The overall prevalence of grade 2 and 3 adult obesity (body mass index, BMI>35 kg/m2
) derived from the 2009–2010 National Health and Nutrition Examination Survey (NHANES) exceeded 15% and grade 3 obesity (BMI>40 kg/m2
) accounted for 6.3%.1
The dietary approach is of limited value in the short term and weight regain is practically the rule in the long run, as a consequence of the poor compliance to the diet shown by obese subjects. In fact, in a recent study,2
where different types of diets were assigned to a population of overweight and obese subjects (BMI from 25 to 40 kg/m2
), an average of 6 kg, corresponding to 7% of initial body weight, was lost in the first 6 months, but most of the weight was regained after 1 year and at 2 years, only 31–37% of the participants had maintained a weight loss of at least 5% of their initial weight.
Bariatric surgery has long been recognised as an effective treatment for grades 3 or 2 obesity associated with complications3
and, accordingly, the number of bariatric operations in the USA is growing over time from ca. 10 000 in the early 1990s to 103 000 in 2003.4
Bariatric surgery may determine type 2 diabetes remission,5
while improving several other serious comorbidities.7
Among bariatric surgery procedures, Roux-en-Y gastric bypass (RYGB) was shown to account for 41% of all bariatric operations at least in the USA.8
Sleeve gastrectomy (SG), which was originally conceived as a first step before performing RYGB or biliopancreatic diversion with duodenal switch in super-obese patients,9
has recently gained a place as first-choice restrictive bariatric procedure.10
It was noted that SG determines weight loss similar to that achieved after RYGB11
and larger than that following laparoscopic adjustable gastric banding.12
Reactive hypoglycaemia is a late complication of RYGB, although it seems to occur also after SG.
After RYGB, early insulin secretion is enhanced during an oral glucose tolerance test (OGTT)14
or after a meal,15
which fact might explain the later reactive hypoglycaemia. An increasing number of reports highlight the occurrence of severe hypoglycaemia after RYGB, including cases of neuroglycopaenia attributed to nesidioblastosis.17–20
Roslin et al21
found that 72%, that is, 26 of 36 patients who underwent RYGB 6 months earlier, had reactive hypoglycaemia at 2 h during OGTT (100 g of glucose), which was defined as ‘an absolute serum glucose level ≤60 mg/dl, or a drop of 100 mg/dl in serum glucose level in 1 h’.
As compared with RYGB, SG seems to have a much lower occurrence of reactive hypoglycaemia, ca. 3%, that is, 1 of 31 patients studied at 6 weeks after the operation in one series.22
Fortunately, the frequency of severe hypoglycaemia or related symptoms requiring hospitalisation after RYGB is pretty low, the adjusted HRs were in fact 2.7 for hypoglycaemia, 2.8 for confusion, 4.9 for syncope, 3.0 for epilepsy and 7.3 for seizures in a Swedish retrospective cohort study on 5040 cases based on national registries.23
However, until now no prospective studies have investigated the incidence of hypoglycaemia after RYGB and no randomised studies have been undertaken to compare the effect of SG to that of RYGB in terms of incidence of hypoglycaemic episodes.
The primary aim of the present study was to conduct a 1-year randomised trial to compare the incidence of hypoglycaemia after RYGB or SG. A secondary objective of great interest is the assessment of the comparative ability of the two surgical procedures in determining the improvement or normalisation of insulin sensitivity in this class of subjects, given the established relevance of insulin resistance in the cardiometabolic syndrome.