Recently, we demonstrated that FVIII knockout (KO) mice had significantly decreased bone mass and bone strength despite the fact that they did not have haemarthroses. The aim of this study was to explore the mechanism of bone disease associated with FVIII deficiency. We compared biochemical markers of bone formation and osteoclastogenesis, inflammatory cytokines, as well as static and dynamic histomorphometry of genetically engineered FVIII KO male mice to those of wild-type (WT) controls.

At 20 weeks of age, FVIII KO mice, as well as WT controls, were sacrificed. Serum and bones were obtained at the time of sacrifice to study biochemical markers of bone formation (osteocalcin) and osteoclastogenesis (receptor

activator of nuclear factor kappa-β and osteoprotegerin), this website levels of inflammatory cytokines (interleukin-1α and interferon-β) and to perform static and dynamic histomorphometry of tibia C646 cancellous bone. There was no difference in the biochemical markers of bone formation or osteoclastogenesis. However, there were differences in the two bone-associated cytokines studied. In addition, histomorphometric examination revealed cancellous osteopenia in FVIII KO mice as evidenced by decreased bone area and trabecular number and increased trabecular separation. Bone formation parameters were normal in FVIII KO mice. In contrast, osteoclast-lined bone perimeter was increased. These data demonstrate that bone disease in FVIII KO mice is due to an increased rate of bone resorption. “
“This chapter contains sections titled: Introduction Incidence and prevalence

Clinical presentation Risk factors Analysis of the immune response selleck chemical to factor VIII in mild/moderate hemophilia A Treatment Conclusion References “
“Summary.  The topic of this monograph is liver cancer associated with chronic HCV infection. We start with some background information on chronic HCV infection and its long-term sequelae, one of which is liver cancer. The rest of the article is concerned with liver cancer or hepatocellular carcinoma (HCC). Epidemiology, risk factors, treatment and outcomes are discussed. We focus on those aspects that are of specific interest in people with haemophilia: studies performed in haemophilia populations, the use of invasive diagnostic and therapeutic tools and the outcome of liver transplantation. Throughout the paper, recommendations are given on surveillance for and diagnosis of HCC and on the practical aspects of invasive procedures. These recommendations are based on professional guidelines, other published evidence and the authors’ experience. In general, diagnostic and therapeutic options are the same in persons with and without haemophilia. Hepatitis C is caused by infection with HCV, an RNA flavivirus. In the haemophilia community, HCV was transmitted through clotting factor concentrates.

Recently, we demonstrated that FVIII knockout (KO) mice had significantly decreased bone mass and bone strength despite the fact that they did not have haemarthroses. The aim of this study was to explore the mechanism of bone disease associated with FVIII deficiency. We compared biochemical markers of bone formation and osteoclastogenesis, inflammatory cytokines, as well as static and dynamic histomorphometry of genetically engineered FVIII KO male mice to those of wild-type (WT) controls.

At 20 weeks of age, FVIII KO mice, as well as WT controls, were sacrificed. Serum and bones were obtained at the time of sacrifice to study biochemical markers of bone formation (osteocalcin) and osteoclastogenesis (receptor

activator of nuclear factor kappa-β and osteoprotegerin), click here levels of inflammatory cytokines (interleukin-1α and interferon-β) and to perform static and dynamic histomorphometry of tibia HIF activation cancellous bone. There was no difference in the biochemical markers of bone formation or osteoclastogenesis. However, there were differences in the two bone-associated cytokines studied. In addition, histomorphometric examination revealed cancellous osteopenia in FVIII KO mice as evidenced by decreased bone area and trabecular number and increased trabecular separation. Bone formation parameters were normal in FVIII KO mice. In contrast, osteoclast-lined bone perimeter was increased. These data demonstrate that bone disease in FVIII KO mice is due to an increased rate of bone resorption. “
“This chapter contains sections titled: Introduction Incidence and prevalence

Clinical presentation Risk factors Analysis of the immune response this website to factor VIII in mild/moderate hemophilia A Treatment Conclusion References “
“Summary.  The topic of this monograph is liver cancer associated with chronic HCV infection. We start with some background information on chronic HCV infection and its long-term sequelae, one of which is liver cancer. The rest of the article is concerned with liver cancer or hepatocellular carcinoma (HCC). Epidemiology, risk factors, treatment and outcomes are discussed. We focus on those aspects that are of specific interest in people with haemophilia: studies performed in haemophilia populations, the use of invasive diagnostic and therapeutic tools and the outcome of liver transplantation. Throughout the paper, recommendations are given on surveillance for and diagnosis of HCC and on the practical aspects of invasive procedures. These recommendations are based on professional guidelines, other published evidence and the authors’ experience. In general, diagnostic and therapeutic options are the same in persons with and without haemophilia. Hepatitis C is caused by infection with HCV, an RNA flavivirus. In the haemophilia community, HCV was transmitted through clotting factor concentrates.

