However, there remains concern over the potential for increased difficulty of transplantation following a prior resection and postoperative complications to negate the benefits of an SLT. We propose to evaluate the outcomes of SLT for patients with recurrent HCC following initial treatment with primary hepatic resection. In this review, we seek to investigate using a systematic literature examination the morbidity,

mortality, and survival outcomes of this therapeutic Hormones antagonist strategy. A literature search was last conducted on December 1, 2012 using Pubmed, Embase, and Medline databases (January 2000–November 2012). The search terms used to locate studies were “salvage,” “secondary,” “liver transplant,” “liver transplantation,” and “recurrent hepatocellular carcinoma.” The search was limited

to English-language articles and to humans. All relevant journal articles and conference abstracts identified were assessed with application of inclusion and exclusion criteria. Where there was insufficient information provided by the abstract or ambiguity of inclusion criteria, full-text articles were retrieved for further assessment. The reference lists of articles identified were manually searched to locate other articles of relevance. Selection criteria www.selleckchem.com/products/mi-503.html were as follows: (i) all studies > 5 patients, (ii) initially treated with hepatic resection, (iii) adopting SLT for recurrent HCC, and (iv) sufficient data to be included in either perioperative morbidity and mortality or longer-term survival tabulation. Where multiple treatments for primary disease

recurrence was employed, reporting of outcome data must be separate. We excluded review articles, case reports, editorials, and letters. Where multiple publications from the same institution were identified, only the most recent update with the largest number of patients or longer follow-up group was included. Where conference abstracts and publications employed the same study cohort, the more recent was included. Studies were evaluated and categorized according to their level of evidence, where level I evidence: medchemexpress randomized controlled trials; level II evidence: nonrandomized controlled clinical trials or well-designed cohort studies; and level III evidence: observational studies, as described by the US Preventive Services Task Force. The studies were independently and critically appraised by two reviewers (DLC and TCC). Data of interest included study characteristics, patient demographics, disease characteristics, perioperative morbidity and mortality, disease recurrence, disease-free survival, and overall survival data. All data were extracted and tabulated from the relevant articles’ texts, tables, and figures. Data were presented as median (range). Discrepancies were resolved by discussion and consensus. Meta-analysis was inappropriate due to the lack of a comparative arm in most studies.

However, several national and international registries dedicated to the study of RBDs are becoming increasingly available. Ongoing and future studies from these registries will hopefully learn more fill the gap in knowledge concerning these orphan disorders. With this background, we herein highlight recent advances in understanding three such congenital RBDs: FXI, FVI and fibrinogen deficiencies. Paula Bolton-Maggs FXI is stimulating current research interest both because of its minor role in haemostasis

and also for the potential role of FXI inhibitors for prevention of thrombosis. An absolute deficiency of FXI in man is associated with a mild bleeding risk, such that individuals may be diagnosed incidentally or late in life, and the bleeding pattern is very

different from severe deficiency of other coagulation factors (such as FVIII and FIX, or the rare factor deficiencies including FVII). Animal experiments have demonstrated that knock-out mice for FXI or FXII have Selleck Fulvestrant no bleeding tendency and thrombosis is abolished, leading to the interesting proposal that FXI inhibitors in humans may prevent thrombosis without increased bleeding risk [6]. Humans with inherited FXI deficiency are protected against stroke [7], but not myocardial infarction [8], and have a reduced incidence of venous thrombosis [9]. FXI has a unique structure among coagulation factors as a dimer, and participates in coagulation by reinforcement of the intrinsic pathway and inhibition of fibrinolysis. MCE公司 It is activated by thrombin [10] and may be important in low tissue factor environments [6]. Inherited factor XI deficiency is associated with a mild bleeding tendency (and an absence of spontaneous bleeding) which is not easily predicted from the FXI level [11]. Most individuals with severe deficiency (i.e. FXI level below

about 15 IU/dl and two gene mutations) are at risk of bleeding. Bleeding characteristically occurs after accidents or surgery in areas of high fibrinolysis, particularly the mouth and genitourinary systems. Excessive bleeding may occur in individuals with mild as well as severe deficiency unrelated to the FXI level, suggesting that additional factors are implicated. Recent data from the European Network of Rare Bleeding Disorders (EN-RBD) confirmed this observation, by absence of correlation between FXI activity level and the severity of clinical bleeding [12]. There is increasing evidence that the overall balance of haemostasis is relevant, as has been found in von Willebrand disease [13]. It is likely that the interaction of platelets and other coagulation factors can modulate the bleeding risk. There is current interest in determining whether or not global tests of haemostasis such as thrombin generation tests and thromboelastography give more indication of the bleeding risk, but to date results are conflicting, which may be due to the lack of standardization of the test parameters [14].