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Background and Objective: The Roux-en-Y duodenal switch (RYDS) is one of the most efficient forms of bariatric surgery. However, diarrhea, malnutrition, ulcers, and internal hernias have hampered its widespread adoption. The stomach intestinal pylorus-sparing (SIPS) procedure was developed to alleviate these sequelae while retaining the same weight loss as the RYDS. In this study, we report our midterm experience with this novel technique., Methods: Retrospective analysis was performed on data from 225 patients who underwent a primary SIPS procedure by 2 surgeons at a single center from October 2013 through December 2016., Results: Two hundred twenty-five patients were identified for analysis. The mean preoperative body mass index (BMI) was 52.4 ± 9.1 kg/m 2 . Forty-eight patients were beyond 2 years after surgery, with data available for 30 patients (62.5% follow-up). Three patients were lost to follow-up. At 2 years, the patients had an average change in BMI of 26.6 U (kg/m 2 ) with an average of 88.7% of excess weight loss. Three deaths were related to the surgery. The most common short-term complication was a leak (2.2%), whereas the most common long-term complication was diarrhea (2.2%)., Conclusion: In conclusion, SIPS surgery is a safe procedure with favorable weight loss outcomes at 2 years.

Ascending thoracic aortic aneurysms leading to type A dissections can be inherited in an autosomal dominant manner with variable age of onset and decreased penetrance, primarily in women. Three families are described with autosomal dominant inheritance of either ascending aortic aneurysms leading to type A dissections or type B dissections, and a young age of onset of aortic dissections in both men and women. Pedigree analysis suggests that a de novo mutation is responsible for the disease in one family. The discordant age of onset of aortic disease in a monozygotic twin pair in a different family indicates that environmental or stochastic factors may influence the variable expression of disease. Genetic analysis of one family excluded linkage to known loci for TAAD (TAAD1, TAAD2, FAA1, or FBN1) and sequence analysis failed to identify mutations in TGFBR2, the gene encoding transforming growth factor beta receptor type II. Thus, a novel unidentified loci may be responsible for the phenotype in these three families., (Copyright 2006 Wiley-Liss, Inc.)