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)

In view of the substantial, at times conflicting, literature on conversion to open surgery during laparoscopic cholecystectomy (LC), we have considered it timely to review the subject to identify the risk factors for conversion and its consequences. The review is based on a complete literature search covering the period 1990 to 2005. The search identified 109 publications on the subject: 68 retrospective series, 16 prospective nonrandomized studies, 8 prospective randomized clinical trials, 5 prospective case-controlled studies, 5 reviews and 7 others (3 observational, 2 population-based studies, 1 national survey, and 1 editorial). As the majority of reported studies are retrospective, firm conclusions cannot be reached. Single factors that appear to be important include male gender, extreme old age, morbid obesity, cirrhosis, previous upper abdominal surgery, severe/advanced acute and chronic disease, and emergency LC. The combination of patient- and disease-related risk factors increases the conversion risk. In the training of residents, the number of cases needed for reaching proficiency exceeds 200 cases. The value of predictive scoring systems is important in the selection of cases for resident training. Conversion exerts adverse effects on operating time, postoperative morbidity, and hospital costs, especially when it is enforced. There appears to be no absolute contraindication to LC that is agreed upon by all. There is consensus on certain individual risk factors and their additive effect on the likelihood of conversion. Predictive systems based on these factors appear to be useful in selection of cases for resident training.
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PMID:Conversions during laparoscopic cholecystectomy: risk factors and effects on patient outcome. 1684 80

In Germany up to 800,000 persons are chronically infected with the hepatis C virus. This chronic disease is correlated with a significant morbidity and mortality. This is a consequence of the development of liver cirrhosis and hepatocellular carcinoma in a substantial proportion of the patients. Health quality of life is also affected by the infection. There are reliable standards available for diagnosis and treatment. Antiviral treatment is highly effective and the combination of pegylated interferon alpha with ribavirin leads to a sustained viral eradication in about 60% of the cases. The treatment is also cost-effective and results in an increased life expectancy. Costs for HCV treatment are favourable in comparison to other well accepted therapies and interventions and a reduction of future costs can be expected.Thus, active screening for HCV infected persons should be intensified to improve the quality of medical care. Early and broad treatment is potentially able to reduce the future burden of HCV-related diseases.
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PMID:[Chronic HCV infections. A model disease for therapy, economics and social-medical aspects]. 1744 Aug 44

Liver cirrhosis, a highly prevalent chronic disease, is frequently associated with endocrine dysfunctions, notably in the gonadal axis. We evaluated lactotroph population by immunohistochemistry, gonadotropins and prolactin by immunoradiometric assay and testosterone and estradiol by radioimmunoassay in adult male Wistar rats with cirrhosis induced by carbon tetrachloride. No significant difference in mean +/- SEM percentages of lactotrophs was found between cirrhotic animals and controls (N = 12, mean 18.95 +/- 1.29%). Although there was no significant difference between groups in mean serum levels of prolactin (control: 19.2 +/- 4 ng/mL), luteinizing hormone (control: 1.58 +/- 0.43 ng/mL), follicle-stimulating hormone (control: 19.11 +/- 2.28 ng/mL), estradiol (control: 14.65 +/- 3.22 pg/mL), and total testosterone (control: 138.41 +/- 20.07 ng/dL), 5 of the cirrhotic animals presented a hormonal profile consistent with hypogonadism, all of them pointing to a central origin of this dysfunction. Four of these animals presented high levels of estradiol and/or prolactin, with a significant correlation between these two hormones in both groups (r = 0.54; P = 0.013). It was possible to detect the presence of central hypogonadism in this model of cirrhotic animals. The hyperestrogenemia and hyperprolactinemia found in some hypogonadal animals suggest a role in the genesis of hypogonadism, and in the present study they were not associated with lactotroph hyperplasia.
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PMID:Male gonadal function, prolactin secretion and lactotroph population in an experimental model of cirrhosis. 1771 59

