Postoperative Complication Burden, Revision Risk, and Health Care Use in Obese Patients Undergoing Primary Adult Thoracolumbar Deformity Surgery

Study Design: This is a retrospective cohort study using a nationally representative administrative database. Objective: To identify the impact of obesity on postoperative outcomes in patients undergoing thoracolumbar adult spinal deformity (ASD) surgery. Background: The obesity rate in the United States remains staggering, with approximately one-third of all Americans being overweight or obese. However, the impact of elevated body mass index on spine surgery outcomes remains unclear. Methods: We queried the MarketScan database to identify patients who were diagnosed with a spinal deformity and underwent ASD surgery from 2007 to 2016. Patients were then stratified by whether or not they were diagnosed as obese at index surgical admission. Propensity score matching (PSM) was then utilized to mitigate intergroup differences between obese and nonobese patients. Patients <18 years and those with any prior history of trauma or tumor were excluded from this study. Baseline demographics and comorbidities, postoperative complication rates, and short- and long-term reoperation rates were determined. Results: A total of 7423 patients met the inclusion criteria of this study, of whom 597 (8.0%) were obese. Initially, patients with obesity had a higher 90-day postoperative complication rate than nonobese patients (46.1% vs 40.8%, P < .05); however, this difference did not remain after PSM. Revision surgery rates after 2 years were similar across the 2 groups following primary surgery (obese, 21.4%, vs nonobese, 22.0%; P = .7588). Health care use occurred at a higher rate among obese patients through 2 years of long-term follow-up (obese, $152 930, vs nonobese,$140 550; P < .05). Conclusion: Patients diagnosed with obesity who underwent ASD surgery did not demonstrate increased rates of complications, reoperations, or readmissions. However, overall health care use through 2 years of follow-up after index surgery was higher in the obesity cohort

Validation of Myc-Associated Protein X (MAX) regulation in growth hormone secreting and nonfunctional pituitary adenoma.

IntroductionMany patients with growth hormone-secreting pituitary adenoma (GHPA) fail to achieve biochemical remission, warranting investigation into epigenetic and molecular signatures associated with tumorigenesis and hormonal secretion. Prior work exploring the DNA methylome showed Myc-Associated Protein X (MAX), a transcription factor involved in cell cycle regulation, was differentially methylated between GHPA and nonfunctional pituitary adenoma (NFPA). We aimed to validate the differential DNA methylation and related MAX protein expression profiles between NFPA and GHPA.MethodsDNA methylation levels were measured in 52 surgically resected tumors (37 NFPA, 15 GHPA) at ~100,000 known MAX binding sites derived using ChIP-seq analysis from ENCODE. Findings were correlated with MAX protein expression using a constructed tissue microarray (TMA). Gene ontology analysis was performed to explore downstream genetic and signaling pathways regulated by MAX.ResultsGHPA had more hypomethylation events across all known MAX binding sites. Of binding sites defined using ChIP-seq analysis, 1,551 sites had significantly different methylation patterns between the two cohorts; 432 occurred near promoter regions potentially regulated by MAX, including promoters of TNF and MMP9. Gene ontology analysis suggested enrichment in genes involved in oxygen response, immune system regulation, and cell proliferation. Thirteen MAX binding sites were within coding regions of genes. GHPA demonstrated significantly increased expression of MAX protein compared to NFPA.ConclusionGHPA have significantly different DNA methylation and downstream protein expression levels of MAX compared to NFPA. These differences may influence mechanisms involved with cellular proliferation, tumor invasion and hormonal secretion