Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis C virus (HCV)-related end-stage liver disease is the main indication for liver transplantation performed in Europe and the United States. Recurrence of hepatitis C in the graft is universal and may lead to chronic hepatitis in most patients and to cirrhosis in 20-30% of patients within 5-10 years of transplantation. The natural history of HCV recurrence is highly variable but leads to a lower survival rate than other recurrent liver diseases. The immunosuppressed status and several other factors have been linked with the pattern and severity of recurrence. What remains controversial are those factors associated with fibrosis progression and how these could be modified to improve outcome of recurrent hepatitis C. No single factor but a combination of several factors is associated with fibrosis progression on the graft. The major factors associated with accelerated disease recurrence include: high viral load pre- (>10(6) IU / mL) and / or early post-transplantation (>10(7) IU / mL at 4 months), donor older than 40-50 years, prolonged ischaemic time, cytomegalovirus coinfection, over immunosuppression and / or abrupt changes in immunosuppression, HIV coinfection, infection by genotype 1b. Cautious follow-up of the pathology of the graft is mandatory including routine biopsies and / or noninvasive monitoring of fibrosis.
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PMID:Risk factors for hepatitis C recurrence after liver transplantation. 1795 49

A 72-year-old male with liver cirrhosis and hepatocellular carcinoma experienced general fatigue. Four days later he was admitted to our hospital because of dizziness, dysbasia and left facial palsy (day 1). On day 6, a neurological examination revealed left trigeminal neuralgia, left medial longitudinal fasciculus (MLF) syndrome, skew deviation, hypacusia, tongue deviation and left limb ataxia. Magnetic resonance imaging of the brain including diffusion-weighted imaging showed previous lacunar infarctions at the left thalamus and pons. The immunological investigation for viral infection in his serum samples showed high titers of IgM antibody against cytomegalovirus (CMV). Cerebrospinal fluid (CSF) investigation revealed mononuclear pleocytosis, elevated protein levels and high titers of IgG antibody against the varicella-zoster virus (VZV). Anti-CMV antibody measurement and CMV-DNA detection by the polymerase chain reaction in CSF revealed that the central nervous system (CNS) was not infected by CMV. We diagnosed this case as brainstem encephalitis following multiple cranial neuropathy associated with CMV and VZV infections. The neurological symptoms gradually improved with aciclovir and prednisolone therapy. The titers of antibody for CMV in his serum samples normalized 4 months later after onset. Although there was no evidence of CMV infection in the CNS was obtained, parainfection or autoimmune mediated responses followed by viral infections might have led to brainstem encephalitis with multiple cranial nerve involvements in our patient.
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PMID:[A case of brainstem encephalitis following multiple cranial neuropathy in a hepatocellular carcinoma patient--association with cytomegalovirus and varicella-zoster virus infection]. 1804 5

Chronic graft dysfunction, manifesting with elevated liver enzymes and histological features of interface hepatitis (IH), is being increasingly recognized as a long-term problem after liver transplantation. The aim of this study was to characterize our group of post-orthotopic liver transplantation (OLT) patients with respect to clinical, laboratory, and histological signs of IH. A retrospective study of charts and liver biopsy specimens from patients transplanted between 1986 and 1999 was used. Histological features of IH were found in 29/119 patients at a median interval of 23.9 months (95% confidence interval -28.2 to 52.6) after OLT. All patients with IH had risk factors for chronic rejection, such as steroid-resistant rejection, acute rejection later than 3 months post-OLT, female receiver of male graft, or pretransplant cytomegalovirus (CMV)-positive serology with a CMV-negative donor liver. None of the 29 had features favoring a diagnosis of de novo autoimmune hepatitis, but 4 had isolated hypergammaglobulinemia, and 4 had non-organ-specific autoantibodies without hyperimmunoglobulin G. Sixteen of 29 patients also had features of chronic rejection, such as foam cell arteriopathy, loss of bile ducts, or pericentral fibrosis. After abnormal biopsy, all but 1 patient were switched to tacrolimus. During a median follow-up of 12 years, death occurred in 5, retransplantation occurred in 7, and definite cirrhosis occurred in 4. In conclusion, IH was detected in 24.4% of our patients and was associated with a high degree of fibrosis development. Most likely, IH represents a form of chronic rejection directed against periportal hepatocytes.
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PMID:Interface hepatitis is associated with a high incidence of late graft fibrosis in a group of tightly monitored pediatric orthotopic liver transplantation patients. 1858 76

