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Alcoholic Liver Disease. IN: Hauser, S., ed. Mayo Clinic Gastroenterology and Hepatology Board Review. 3rd ed. New York, NY: Informa Healthcare USA. 2008. pp 325-336.
This chapter on alcoholic liver disease is from a comprehensive textbook that provides an in-depth examination of essential knowledge in gastroenterology, hepatology, and the related areas of pathology, endoscopy, nutrition, and radiology. Alcohol is implicated in more than 50 percent of the liver-related deaths that occur in the United States. Alcoholic liver disease is a major health cost expenditure, accounting for nearly $3 billion annually. The author notes that the clinical spectrum of alcoholic liver disease includes fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. The chapter covers epidemiology, risk factors, ethanol metabolism, pathophysiology, fatty liver, alcoholic hepatitis, alcoholic cirrhosis, alcohol and hepatitis C, and risk for acetaminophen toxicity in people with alcoholism. For each of the liver diseases, the author presents and discusses a case study, including history and physical examination, laboratory and radiographic features, histologic features, prognosis, and treatment. 3 figures. 1 table. 7 references.
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Antimitochondrial Antibody-Negative Primary Biliary Cirrhosis. Gastroenterology Clinics of North America. 37(2): 479-484. June 2008.
This article about antimitochondrial antibody-negative primary biliary cirrhosis (PBC) is from an issue of Gastroenterology Clinics of North America that focuses on eosinophilic and autoimmune gastrointestinal disease. The authors describe PBC as a chronic cholestatic liver disease of unclear cause, characterized by nonsuppurative destruction of the bile ducts and serologically by the presence of antimitochondrial antibodies (AMA). The authors briefly review the controversy and uncertainty regarding AMA-positive and AMA-negative types of PBC, noting that recent developments strengthen the idea that they are truly one condition. The authors review the clinical, biochemical, serologic, and histopathologic features and treatment approach and outcomes in patients who have AMA-negative PBC. The authors conclude that AMA-negative PBC shares similar clinical, biochemical, histologic, and prognostic features with classic PBC. Management of AMA-negative PBC should not differ from treatment of AMA-positive disease. 1 figure. 1 table. 20 references.
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Approach to the Patient with Abnormal Liver Tests and Fulminant Liver Failure. IN: Hauser, S., ed. Mayo Clinic Gastroenterology and Hepatology Board Review. 3rd ed. New York, NY: Informa Healthcare USA. 2008. pp 283-292.
This chapter on managing patients with abnormal liver tests and fulminant liver failure is from a comprehensive textbook that provides an in-depth examination of essential knowledge in gastroenterology, hepatology, and the related areas of pathology, endoscopy, nutrition, and radiology. This chapter includes a general discussion of commonly used liver tests; the differential diagnosis and discussion of diseases characterized by an increase in hepatocellular enzyme levels; differential diagnosis and discussion of diseases characterized by an increase in cholestatic enzyme levels; the evaluation of patients who have jaundice; and the management of patients who have fulminant liver failure. In general, a patient with liver test abnormalities that are less than twice normal may be followed as long as the patient is asymptomatic and the albumin level, prothrombin time, and bilirubin concentration are normal. Clinical syndromes that contribute to abnormal liver tests include acute hepatitis, chronic hepatitis, cholestasis without hepatitis or jaundice, jaundice, and cirrhosis or portal hypertension. Fulminant liver failure can be defined as the presence of acute liver failure, including the development of hepatic encephalopathy, within 8 weeks after the onset of jaundice in a patient without a previous history of liver disease. Liver transplantation has revolutionized the management of fulminant liver failure, which without transplantation has a low survival rate. The author stresses that transplantation should be performed when a poor outcome is anticipated, before the patient has uncontrolled sepsis or prolonged periods of increased intracranial pressure. The chapter includes diagnostic algorithms for evaluating patients who have abnormal liver tests. 4 figures. 6 tables. 7 references.
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Ascites, Hepatorenal Syndrome, and Encephalopathy. IN: Hauser, S., ed. Mayo Clinic Gastroenterology and Hepatology Board Review. 3rd ed. New York, NY: Informa Healthcare USA. 2008. pp 351-362.