This paper describes a prospective study of the clinical course and outcome of a nosocomial outbreak of hepatitis C virus (HCV) infection in six male urology patients at a hospital in Stara Zagora, Bulgaria. These patients had been previously hospitalised in the urology ward, during which all had received intravenous therapy. Approximately three weeks later, all six were admitted to the infectious diseases unit with acute hepatitis, shown to be caused by HCV genotype 1b. The diagnosis was confirmed by polymerase chain reaction during the first week of their hospital stay. Infected patients were followed up for 30 months following diagnosis and 54 potential contacts for 6 months post-exposure. Four patients recovered completely; one developed chronic HCV infection and one died. The latter already had cirrhosis due to co-infection with hepatitis B virus. The investigation established the index case as a patient with chronic hepatitis C, who had been an in-patient on the same ward at the same time. The most likely route of transmission was intravenous heparin flushes administered with a common syringe. Contrary to the common assumption that acute HCV infection often leads to chronic disease, only one chronic case was observed during the 30-month period of investigation.
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PMID:Clinical course and outcome of a nosocomial outbreak of hepatitis C in a urology ward. 1771 79

Portal or/and mesenteric vein thrombosis is a rare condition with high mortality in an acute form. Therapy of thrombosis is not well defined, although there are some general guidelines that differ according to disease onset and clinical presentation. In acute thrombosis with bowel infarction, surgical resection with possible thrombolysis is advised. The best therapy for the subacute form is not known and the approach differs between centers. For chronic disease, prolonged anticoagulant therapy is recommended. Thrombolysis is well recognized in the treatment of acute ischemic coronary or cerebral diseases. Success of treatment is better if therapy is introduced within a few hours after symptoms have begun. We describe a 25-year-old patient with the subacute form of extensive portal, mesenteric and ileocolic vein thrombosis in the setting of underlying liver cirrhosis due to autoimmune disease. An aggressive therapeutic approach is advised, especially in patients who will eventually undergo liver transplantation, since portal and/or mesenteric vein thrombosis is relative contraindication for liver transplantation in the majority of transplant centers.
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PMID:Treatment of extensive subacute portal, mesenteric and ileocolic vein thrombosis with recombinant tissue plasminogen activator. 1776 37

Liver fibrosis is a chronic disease that results from hepatitis B and C infections, alcohol abuse or metabolic and genetic disorders. Ultimately, progression of fibrosis leads to cirrhosis, a stage of the disease characterized by failure of the normal liver functions. Currently, the treatment of liver fibrosis is mainly based on the removal of the underlying cause of the disease and liver transplantation, which is the only treatment for patients with advanced fibrosis. Hepatic stellate cells (HSC) are considered to be key players in the development of liver fibrosis. Chronically activated HSC produces large amounts of extracellular matrix and enhance fibrosis by secreting a broad spectrum of cytokines that exert pro-fibrotic actions in other cells, and in an autocrine manner perpetuate their own activation. Therefore, therapeutic interventions that inhibit activation of HSC and its pro-fibrotic activities are currently under investigation worldwide. In the present study we applied targeted liposomes as drug carriers to HSC in the fibrotic liver and explored the potential of these liposomes in antifibrotic therapies. Moreover, we investigated effects of bioactive compounds delivered by these liposomes on the progression of liver fibrosis. To our knowledge, this is the first study demonstrating that lipid-based drug carriers can be selectively delivered to HSC in the fibrotic liver. By incorporating the bioactive lipid DLPC, these liposomes can modulate different processes such as inflammation and fibrogenesis in the fibrotic liver. This dual functionality of liposomes as a drug carrier system with intrinsic biological effects may be exploited in new approaches to treat liver fibrosis.
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PMID:Addressing liver fibrosis with liposomes targeted to hepatic stellate cells. 1802 41

Wilson's disease is an inherited disorder of copper metabolism, presenting with prominent hepatic and neurologic manifestations. There is an established place for liver transplantation in the presence of liver disease, while the indication for neurologic manifestations is debated. Between 1993 and 2005, 11 patients were liver transplanted for Wilson's disease at our institution. We retrospectively reviewed the medical records of the patients. The pathology of the explanted livers was analyzed. The patients were divided into three groups based on the evolution of the disease. Postoperative data gathered included patient and graft outcome, complications, neurologic status, and copper metabolism. Six males and five females were transplanted at a mean age of 29.7 yr (range 15-48 yr). Three patients had a fulminant presentation, two patients had decompensation of established disease, and six patients had chronic disease. Neurologic features were prominent in five patients. The pathologic analysis of the explanted graft showed cirrhosis in all patients. The five patients with fulminant and acute on chronic presentations also showed necrosis in the explant. The mean postoperative follow-up was 56.8 months (range 10-129 months). Two patients were re-transplanted. One patient died because of severe sepsis. Two patients with severe neurologic dysfunction showed significant remission of symptoms. Liver transplantation is a safe and effective treatment for both acute and chronic presentations of Wilson's disease. Acute presentation correlates with the presence of necrosis in the explanted liver. In our series, there was a relevant improvement of the neurologic features after transplantation.
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PMID:A single-center experience with liver transplantation for Wilson's disease. 1833 42

