Luca Prevedello

Sleeve gastrectomy as revisional procedure for failed gastric banding or gastroplasty

BACKGROUND Laparoscopic sleeve gastrectomy (LSG) is considered an effective multipurpose operation for morbid obesity, although long-term results are still lacking. Also, the best procedure to be offered in the case of failed restrictive procedures is still debated. We here reported our results of LSG as a revisional procedure for inadequate weight loss and/or complications after adjustable gastric banding or gastroplasty. METHODS Since April 2005, 57 patients (20 men and 37 women), with a mean age of 49.9 +/- 11.9 years, underwent revisional LSG, 52 after laparoscopic adjustable gastric banding/adjustable gastric banding and 5 after vertical banded gastroplasty at our institution. The mean interval from the primary procedure to LSG was 7.54 +/- 4.8 years. The LSG was created using a 34F bougie with an endostapler, after removing the laparoscopic adjustable gastric band or the anterior portion of the band in those who had undergone vertical banded gastroplasty. An upper gastrointestinal contrast study was performed within 3 days after surgery and, if the findings were negative, a soft diet was promptly started. RESULTS A total of 41 patients had undergone concurrent band removal and LSG and 16 had undergone band removal followed by an interval LSG. Three cases required conversion to open surgery because of a large incisional hernia. The mean operative time was 120 minutes (range 90-180). One patient died of multiple organ failure from septic shock. Three patients (5.7%) developed a perigastric hematoma, 3 (5.7%) had leaks, and 1 had mid-gastric short stenosis. The median hospital stay was 5 days. The mean body mass index at revisional LSG was 45.7 +/- 10.8 kg/m(2) and had decreased to 39 +/- 8.5 kg/m(2) after 2 years, with a mean percentage of the estimated excess body mass index lost of 41.6% +/- 24.4%. Two patients required a duodenal switch for insufficient weight loss. CONCLUSION LSG seems to be effective as revisional procedure for failed LAGB/vertical banded gastroplasty, although with greater complication rates than the primary procedures. Larger series and longer follow-up are needed to confirm these promising results.

Weight loss reduces anti-ADAMTS13 autoantibodies and improves inflammatory and coagulative parameters in obese patients.

Obese patients have been described at increased risk of thrombotic thrombocytopenic purpura, a disease caused by anti-ADAMTS13 autoantibodies. ADAMTS13 has a structure homology with the adipokine thrombospondin-1. We previously demonstrated an increased presence of anti-ADAMTS13 antibodies in obese patients. We aimed to study the changes induced by weight loss after bariatric surgery on some inflammatory and coagulative parameters and their link with anti-ADAMTS13 autoantibodies. We studied 100 obese patients before and after weight loss induced by bariatric surgery and 79 lean volunteers as controls. We measured anthropometric, metabolic and inflammatory parameters, thrombospondin-1, ADAMTS13 activity, anti-ADAMTS13 autoantibodies, Von Willebrand factor. At baseline, 13 % of patients was positive for anti-ADAMTS13 autoantibodies, while all controls were negative. Thrombospondin-1 levels were higher in obese subjects with than without antibodies, with a positive correlation between the two parameters. In multiple logistic regression analysis only thrombospondin-1 levels predicted positivity for anti-ADAMTS13 antibodies. After weight loss both anti-ADAMTS13 antibodies and thrombospondin-1 reduced significantly. Weight loss in obesity improves the inflammatory and coagulative profile, and in particular anti-ADAMTS13 autoantibodies, ADAMTS13 activity and thrombospondin-1.

CK2 modulates adipocyte insulin-signaling and is up-regulated in human obesity

Insulin plays a major role in glucose metabolism and insulin-signaling defects are present in obesity and diabetes. CK2 is a pleiotropic protein kinase implicated in fundamental cellular pathways and abnormally elevated in tumors. Here we report that in human and murine adipocytes CK2-inhibition decreases the insulin-induced glucose-uptake by counteracting Akt-signaling and GLUT4-translocation to the plasma membrane. In mice CK2 acts on insulin-signaling in adipose tissue, liver and skeletal muscle and its acute inhibition impairs glucose tolerance. Notably, CK2 protein-level and activity are greatly up-regulated in white adipose tissue from ob/ob and db/db mice as well as from obese patients, regardless the severity of their insulin-resistance and the presence of pre-diabetes or overt type 2 diabetes. Weight loss obtained by both bariatric surgery or hypocaloric diet reverts CK2 hyper-activation to normal level. Our data suggest a central role of CK2 in insulin-sensitivity, glucose homeostasis and adipose tissue remodeling. CK2 up-regulation is identified as a hallmark of adipose tissue pathological expansion, suggesting a new potential therapeutic target for human obesity.