This chapter on ascites, hepatorenal syndrome, and hepatic encephalopathy is from a comprehensive textbook that provides an in-depth examination of essential knowledge in gastroenterology, hepatology, and the related areas of pathology, endoscopy, nutrition, and radiology. The author describes these conditions as the three main complications that occur with portal hypertension and hepatic synthetic dysfunction of cirrhosis as liver disease progresses. For each condition, the chapter covers pathogenesis, patient evaluation, and treatment strategies, including dealing with refractory conditions. The chapter also covers spontaneous bacterial peritonitis and the prognostic indicators for survival in cirrhosis. Hepatorenal syndrome requires the presence of five conditions for diagnosis: chronic or acute liver disease with advanced liver failure and portal hypertension; low glomerular filtration rate; absence of shock, bacterial infection, nephrotoxic drugs, or significant fluid loss; no sustained improvement in renal function following diuretic withdrawal or plasma volume expansion; and proteinuria of less than 500 milligrams per deciliter and no ultrasonographic evidence of obstructive uropathy or parenchymal renal disease. The only proven treatment for hepatorenal syndrome is liver transplantation. 1 figure. 1 table. 9 references.
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Cholestasis Post Liver Transplantation. IN: Lindor, K.; Talwalkar, J., eds. Cholestatic Liver Disease. Totowa, NJ: Humana Press. 2008. pp 171-182.
This chapter on cholestasis that occurs after liver transplantation is from a book that offers health care providers an overview of cholestatic liver disease; cholestasis is defined as a liver disorder characterized by impaired bile flow. The chapter covers biliary complications, preservation or reperfusion injury and ABO incompatibility, small-for-size syndrome, hepatic artery thrombosis, infectious complications, drug-induced acute cellular rejection, chronic rejection, and recurrent disease, including primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), and viral hepatitis. The authors caution that cholestasis can occur anytime throughout the posttransplant period, may be intrahepatic or extrahepatic in origin, and has a very broad differential diagnosis. Careful diagnostic imaging of the biliary tree is an important first step in the workup, followed by liver biopsy if clinically indicated. 1 table. 50 references.
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Cholestatic Liver Disease. Totowa, NJ: Humana Press. 2008. 188 p.
This book offers health care providers an overview of cholestatic liver disease; cholestasis is defined as a liver disorder characterized by impaired bile flow. The text includes 10 chapters: the diagnosis of cholestasis, drug-induced cholestasis, primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), overlap syndrome with autoimmune hepatitis, rare causes of cholestasis, cholestatic variants of viral disease and alcohol, cholestasis from systemic disorders, complications of cholestasis, and posttransplantation cholestasis. Specific topics include liver tests and antibodies, cross-sectional studies, liver biopsy, other diagnostic tests, endoscopic ultrasound, herbal remedies, the risk of colon cancer with inflammatory bowel disease (IBD), colon cancer posttransplant, and cholangiocarcinoma, genetic disorders, viral hepatitis, sarcoid disease, lymphoma, granulomatous disease, cystic fibrosis, rheumatologic diseases, osteoporosis, pruritus, hyperlipidemia, strictures, viral disease, and recurrent cholestatic liver disease. Each chapter begins with a brief outline and concludes with a summary and a list of references. The text concludes with a subject index.
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Cholestatic Liver Disease: Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis, and AIDS-Associated Cholangiopathy. IN: Hauser, S., ed. Mayo Clinic Gastroenterology and Hepatology Board Review. 3rd ed. New York, NY: Informa Healthcare USA. 2008. pp 377-382.
This chapter on cholestatic liver disease is from a comprehensive textbook that provides an in-depth examination of essential knowledge in gastroenterology, hepatology, and the related areas of pathology, endoscopy, nutrition, and radiology. This chapter covers primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), and AIDS-associated cholangiopathy. The author notes that drug-induced cholestasis may be the most common explanation for cholestasis in patients without biliary obstruction. The author briefly reviews the differential diagnosis. The author outlines the recommended treatment for each of these conditions, including the management of the complications of cholestasis, such as malabsorption, pruritus, and bone disease. PBC involves women in 90 percent of cases and is characterized by antimitochondrial antibodies, fatigue, and pruritus. Treatment usually involves ursodiol for patients at any stage of PBC who have abnormal findings on liver tests. Ursodiol improves survival free of transplantation, decreases the risk of the development of cirrhosis and varices, and lowers lipid levels. PSC is the next most common cholestatic condition in adults. About 70 percent of these patients have inflammatory bowel disease. Unfortunately, no effective therapy is available for PSC. AIDS-associated cholangiopathy is defined as biliary obstruction due to infections that lead to biliary strictures. Treatment with highly active retroviral therapy decreases the percentage of patients with HIV infection that progresses to AIDS and may eventually prevent the development of biliary complications. 2 figures. 1 table. 26 references.
