The gold standards for the final diagnosis were


The gold standards for the final diagnosis were

histologic findings of surgically resected specimen. Additionally, immunophenotyping of specimens obtained by EUS-FNA and surgical resection specimens were compared. Results: Postoperative histological diagnosis were 109 GISTs (85.8%), 7 neurinomas (5.5%), 5 SMT like cancers (3 primary gastric cancers and 2 metastatic cancers) (3.9%), 2 leiomyomas (1.6%), 2 Glomus tumors (1.6%), 1 accessory spleen (0.8%), check details and 1 gauzeoma (0.8%). In 4 cases puncture was not performed because of anatomical problems. The diagnostic rate of the gastric hypoechoic solid SMT by EUS-FNA was 93.7% (119/127). In 119 surgically resected cases who were conclusively diagnosed by preoperative EUS-FNA, the diagnostic accuracy of EUS-FNA using immunohistochemical analysis of gastric hypoechoic solid SMT was 95.7% (114/119). No major complications were encountered. Conclusion: EUS-FNA with immunohistochemical analysis is an Selleckchem Hydroxychloroquine accurate and safe preoperative histologic test of differential diagnosis of Gastric SMT. Key Word(s): 1. EUS-FNA; 2. GIST; 3. SMT;

4. stomach; 5. immunohistochemical analysis; 6. histology Presenting Author: TEPPEI AKIMOTO Additional Authors: KAZUMASA MIYAKE, YUTA MARUKI, HIROSHI YAMAWAKI, YASUHIRO KODAKA, HIROYUKI NAGOYA, NOBUE UEKI, TETSURO KAWAGOE, SEIJI FUTAGAMI, CHOITSU SAKAMOTO Corresponding Author: TEPPEI AKIMOTO Affiliations: Nippon Medical School, Nippon Medical School, Nippon Medical School, Nippon Medical School, Nippon Medical Schoo, Nippon Medical School, Nippon Medical School, Nippon Medical School, Nippon Medical School Objective: It has been recommended, if antithrombotic treatment is

at least a single use, to perform endoscopic biopsy without cessation of antithrombotic agents, also in the guideline of Japan since 2012. Past reports supporting the guidelines, have indicated the safety of biopsy Fludarabine supplier for these patients by evaluating the development of severe gastrointestinal bleeding complication. However, since such patients are basically elderly, and have comorbidity of cerebro-cardiovascular disease, even if there is no severe bleeding complication after biopsy, anemia due to asymptomatic potential bleeding could lead to serious condition. Therefore, we investigated the development of bleeding complication after biopsy, containing asymptomatic potential bleeding. Methods: This prospective cohort study entered consecutive outpatients who needed esophagogastroduodenoscopy without cessation of antithrombotic agents in our institution, and hemoglobin levels were checked just before endoscopy. Patient performed biopsies among these patients were re-checked hemoglobin levels 1 to 2 weeks later, and were asked about episodes of bleedig and thrombosis.

[24] Thus, the efficacy of Peg-IFNα-2a therapy on patients with H

[24] Thus, the efficacy of Peg-IFNα-2a therapy on patients with HBeAg negative chronic hepatitis B can be considerably improved by extending the therapy period. In Japan however there is no national medical insurance approval for treatment regimens longer than 48 weeks. Recommendation A clinical study in Japan reported that 38% of patients with HBeAg negative chronic hepatitis B administered Peg-IFNα-2a at either 90 or 180 μg

find more dosage for 48 weeks achieved the virological target of a HBV DNA levels <4.3 log copies/mL 24 weeks after the end of treatment. It was demonstrated that IFN treatment of compensated HBV cirrhosis produced much the same outcomes and adverse effects to IFN therapy as in non-cirrhotic check details patients, and in Asian patients in whom HBeAg had been successfully eliminated the HBsAg elimination rate was boosted by a factor of 6.63 times, effectively suppressing progression of liver fibrosis and hepatocarcinogenesis.[101] A study of 24 patients with HBeAg positive compensated cirrhosis administered

