The Experts below are selected from a list of 300 Experts worldwide ranked by ideXlab platform
Stephen H. Caldwell - One of the best experts on this subject based on the ideXlab platform.
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Nonalcoholic steatohepatitis and cryptogenic Cirrhosis within kindreds
American Journal of Medicine, 2000Co-Authors: Veerle Margrethe Diane Struben, Elizabeth Erickson Hespenheide, Stephen H. CaldwellAbstract:PURPOSE: Familial forms of cryptogenic Cirrhosis have been described. We have cared for families in which several members were afflicted with cryptogenic Cirrhosis as well as the more recently recognized entity of nonalcoholic steatohepatitis. To examine the familial patterns of these disorders, we reviewed patients with nonalcoholic steatohepatitis, with and without Cirrhosis, or cryptogenic Cirrhosis to assess how frequently their relatives were afflicted with these disorders. SUBJECTS AND METHODS: Eighteen members of eight kindreds containing 2 or more afflicted members were studied. Diagnoses were based on histology in all but 3 patients (2 elderly women with liver atrophy and severe cirrhotic ascites diagnosed clinically with cryptogenic Cirrhosis and 1 adult man with abnormal serum aminotransferase levels and hepatomegaly that was diagnosed as fatty liver by ultrasound). Other forms of liver disease were excluded by extensive serologic testing. RESULTS: There were 8 index patients (1 man, 7 women; 2 with cryptogenic Cirrhosis, 4 with nonalcoholic steatohepatitis with Cirrhosis, and 2 with nonalcoholic steatohepatitis without Cirrhosis) and 10 relatives (4 men, 6 women; 2 with cryptogenic Cirrhosis and 8 with nonalcoholic steatohepatitis). Nonalcoholic steatohepatitis and nonalcoholic steatohepatitis with Cirrhosis coexisted within four kindreds, one of which also had an afflicted member with cryptogenic Cirrhosis. Nonalcoholic steatohepatitis and cryptogenic Cirrhosis coexisted within three additional kindreds. Patterns of afflicted patients included mother-daughter, sister-sister, sister-brother, father-daughter, and male-female cousins. Fifteen (83%) of the 18 subjects were obese, and 11 (61%) had type 2 diabetes mellitus. CONCLUSIONS: The coexistence of nonalcoholic steatohepatitis with and without Cirrhosis and cryptogenic Cirrhosis within these kindreds suggests a common pathogenesis and possible genetic risk. These disorders were frequently but not invariably associated with female sex, obesity, and type 2 diabetes. Copyright (C) 2000 Excerpta Medica Inc.
Morris Sherman - One of the best experts on this subject based on the ideXlab platform.
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Regression of Human Cirrhosis
2009Co-Authors: Ian R. Wanless, Eisuke Nakashima, Morris ShermanAbstract:Abstract Context.—Cirrhosis is widely regarded as being irreversible. Recent studies have demonstrated that fibrosis may decrease with time in humans and experimental animals if the disease activity becomes quiescent. The histologic appearance of regressing Cirrhosis in the human has not been described in detail. Objectives.—To define histologic parameters that indicate regression of Cirrhosis and to provide an interpretation of how regression occurs from a histologic point of view. Design.—A patient who underwent a series of biopsies that showed apparent regression of hepatitis B Cirrhosis is presented. In addition, 52 livers removed at transplantation having Cirrhosis or incomplete septal Cirrhosis were graded for histologic parameters that suggest progression or regression of fibrosis. Progression parameters were steatohepatitis, inflammation, bridging necrosis, and piecemeal necrosis. The regression parameters (collectively called the hepatic repair complex) were delicate perforated septa, isolated th...
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management of hepatocellular carcinoma
Hepatology, 2005Co-Authors: Jordi Bruix, Morris ShermanAbstract:The incidence of hepatocellular carcinoma (HCC) has increased worldwide and is now the 5th most frequent cancer representing approximately 5% of all cancers worldwide. More than 500,000 new cases are diagnosed per year and it is the third cause of cancer-related death and the first cause of death in patients with Cirrhosis [1]. The incidence of HCC has major geographical differences, but most patients diagnosed with HCC have underlying Cirrhosis. The highest risk is observed in Cirrhosis from chronic infection by the hepatitis B virus (HBV) or hepatitis C virus (HCV) [2]. In patients with HCV infection the risk increases with the confirmation of Cirrhosis, when the yearly incidence varies between 3-5% and the 5-year cumulative incidence ranges from 15-20% [2]. Since vaccination against HCV is not available, prevention of HCV infection is based on preventing transmission by blood products. Progression from chronic HCV infection to advanced fibrosis or Cirrhosis may be prevented in 40% of patients who are sustained responders to new antiviral strategies, such as pegylated interferon and ribavirin [3]. Thus, the prevention of Cirrhosis can prevent the development of HCC. On the other hand, in patients with confirmed Cirrhosis, the preventive effect of these agents has not been proven [4].