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Cholestatic Variants of Viral Disease and Alcohol. IN: Lindor, K.; Talwalkar, J., eds. Cholestatic Liver Disease. Totowa, NJ: Humana Press. 2008. pp 119-134.
This chapter on cholestatic variants of viral disease and alcohol is from a book that offers health care providers an overview of cholestatic liver disease; cholestasis is defined as a liver disorder characterized by impaired bile flow. The chapter focuses on the cholestatic variants of viral hepatitis and of alcoholic liver disease. The authors note that hepatitis, or liver inflammation, of any etiology routinely presents with elevated transaminases. However, the presence of cholestasis does not necessarily rule out the presence of viral or alcoholic hepatitis. Specific diseases covered include hepatitis A, B, C, D, and E; cytomegalovirus; and Epstein-Barr virus. A careful clinical history, viral serologies, and in some cases, a liver biopsy can clarify and diagnose these disease states. The authors conclude that recognition of these variants may be crucial to the timely diagnosis and therapy of these disease states. 1 table. 134 references.
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Chronic Viral Hepatitis. IN: Hauser, S., ed. Mayo Clinic Gastroenterology and Hepatology Board Review. 3rd ed. New York, NY: Informa Healthcare USA. 2008. pp 293-306.
This chapter on chronic viral hepatitis is from a comprehensive textbook that provides an in-depth examination of essential knowledge in gastroenterology, hepatology, and the related areas of pathology, endoscopy, nutrition, and radiology. The author notes that viral infections are major causes of liver disease worldwide. The five primary hepatitis viruses that have been identified are A, B, C, D (or delta), and E. This chapter focuses on the primary hepatitis viruses, covering epidemiology, clinical presentation and natural history, diagnostic tests, treatment, and prevention of each type. The major routes of transmission of hepatitis A virus are ingestion of contaminated food or water and contact with an infected person. The treatment of acute hepatitis A is supportive; a vaccine is available and should be offered to travelers to areas with an intermediate or high prevalence of hepatitis A, intravenous drug users, and other selected populations. Hepatitis B is usually transmitted through sexual activity or intravenous drug use. Hepatitis B infection is treated with interferon or an oral agent. Hepatitis B vaccine is given to infants and previously unvaccinated young adolescents. Hepatitis C is a factor in 40 percent of all cases of chronic liver disease and is the leading indication for liver transplantation. Most people with hepatitis C present with chronic hepatitis, with a mild-to-moderate increase in ALT levels. Treatment is successful in many patients with hepatitis C infection and can be useful to prevent complications, notably cirrhosis. A final section of the chapter considers the interplay between viral hepatitis and human immunodeficiency virus (HIV) infection. Patient care algorithms are provided. 6 figures. 7 tables. 7 references.
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Cirrhosis. Bethesda, MD: National Digestive Diseases Information Clearinghouse. 2008. 8 p.
