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Background: Emergency surgery for malignant colon obstruction entails relatively high morbidity and mortality rates and typically necessitates a 2-step resection. These problems might be potentially mitigated by placement of a self-expanding metal stent (SEMS) as a bridge to surgery. A nitinol colorectal SEMS may offer several advantages, but available evidence on the utility of this SEMS type remains highly limited., Objective: Our purpose was to evaluate the effectiveness and safety as a bridge to surgery of a nitinol SEMS designed for colorectal use., Design: Prospective and retrospective multicenter clinical study., Setting: Sixteen European study centers., Patients: Thirty-six patients with malignant colonic obstruction., Interventions: Nitinol colorectal SEMS placement., Main Outcome Measures: Technical success in accurate SEMS placement with coverage of the entire stricture length, clinical success in alleviating colonic obstructive symptoms, and bridging to elective surgery., Results: Technical success was achieved in 97% of patients with a 95% CI of 85% to 100% and clinical success in 81% (95% CI, 64%-92%). Elective surgery was performed in 94% (95% CI, 81%-99%) of patients at a median of 11 days (95% CI, 7-15 days) after SEMS placement. SEMS-related perforation occurred in 3 patients., Limitations: No control group was included in this nonrandomized cohort study., Conclusions: In this first comparatively large clinical study of a nitinol colorectal SEMS as a bridge to surgery, a high proportion of patients successfully proceeded to elective surgery after prior decompression by SEMS placement.

The clinical course, changes in liver function tests and the behaviour of viral markers over the course of time have been examined in 45 patients with acute hepatitis B and 14 patients with acute hepatitis caused by B and D viruses coinfection. There were no significant differences either in the clinical course or in the liver function tests, in the two groups. The changes in serum viral markers were as follows: HBV-DNA was the first marker to disappear; this was closely followed by HBeAg, and HBsAg was the last marker to become negative, during convalescence. This pattern was not altered by Delta coinfection. When we quantified serum HBV-DNA in both groups of patients, we found that Delta virus infection led to parital inhibition of HBV replication, so that serum HBV-DNA levels were significantly lower in those patients with acute hepatitis B who were simultaneously infected with Delta virus.