Markers of Bone Metabolism in Obese Individuals Undergoing Laparoscopic Sleeve Gastrectomy.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
laparoscopic sleeve gastrectomy (LSG) | decrease | excess weight loss (EWL) | obese patients | 54 ± 20 % | caused | #1 |
- | decrease | 25-hydroxyvitamin D (25(OH)D) | subjects | 80 % | found decreased levels | #2 |
- | decrease | calcium | subjects | 5 % | found decreased levels | #3 |
- | increase | parathyroid hormone (PTH) | subjects | 39 % | found increased levels | #4 |
- | increase | bone alkaline phosphatase (BAP) | subjects | 28 % | found increased levels | #5 |
- | increase | N-telopeptides crosslinks (NTx) | subjects | 21 % | found increased levels | #6 |
laparoscopic sleeve gastrectomy (LSG) | increase | mean levels of NTx | - | - | increased | #7 |
laparoscopic sleeve gastrectomy (LSG) | increase | prevalence of elevated levels of NTx | - | - | increased | #8 |
laparoscopic sleeve gastrectomy (LSG) | no change | mean blood concentrations of 25(OH)D, calcium, PTH, and BAP | - | - | did not change | #9 |
laparoscopic sleeve gastrectomy (LSG) | no change | relative prevalence of deficiencies regarding these markers | - | - | did not change | #10 |
calcium and vitamin D supplementation | increase | supplementation rates | - | - | increased | #11 |
laparoscopic sleeve gastrectomy (LSG) | no change | vitamin D metabolism | - | - | did neither aggravate nor ameliorate | #12 |
laparoscopic sleeve gastrectomy (LSG) | increase | bone resorption | - | - | led to increased | #13 |
routine supplementation of calcium and vitamin D | no change | obesity-associated deficiencies in bone metabolism | - | - | is not likely sufficient to compensate | #14 |
BACKGROUND: Besides its advantages, bariatric surgery implicates a risk of nutritional deficiencies, which might result in impaired bone metabolism. We assessed the effect of laparoscopic sleeve gastrectomy (LSG) on blood markers of bone metabolism in obese patients during a 3-year observation period. METHODS: In 39 obese patients (29 women, 10 men, mean BMI 51.8 ± 6.8 kg/m(2)) undergoing LSG, we measured blood concentrations of 25-hydroxyvitamin D (25(OH)D), calcium, parathyroid hormone (PTH), bone alkaline phosphatase (BAP), and N-telopeptides crosslinks (NTx) before LSG and up to 3 years postoperatively. Vitamin D and calcium supplementations were recorded. RESULTS: LSG caused an excess weight loss (EWL) of 54 ± 20 % after 3 years. Before surgery, we found decreased levels of 25(OH)D and calcium in 80 and 5 % of the subjects, respectively, while increased levels of PTH, BAP, and NTx were found in 39, 28, and 21 %, respectively. Mean levels of NTx and the prevalence of elevated levels of NTx increased within 2 years (p < 0.001 and p < 0.01). Neither mean blood concentrations of 25(OH)D, calcium, PTH, and BAP nor relative prevalence of deficiencies regarding these markers changed during the study period. The supplementation rates of calcium and vitamin D increased postoperatively. CONCLUSIONS: Morbid obesity is associated with pronounced changes of markers of bone metabolism; LSG did neither aggravate nor ameliorate vitamin D metabolism within a 3-year time period, but led to increased bone resorption 2 years postoperatively. Routine supplementation of calcium and vitamin D is not likely sufficient to compensate the obesity-associated deficiencies in bone metabolism.