Abstract
To discuss the clinical scope and frequency of hypoglycemia following bariatric surgery, and possible mechanisms mediating this potentially life-threatening complication. Consequent to the rise in severe obesity, bariatric surgery is being performed with ever increasing frequency. Although data continue to accumulate supporting the myriad metabolic and other health benefits of bariatric surgery, there are also concerns regarding the mounting reports of severe hypoglycemia. The problem is particularly significant following gastric bypass, with the first concerns raised in 2005 following a case series reported from the Mayo Clinic. A Swedish nationwide cohort study recently estimated the frequency of this complication suggesting it was less than 1%. Hypotheses regarding the mechanism(s) by which hypoglycemia arise following gastric bypass range from beta cell expansion to altered beta cell function as well as nonbeta cell factors. Regardless of the incidence, the severity of hypoglycemia for select patients following gastric bypass necessitates that we strive to gain a better understanding of the underlying mechanisms. With such knowledge, those patients at greater risk for this complication might be identified preoperatively, and decisions regarding their surgical management optimized to reduce this risk.
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