This fact sheet describes cirrhosis, a condition in which the liver slowly deteriorates and malfunctions due to chronic injury. In cirrhosis, scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. Scarring impairs the liver’s ability to control infections, remove bacteria and toxins from the blood, process nutrients and drugs, make proteins that regulate blood clotting, and produce bile to help absorb fats and fat-soluble vitamins. Written in nontechnical language, the fact sheet describes the causes of cirrhosis, symptoms, complications, diagnosis, measurement of severity, treatment options, and indications for liver transplantation. In the United States, heavy alcohol consumption and chronic hepatitis C have been the most common causes of cirrhosis. Obesity is becoming a common cause of cirrhosis, either as the sole cause or in combination with alcohol, hepatitis C, or both. Other causes of cirrhosis include hepatitis B, hepatitis D, and autoimmune hepatitis; diseases that damage or destroy bile ducts; inherited diseases; nonalcoholic fatty liver disease; drugs; toxins; and infections. Many people with cirrhosis have no symptoms in the early stages of the disease. As the disease progresses, symptoms may include weakness, fatigue, loss of appetite, nausea, vomiting, weight loss, abdominal pain and bloating, itching, and spiderlike blood vessels on the skin. The goals of treatment are to stop the progression of scar tissue in the liver and prevent or treat complications. Treatment for cirrhosis includes avoidance of alcohol and other drugs, nutrition therapy, and other therapies that treat specific complications or causes of the disease. A liver transplant may be considered when complications of cirrhosis cannot be controlled by treatment. Readers are referred to three resource organizations for more information: the American Liver Foundation (www.liverfoundation.org and 1–800–465–4837), Hepatitis Foundation International (www.hepfi.org or 1–800–891–0707), and the United Network for Organ Sharing (www.unos.org or 1–888–894–6361). The fact sheet briefly describes the work of the National Digestive Diseases Information Clearinghouse, which provides information about digestive diseases to people with digestive disorders and to their families, health care professionals, and the public. 1 figure.
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Diagnosis and Treatment of Autoimmune Hepatitis. Gastroenterology Clinics of North America. 37(2): 461-478.June 2008.
This article about the diagnosis and treatment of autoimmune hepatitis is from an issue of Gastroenterology Clinics of North America that focuses on eosinophilic and autoimmune gastrointestinal disease. The authors describe autoimmune hepatitis (AIH) as a hepatitis of unknown cause, known as idiopathic, characterized by inflammation of the liver, presence of auto-antibodies, and evidence of increased gamma globulins in the serum. AIH is considered to be an interaction between the immune system, auto-antigens, and unknown triggering factors. The authors provide a brief summary of the diagnosis of AIH, epidemiologic factors, the natural history of AIH, an approach to the treatment and follow-up of AIH, and the role of liver transplantation in the treatment of AIH. This immune disease affecting the liver responds well to prednisone or a combination of prednisone and azathioprine; most patients can be brought into remission, although many will require maintenance therapy with low-dose levels of these drugs. The authors stress that not all patients with AIH need to be treated, even once the diagnosis is confirmed. Drug therapy should be considered in patients who have cirrhosis if biopsy demonstrates considerable inflammation. Liver transplantation should be considered in patients who have decompensated cirrhosis from AIH or in those patients who have severe fulminant hepatitis who fail to respond to initial therapy. 3 figures. 3 tables. 60 references.
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Diagnosis and Treatment of Wilson Disease: An Update. Hepatology. 47(6): 2089-2111. June 2008.
This article presents the American Association for the Study of Liver Diseases (AASLD) practice guidelines on the diagnosis and treatment of Wilson disease. The recommendations are based on formal review and analysis of the recent literature, the American College of Physicians Manual for Assessing Health Practices and Designing Practice Guidelines[bam1], guideline policies, and the experience of the authors in the specified topic. Wilson disease is a genetic condition characterized by the collection of copper in the liver, which results in damage to the liver and eventually in release of copper into the bloodstream. The copper is subsequently deposited in other organs, notably the brain, kidneys, and cornea. Wilson disease is usually treated with a chelating agent, D-penicillamine. Other treatments are available, including liver transplantation, which may be lifesaving and curative for this disorder. The guidelines cover clinical features, diagnostic approaches and laboratory tests, diagnosis in specific target populations such as patients in acute liver failure, and available treatments, including D-penicillamine, trientine, zinc, antioxidants, diet, and ammonium tetrathiomolybdate. The guidelines consider treatment in specific clinical situations, including asymptomatic patients, maintenance therapy, decompensated cirrhosis, acute liver failure, and pregnancy. A final section briefly considers treatment targets and monitoring of treatment. 3 figures. 3 tables. 253 references.
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Hepatitis C. Annals of Internal Medicine. 148(11): 1-16. June 2008.