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Regression of human Cirrhosis: Morphologic features and the genesis of incomplete septal Cirrhosis
Archives of Pathology & Laboratory Medicine, 2000Co-Authors: Ian R. Wanless, Eisuke Nakashima, Morris ShermanAbstract:○ Context.-Cirrhosis is widely regarded as being irreversible. Recent studies have demonstrated that fibrosis may decrease with time in humans and experimental animals if the disease activity becomes quiescent. The histologic appearance of regressing Cirrhosis in the human has not been described in detail. Objectives.-To define histologic parameters that indicate regression of Cirrhosis and to provide an interpretation of how regression occurs from a histologic point of view. Design.-A patient who underwent a series of biopsies that showed apparent regression of hepatitis B Cirrhosis is presented. In addition, 52 livers removed at transplantation having Cirrhosis or incomplete septal Cirrhosis were graded for histologic parameters that suggest progression or regression of fibrosis. Progression parameters were steato-hepatitis, inflammation, bridging necrosis, and piecemeal necrosis. The regression parameters (collectively called the hepatic repair complex) were delicate perforated septa, isolated thick collagen fibers, delicate periportal fibrous spikes, portal tract remnants, hepatic vein remnants with prolapsed hepatocytes, hepatocytes within portal tracts or splitting septa, minute regenerative nodules, and aberrant parenchymal veins. Results and Conclusions.-Regression parameters were found in all livers and were prominent in the majority. Livers with micronodular Cirrhosis, macronodular Cirrhosis, and incomplete septal Cirrhosis demonstrate a histologic continuum. A continuum of regressive changes was also seen within individual livers. These appearances allow one to understand visually how fibrous regions of hepatic parenchyma can be returned toward a normal appearance. Many examples of incomplete septal Cirrhosis could be the product of regressed Cirrhosis.
Robert A Fisher - One of the best experts on this subject based on the ideXlab platform.
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similarities and differences in outcomes of Cirrhosis due to nonalcoholic steatohepatitis and hepatitis c
Hepatology, 2006Co-Authors: Arun J Sanyal, Colin Banas, Carol Sargeant, Velimir A Luketic, Richard K Sterling, Richard T Stravitz, Mitchell L Shiffman, Douglas M Heuman, Adrian Coterrell, Robert A FisherAbstract:The objective of this study was to prospectively define outcomes of Cirrhosis due to nonalcoholic steatohepatitis (NASH) and compare them with those associated with hepatitis C virus (HCV) infection. We compared 152 patients with Cirrhosis due to NASH with 150 matched patients with Cirrhosis due to HCV. Over 10 years, 29/152 patients with Cirrhosis due to NASH died compared with 44/150 patients with HCV (P < .04). This was mainly due to the lower mortality rate in patients with Child class A Cirrhosis due to NASH versus HCV (3/74 vs. 15/75; P < .004). There were no significant across-group differences in mortality in patients with Child class B or C Cirrhosis. Sepsis was the most common cause of death in both groups; patients with NASH had a higher cardiac mortality (8/152 vs. 1/150; P < .03). Patients with Child class A Cirrhosis due to NASH also had a significantly lower risk of decompensation, defined by a 2-point increase in Child-Turcotte-Pugh score (P < .007). Cirrhosis due to NASH was associated with a lower rate of development of ascites (14/101 vs. 40/97 patients at risk; P < .006). NASH also had a significantly lower risk of development of hepatocellular carcinoma (10/149 vs. 25/147 patients at risk; P < .01). In conclusion, compensated Cirrhosis due to NASH is associated with a lower mortality rate compared with that due to HCV. It is also associated with a lower rate of development of ascites, hyperbilirubinemia, and hepatocellular carcinoma. However, cardiovascular mortality is greater in patients with NASH. (HEPATOLOGY 2006.)
Andrew K. Burroughs - One of the best experts on this subject based on the ideXlab platform.
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Liver Cirrhosis.
Lancet (London England), 2014Co-Authors: Emmanuel A Tsochatzis, Jaime Bosch, Andrew K. BurroughsAbstract:Cirrhosis is an increasing cause of morbidity and mortality in more developed countries, being the 14th most common cause of death worldwide but fourth in central Europe. Increasingly, Cirrhosis has been seen to be not a single disease entity, but one that can be subclassified into distinct clinical prognostic stages, with 1-year mortality ranging from 1% to 57% depending on the stage. We review the current understanding of Cirrhosis as a dynamic process and outline current therapeutic options for prevention and treatment of complications of Cirrhosis, on the basis of the subclassification in clinical stages. The new concept in management of patients with Cirrhosis should be prevention and early intervention to stabilise disease progression and to avoid or delay clinical decompensation and the need for liver transplantation. The challenge in the 21st century is to prevent the need for liver transplantation in as many patients with Cirrhosis as possible.
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Muscle cramps in Cirrhosis: the therapeutic value of quinine. Is it underused?
