causes greater variability in glycaemic and insulinemic responses and development of PRHS symptoms (but also symptoms of early dumping) than a SMMTT, both tests do not differ in nadir glucose levels or frequency of hypoglycaemia. In addition, neither tests cause hypoglycaemic values in control subjects making them possible diagnostic tools for PHRS in post-GBS subjects.