Peg-IFNα-2b (with or without lamivudine) for 52 weeks reported 30% efficacy (defined as HBeAg seroconversion and HBV DNA <4.0 log copies/mL) at 26 weeks after finishing treatment. This figure is significantly higher than the corresponding 14% for non-cirrhotic cases. Histological improvement was observed in 66% of cases, also significantly higher than the 22% for non-cirrhotic cases, with similar adverse reactions.[102] It should be noted however that IFN, unlike NAs, has an immunopotentiation effect that can increase the risk of acute exacerbation of hepatitis through immunological destruction of HBV infected cells. IFN therapy is contraindicated for HBV-associated decompensated cirrhosis patients in particular, who are at risk of potentially fatal adverse reactions such as deterioration of liver function.[103] In Japan there is insufficient evidence regarding the efficacy and safety of IFN therapy for HBV associated cirrhosis, and consequently this is not approved by national medical insurance. Hence HBV-associated cirrhosis should be treated with

NAs. Recommendation There is insufficient evidence in Japan on the efficacy and safety of IFN therapy for HBV-associated compensated cirrhosis, and NA therapy is recommended instead. IFN treatment oxyclozanide is contraindicated for patients with HBV decompensated cirrhosis. IFN administered in combination with lamivudine produces improved HBV DNA negative conversion and ALT normalization outcomes compared to lamivudine alone, for both HBeAg positive and negative patients. Meanwhile, studies comparing IFN plus lamivudine combination therapy with IFN monotherapy found similar therapeutic effects[8, 22, 104] and similar persistent benefits.[96, 105, 106] IFN in combination with adefovir was likewise found to have roughly the same therapeutic effect six months after treatment as IFN alone.

At the HLA region, the variants showing the strongest association

At the HLA region, the variants showing the strongest associations with PBC were similar between the two data sets, with almost complete overlap of the strongest association observed between the DQB1 and find more DQA2 loci (Fig. 2B). Importantly, the association with HLA region were also confirmed and strengthened by a third GWAS, recently conducted in a very large cohort of 1840 UK PBC cases and 5163 population controls17 (Table 2). Taken together, these three GWAS identified a number of non-HLA loci, with plausible candidate genes that indicate the involvement of the innate and adaptive immune systems in the etiopathogenesis of PBC (Table 2). In particular, these findings support the role for the Toll-like

receptor, TNF, and nuclear factor kappa B (NF-κB) pathways. Among the associations consistently reported are, notably, those with the IL-12A and IL-12RB2 loci, the gene encoding the SPi-B transcription factor (SPIB), as well as two other loci, the gene click here encoding interferon regulatory factor 5 (IRF5) and the gene encoding the IKAROS family zinc finger 3 (IKZF3), and that encoding ORM1-like 2 (ORMDL3) also implicated in risk for other autoimmune diseases such as lupus and asthma, respectively. Suggestive associations were also observed between

PBC and two other loci associated with other autoimmune conditions, the signal transducer and activator of transcription 4 (STAT4) and DENND1B. Finally, the most recent UK GWAS identified novel associations between PBC and loci, such as CD80, NF-κB1, IL-7R, CXCR5, and TNFAIP217 (Table 2). These studies clearly identified PBC association with several novel non-HLA loci and added evidence of overlaps in the risk loci predisposing to PBC and other autoimmune diseases. However, all these novel genetic data allow us to make some observations. First, a greater number of studies and of subjects Alectinib nmr (cases and controls) who are studied results in a greater number of common genetic

variants associated with PBC. This suggests caution in some way and the reasonable need to redirect our future research studies, for example, to rare variants or to copy number variants or to gene expression. The second observation is the strong consistency among the findings of these three GWAS, thus suggesting the presence of a common genetic pattern for PBC. This finding is very positive, but again, caution is needed, because the first three GWAS have been performed in populations of European ancestry, and it will be important also to replicate the reported associations in non-European populations. Indeed, a recent study from Japan failed to confirm some GWAS-associated variants.84 It is currently believed the development of PBC requires that an environmental factor, particularly an infection, initiates an autoimmune reaction in a genetically predisposed individual.