Worldwide, one of the most prevalent forms of chronic disease is alcoholic fatty liver, which may progress to more severe forms of liver injury including steatohepatitis, fibrosis, and cirrhosis. The molecular mechanisms by which ethanol consumption causes accumulation of hepatic lipid are multiple and complex. Chronic ethanol exposure is thought to cause enhanced hepatic lipogenesis and impaired fatty acid oxidation by inhibiting key hepatic transcriptional regulators such as AMP-activated kinase (AMPK), sirtuin 1 (SIRT1), PPAR-gamma coactivator alpha (PGC-1alpha), peroxisome proliferator-activated receptor alpha (PPARalpha), and sterol regulatory element-binding protein 1 (SREBP-1). Adiponectin is an adipose-derived hormone with a variety of beneficial biological functions. Increasing evidence suggests that altered adiponectin production in adipose tissue and impaired expression of hepatic adiponectin receptors (AdipoRs) are associated with the development of alcoholic liver steatosis in several rodent models. More importantly, studies have demonstrated a protective role of adiponectin against alcoholic liver steatosis. The hepato-protective effect of adiponectin is largely mediated by the coordination of multiple signaling pathways in the liver, leading to enhanced fat oxidation, reduced lipid synthesis and prevention of hepatic steatosis. This review begins with an assessment of the current understanding of the role of adiponectin and its receptors in the regulation of lipid homeostasis in liver, with emphasis on their relationship to the development of alcoholic liver steatosis. Following sections will review hepatic signaling molecules involved in the protective actions of adiponectin against alcoholic fatty liver and summarize the current knowledge of regulatory mechanisms of adiponectin expression and secretion in response to chronic ethanol exposure. We will conclude with a discussion of potential strategies for treating human alcoholic fatty liver disease (AFLD), including nutritional and pharmacological modulation of adiponectin and its receptors.
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PMID:Adiponectin and alcoholic fatty liver disease. 1870 50

Liver cirrhosis secondary to HCV infection is a chronic disorder that carries high morbidity and mortality. Approved antiviral treatment for this condition at present includes peginterferon in combination with ribavirin. Treatment is only recommended for a well-compensated liver cirrhosis, whereas antiviral therapy is commonly not implemented in cirrhotics with signs of liver decompensation, over the concern that the use of peginterferon and ribavirin might expose patients to severe treatment-related side effects. This review focuses on data available to support both efficacy and safety of antiviral therapy in both compensated and decompensated cirrhotic patients.
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PMID:Antiviral therapy in compensated and decompensated cirrhotic patients with chronic HCV infection. 1956 72

Alcoholic liver disease (ALD) and hepatitis C virus (HCV) infection represent, either alone or in combination, more than two thirds of all patients with liver disease in the Western world. This review discusses the epidemiology and combined impact of ALD and HCV on the progression of liver disease. ALD and HCV affect the progression of liver disease to liver cirrhosis and hepatocellular carcinoma (HCC) in a synergistic manner. Thus, the risk for HCC increases five times with a daily alcohol consumption of 80 g; in the presence of HCV it is increased 20-fold, and a combination of both risk factors leads to a more than 100-fold risk for HCC development. Alcohol consumption also decreases the response to interferon treatment which is probably due to a lack of compliance than a direct effect on HCV replication. Several molecular mechanisms are discussed that could explain the synergistic interaction of alcohol and HCV on disease progression. They include modulation of the immune response and apoptosis, increased oxidative stress via induction of CYP2E1 and the hepatic accumulation of iron. Thus, both HCV and alcohol independently cause hepatic iron accumulation in > 50% of patients probably due to suppression of the liver-secreted systemic iron hormone hepcidin. A better understanding of hepcidin regulation could help in developing novel therapeutic approaches to treat the chronic disease in the future. For now, it can be generally concluded that HCV-infected patients should abstain from alcohol and alcoholics should be encouraged to participate in detoxification programs.
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PMID:Alcoholic liver disease and hepatitis C: a frequently underestimated combination. 1963 99


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