Does Early Endoscopy Improve Mortality in Patients with Acute Non-variceal Gastrointestinal Bleeding? A Retrospective review.

Introduction Initial management of acute upper gastrointestinal bleeding (UGIB) aims towards aggressive fluid resuscitation to maintain hemodynamic stability. Existing evidence regarding the benefit of early endoscopy is unclear with some studies suggesting mortality benefits and some suggesting otherwise. The purpose of this study is to evaluate if there is any mortality benefit of doing early endoscopy within 24 hours of presentation. Methods From July 2013 to July 2016, 179 patients admitted with a diagnosis of non-variceal UGIB were retrospectively reviewed. Clinical variables including 30-day mortality were then compared between the patients who had endoscopy within 24 hours with those who had endoscopy after greater than 24 hours. Results Out of 179 patients admitted for non-variceal UGIB, 146 underwent endoscopy within 24 hours of presentation and 33 underwent endoscopy after 24 hours. The overall mortality associated with UGIB was 6.7% (12/179). There was no statistically significant difference found in 30-day mortality between the two groups (6.8% within 24 hours vs 6.1% after 24 hours). There was also no difference in 30-day readmission or rates of rebleeding among the two groups. The length of stay was also similar in both groups (6.0 days vs 6.1 days). Conclusion This study did not find any advantage of endoscopy within 24 hours on length of stay, rate of complications, and 30-day mortality. As hemostasis is achieved in almost 90% of patients with supportive management without any endoscopic intervention, focus should be made on aggressive fluid resuscitation to achieve hemodynamic stability before endoscopy.

Effect of median household income on surgical approach and survival in renal cell carcinoma.

PURPOSE: We sought to determine whether median household income (MHI) independently predicts surgical approach (partial vs. radical nephrectomy) and survival in patients with renal cell carcinoma. METHODS: The U.S. Surveillance Epidemiology and End Results Database (1988-2011) was queried to examine kidney cancer cases and linked to the Area Health Resources File. We correlated surgical approach and survival, both overall and cancer-specific, with tumor stage, age, race, sex, and income data. RESULTS: Of 152,589 patients diagnosed with renal cell carcinoma, 24,221 (16%) patients underwent partial nephrectomy, 102,771 (67%) patients underwent radical nephrectomy, and 25,597 (17%) patients had no surgery. There was no significant difference in stage of presentation between the wealthiest and poorest MHI quartiles, with approximately 35% of patients in each quartile presenting with T1aN0M0 disease and 17% of patients presenting with metastatic disease. Despite this, 18% of patients in the wealthiest quartile underwent partial nephrectomy compared to 14% of patients in the poorest quartile. Although the percentage of patients undergoing partial nephrectomy rose over the timeframe studied in both the wealthiest and poorest quartiles, the rate of rise was highest in the wealthier group. Those in the poorest quartile were 0.10 times more likely to die of all causes (95% CI: 1.09-1.11, P<0.001) and 0.09 times more likely to die of kidney cancer (95% CI: 1.05-1.10, P<0.001) than those in the wealthiest quartile over the timeframe studied. CONCLUSIONS: Despite presenting with similar stage, patients with lower MHI less commonly undergo partial nephrectomy and are more likely to die of kidney cancer than those in the highest MHIs.

Anticancer peptide PNC-27 adopts an HDM-2-binding conformation and kills cancer cells by binding to HDM-2 in their membranes.

The anticancer peptide PNC-27, which contains an HDM-2-binding domain corresponding to residues 12-26 of p53 and a transmembrane-penetrating domain, has been found to kill cancer cells (but not normal cells) by inducing membranolysis. We find that our previously determined 3D structure of the p53 residues of PNC-27 is directly superimposable on the structure for the same residues bound to HDM-2, suggesting that the peptide may target HDM-2 in the membranes of cancer cells. We now find significant levels of HDM-2 in the membranes of a variety of cancer cells but not in the membranes of several untransformed cell lines. In colocalization experiments, we find that PNC-27 binds to cell membrane-bound HDM-2. We further transfected a plasmid expressing full-length HDM-2 with a membrane-localization signal into untransformed MCF-10-2A cells not susceptible to PNC-27 and found that these cells expressing full-length HDM-2 on their cell surface became susceptible to PNC-27. We conclude that PNC-27 targets HDM-2 in the membranes of cancer cells, allowing it to induce membranolysis of these cells selectively.