Due to the increased risk of CRC in Crohn colitis, patients with

Due to the increased risk of CRC in Crohn colitis, patients with PSC who have CD are LEE011 recommended to be surveyed similarly to patients with UC.80, 98 Ursodeoxycholic acid (UDCA) has been suggested to decrease the risk of colorectal dysplasia in patients with PSC and UC.99, 100 Treatment with UDCA was associated with a decreased prevalence of colonic dysplasia (OR 0.18, 95% CI 0.05–0.61) in a cross-sectional study of 59 PSC patients with UC100 and significantly decreased the risk for developing colorectal dysplasia or cancer (relative

risk, 0.26; 95% CI, 0.06–0.92) in a follow-up of 52 patients with PSC and UC after a randomized, placebo-controlled trial of UDCA.99 In a study comparing 28 patients with PSC and UC treated with UDCA for at least 6 months with 92 untreated patients, UDCA did not decrease the risk of cancer or dysplasia.101

All of these studies have been based on retrospective analysis with its inherent limitations. Furthermore, high dose UDCA can be problematic in PSC patients.102 UDCA use as a chemopreventative CAL-101 order agent in PSC patients can not be routinely recommended given the limited information available. PSC patients who have an ileostomy after proctocolectomy and who develop portal hypertension, are prone to develop peristomal varices.103 Bleeding from these often is recurrent and difficult to treat.103 This complication can be controlled with a portosystemic shunt or transjugular intrahepatic portosystemic shunt (TIPS), but liver transplantation may be considered.79 IPAA is less complicated with variceal formation86 and PSC patients undergoing IPAA have good functional results.104 Recommendations: 18 We recommend full colonoscopy with biopsies in patients with a new diagnosis of PSC and no previous history or symptoms of IBD (1A). Gallbladder abnormalities are frequently observed in PSC patients. In an early study of 121 cases, 41% had one or more gallbladder abnormalities, including gallstones (26%), probable

PSC involving the gallbladder (15%), and benign or malignant neoplasms (4%).105 Although gallstones as a cause of SSC must be considered, PSC patients seem to be predisposed to gallstone disease, including both the gallbladder and the biliary tract. ifenprodil In a review of the records of 286 PSC patients, gallstones (confirmed by one or more radiological modalities) were found in 25% of the cases.17 Gallbladder stones were diagnosed at a mean of 5 years (±6.4 years) after the diagnosis of PSC. Treatment with UDCA or the presence of IBD did not influence the frequency of gallstones. In the above study of 286 patients with PSC, a gallbladder mass lesion (mean size 21±9 mm) was found in 18 (6%) cases.17 Among these, 10 (56%) proved to be a gallbladder carcinoma. Nine patients without a mass lesion, had epithelial dysplasia of the gallbladder on histological examination.

This AASLD statement is only “Grade II” The effectiveness of tra

This AASLD statement is only “Grade II”. The effectiveness of transplantation versus resection or percutaneous ablation still needs randomized controlled trials (RCTs). This need is not futile: (1) From the French national database, survival after transplantation for patients with HCC is

lower than for other indications (less than 70% versus more than 80% at 2 years, respectively) and at 5 years, survival after transplantation for HCC is 65%, a very serious issue considering the shortage of organs.2 (2) Resection for small solitary HCC in compensated cirrhosis yields an overall survival rate comparable to upfront transplantation.3 Surgery substantially contributes to improve health, but needs high-quality outcome data. Complex mathematical models cannot be used to bypass the complexities of the surgical

research framework. To limit complexity, we must begin at the beginning, namely, RCTs investigating the effectiveness of transplantation versus ablation and/or resection, or at least, the full find more publication of national series which are more relevant than short series of selected cases from a few leading centers. Hepatocellular carcinoma is a major health care issue which deserves both evidence-based medicine and evidence-based surgery.4 Alain Braillon*, * Public Health, University Hospital, Amiens, France. “
“Liposarcoma frequently

