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Endocrine Abstracts (2014) 34 CMW1.3 | DOI: 10.1530/endoabs.34.CMW1.3

1University College Hospitals, London, London, UK; 2National Centre for Cardiovascular Prevention and Outcomes, UCL Institute of Cardiovascular Science, London, UK.


The growing adoption of bariatric surgery (BS) as treatment for severe and complex obesity, is resulting in the emergence of both iatrogenic and nosohypokatastatic (disease substitution) diseases. Malabsorption (an integral part of gastric bypass surgery) may compound mineral, vitamin and trace element deficiencies that also result from poor nutrition that can be worsened by the restricted intake imposed by BS. Thiamine deficiency (especially in those who have frequent vomiting) can produce Wernicke encephalopathy. Vitamin D deficiency affects most patients with morbid obesity before BS. Bone loss is likely to occur after BS and fracture risk is increased, although possibly not related to the surgery per se. There is particular concern of the impact of BS in women of childbearing age who subsequently become pregnant. While BS is it is protective against infant macrosomia in obese mothers, it has been associated with multiple negative maternal and fetal outcomes. While one of the major benefits of bariatric surgery is to improve glycaemic control in patients with diabetes, with marked reductions in A1c even after withdrawal of hypoglycaemic therapy, it does not normalise blood glucose profiles. The significance of the (inevitable) excessive rises in post-prandial glucose levels to long-term micro- and macrovascular disease is unclear. However, an increasingly recognised metabolic consequence is ‘reactive’ hypoglycaemia that appears to result from the hyper-responsiveness of incretin response to meals. There continues to be debate as to whether nesidioblastosis or insulinoma can result from the continued exposure of the β-cell to incretins, but if this does occur it is rare. Some evidence points to an acquired hypothalamic unresponsiveness to hypoglycaemia as a contributory factor. Increased absorption of calcium oxalate can lead to deposition in the renal parenchyma, resulting in oxalate nephropathy and renal failure as well as an increased incidence of ureteric renal stones.

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