Predictable pharmacokinetics and pharmacodynamics allow a fixed dose of rivaroxaban without coagulation monitoring.[2] It has a half-life of up to 12 hours, its absorption is not affected by food, and one-third of the drug is eliminated by the kidneys, while two-thirds undergo metabolism in the liver.[2] Specific labeling restrictions for rivaroxaban regarding impaired hepatic function are based

on both the Child-Pugh classification and liver-related exclusion criteria applied in pivotal trials.[2] It is currently contraindicated in patients with liver disease associated with coagulopathy, cirrhosis Child Class B or C, and clinically relevant bleeding risk.[2] When compared to warfarin, rivaroxaban’s acquisition cost is higher, but this may be counterbalanced by costs of monitoring, patient’s inconvenience, and healthcare provider’s time required for managing test http://www.selleckchem.com/products/abt-199.html results.[2] Selleckchem GSI-IX In fact, a recent study showed that rivaroxaban is more cost-effective than warfarin for prevention of recurrent venous thromboembolism.[4] Although major and clinically relevant nonmajor bleeding rates were similar between warfarin and rivaroxaban, the rates of intracranial bleeding were significantly lower in the rivaroxaban group, but significantly higher with regard to gastrointestinal bleed.[5] Current concerns about the lack of an antidote for rivaroxaban may be alleviated

when a promising agent such as Andexanet Alfa (Clinicaltrials.gov: NCT01758432) gains regulatory approval. Premature discontinuation of rivaroxaban, like any anticoagulant, can increase the risk of thrombotic events and therefore documentation of complete clot resolution is essential.[2] “
“Despite standardization of surgical ADP ribosylation factor methods in biliary reconstruction, immunosuppression and post-operative management, biliary complications continue to be a major cause of morbidity

and mortality after liver transplantation (LT). Early identification of biliary complications after LT is critical due to the potential for graft and patient injury. Biliary complications include biliary strictures, bile leaks, biliary stones/debris, sphincter of Oddi dysfunction, mucoceles and hemobilia. Many of these complications can be managed with a combination of endoscopic and percutaneous therapy and this has minimized the need for post-transplant biliary surgery. “
“Superior mesenteric artery (SMA) syndrome, a rare form of proximal intestinal obstruction, occurs when the third portion of duodenum passes through a narrowed opening between the SMA and abdominal aorta. It has been described in association with anorexia nervosa, burns as well as severe weight loss due to various etiologies. The mechanism is a loss of the mesenteric fat pad from undue weight loss. The course may be acute or insidious with nonspecific presentations of postprandial epigastric pain, nausea, and vomiting. Panendoscopy usually identifies reflux-related injury.