A detailed examination of the literature reveals considerable heterogeneity in the phenotypic descriptions labelled as NDPH. The first effort in a patient with a NDPH presentation is to discern if secondary causes are present; some are obvious, such as subarachnoid bleeds and some can be more troublesome, such as syndromes of abnormal CSF pressure/volume, either high or low. A cohort of primary NDPH headaches can be seen in practice and in the literature and these should be sub-divided into a migrainous type, with appropriate phenotypic manifestations and a featureless type. Patients with any one of the NDPH presentations are best managed according to the more detailed

pathophysiology-based diagnosis then lumped together into a single group, since a single disorder is unlikely to exist. “
“Objective.— To assess the psychometric properties of a new patient-reported migraine instrument, the Completeness SCH772984 order of Response Survey (CORS), which measures a comprehensive set of factors

important to patients’ decisions regarding the initiation and continuation of treatment. Background.— Traditionally, migraine treatments and the instruments used to demonstrate their efficacy have focused on the relief of headache pain. As new treatments emerge with the potential for more complete and consistent migraine relief, more comprehensive tools are needed to demonstrate these benefits. The CORS includes 2 modules, the static CORS, which comprehensively evaluates one treatment at one time point, and the comparative CORS, which provides a more global comparison between 2 treatments at one time point. Together, Alvelestat in vitro the 2 modules can measure unmet treatment needs and improvements over the course of a clinical study. Methods.— Data from an 8-site study comparing 147 patients’ recent experiences with their current triptan therapy and 2 months of study treatment with a single-tablet formulation of sumatriptan/naproxen sodium were used to conduct a preliminary psychometric evaluation of the CORS. The study included

both modules of the CORS, the Headache Impact Test, the revised Patient Perception of Migraine Questionnaire, and a migraine diary. Results.— The CORS response categories find more in both the static and comparative modules demonstrated limited floor or ceiling effects and few missing values (<3%). Inter-item correlations, principal components analysis (component loading range: 0.62 to 0.95), and high estimates of internal consistency (alpha range: 0.88 to 0.94) for each composite score supported the structure and proposed scoring algorithm for the static module. The pattern of correlations between the CORS static and comparative items and composites with the revised Patient Perception of Migraine Questionnaire items and subscales, as well as the relationships between responses to selected static CORS items and the migraine diary, supported the construct validity of the CORS.

Nagorney, MD Session II: Adenoma 3:50 – 4:10 PM Imaging Characteristics of Adenomas BachirTaouli, MD 4:10 – 4:30 PM How Molecular and Immunohistochemical Analyses Can Help Us Guide Therapy For Hepatic Adenomas and FNH Jessica Zucman-Rossi, MD, PhD 4:30 – 4:50

PM Resection, Transplantation and Local Regional Therapies For Adenomas Jacques Belghiti, MD 4:50 – 5:10 PM Break Session III: Neuroendocrine Tumors 5:10 – 5:30 PM Imaging Characteristics of Neuroendocrine Tumors Bachir Taouli, MD 3-MA chemical structure 5:30 – 5:50 PM Current NANETS and ENETS Guidelines for Management Of Neuroendocrine Tumors Diane Reidy, MD 5:50 – 6:10 PM Liver Transplantation for Neuroendocrine Tumors Vincenzo Mazzaferro, MD 6:10 – 6:30 PM Liver Resection and Local Regional Therapies for Neuroendocrine Tumors Timothy M. Pawlik, MD, PhD 6:30 – 6:40 PM Debate: Patients with Neuroendocrine Tumors Will Do Well No Matter What We Do – So Why Treat Them? Vincenzo Mazzaferro, MD 6:40 – 6:50

