Bariatric Surgery and Calcium and Vitamin D Metabolism

Bariatric surgery has been reported to be closely associated with altered calcium metabolism and changes in the bone mineral density [15, 16]. Bypass of the duodenum and/or nutritional inadequacy in the immediate post-operative period are the main factors that lead to calcium malabsorption which could potentiate secondary hyperparathyroidism.

After bariatric surgery low levels of circulating calcium leads to increased parathyroid hormones and a reduction in bone mass, particularly a depletion of calcium and phosphorous in order to increase the blood calcium levels. At the same time, the kidney increases the phosphorus and calcitrol excretion and reduces calcium excretion. This whole mechanism causes secondary hyperparathyroidism [16]. Vitamin D deficiency secondary to less sunlight exposure and inadequate vitamin D rich food intake may worsen secondary hyperparathyroidism.

Studies have shown a significant fall in bone mineral density (BMD), bone mineral content (BMC) and increased bone remodeling within the first year postbariatric surgery [17]. This fall in BMD has been demonstrated after all kinds of bariatric procedures [18-20]. It has been noted that these changes in BMD are closely associated with the change in body composition following weight loss. For non-surgical weight loss therapies every 10 % weight loss leads to a bone mass reduction by 1-2 % [21]. But with more significant weight loss following bariatric surgery this fall has been found to be significantly higher [22]. It has also been demonstrated that this fall in BMD persisted beyond the first year, with bone loss continuing throughout the second year at all skeletal sites with the serum calcium levels, vitamin D3 and PTH levels maintained within normal limits during this period [21].

Thus, several mechanisms have been suggested for changes in BMD besides nutritional inadequacy. One mechanism suggested is that a reduced mechanical load on the skeleton leads to secondary reduction in bone mass [21]. The other possible explanations are alterations in gut derived hormones like GLP-1, Peptide YY and Ghrelin which can lead to bone loss in association with fall in levels of leptin and elevated adiponectin [23-26].

The distribution of BMD reduction has been researched in several studies. A recent meta-analysis comparing all kinds of bariatric procedures showed that this BMD was significantly low only at the femoral neck and not at the lumbar spine [27]. Another study in post sleeve gastrectomy patients also showed significant fall in BMD in the hip and femoral neck and not in the spine [19]. The clinical implications of this distribution are uncertain. A recent population based study showed that following bariatric surgery the risk of fracture was increased two fold [28]. A population based retrospective study from UK showed that bariatric surgery increased fracture risk at 3-5 years after surgery, but this was not statistically significant [29]. In another study on bariatric surgery and bone loss it was demonstrated that there was no increased risk of fractures [30].

This stresses the importance of adequate replacements of calcium and vitamin D3 that needs to be initiated in the first months of surgery itself, which is the period, associated with severe muscle loss and increased bone turnover [31]. The BABS study (Bone metabolism after bariatric surgery) demonstrated that pre-operative loading of vitamin D along with ongoing vitamin D and calcium supplementation with adequate protein supplementation with physical exercise decelerates the loss of both BMD and LBM (lean body mass) after bariatric surgery [32].

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