This continuing education program, an In The Clinic supplement to the Annals of Internal Medicine, reviews the prevention, screening, diagnosis, and treatment of hepatitis C. The material presents the answers to common questions in each of these areas, supplemented by evidence from clinical studies that supports the implementation of best practices. Topics include the risk factors for hepatitis C virus (HCV) infection; how to reduce the risk of HCV transmission, particularly in the health care setting; screening and diagnostic tests for HCV infection; the symptoms of HCV, which range from asymptomatic individuals to chronic infection to liver cirrhosis; the indications for liver biopsy; the use of dietary and other lifestyle interventions in the management of HCV infection, including complementary and alternative medicine (CAM) approaches; when drug therapy for HCV is appropriate and the contraindications for drug therapy; treatment regimens and how to choose which drug regimen is appropriate for which patient; vaccinating patients with HCV; the clinical management of patients who do not respond to hepatitis C therapy or who relapse after an initial response; the side effects of hepatitis C drugs and strategies to minimize and manage side effects; how to evaluate the response to hepatitis C drug therapy; liver transplantation in patients with HCV infection; and the risks for hepatocellular carcinoma in patients with HCV infection, including the indications for routine screening for this cancer. A final section considers strategies for practice improvement. Appended to the instructional materials is a patient handout with basic information about hepatitis C, as well as a posttest with which readers can obtain continuing medical education (CME) credits. 1 figure. 4 tables. 53 references.
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Impact of Non-Alcoholic Fatty Liver Disease on Chronic Hepatitis B and C. Practical Gastroenterology. 32(7): 14-28. July 2008.
This article reviews the impact of nonalcoholic fatty liver disease (NAFLD) on chronic hepatitis B and C. The authors note that the prevalence of NAFLD is increasing due to the worldwide epidemic of obesity and diabetes. Metabolic conditions such as central obesity, insulin resistance, dyslipidemia, and hypertension are strongly associated with NAFLD. The article covers the pathogenesis of NAFLD; NAFLD, insulin resistance, and hepatitis C; hepatitis C and hepatic steatosis interaction; host and viral-induced steatosis in patients with hepatitis C virus (HCV); mechanisms underlying the interaction of these conditions and disease progression; the impact of hepatic steatosis on fibrosis progression; the impact of NAFLD on HCV treatment options and results; NAFLD and hepatitis B virus (HBV); and the impact of treating components of the metabolic syndrome on outcomes related to hepatitis B and C. Nonalcoholic steatohepatitis (NASH) is defined as a histologic subtype of NAFLD that may progress to cirrhosis, advanced liver disease, or hepatocellular carcinoma (HCC). Although simple hepatic steatosis may not lead to progressive liver disease, it increases the risk of coronary artery disease. In addition, hepatic steatosis and conditions associated with metabolic syndrome seem to aggravate other liver diseases such as hepatitis B and C. The authors conclude by calling for a better definition and understanding of the impact of superimposed NAFLD and its risk factors on HBV and HCV, which is particularly crucial as the rates of obesity and NAFLD continue to increase. 1 table. 57 references.
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Liver Disease and Pregnancy. IN: Hauser, S., ed. Mayo Clinic Gastroenterology and Hepatology Board Review. 3rd ed. New York, NY: Informa Healthcare USA. 2008. pp 419-430.
This chapter on liver disease and pregnancy is from a comprehensive textbook that provides an in-depth examination of essential knowledge in gastroenterology, hepatology, and the related areas of pathology, endoscopy, nutrition, and radiology. The author notes that because most pregnant women are young and healthy, liver disease is uncommon in this patient population. The presence of liver disease should not be confused with some of the physiologic changes of pregnancy that mimic features commonly associated with liver dysfunction. The chapter divides liver diseases during pregnancy into three categories: chronic liver disease and portal hypertension, liver disease coincidental with pregnancy, and liver disease unique to pregnancy. Specific conditions covered include chronic hepatitis B, hepatitis C, autoimmune disease, Wilson’s disease, cirrhosis of any cause, extrahepatic portal hypertension, acute viral hepatitis, Budd-Chiari syndrome, gallstones, drug-induced liver disease, intrahepatic cholestasis of pregnancy, hyperemesis gravidarum, preeclampsia, HELLP syndrome, and acute fatty liver of pregnancy. For each condition, particularly those in the last category, the author discusses clinical features and diagnosis, incidence and cause, and patient care management, including concerns for both mother and fetus. 2 figures. 4 tables. 7 references.