PM Debate: Patients with Neuroendocrine Tumor Will Do Better With Aggressive Treatment Timothy M. Pawlik, MD, PhD 6:50 – 7:00 PM Closing Remarks AASLD BUSINESS MEETING (MEMBERS ONLY) Saturday, MG-132 in vitro November 2 5:15 – 6:15 PM Hall E – General Session Room J. Gregory Fiz, MD, presiding Early Morning Workshops Sunday, November 3 6:45 – 7:45 AM Refer to your luncheon ticket for meeting room location. Sunday Basic Early Morning Workshops Goals and Objectives: Bring together investigators in a specific area of research to discuss their ongoing work. Focus of discussions is on new work and not a review of previous studies. Allow ample time for questions from the audience. EMW-1 Artificial Liver Support Systems Jayanta Roy-Chowdhury, MD and Vicente Arroyo, EMW-2 HCV Replication Andrew H. Talal, MD and Raymond T.

Chung, MD EMW-3 Triggers of Fibrosis in NASH Ariel E. Feldstein, MD and Detlef Schuppan, MD, PhD EMW-4 Cholangiocyte Pathobiology Gianfranco Alpini, PhD and Marco Marzioni, MD EMW-5 Microbiome and the Liver Bernd Schnabl, MD and David Brenner, MD EMW-6 Animal Models of NAFLD Rohit Kohli, MD and Michael R. Charlton, MD click here Sunday Clinical Early Morning Workshops Goals and Objectives: Discuss difficult management issues utilizing acknowledged experts in the area. Provide an overview of the current state-of-the-art in each area. Allow ample time for questions from the audience. EMW-7 Imaging of Liver Tumors Claude B. Sirlin, MD and Laura M. Kulik, MD EMW-8 Liver Transplantation for Hepatitis C Xavier Forns, MD and Norah Terrault, MD EMW-9 New Anti-Tumor Agents in Development for HCC Jorge A. Marrero, MD and Josep M.

Nagorney, MD Session II: Adenoma 3:50 – 4:10 PM Imaging Characteristics of Adenomas BachirTaouli, MD 4:10 – 4:30 PM How Molecular and Immunohistochemical Analyses Can Help Us Guide Therapy For Hepatic Adenomas and FNH Jessica Zucman-Rossi, MD, PhD 4:30 – 4:50

PM Resection, Transplantation and Local Regional Therapies For Adenomas Jacques Belghiti, MD 4:50 – 5:10 PM Break Session III: Neuroendocrine Tumors 5:10 – 5:30 PM Imaging Characteristics of Neuroendocrine Tumors Bachir Taouli, MD see more 5:30 – 5:50 PM Current NANETS and ENETS Guidelines for Management Of Neuroendocrine Tumors Diane Reidy, MD 5:50 – 6:10 PM Liver Transplantation for Neuroendocrine Tumors Vincenzo Mazzaferro, MD 6:10 – 6:30 PM Liver Resection and Local Regional Therapies for Neuroendocrine Tumors Timothy M. Pawlik, MD, PhD 6:30 – 6:40 PM Debate: Patients with Neuroendocrine Tumors Will Do Well No Matter What We Do – So Why Treat Them? Vincenzo Mazzaferro, MD 6:40 – 6:50

PM Debate: Patients with Neuroendocrine Tumor Will Do Better With Aggressive Treatment Timothy M. Pawlik, MD, PhD 6:50 – 7:00 PM Closing Remarks AASLD BUSINESS MEETING (MEMBERS ONLY) Saturday, check details November 2 5:15 – 6:15 PM Hall E – General Session Room J. Gregory Fiz, MD, presiding Early Morning Workshops Sunday, November 3 6:45 – 7:45 AM Refer to your luncheon ticket for meeting room location. Sunday Basic Early Morning Workshops Goals and Objectives: Bring together investigators in a specific area of research to discuss their ongoing work. Focus of discussions is on new work and not a review of previous studies. Allow ample time for questions from the audience. EMW-1 Artificial Liver Support Systems Jayanta Roy-Chowdhury, MD and Vicente Arroyo, EMW-2 HCV Replication Andrew H. Talal, MD and Raymond T.

Chung, MD EMW-3 Triggers of Fibrosis in NASH Ariel E. Feldstein, MD and Detlef Schuppan, MD, PhD EMW-4 Cholangiocyte Pathobiology Gianfranco Alpini, PhD and Marco Marzioni, MD EMW-5 Microbiome and the Liver Bernd Schnabl, MD and David Brenner, MD EMW-6 Animal Models of NAFLD Rohit Kohli, MD and Michael R. Charlton, MD selleck chemicals Sunday Clinical Early Morning Workshops Goals and Objectives: Discuss difficult management issues utilizing acknowledged experts in the area. Provide an overview of the current state-of-the-art in each area. Allow ample time for questions from the audience. EMW-7 Imaging of Liver Tumors Claude B. Sirlin, MD and Laura M. Kulik, MD EMW-8 Liver Transplantation for Hepatitis C Xavier Forns, MD and Norah Terrault, MD EMW-9 New Anti-Tumor Agents in Development for HCC Jorge A. Marrero, MD and Josep M.