The objective of this study was to investigate the role of chronic viral infections in development of the atypical and complicated forms of tuberculosis. Were investigated human herpes virus-2 (HHV-2), cytomegalovirus (CMV) and hepatitis C virus (HCV). Chronic viral infections have been identified as a risk factor for developing and complicated tuberculosis. Research has been shown, that infection of chronic virus diseases in patients with tuberculosis is rather significant and in several times exceeds similar parameters in healthy persons (CMV: 5.8% in healthy persons and 68.5% in patients with tuberculosis; HHV-2: 39% in healthy persons, 92%in patients with tuberculosis; HCV: in 36.4% patients with tuberculosis complicated with cirrhosis). The high level of chronic virus diseases and/or high frequency of their activization at patients with tuberculosis of various forms testify to interrelation between them. Increased level of chronic viral infections in patients with tuberculosis explained by the social factors and tuberculosis-induced immunodeficiency.
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PMID:[Chronic virus infections in combination with tubercular process]. 1863 50

Patients with advanced liver disease are at increased risk of cardiovascular events, especially following orthotopic liver transplantation (OLT). Coronary artery calcification (CAC) is a novel and independent predictor of cardiovascular risk, but its prevalence and utility in patients with cirrhosis are unknown. The aim of this study was to define the prevalence of CAC and its association with markers of disease severity and standard measures of cardiovascular risk in a large cohort of patients undergoing OLT assessment. A single-center, prospective, observational study of 147 consecutive patients undergoing assessment for OLT was performed. CAC scores were derived with the Agatston method from thoracic computed tomography scans and correlated with cardiovascular risk factors and measures of liver disease severity. There were 101 patients (66 males) with a mean age of 53.2 years; 46 patients were excluded because the CAC score was not reported. The median CAC score was 40 HU (range, 0-3533). Correlations were identified between the CAC score and age (r = 0.477; P < 0.001), male sex (r = 0.262; P = 0.008), family history of cardiovascular disease (r = 0.208; P = 0.036), Framingham risk score (r = 0.621; P < 0.001), Model for End-Stage Liver Disease score (r = 0.221; P = 0.027), systolic blood pressure (r = 0.285; P = 0.004), diastolic blood pressure (r = 0.267; P = 0.007), cytomegalovirus status (r = 0.278; P = 0.005), fasting glucose (r = 0.330; P = 0.001), number of coronary vessels involved (r = 0.899; P < 0.001), and components of the metabolic syndrome (r = 0.226; P = 0.026). After multivariate analysis, age, systolic blood pressure, fasting glucose, number of features of metabolic syndrome, and number of vessels involved remained significantly associated with CAC. In conclusion, this study identified a high prevalence of occult coronary artery disease in patients undergoing OLT assessment and identified a strong relationship between CAC scores and a limited number of specific cardiovascular risk factors. The usefulness of these factors in predicting perioperative and postoperative cardiovascular events in patients undergoing OLT requires prospective evaluation.
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PMID:Prevalence of coronary artery calcification in patients undergoing assessment for orthotopic liver transplantation. 1902 24

1. Hepatitis C virus (HCV) RNA+ liver allograft recipients invariably reinfect the liver allograft within hours after transplantation, and the majority (>70%) develop chronic hepatitis. The rate at which these patients experience progression to cirrhosis and the overall percentage are significantly increased in comparison with HCV infection in the nontransplant setting. 2. Core needle biopsy evaluation is used to establish the diagnosis of recurrent HCV, which can be difficult to distinguish from acute cellular rejection and other causes of allograft dysfunction. In the vast majority of cases, however, distinguishing recurrent HCV from other posttransplant syndromes is reliably achieved by a careful examination of hematoxylin and eosin-stained sections and correlation with clinical and serological data. 3. Recurrent HCV often coexists with other causes of liver allograft dysfunction, and the determination of the most important cause of injury and whether other causes of injury are present is important. Included are residual changes of preservation/reperfusion injury, biliary sludging/structuring, acute cellular and chronic rejection, and autoimmune hepatitis. 4. The complex interplay between immunosuppression management, viral replication, and the recipient immune system results in distinct patterns of recurrent chronic HCV in the liver allograft: (1) conventional or usual acute and chronic HCV, which resembles that seen in the general population with HCV; (2) fibrosing cholestatic hepatitis; and (3) plasma cell-rich HCV, which might represent a variant of, or overlap with, autoimmune hepatitis and rejection. 5. The variable but usually hastened histopathological progression toward cirrhosis in HCV+ allografts is similar to that seen in the nontransplant setting, but in allografts, the overall severity of lymphocytic inflammation is less, and ductular reactions, stellate cell activation, and subsinusoidal fibrosis are accentuated. Hepatic stressors and causes of an impaired ability of hepatocytes to replicate include persistently high levels of viral replication, HCV-specific CD4+ T responses, advanced donor age, high levels or rapid withdrawal of immunosuppression, and coexistent liver damage from preservation/reperfusion injury, biliary structuring, or coexistent cytomegalovirus or herpes 6 viral infection. 6. Immunological effector mechanisms involved in the rejection and control of HCV replication/HCV elimination show significant overlap. Patients with very high levels of HCV RNA rarely show significant clinically significant acute or chronic rejection, whereas their occurrence is frequently associated with very low levels or clearance of HCV RNA. Studying the evolution from recurrent HCV to acute rejection in patients treated with interferon and/or weaned from immunosuppression might provide valuable insights into the relationship between these 2 processes as well as liver allograft acceptance.
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PMID:Evolution of hepatitis C virus in liver allografts. 1987 40

