Post-Prandial Hypoglycemia Can be a Manifestation of Impaired Glucose Tolerance

Presentation Number: MON 608
Date of Presentation: April 3rd, 2017

Chong Yau Ong*1, Pelicano Ma Donna Balagapo1, Shengyong Su1 and Yu Kwang Tay Donovan2
1Sengkang Hospital, Singapore, Singapore, 2Sengkang Hospital and Singapore General Hospital, Singapore, Singapore

Abstract

Introduction

Although the underlying etiology for post prandial hypoglycemia is well defined, evaluation of this problem can poses a diagnostic conundrum to clinicians. We present a case of post- prandial hypoglycemia that was eventually attributed to impaired glucose tolerance to highlight the diagnostic difficulty.

Clinical Case

A 36 year old, Filipino lady, who was previously well, presented to our institution for evaluation of recurrent hypoglycemia. Her symptoms were exclusively post-prandial manifesting 3 to 5 hours post carbohydrate rich meals/beverage and consist of hunger pangs, headache, disorientation, blurred vision and diaphoresis. Occurrence of symptoms were accompanied by documented capillary blood glucose readings of 2.7 to 3.8 mmol/L and were relieved by frequent food ingestion resulting in a significant weight gain of 13kg over that past few years. She revealed a strong family history of diabetes mellitus. She weighed 65kg (BMI 28.9kg/m2) and had no evidence of acanthosis nigricans or hyperandrogenism. Renal and liver function test and short synacthen test were normal.

She underwent a supervised 72 hr fast test. At 63 hours into fast, she developed symptomatic hypoglycemia (plasma glucose: 2.4 mmol/L) with corresponding C-peptide 0.69 ug/L (<0.6) and insulin 2.67 mIU/L (<3). βOHB at end of fast was elevated at 3.3 mmol/L (>2.7) and there was a 0.5 mmol/L rise in glucose with 1mg glucagon. Drug screen for sulphonylurea and metglitinides were negative.

In view of the inappropriate elevated C-peptide, she underwent a second 72 hr fast test which provoked asymptomatic hypoglycemia (plasma glucose: 2.3 mmol/L) with corresponding suppressed C-peptide 0.46 ug/L and insulin 0.36 mIU/L. βOHB was elevated at 3.8 mmol/L and there was a 0.6 mmol/L rise in glucose with 1mg glucagon at the end of the test consistent with an insulinopenic state. She also underwent mixed meal testing with no occurrence of hypoglycemia or symptoms over 5 hours. A negative 72hr fast and mixed meal testing excluded endogenous hyperinsulinemia. Further workup showed an Hba1c of 5.3% and a 75g OGTT revealed a fasting glucose of 5.3 mmol/L and a 2hr reading of 10.6 mmol/L consistent with impaired glucose tolerance. No lesion was found on CT imaging of the pancreas. Her symptoms resolved with acarbose in addition to dietary modification. 

 Conclusion

Reactive or post-prandial hypoglycemia can be a result of an inappropriate and dyssynchronous pancreatic β-cell insulin response to a post absorptive plasma glucose surge where the insulin peak is delayed and occurs with a declining glucose. This has been reported in patients with early diabetes mellitus yet to develop significant peripheral insulin resistance as in our patient. Patient should be thoroughly investigated and organic causes of endogenous hyperinsulinaemia be excluded before attributing symptoms to diabetes mellitus.

 

Nothing to Disclose: CYO, PMDB, SS, YKT