[12] This was the missing piece that revealed that NANBH had severe, and sometimes fatal, consequences. Throughout the 1980s, I continued to prospectively follow blood recipients, track hepatitis incidence and investigate donor screening interventions that might reduce risk. By 1980, TAH incidence had fallen to about 6% as the consequence of lessened blood use in cardiovascular surgery. In trying to further reduce risk, we did a retrospective analysis that predicted that the introduction of ALT testing of blood donors might reduce TAH incidence by 30%,[13] as did a similar study by Aach et al.[14] Hence, in 1981, we began

routine ALT testing of donors, but despite predictions, this did not have a measurable effect on hepatitis outcomes. beta-catenin inhibitor A similar retrospective analysis predicted that hepatitis B core antibody (anti-HBc) testing of donors could serve as a surrogate for NANBH virus carriers and reduce TAH by 30%-40%.[15] This confirmed results from a multicenter, prospective study (Transfusion-Transmitted Virus) sponsored by the National Heart, Lung and Blood Institute.[16] Kinase Inhibitor Library in vitro I

am proud of the fact that, in 1986, I presented data at the annual meeting of the American Association of Blood Banks, and then separately to each of the major blood organizations, in which I urged the introduction of routine anti-HBc donor screening. Such testing was introduced nationally in 1987 and not only prevented some cases of NANBH, but also detected occult hepatitis B carriers and served as a surrogate for human immunodeficiency virus carriers. Our ongoing prospective studies showed that subsequent to anti-HBc testing, TAH incidence fell to about 4% by 1989. This was quite gratifying, but we continued to be frustrated by our inability to find the NANB agent, despite extensive efforts. Together with Dr. Purcell’s lab,

we utilized highly pedigreed infectious sera and attempted every serologic approach known at the click here time. In addition, Steve Feinstone was experimenting with subtractive hybridization in these very early days of emergent molecular biology. This frustration spilled out in a poem that I wrote in 1988, which I titled, “I Can’t See the Forest for the HBsAgs”: I think that I shall never see This virus called non-A, non-B A virus I cannot deliver And yet I know it’s in the liver A virus that we often blame, But which exists alone by name No antigen or DNA No little test to mark its way. A virus which in our confusion Has forced us into mass collusion To make exist just by exclusion But is it real or an illusion? Oh GREAT LIVER in the sky, Show us where and tell us why Send us thoughts that will inspire us Let us see this elusive virus If we don’t publish soon, They’re going to fire us! I think it was this poem that pushed the field forward, because in 1988, I received a call from George Kuo suggesting that Chiron had cloned the NANB agent and developed an Ab assay.

[12] This was the missing piece that revealed that NANBH had severe, and sometimes fatal, consequences. Throughout the 1980s, I continued to prospectively follow blood recipients, track hepatitis incidence and investigate donor screening interventions that might reduce risk. By 1980, TAH incidence had fallen to about 6% as the consequence of lessened blood use in cardiovascular surgery. In trying to further reduce risk, we did a retrospective analysis that predicted that the introduction of ALT testing of blood donors might reduce TAH incidence by 30%,[13] as did a similar study by Aach et al.[14] Hence, in 1981, we began

routine ALT testing of donors, but despite predictions, this did not have a measurable effect on hepatitis outcomes. Epacadostat in vivo A similar retrospective analysis predicted that hepatitis B core antibody (anti-HBc) testing of donors could serve as a surrogate for NANBH virus carriers and reduce TAH by 30%-40%.[15] This confirmed results from a multicenter, prospective study (Transfusion-Transmitted Virus) sponsored by the National Heart, Lung and Blood Institute.[16] this website I