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Nonalcoholic Fatty Liver Disease. IN: Hauser, S., ed. Mayo Clinic Gastroenterology and Hepatology Board Review. 3rd ed. New York, NY: Informa Healthcare USA. 2008. pp 407-418.
This chapter on nonalcoholic fatty liver disease (NAFLD) is from a comprehensive textbook that provides an in-depth examination of essential knowledge in gastroenterology, hepatology, and the related areas of pathology, endoscopy, nutrition, and radiology. The author defines NAFLD as the accumulation of fat, mainly triglycerides, in hepatocytes that results from insulin resistance. NAFLD includes a wide range of disease, from bland hepatic steatosis, which is generally benign, to nonalcoholic steatohepatitis (NASH), which may progress to cirrhosis and liver failure. The chapter covers clinical manifestations, imaging features, diagnosis, staging with liver biopsy, prognosis, drug therapy, treatment of associated conditions, and prevention strategies. The author cautions that weight gain and obesity resulting from an increased sedentary lifestyle and diets with a high content of fat and carbohydrates seem to be key factors in the development of insulin resistance and NAFLD. The chapter includes full-color and black-and-white illustrations. 4 figures. 4 tables. 20 references.
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Overlap Syndromes with Autoimmune Hepatitis. IN: Lindor, K.; Talwalkar, J., eds. Cholestatic Liver Disease. Totowa, NJ: Humana Press. 2008. pp 85-104.
This chapter on overlap syndromes with autoimmune hepatitis is from a book that offers health care providers an overview of cholestatic liver disease; cholestasis is defined as a liver disorder characterized by impaired bile flow. The author of this chapter notes that autoimmune hepatitis, or some features thereof, may coexist with primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). The overlapping symptoms can include significant elevations of serum aminotransferase, immunoglobulin G, and total protein concentrations, additional circulating antibiotics, and intense, plasma-cell-predominant interface inflammation––hepatitis––that is responsive to systemic immunosuppressive therapy. The chapter covers nomenclature, the interplay of PBC and autoimmune hepatitis, and the overlap between PSC and autoimmune hepatitis. The author concludes that although there is a lot of debate about how autoimmune overlap syndromes should be defined, their existence is not in doubt. The chapter is illustrated with black-and-white photographs. 3 figures. 4 tables. 74 references.
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Preventive Approaches in Chronic Diseases Part III: Decompensated Liver Cirrhosis. Practical Gastroenterology. 32(6): 32-41. June 2008.
This article is the third part of a series of articles about compensated liver disease. Compensated liver disease becomes decompensated at a rate of 5 to 10 percent yearly. Liver cirrhosis is considered decompensated when patients develop at least one complication of the disease, including hepatic encephalopathy, gastrointestinal bleeding due to portal hypertension, ascites, coagulopathies, hepatocellular carcinoma, or severe infections. Liver transplantation is the only prospect for long-term survival in patients with decompensated cirrhosis. The authors provide strategies to the caregiver that will help to detect and avoid complications in patients before liver transplantation. Two grams of sodium and 1 to 1.5 grams of protein per kilogram of body weight per day diet is recommended. The use of prophylactic antibiotics in patients with spontaneous bacterial peritonitis (SBP) is considered only in selected cases, and never exceeding 6 months. A maximum dose of furosemide 40 milligrams per day and spironolactone up to 300 milligrams per day is recommended to prevent hepatorenal syndrome (HRS). HRS is characterized by kidney failure in patients with chronic liver disease due to severe vasoconstriction of the renal circulation. Patients presenting with severe acute alcoholic hepatitis should be considered for pentoxifylline. Other management strategies may need to include magnesium supplementation for the prevention of muscle cramps; end-of-life discussions if the patient is not a candidate for liver transplantation; the use of urea-containing moisturizers to prevent lower extremities cellulitis; and intermittent histamine H1 blockers to help with sleep disturbances. 2 tables. 48 references.
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Preventive Approaches in Chronic Liver Diseases Part II: Compensated Liver Cirrhosis. Practical Gastroenterology. 32(5): 49-60. May 2008.