occurs in the retroperitoneum and lower extremities, accounting for 9.8–16% of all soft tissue sarcomas. Liposaromas vary by histology and can be classified into four types. Those four types are well differentiated, myxoid/round cell, pleomorphic and dedifferentiated. This classification corresponds to the clinical aspect and prognosis of patients. Dedifferentiated liposarcoma (DDL) has both a well differentiated liposarcoma and a high grade nonlipogenic sarcoma within the tumor. It is difficult to diagnose DDL histologically. DDL can show a variety of histological appearances. The most common phenotype is malignant fibrous histiocytoma. Other phenotypes include leiomyosarcoma, osteosarcoma, rhabdomyosarcoma, and angiosarcoma. For DDL, prognosis is generally ZD1839 solubility dmso poor compared with the other types of liposarcoma. It shows high recurrence rate of 40-83%, metastasis rate of 15–30%, and the overall 5-year survival rate of 20%. DDLs often originate in the retroperitoneum, extremities, trunk, testis, and spermatic cord. A 61-year-old man was admitted to our hospital with 38.8°C of fever and general weakness. He had a history of a 20 × 10 cm well-differentiated retroperitoneal liposarcoma and underwent debulking surgery and intraoperative radiotherapy eight years previously. After surgery, there was no remnant mass visible on the abdominal computed tomography (CT) scan.

This facilitates identification of carriers and prenatal diagnosi

This facilitates identification of carriers and prenatal diagnosis for male fetuses. Genetic counseling is key to helping people with hemophilia, carriers, and their families make more informed choices. Prenatal diagnosis is usually offered when termination of the pregnancy would be considered if an affected fetus was identified. However, it may also be done to help the family prepare and to plan delivery. Assisted delivery is best avoided in an affected fetus. Fetal gender can be determined using Y chromosome-specific PCR in maternal plasma/serum after 7–9 weeks of gestation [7, 8] or by ultrasonography

beginning week 11 of gestation [9]. Chorionic villus sampling (CVS), or biopsy, is the main method of prenatal diagnosis and is best done between 9 and 14 weeks of gestation. Biopsy carried out earlier Buparlisib may be associated with increased complications including fetal limb abnormalities. (Level 1) [ [10-13] ] Amniocentesis can be done at 15–17 weeks of gestation [11]. It is important to be aware of and to follow the relevant laws governing such procedures in the country

where the service is being provided. For carriers with low factor levels (<50 IU dL−1), hemostatic support may be required to prevent maternal bleeding during prenatal diagnosis procedures. All invasive methods used for prenatal diagnosis may cause feto-maternal hemorrhage. Anti-D immunoglobulin should be given if the mother is RhD negative. (Level 3) [ [14] ] Preimplantation genetic diagnosis allows selection of embryos without specific mutation to be implanted into the uterus. [15] FVIII levels usually rise

into the normal range during the second and third trimesters and should therefore be measured in carriers selleck kinase inhibitor during the third trimester of pregnancy to inform decisions for factor coverage during delivery. (Level 3) [ [4] ] In carriers with significantly low factor levels (<50 IU dL−1), clotting factor replacement is necessary for surgical or invasive procedures including delivery. (Level 3) [[4]] The need for clotting factor replacement should be planned in the prenatal period. Route of delivery in carriers with a normal fetus should be as per obstetric indications. Delivery of infants with known or suspected hemophilia should be atraumatic, regardless of whether it is vaginal or cesarean, to decrease the risk of bleeding. (Level 3) [ [4] ] Forceps and vacuum extraction should be avoided in vaginal delivery, as well as invasive procedures to the fetus such as fetal scalp blood sampling and internal fetal scalp electrodes [16]. Persons with bleeding disorders should be vaccinated, but should preferably receive the vaccine subcutaneously rather than intramuscularly or intradermally, unless covered by infusion of clotting factor concentrates.

Our results demonstrate that miR-1 acts as a positive regulator o

Our results demonstrate that miR-1 acts as a positive regulator of HBV replication and transcription through regulating the cellular gene expression. MiR-1 has been shown to play an important role in many cellular and biological functions of the cardiovascular system. The presence of miR-1 in liver tissues and hepatoma cells has been reported.21, 29 By real-time PCR, we confirmed the expression of miR-1 in primary hepatocytes and hepatoma cell lines (Supporting Information Fig. 9), indicating that miR-1 may play a role in the regulation of hepatic

gene expression, as well as HBV replication. It is has been suggested that miRNAs may not only regulate gene expression at the posttranscriptional level, but that they are also capable of modifying chromatin.30 Because HBV covalently closed circular DNA (cccDNA) forms a viral minichromosome in infected hepatocytes as a template for the transcription of viral mRNAs, epigenetic modifications of the HBV cccDNA, AUY-922 purchase such as the deacetylation of cccDNA-bound histones by HDACs, might regulate the transcription of viral chromatin and thereby viral replication.31 A recent study revealed that HBV replication is regulated by the acetylation status of H3/H4 histones bound to the HBV cccDNA, both in cell-based replication systems

