Bariatric surgery, bone loss, obesity and possible mechanisms.

Bariatric surgery remains the most effective treatment for severely obese patients. However, the potential long-term effects of bariatric surgical procedures on health, including bone health, are only partially understood. The goal of this review was to present data on the impact of bariatric surgery on bone metabolism and to analyse possible reasons for the loss of bone mass that frequently occurs after bariatric surgery. Such factors include nutritional deficiencies, rapid weight loss per se, effects of fat-derived adipokines and gut-derived appetite-regulatory hormones. However, the relative roles of these factors in skeletal regulation and the mechanisms by which they work are not yet fully defined. Our review was focussed on the complex relationship between body weight, fat mass and bone mass, as well as peripheral and central mediators potentially involved in the dual regulation of both energy and bone homeostasis. We also review the data on the inverse relationship between central obesity, bone marrow fat and osteoporosis. As the number of bariatric operations increases, it is imperative to recognize mechanisms responsible for bariatric surgery-induced bone loss, with careful monitoring of bone health including long-term fracture incidence in patients undergoing these procedures.

Hypercalcaemia caused by a carcinoid tumour.

Humoral hypercalcaemia resulting from carcinoid tumours is uncommon. We report a case of hypercalcaemia because of excessive secretion of parathyroid hormone-related protein (PTHrP) in a 77-year-old woman with an advanced carcinoid tumour. Fibroblast growth factor 23 levels were also elevated. The hypercalcaemia responded to adjunctive therapy with long-acting octreotide analogue therapy, bisphosphonates and steroids. The role of PTHrP in humoral hypercalcaemia of malignancy, its association with neuroendocrine tumours, as well as the therapeutic use of somatostatin analogues are reviewed.