am proud of the fact that, in 1986, I presented data at the annual meeting of the American Association of Blood Banks, and then separately to each of the major blood organizations, in which I urged the introduction of routine anti-HBc donor screening. Such testing was introduced nationally in 1987 and not only prevented some cases of NANBH, but also detected occult hepatitis B carriers and served as a surrogate for human immunodeficiency virus carriers. Our ongoing prospective studies showed that subsequent to anti-HBc testing, TAH incidence fell to about 4% by 1989. This was quite gratifying, but we continued to be frustrated by our inability to find the NANB agent, despite extensive efforts. Together with Dr. Purcell’s lab,

we utilized highly pedigreed infectious sera and attempted every serologic approach known at the selleck inhibitor time. In addition, Steve Feinstone was experimenting with subtractive hybridization in these very early days of emergent molecular biology. This frustration spilled out in a poem that I wrote in 1988, which I titled, “I Can’t See the Forest for the HBsAgs”: I think that I shall never see This virus called non-A, non-B A virus I cannot deliver And yet I know it’s in the liver A virus that we often blame, But which exists alone by name No antigen or DNA No little test to mark its way. A virus which in our confusion Has forced us into mass collusion To make exist just by exclusion But is it real or an illusion? Oh GREAT LIVER in the sky, Show us where and tell us why Send us thoughts that will inspire us Let us see this elusive virus If we don’t publish soon, They’re going to fire us! I think it was this poem that pushed the field forward, because in 1988, I received a call from George Kuo suggesting that Chiron had cloned the NANB agent and developed an Ab assay.

The GPRD

is not population-based; therefore, its incidence estimate represents that of the GPRD and not the general population. Moreover, the code for PSC was not validated, and this poses additional challenges to its validity. These two studies were not fully comparable with the other studies included in the analysis. The incidence of PSC appears to be increasing; however, additional studies are necessary to confirm this observation. This increase in PSC incidence may be a direct result of its link to IBD because recent evidence suggests that the incidence of IBD is still increasing in many regions of the world.26, 29-32 Studies investigating the incidence of PSC with and without IBD may help to resolve this issue; however, the decrease in power when these analyses Opaganib purchase are conducted may hinder the finding of statistical evidence. One study reported

time trends in PSC with and without IBD but failed to find a statistically significant increase.9 Additionally, the observed increase may be due to improvements in the diagnostic abilities of physicians and diagnostic tools such as noninvasive imaging (i.e., selleck inhibitor magnetic resonance cholangiopancreatography).33, 34 Magnetic resonance cholangiopancreatography permits fast and highly accurate imaging of the biliary tree and has been used with increasing frequency as a noninvasive alternative to endoscopic retrograde cholangiopancreatography.33, 35-37 Furthermore, the increasing use of biological therapies (e.g., infliximab) and immunosuppressants (e.g., azathioprine

and methotrexate), particularly in those with IBD,38-40 may have contributed to the greater detection of PSC over time. Biologics and immunosuppressants have been associated with drug-induced liver complications, hepatobiliary disease, and liver toxicity41, 42; therefore, the routine screening of liver function profiles for individuals taking these therapies has increased. Studies investigating the incidence of PSC should consider assessments of diagnostic tool utilization over time. Moreover, this increase in incidence may be a result of biases in observational studies. In particular, the study by Escorsell et al.7 learn more had an unrealistically high AAPC of 27%. Many factors likely contributed to the obvious bias of this estimate. The population estimate used to calculate the incidence was taken from the end of the study period. An increase in the study population (i.e., 12 regions in Spain)43 over the time interval would have overestimated the increase in IR. Additionally, because of the retrospective nature of the study and the need for physicians to respond to a questionnaire, the response rate could have been lower for earlier time periods. Finally, detection bias could have been more pronounced at the end of the study period because of the increased availability and use of diagnostic technologies.

As the host components required for HCV assembly in human liver cells are discerned, the ability of other cell types and species to produce infectious particles remains an open question. Mouse cells, which are of particular interest to animal model developers, show

restrictions in HCV entry and replication; the ability of these cells Dabrafenib in vivo to support assembly is not known. This question was addressed by Long et al. in a recent issue of Gastroenterology.8 Using murine hepatic cell lines, the investigators first sought to bypass known roadblocks to HCV life-cycle steps preceding assembly. To avoid limited HCV production yielded by transient genome transfection and unwanted structural protein deletions found in selectable genomes, they devised a transcomplementation VX-770 manufacturer system to exogenously express HCV core, E1, E2, p7, and NS2 proteins in murine cells harboring subgenomic HCV replicons, which replicate autonomously under antibiotic selection. Limited particle production prompted a comparative transcriptome analysis between naïve mouse cells and those