and in the liver of HBV chronically infected patients.23 We confirmed that HDAC4 expression is down-regulated by miR-1. Silencing of HDAC4 by siRNA or histone deacetylase inhibitors selleck inhibitor TSA treatment led to the enhancement of HBV replication. Our results are consistent with previous findings and suggest selleck chemicals llc the significance of epigenetic modifications for HBV replication. A direct link from miR-1 action to HBV replication is the

regulation of HBV core promoter activity by augmenting FXRA expression. Several studies have described the essential role of FXRA/RXRA in the HBV life cycle in detail. FXRA forms a heterodimer with RXRA and binds to the regulatory sequences in the HBV core promoter. Activation of the FXR/RXR pathway by bile acids can enhance HBV transcription and replication.24, 32 Ectopic expression of FXRA/RXRA can establish HBV replication in nonhepatoma cells.15 In our study, FXRA was significantly up-regulated by miR-1. Furthermore, the FXRA antagonist GGS and FXRA-specific siRNA partially attenuated the miR-1 effect on HBV replication. Our results strongly suggested that FXRA may contribute to the modulation of HBV core promoter activity and subsequently to the level of viral replication by miR-1 expression. However, the mechanism of miR-1 regulation in FXRA expression remains to be clarified. The ability of miRNAs to regulate the expression of multiple target genes implies the influence of miRNAs on global biological processes in cells. As shown previously, miR-1 expression was reduced in primary human hepatocellular carcinomas compared with matching normal liver tissue.

The clinical presentation of a severe factor deficiency is sponta

The clinical presentation of a severe factor deficiency is spontaneous

bleeding or excessive bleeding following minor trauma in otherwise healthy infants. ICH may be the presenting symptom. Facial purpura following birth is usually associated with severe platelet dysfunction or thrombocytopenia. Oral mucous membrane bleeding is common for thrombocytopenic infants; however, gum bleeding and epistaxis hardly ever present in neonates. Joint haemarthroses, typical for severe factor deficiencies, rarely occur before ambulation. Persistent oozing from the umbilical stump is typical for infants click here with defective fibrinogen production or function and FXIII deficiency. The correct diagnostic assays and appropriate management vary according to the underlying basic disorder. Most forms of von Willebrand’s disease (VWD) cannot be diagnosed in newborns, as physiological concentrations of VWF and the proportion of high molecular weight multimers of VWF are increased [10]. Thus, type 3 VWD (the severe form, complete factor deficiency) can be diagnosed in neonates, whereas the diagnoses of mild or qualitative deficiencies (type 1 or 2 VWD,

respectively) are troublesome and require repeated testing for confirmation in later infancy. Severe FXI deficiency, a genetic disorder that prevails among Ashkenazi Jews, can present in newborns following haemostatic challenges, such as circumcision [35]. As physiological FXI levels may be low after birth, infants with borderline FXI levels EPZ-6438 solubility dmso should be retested prior to any elective surgical procedures, for

treatment of bleeding episodes, or during surgery and treated accordingly, if required. Severe homozygous FVII deficiency (plasma levels <0.03 units mL−1) can present with ICH following birth (r). Milder deficiencies are usually diagnosed at older ages, as a result of lower boundaries of the vitamin K-dependant FVII at birth as well as more selleck kinase inhibitor subtle bleeding manifestations. Deficiencies of factor XII, prekalikrein and high molecular weight kininogen are of no clinical significance in newborns. Rare autosomal recessive homozygous severe FV deficiency (diagnosed by plasma concentrations <0.1 units mL−1) as well as homozygous severe FII or FX deficiencies (plasma concentrations lower than 0.2 and 0.1 units mL−1, respectively) can cause haemorrhagic symptoms. The exact prevalence of these disorders is unknown. All infants suffering these disorders demonstrate abnormal coagulation screening tests, with prolonged PT and PTT. Whereas FV deficiency is easily diagnosed in neonates, FII or FX (both vitamin K-dependant factors) borderline-low levels may overlap with neonatal physiological levels, making the diagnosis difficult.

