Duodenal self-expandable metal stents (SEMS) are designed for palliation and prompt relief of malignant gastric outlet obstruction (GOO). This mini-invasive endoscopic treatment is preferable to surgery due to its lower morbidity and mortality, shorter hospitalization, and earlier symptoms relief; furthermore endoscopic enteral stenting can be performed under conscious sedation, reducing the risk of general anesthesia in these already fragile patients. The stent placement technique is well established and should be performed in referral centers with adequate materials and equipment. Duodenal stents can be covered and uncovered. Nitinol stents have almost replaced other materials, being more flexible with a satisfactory axial and radial force. Common duodenal SEMS-related complications are recurrence of GOO symptoms due to stent clogging (tissue ingrowth/overgrowth and food impaction) and stent migration. These complications can be usually managed endoscopically. Perforation and bleeding are the most severe, but rare, complications. After stent placement, malignant GOO patients usually have improvement of the GOO symptoms with good resumption of fluids and solids. Choosing the most appropriate type of stent is arduous and should be done mainly in relation to the morphological aspects of the stricture. Endoscopic duodenal SEMS placement is indicated in symptomatic GOO patients suffering from unresectable malignancy or those inoperable due to advanced age or comorbidities. The absence of peritoneal carcinomatosis and multiple small bowel strictures is a key point for the clinical success of duodenal SEMS. Almost all symptomatic malignant GOO patients are candidates for the duodenal SEMS procedure; resolution of GOO, avoiding the need for a permanent naso-gastric or percutaneous endoscopic gastrostomy tube, significantly improves the patients’ quality of life and dignity, even if life expectancy is short. Endoscopic duodenal SEMS insertion, after an adequate training, is a reproducible, simple, safe, and cost-effective procedure.

Morphine and other opioids increase tone and reduce propulsive motility in several segments of the gut, enhance absorption of fluids, and inhibit secretion. This opioid-induced bowel dysfunction may present as infrequent stools, hard stools, difficult defecation, bloating, and sense of incomplete emptying of the bowels, but also dry mouth, gastroesophageal reflux, epigastric fullness, and abdominal cramping. It afflicts about one-third of patients on opioid treatment. Lifestyle measures, such as regular toilet visits, physical activity, and fiber-rich diet, are very unlikely to be successful. Laxatives, such as bisacodyl, sodium picosulfate, sennosides, macrogols, and prucalopride, may relieve opioid-induced constipation (OIC) in a proportion of patients only. A new approach to counteract OIC is the coadministration of an opioid antagonist devoid of the potential to penetrate the brain. In the EU, an oxycodonenaloxone combination has been approved for this purpose. Both components are included in an oral extended-release preparation. Following its release, naloxone acts locally on the gut and antagonizes the inhibitory effect of the opioid. After being absorbed in parallel with oxycodone, naloxone is rapidly and completely inactivated by a high firstpass effect in the liver. In a 2:1 dose ratio it may improve OIC without interfering with the analgesic effect.

More than 180 million people worldwide have chronic hepatitis C (CHC) virus infection, a major cause of liver cirrhosis and its life-threatening complications including liver failure, portal hypertension, and hepatocellular carcinoma. With the current standard of care of pegylated interferon-alpha and ribavirin (PEG-IFN-α/RBV), the chances of sustained viral clearance or “cure” are only 40%-50% for genotype 1 infection, which is the most common genotype in western populations. Consequently, there has been a drive to develop new agents specifically targeting essential components of the viral life cycle, such as the hepatitis C virus (HCV) NS3/4A serine protease. Perhaps the most advanced HCV protease inhibitor in clinical development is telaprevir, which has been shown to improve treatment outcomes when combined with PEG-IFN-α/RBV in genotype 1 infection, and is currently undergoing phase 3 study. In this review, we summarize the pharmacology, pharmacokinetics, and results of phase 1 and 2 clinical trials of telaprevir, and discuss the likely role of this agent in the future management of CHC.