End stage liver disease from hepatitis C is the leading indication for liver transplantation (LT) in the United States. Recurrent hepatitis C after LT is universal and causes substantial morbidity and mortality with up to 30% patients developing cirrhosis by the fifth postoperative year. Once cirrhosis is established, the risk of hepatic decompensation is approximately 40% per year. Risk factors associated with accelerated disease recurrence are elevated high viral load prior to transplantation, older donor age, prolonged ischemic time, cytomegalovirus coinfection, intensity of immunosuppression and HIV coinfection. Although the mechanisms of accelerated HCV-induced liver damage after transplantation are poorly understood, strategies employed to limit severe recurrence include avoidance of older donors, early recognition of cytomegalovirus, minimization of immunosuppression, particularly T-cell depleting therapies and pulsed steroids for acute cellular rejection. Treatment of recurrent hepatitis C post-transplant is also problematic and fraught with controversy. As there is a paucity of evidence on when treatment should be initiated, out of necessity treatment has been empiric and often varies between centers. As prophylactic treatment immediately after transplantation is rarely effective and associated with numerous side effects, most clinicians acknowledge that treatment should be initiated once early fibrosis has developed although sustained viral rates with pegylated interferon and ribavirin are frequently less than 30%. Side effects are common and can lead to dose reduction or discontinuation of treatment. For those patients who develop develop decompensated cirrhosis from recurrent hepatitis C, retransplantation may be considered.
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PMID:Hepatitis C recurrence after liver transplantation. 2019 34

We have described a fatal case of interstitial pneumonia with pleuritis in woman, 54 years old, suffered from end stage liver disease caused by ethanolic hepatic cirrhosis. Broncholavage microbiological culture was negative but biomolecular assays with polymerase chain reaction demonstred Pneumocystis jiroveci and Cytomegalovirus. She died despite aetiological therapy with cotrimoxazole and gancyclovir. Immunodeficiency of the delayed immune response, related to the severe liver disease and ethanol use, explains the occurrence of these opportunistic infections in ethanolic cirrhotic patients too.
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PMID:[Pneumocystis jiroveci and cytomegalovirus pneumonia in patients with alcoholic hepatic cirrhosis]. 2061 Sep 36

Living donor liver transplantation (LDLT) has become one of the chief methods of saving patients with end-stage liver disease due to liver cirrhosis. Accumulation of knowledge about indication and perioperative managements improve outcome of this treatment. In this study, we elucidate the risk factors of LDLT, which still exist today. Sixty-one patients received LDLT in our institute between 2003 and 2009 were included in this study. Recipient age and sex, donor age and sex, etiology, preoperative model of end-stage liver disease (MELD) score, hepatocellular carcinoma (HCC), graft versus recipient weight ratio (GRWR), cold and warm ischemic time, operation time, blood loss, ABO compatibility, rejection, cytomegalovirus (CMV) infection, biliary stricture, and calcineurin inhibitor (FK506 or cyclosporin A) were the factors investigated. p < 0.05 was considered as statistically significant in the proportional hazard model. In univariate analysis, the recipients' age (p = 0.024) and rejection episode (p = 0.046) were selected as significant risk factors. In multivariate analysis including the factors that showed p < 0.2 (recipient age, GRWR, ABO compatibility, rejection episode) in univariate analysis, recipient age (p = 0.008, HR: 1.40; 95% CI: 1.09-1.80) and rejection episodes (p = 0.002, HR: 13.33; 95% CI: 2.53-71.43) were still selected as significant independent risk factors after LDLT. Recipient age was shown to be 1.40 times risk per 1 year older and the rejection episode was shown to be 13.33 times risk in the recent era with comprehensive indication and preoperative management for LDLT. Indication must be cautious for elderly patients, and prevention of rejection is crucial for the improvement of results for LDLT.
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PMID:Risk factors of recipient receiving living donor liver transplantation in the comprehensive era of indication and perioperative managements. 2094 66

Polyarteritis nodosa is a systemic necrotizing vasculitis that affects small- and medium-sized arteries. Liver involvement in patients with polyarteritis nodosa has been described, and ranges from asymptomatic elevation of aminotransferases to hepatic aneurysm rupture. We describe the case of a patient with type 1 autoimmune hepatitis and compensated liver cirrhosis who developed classic polyarteritis nodosa, complicated with cytomegalovirus and repeated urinary tract infections. After a long bedridden hospitalization, the patient's condition was stabilized. She is currently in good health, with well-controlled blood pressure, and stable kidney and liver function. To our knowledge, this is the first case report in the literature with concurrent appearance of both diseases.
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PMID:Polyarteritis nodosa in a patient with type 1 autoimmune hepatitis. 2111 56


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