Dig Liver Dis, 2008Co-Authors: Andrew K. BurroughsAbstract:Muscle cramps are a common and recurring symptom in patients with Cirrhosis. Although, the pathophysiology has not been specifically studied in Cirrhosis, this is thought to be the same for cramps in general, originating in the motorneurone, with high frequency firing of motor unit action potentials. However precise pathophysiological mechanisms are not known. Risk factors in Cirrhosis have been little studied. Neither aetiology, nor pre-ascitic or ascitic stage, nor electrolyte disturbances, nor use of diuretic therapy has been found to have a statistical association with cramps in patients with Cirrhosis. Effective treatments, from this literature review, are albumin, which however is expensive and has little applicability as preventative therapy and oral quinine or quinidine. Quinine is little used in Italy but licensed in the UK for the therapy of muscle cramps. There is evidence for the efficacy of quinine in patients without Cirrhosis and in healthy subjects. In Cirrhosis quinidine (isomer of quinine) has also been shown to be effective versus placebo. Its major effect is in the prevention of cramps. More widespread use of quinine and further studies are needed, particularly in Italy and other countries, in which its use has been limited, as it is effective therapy in many patients with Cirrhosis.
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hypercoagulability in patients with primary biliary Cirrhosis and primary sclerosing cholangitis evaluated by thrombelastography
Journal of Hepatology, 1997Co-Authors: Ziv Benari, Manos Panagou, David Patch, Steven Bates, Elsir Osman, John Pasi, Andrew K. BurroughsAbstract:Abstract Background/Aims: Patients with primary biliary Cirrhosis and primary sclerosing cholangitis survive variceal bleeding better than patients with alcoholic Cirrhosis and have less bleeding at liver transplantation. Recently, patients with primary biliary Cirrhosis have been found to have a higher incidence of thrombosis in the portal venous tree. We hypothesized that primary biliary Cirrhosis and primary sclerosing cholangitis patients may be hypercoagulable. Methods: We used thrombelastography, which is a simple technique for evaluating whole blood clotting and fibrinolysis, to establish if hypercoagulability was present, defined by thrombelastography values greater than 2SD over controls: r 60 mm, and alpha angle > 43° (these reflect platelets and fibrinogen levels). We evaluated 47 primary biliary Cirrhosis and 21 primary sclerosing cholangitis patients, 40 with non-cholestatic Cirrhosis and 40 healthy subjects as control groups with thrombelastography, full blood count, prothrombin time, partial thromboplastin time and, fibrinogen concentrations. In those with hypercoagulability we evaluated protein S, C, anti-thrombin III levels and activated protein C phenotype. Results: All three thrombelastography abnormalities present together defined hypercoagulability: these were found in 13 of 47 (28%) primary biliary Cirrhosis and in nine of 21 (43%) primary sclerosing cholangitis patients independent of Cirrhosis, and bilirubin concentration, but in only 2 of 40 (5%) patients with non-cholestatic Cirrhosis and in none of the healthy controls ( p p Conclusions: This difference between biliary and parenchymal liver disease may have clinical implications, which need to be defined.
Spiros D. Ladas Garyfallia Kaltsa, Giorgos Bamias, Spyros I. Siaka - One of the best experts on this subject based on the ideXlab platform.
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Systemic levels of human β-defensin 1 are elevated in patients with Cirrhosis
Annals of Gastroenterology, 2016Co-Authors: Spiros D. Ladas Garyfallia Kaltsa, Giorgos Bamias, Spyros I. SiakaAbstract:Background Bacterial translocation (BT) commonly occurs in Cirrhosis. Reliable biomarkers for BT are currently lacking. Human beta defensin-1 (hBD-1) is a member of the family of natural antimicrobial peptides produced by epithelial cells and participates in the mucosal defensive mechanisms that prevent BT. The aim of the present study was to examine the local and systemic expression of hBD-1 in patients with Cirrhosis. Methods Plasma concentrations of hBD-1 and of soluble CD14 (sCD14) proteins were measured by ELISA in patients with chronic viral hepatitis, Cirrhosis, and healthy controls. Relative mRNA expression of various natural antimicrobial peptides was determined by real-time PCR in biopsies from the terminal ileum and colon. Results We found significant upregulation of hBD-1 and sCD14 in the peripheral blood of patients with Cirrhosis compared to patients with chronic viral hepatitis and healthy controls. The etiology of Cirrhosis did not affect the concentration of either protein. The levels of hBD-1 protein correlated significantly with the levels of sCD14 in blood collected from hepatic veins of cirrhotic patients. In contrast, no significant differences were observed in the intestinal mucosal mRNA expression of the Paneth cell specific defensin A5 or hBD-1 between patients with Cirrhosis and healthy controls. Conclusions hBD-1 is upregulated in patients with Cirrhosis and highly correlates with the lipopolysaccharide-induced protein sCD14. hBD-1 may serve as a biomarker of BT in patients with Cirrhosis.