Predictors of venous thromboembolism in hospitalized patients with inflammatory bowel disease and colon cancer: A retrospective cohort study.

INTRODUCTION: Venous thromboembolism (VTE) in patients with inflammatory bowel disease (IBD) and colon cancer (CC) increases morbidity and mortality. Risk of thrombosis in IBD and CC is well established. Still, it remains unclear how interaction of thrombotic properties in patients with both diseases predict development of VTE. MATERIALS AND METHODS: The Nationwide Inpatient Sample was sourced (2005-2014) for data on patients admitted with IBD-CC who developed VTE. The main outcome was predictors of VTE. Secondary outcomes were length of stay and total charge of admission. RESULTS: 7625 adults were admitted from 2005 to 2014 with a co-diagnosis of IBD and CC. 197 (2.6%) were coded to have VTE as a top three diagnosis. Multivariate logistic regression showed that black patients (11.9% vs 6.0%; aOR 2.04, 95% CI = 1.26-3.31, P < 0.004) and patients with metastatic disease (27.9% vs 16.7%; aOR 1.77, 95% CI = 1.27-2.47, P = 0.001) had higher odds of having VTE. Patients with uncomplicated diabetes (8.1% vs 15.5%; aOR 0.48, 95% CI = 0.28-0.84, P = 0.010) had lower odds. Obesity and anemia were significantly associated with VTE in univariate logistic regression, but lost significance after multivariate regression. Additionally, VTE was associated with increased length of stay (8.41 vs 6.87 days, P = 0.006) and admission cost ($64,388 vs $50,874, P = 0.010). CONCLUSIONS: Patients with IBD and CC likely have unique procoagulant properties that differ from patients with IBD or CC alone. Knowledge of these predictors can assist efforts to risk stratify IBC-CC patients, and can aid development of an individualized approach to DVT prophylaxis in this population.

Protein network analysis reveals selectively vulnerable regions and biological processes in FTD.

OBJECTIVE: The neuroanatomical profile of behavioral variant frontotemporal dementia (bvFTD) suggests a common biological etiology of disease despite disparate pathologic causes; we investigated the genetic underpinnings of this selective regional vulnerability to identify new risk factors for bvFTD. METHODS: We used recently developed analytical techniques designed to address the limitations of genome-wide association studies to generate a protein interaction network of 63 bvFTD risk genes. We characterized this network using gene expression data from healthy and diseased human brain tissue, evaluating regional network expression patterns across the lifespan as well as the cell types and biological processes most affected in bvFTD. RESULTS: We found that bvFTD network genes show enriched expression across the human lifespan in vulnerable neuronal populations, are implicated in cell signaling, cell cycle, immune function, and development, and are differentially expressed in pathologically confirmed frontotemporal lobar degeneration cases. Five of the genes highlighted by our differential expression analyses, BAIAP2, ERBB3, POU2F2, SMARCA2, and CDC37, appear to be novel bvFTD risk loci. CONCLUSIONS: Our findings suggest that the cumulative burden of common genetic variation in an interacting protein network expressed in specific brain regions across the lifespan may influence susceptibility to bvFTD.