It is likely that PD-1 can induce tumor-specific CD8+ T-cell apop

It is likely that PD-1 can induce tumor-specific CD8+ T-cell apoptosis34 and PD-1 signaling has been shown to reduce IFN-γ, TNF-α, and IL-2 synthesis.31 Collectively, these studies suggest a pivotal role for the PD-1-PDL1/2 axis during initial viral escape and reduced tumor surveillance. The liver is a preferred site of T-cell see more accumulation and activation, due, in part, to unique architectural features and the abundance of APC. Increased expression of adhesion molecules facilitates the trapping of activated T cells in sinusoids, where they may undergo

apoptosis induced by FasL and Trail on KC or be phagocytosed.32 Moreover, T cells that recognize antigen in the liver are typically exposed to high levels of the suppressive Pifithrin�� cytokines IL-10 and TGF-β; further modulation occurs through PD1-PDL1/2 inhibitory signaling. This T-cell tolerance likely explains the evolutionary need to have a substantial innate component, potentially explaining the abundance of pDC and NK cells. The role and types of immunosuppressive cells that accumulate in chronic infection and HCC remain incompletely understood in the liver. MDSCs are a heterogeneous population of immature myeloid cells,

which can expand and contribute to immune suppression during HCV infection and HCC.37, 38 The liver is a preferred site for homing and expansion of MDSCs.39 this website MDSCs can disrupt immune surveillance mechanisms including

suppressing effector T cells,38 expanding Tregs,40 and impairing NK cell function.41 MDSC-derived ROS can induce oxidative stress and mediate T-cell suppression during chronic HCV infection.37 The presence of intratumoral and circulating Tregs correlates with tumor progression,42 poor prognosis,43 and reoccurrence following surgical resection44 of HCC. Tregs mediate immune suppression through functional modulation of tumor-specific CD8+ and CD4+ T cells and by tumor-specific accumulation mediated through chemokine receptor CCR4.45 However, a recent report from Chen et al.46 identified a selective Treg recruitment pathway facilitated through CCR6-CCL20, selectively promoting HCC progression and predicting poor prognosis. NK and NKT cells represent a major innate immune component in liver, constituting over 50% of hepatic lymphocytes in mice and humans.47 During chronic viral infection, suppression of NK cells can result in reduced surveillance. Recent evidence suggests that once HBV/HCV infections become persistent, NK cells lose their cytotoxic potential and ability to secrete IFN-γ.48 NK cell function is also impaired in nonviral-induced liver cirrhosis.

, MD (AASLD Postgraduate Course, Parallel Session) Nothing to dis

, MD (AASLD Postgraduate Course, Parallel Session) Nothing to disclose Baddour, Larry, MD (SIG Program) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices

or procedure(s) Bajaj, Jasmohan S., MD (AASLD Postgraduate Course, SIG Program) Advisory Committees or Review Panels: Salix, Merz, otsuka, ocera, grifols, american college of gastroenterology Grant/Research Support: salix, otsuka, grifols Content of the presentation does not include discussion CP-673451 order of off-label/investigative use of medicine(s), medical devices or procedure(s) Baliga, Prabhakar, MD (SIG Program) Nothing to disclose Content selleck of the presentation does not include discussion

of off-label/investigative use of medicine(s), medical devices or procedure(s) Bambha, Kiran, MD (Early Morning Workshops, Hepatology Associates Course, Parallel Session) Nothing to disclose Banerjee, Subhas, MD (AASLD/ASGE Endoscopy Course) Grant/Research Support: Boston Scientific Foundation Speaking and Teaching: Pentax Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Baron, Todd H., MD (AASLD/ASGE Endoscopy Course) Consulting: Cook Medicine, Olympus, Merit Endotek Speaking and Teaching: Boston Scientific Corporation, ConMed Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Bataller, Ramón, MD (Federal Focus) check details Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Befeler, Alex, MD (Parallel

Session) Nothing to disclose Belghiti, Jacques, MD (Transplant Surgery Workshop) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Berenguer, Marina, MD (Meet-the-Professor Luncheon) Advisory Committees or Review Panels: Novartis, Astellas, Janssen, BMS Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Berk, Paul D., MD (Early Morning Workshops) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Beutler, Bruce, MD (President’s Choice) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Bezerra, Jorge A.