Objectives To investigate the influences of inflammatory bowel disease (IBD), a rare but morbid disease with increasing incidence, on prostate cancer management decisions. We examined whether prostate cancer treatment differed for men with IBD, and whether treatment choice was associated with risk of IBD flare. Methods Using Veterans Health Administration cancer registry and administrative data, we identified 52,311 men diagnosed with prostate cancer from 2005 through 2008. We used ICD–9 codes, pharmacy and utilization data to identify IBD diagnoses, IBD-directed therapy, and flares (glucocorticoid escalation, hospitalization, surgical intervention). We compared characteristics across men with and without IBD, and used multivariable regression to examine IBD flares after treatment according to treatment type. Results Two hundred and forty men (0.5%) had IBD prior to prostate cancer diagnosis. Compared to non-IBD patients, IBD patients were more likely Caucasian (p<0.001) with lower risk cancer (p=0.02). Surgery was more common in IBD patients (41% vs 28%, p<0.001). In the year following prostate cancer treatment 18% of IBD patients experienced flares. After adjustment, the only predictor of flare in the year after treatment was flare in the year prior to treatment (adjusted odds ratio, 12.5, 95% confidence interval, 5.4–29.2). Conclusions IBD patients were more likely to have lower risk disease and be treated with surgery. Choice of prostate cancer treatment did not predict flares in the subsequent year. Better understanding the intersection of IBD and prostate cancer can help inform treatment decisions for the increasing number of men managing both diseases.

Introduction It is well established that sarcopenic patients are at higher risk of postoperative complications and short-term healthcare utilization. Less well understood is how these patients fare over the long-term after surviving the immediate postoperative period. We explored costs over the first postoperative year among sarcopenic patients. Methods We identified 1,279 patients in the Michigan Surgical Quality Collaborative database who underwent inpatient elective surgery at a single institution from 2006 to 2011. Sarcopenia, defined by gender-stratified tertiles of lean psoas area, was determined from preoperative CT scans using validated analytic morphomics. Data were analyzed to assess sarcopenia’s relationship to costs, readmissions, discharge location, intensive care unit admissions, hospital length of stay, and mortality. Multivariate models adjusted for patient demographics and surgical risk factors. Results Sarcopenia was independently associated with increased adjusted costs at 30, 90, and 180 but not 365 days. The difference in adjusted postsurgical costs between sarcopenic and non-sarcopenic patients was $16,455 at 30 days and $14,093 at one year. Sarcopenic patients were more likely to be discharged somewhere other than home (p <0.001). Sarcopenia was not an independent predictor of increased readmission rates in the postsurgical year. Conclusion The effects of sarcopenia on healthcare costs are concentrated in the immediate postoperative period. It may be appropriate to allocate additional resources to sarcopenic patients in the perioperative setting to reduce the incidence of negative postoperative outcomes.

A major focus of the Comprehensive Care for Joint Replacement bundle is improving cost and quality by limiting readmission rates. TKA readmissions are low and comprise a small percentage of total TKA cost, suggesting that they may not be the optimal measure of quality care or a significant driver of overall cost.

The C-C chemokine ligand 2 (CCL2) stimulates migration, proliferation, and invasion of prostate cancer (PCa) cells, and its signaling also plays a role in the activation of osteoclasts. Therefore targeting CCL2 signaling in regulation of tumor progression in bone metastases is an area of intense research. The objective of our study was to investigate the efficacy of CCL2 blockade by neutralizing antibodies to inhibit the growth of PCa in bone. We used a preclinical model of cancer growth in the bone in which PCa C4-2B cells were injected directly into murine tibiae. Animals were treated for ten weeks with neutralizing anti-CCL2 antibodies, docetaxel, or a combination of both, and then followed an additional nine weeks. CCL2 blockade inhibited the growth of PCa in bone, with even more pronounced inhibition in combination with docetaxel. CCL2 blockade also resulted in increases in bone mineral density. Furthermore, our results showed that the tumor inhibition lasted even after discontinuation of the treatment. Our data provide compelling evidence that CCL2 blockade slows PCa growth in bone, both alone and in combination with docetaxel. These results support the continued investigations of CCL2 blockade as a treatment for advanced metastatic PCa.