This article presents evidence-based strategies that are designed to prevent or detect the early complications of liver cirrhosis (LC). The authors note that the scoring systems described in the article can be used for diagnosis of LC; the clinical severity of LC can subsequently be assessed. The authors focus on treatment considerations. Due to increased risk of perioperative complications or death, patients with LC should only undergo elective surgery after careful consideration. Esophagogastroduodenoscopy screening can be used to detect varices in patients with LC; beta-blockers are the primary choice for preventing bleeding in LC patients diagnosed with esophageal varices. Liver cancer screening with abdominal computerized tomography (CT) scan or ultrasound at least yearly and serum-alpha feto protein levels every 6 months is recommended in patients with LC. Other preventive measures that should be considered in patients with LC include pneumococcus vaccination, yearly influenza vaccine, and osteoporosis screening. This article is the second in a series of three articles about prevention of liver disease. 4 tables. 39 references.
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Primary Biliary Cirrhosis. IN: Lindor, K.; Talwalkar, J., eds. Cholestatic Liver Disease. Totowa, NJ: Humana Press. 2008. pp 45-66.
This chapter on primary biliary cirrhosis (PBC) is from a book that offers health care providers an overview of cholestatic liver disease; cholestasis is defined as a liver disorder characterized by impaired bile flow. Primary biliary cirrhosis is a chronic progressive cholestatic liver disease that primarily affects middle-aged women. The chapter covers pathogenesis, epidemiology, clinical features, diagnosis, treatment, natural history and prognosis, and liver transplantation for PBC. The authors note that the pathogenesis of this disease is unknown, but some research points to genetic and environmental factors that may initiate the autoimmune process. Patients are often asymptomatic at the time of their diagnosis, but as inflammation destroys the bile ducts and fibrosis develops, symptoms of fatigue and pruritus may become present. Ursodeoxycholic acid (UDCA) is the only recommended treatment and may improve liver biochemistries, delay progression of fibrosis and development of esophageal varices, and may improve survival in selected patients. Liver transplantation is the only definitive therapy once end-stage liver disease occurs. 1 table. 153 references.
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Rare Causes of Cholestasis. IN: Lindor, K.; Talwalkar, J., eds. Cholestatic Liver Disease. Totowa, NJ: Humana Press. 2008. pp 105-118.
This chapter on rare causes of cholestasis is from a book that offers health care providers an overview of cholestatic liver disease; cholestasis is defined as a liver disorder characterized by impaired bile flow. The chapter focuses on bile formation and transport, as well as rare cholestatic syndrome. The authors note that intrahepatic cholestasis can result from genetic defects of liver epithelial cells. They discuss specific conditions, including Alagille syndrome, progressive familial intrahepatic cholestasis, benign recurrent intrahepatic cholestasis, Dubin-Johnson syndrome, Crigler-Najjar syndrome, cholestasis-lymphedema syndrome/Aagenaes syndrome, Northern American Indian cirrhosis, and arthrogyposis multiplex congenita, renal dysfunction, and cholestasis syndrome (ARC syndrome). The authors conclude that further characterization of these rare cholestatic diseases and the defective genes associated with them will aid in understanding hepatobiliary biology and other more common causes of intrahepatic cholestasis. 78 references.
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Viral Hepatitis: A Through E And Beyond. Bethesda, MD: National Digestive Diseases Information Clearinghouse. 2008. 6 p.
This fact sheet reviews the different types of viral hepatitis, defined as inflammation of the liver caused by a virus. Several different viruses, named the hepatitis A, B, C, D, and E viruses, cause viral hepatitis. These viruses all cause acute, or short-term, viral hepatitis. The hepatitis B, C, and D viruses can also cause chronic hepatitis, in which the infection is prolonged, sometimes lifelong. Chronic hepatitis can lead to cirrhosis, liver failure, and liver cancer. This fact sheet answers common questions about viral hepatitis, discussing the symptoms of the disease, and, for each type, how it is spread, who is at risk for contracting the disease, how it can be prevented, and treatment options. Depending on the type of virus, viral hepatitis is spread through contaminated food or water, contact with infected blood, sexual contact with an infected person, or from mother to child during childbirth. Vaccines can offer protection from hepatitis A and hepatitis B; no vaccines are available for hepatitis C, D, and E. Reducing exposure to the viruses offers the best protection. The fact sheet concludes with a brief note about research studies in this area and a list of resource organizations through which readers can get additional information. The back cover of the fact sheet provides information about the goals and activities of the National Digestive Diseases Information Clearinghouse (NDDIC).