containing HCV replicons that revealed low levels of apoE in the replicon-containing cells. Remarkably, ectopic expression of human or mouse apoE was sufficient to rescue infectious HCV production from mouse cells, yielding infectious titers similar to those observed in the widely used selleck chemical human hepatoma cell line, Huh-7.5. Notably, Long et al. achieved comparable levels of infectious particle production in cells expressing individual human apoE isoforms (apoE2, E3, and E4). This

corroborates a recent study by Cun et al.,9 suggesting that all isoforms are competent to promote HCV assembly, but contradicts Hishiki et al., who correlated HCV infectivity with isoform affinity for LDLR binding.10 Though the reason for this discrepancy is unclear, this emphasizes the difficulty in separating the role of apoE in particle assembly from its role in entry. It is still unclear whether noninfectious particles can be produced by cells lacking apoE or expressing only a single isoform of the protein. The mechanism of apoE function during HCV assembly in mouse or human cells also remains to be determined. Coaxing HCV assembly in mouse cells adds a new piece to the puzzle in the development of a fully functional rodent model for the virus. HCV has a narrow host range, infecting only humans and chimpanzees, and the lack of a suitable small animal model has limited preclinical testing of drugs and candidate vaccines, as well as hampered mechanistic studies of virus-host interactions. Advances have been made, including murine xenorecipient strains that can be engrafted with human hepatocytes and rendered susceptible to HCV challenge. Liver chimeric mice are, however, a relatively low throughput system with high costs and logistical challenges.

inflammatory marker; 4. ammonia; Presenting Author: KA ZHANG Additional Authors: JING LAI, XIAHAI SUN, YIJIA LIANG, HUANQI XU Corresponding Author: KA ZHANG Affiliations: Department of Infectious Diseases, Third Affiliated Hospital of Sun Yat-sen University Objective: To investigate the correlation between serum-ascites total protein grdient(SATPG)

and Spleen Size Parameters. Methods: 662 liver cirrhosis patients with ascites were examined with color doppler ultrasonography. SATPG was examined with abdominal paracentesis, which was the difference of total protein between serum and ascites. Pearson correlation analysis was used to assess the correlation between SATPG and the thickness of spleen, the length BMN673 of spleen ,and the diameter of splenic vein. Results: Correlations were found between the levels of SATPG and the thickness of spleen, the length of spleen ,and the diameter of splenic vein (r =0.137 P =0.001; r =0.083,P =0.047; r =0.094 P =0.027). The correlation between SATPG levels and the thickness of spleen, the length of spleen ,and the diameter of splenic vein had click here statistical significance(P < 0.05). Conclusion: SATPG levels can reflect the size of spleen

and the diameter of splenic vein. Key Word(s): 1. Total Protein; 2. Liver cirrhosis; 3. Spleen; Presenting Author: RADAN BRUHA Additional Authors: MARIE JACHYMOVA, JAROMIR PETRTYL, LIBOR VITEK, PETR URBANEK, JANA SMALCOVA, KAREL DVORAK Corresponding Author: RADAN BRUHA Affiliations: Charles University in Prague, 1st Faculty of Medicine, 4th Internal Clinic; Charles University see more in Prague, 1st Faculty of

Medicine, Internal clinic of Central Military Hospital Objective: Portal hypertension is a consequence of liver cirrhosis leading to major complications. Non-selective betablocker propranolol plays a crucial role in the prevention of variceal bleeding, but its efficacy is limited and unpredictable. Carvedilol is a new promising combined alfa and nonselective betablocker used in the treatment of portal hypertension. Polymorphism of beta-2 adrenergic receptors was described to influence the response to propranolol treatment. The data regarding carvedilol and beta-2 adrenergic receptors polymorphism are not known. Methods: The aim was to evaluate the relationship between the polymorphisms of beta-2 adrenergic receptors (Gly16Arg, Glu27Gln) and the treatment response to carvedilol in patients with portal hypertension. Patients and methods: 67 patients with liver cirrhosis (47 ethylic, 47 men, age 36-72 years) treated by carvedilol in the prevention of variceal bleeding were examined for Gly16Arg and Glu27Gln polymorphism in the gene for beta-2 adrenergic receptors. The treatment response was evaluated as the decrease in HVPG for more than 20% or below 12 mm Hg. The polymorphisms were examined by standard PCR technique. Results: Complete response to carvedilol treatment was seen in 33 patients (49% of all patients).