A Review of the Use of Acarbose for the Treatment of Post-prandial Syndrome (Reactive Hypoglycemia)

Introduction: The term “reactive” hypoglycemia, also known as post-prandial hypoglycemia has been loosely defined in the literature. The term refers to the occurrence of autonomic symptoms including weakness, perspiration, hunger, nausea, anxiety and tremors occurring one to two hours after ingestion of a meal. This collection of symptoms has been described in various patient groups including patients with impaired glucose tolerance, dumping syndrome following gastric surgeries (e.g. Nissen fundoplication, Billroth II and Roux en Y gastric bypass) and in patients in whom no specific cause has been identified. These autonomic symptoms have been reported in patients with and without documented hypoglycemia. This suggests that factors other than hypoglycemia may also be involved in the pathogenesis of this disorder. Data extraction: English-language articles that presented data relevant to the treatment of reactive hypoglycemia were identified in a MEDLINE search from 1966 to 2011. References of these articles and other publications were also reviewed. Search terms were reactive hypoglycemia, functional hypoglycemia, post-prandial hypoglycemia, Nissen fundoplication, Billroth procedure, gastric banding, Roux en Y occurring in association with the term hypoglycemia. Studies were included for review if they evaluated the clinical use of acarbose for the treatment of this syndrome and did not meet our exclusion criteria. Evidence synthesis: Five case reports and four small controlled trials met our inclusion criteria which examined the use of acarbose in the treatment of reactive hypoglycemia. Conclusion: We suggest the term Post-Prandial Syndrome (PPS) rather than reactive hypoglycemia since hypoglycemia is often not documented in patients who nevertheless experience postprandial autonomic symptoms. Acarbose is often used for the treatment of postprandial syndrome, but the evidence for its effectiveness is sparse and not definitive. Although acarbose does cause a statistically significant increase in the post-prandial glucose nadir after sucrose ingestion under experimental conditions, the effect is minimal and may not be clinically significant. There are currently no high-quality placebo-controlled clinical trials for the treatment of this syndrome. Further studies are needed to evaluate the potential therapeutic benefit of acarbose in the treatment of PPS. *Corresponding author: Tharsan Sivakumar, LMC Endocrinology Centers, Dartmouth-Hitchcock Medical Center / Dartmouth Medical School, USA, E-mail: [email protected] Received October 24, 2011; Accepted January 28, 2012; Published January 31, 2012 Citation: Sivakumar T, Sivakumar S, Chaychi L, Comi RJ (2012) A Review of the Use of Acarbose for the Treatment of Post-prandial Syndrome (Reactive Hypoglycemia). Endocrinol Metabol Syndrome S1:010. doi:10.4172/2161-1017. S1-010 Copyright: © 2012 Sivakumar T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Introduction The term “reactive” hypoglycemia, also known as post-prandial hypoglycemia or functional hypoglycemia has been loosely defined in the literature. This phenomenon was first described by Harris in 1924 who reported five cases of hypoglycemia following a meal which he called reactive hypoglycemia [1]. The term refers to the occurrence of autonomic symptoms including weakness, perspiration, hunger, nausea, anxiety and tremors occurring one to two hours after ingestion of a meal. This collection of symptoms has been described in various patient groups including patients’ with impaired glucose tolerance, dumping syndrome following gastric surgeries (e.g. Nissen fundoplication, Billroth II and gastric bypass) and in patients in whom no specific cause has been identified. These autonomic symptoms have been reported in patients with and without documented hypoglycemia. This suggests that factors other than hypoglycemia may also be involved in the pathogenesis of this disorder. The prevalence of this condition is difficult to ascertain since the symptoms are subjective and there are no formal criteria for diagnosis. To evaluate the prevalence of symptoms attributed to hypoglycemia, a British trial randomly selected 2000 women between the ages of 17-50 and mailed them a health and well-being questionnaire. The women were unaware of the specific focus of the study. The authors report that 37.9% of the participants experienced symptoms attributed to hypoglycemia approximately four times per month [2]. This study did not assess whether the individuals were actually experiencing hypoglycemia but aimed to investigate the percentage of women from a random sample in the UK reporting symptoms which they ascribed to low blood sugar. Only 0.5% of those reporting symptoms in this survey had sought medical advice for their symptoms. However, other studies have shown that many patients attribute their symptoms to hypoglycemia, but do not have “true hypoglycemia” as defined the by American Diabetes Association requiring plasma glucose value < 3.9 mmol/L (<70 mg/dL) [3]. Thus the term Post-Prandial Syndrome (PPS) maybe a better term than the commonly used “reactive hypoglycemia” since it describes a collection of post-prandial symptoms but does not require documented hypoglycemia. Several case reports, and a few small placebo-controlled trials have examined the use of acarbose in the treatment of reactive hypoglycemia. Acarbose is an alpha-glucosidase inhibitor which prevents the hydrolysis of di-, triand oligosaccharides to monosaccharides in the intestinal brush border, thereby slowing their absorption. This leads attenuation of post-prandial hyperglycemia which may be related to Citation: Sivakumar T, Sivakumar S, Chaychi L, Comi RJ (2012) A Review of the Use of Acarbose for the Treatment of Post-prandial Syndrome (Reactive Hypoglycemia). Endocrinol Metabol Syndrome S1:010. doi:10.4172/2161-1017.S1-010