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Alcohol-Induced Liver Disease: What You Need to Know About This Dangerous But Preventable Liver Disease. New York, NY: American Liver Foundation. 2007. 2 p.
This brochure from the American Liver Foundation reviews alcohol-induced liver disease, including fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Written in a question-and-answer format, the brochure discusses the liver’s role in digesting alcohol, the details of these three kinds of liver disease related to alcohol consumption, the complications of alcohol-induced liver disease, diagnostic tests that may be used to confirm the presence of alcohol-induced liver disease, safe levels of drinking alcohol, other risks to the liver from alcohol, treatment options, and prognosis for people with alcohol-induced liver disease. The brochure stresses that for people with chronic liver disease even small amounts of alcohol can make their disease worse. Patients with alcohol-induced liver disease and those with cirrhosis from any cause must abstain from alcohol completely. The back cover of the brochure lists facts about alcohol-induced liver disease in a summarized format. Contact information for the American Liver Foundation is provided.
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Catheter-Related Complications of Total Parenteral Nutrition. American Journal of Gastroenterology. 102: S97-S101. 2007.
This article describes the hepatobiliary complications that can occur with the use of total parenteral nutrition (TPN). The author reviews the background and incidence of TPN-associated liver disease; the risk factors associated with the development of TPN-associated liver disease; potential etiologies of TPN-associated liver disease including malnutrition, overnutrition, carnitine deficiency, choline deficiency, bacterial overgrowth, and methionine toxicity; and treatment options including medical treatment and nutritional treatment. Patients can only prevent hepatobiliary complications, including hepatic steatohepatitis, cirrhosis, and liver failure, if they eat. Eating allows the patient to preserve as much portal nutrient absorption as possible. A final section considers the problem of TPN-associated biliary disease, notably biliary tract stones and gallstones. 5 figures. 53 references.
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Chronic Hepatitis B: Who And How to Treat. Practical Gastroenterology. 31(11): 25-30, 35-40. November 2007.
This article reports on the use of drug therapies for hepatitis B and how to determine which patients can and should be treated. The author considers factors such as the natural history of hepatitis B, the variability in disease progression, variable individual patient response, and the advantages and disadvantages of each treatment modality. Patient selection is the key to having the best chance at a remission or cure with treatment. Specific topics include patient evaluation, the immune tolerant phase of the disease, the immune reactive phase of the disease, the inactive carrier phase, the e-antigen negative reactivation phase, treatment goals, treatment options currently approved by the Food and Drug Administration (FDA), and choosing a therapy for an individual patient. The six treatment approaches discussed are interferon alfa-2b, pegylated interferon alfa, lamivudine, adefovir dipivosil, entecavir, and L-deoxythymidine (telbivudine). The author concludes that the goal of treatment for chronic hepatitis B virus (HBV) is to prevent progressive liver disease, cirrhosis, and hepatocellular carcinoma. These goals are achieved through suppression of viral replication. An individual approach should be taken with each patient, and biopsy should be considered in some patients to evaluate for inflammation and fibrosis. 5 tables. 37 references.
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Cirrhosis: What You Need to Know About This Potentially Life-Threatening Liver Condition. New York, NY: American Liver Foundation. 2007. 2 p.
This brochure from the American Liver Foundation reviews the physiology of the liver and the problems associated with cirrhosis, which is defined as the replacement of normal liver tissue with nonliver scar tissue. As cirrhosis continues, the liver is left without enough functioning tissue to perform properly. The liver is needed to convert food into nutrients and stored energy, detoxify substances that are harmful to the body, process medications, store vitamins and minerals, and make bile, which is used for the digestion of fats. Written in a question-and-answer format, the brochure discusses the causes of cirrhosis; alcoholism and cirrhosis; other causes of cirrhosis, including chronic viral hepatitis, nonalcoholic steatohepatitis (NASH), and bile duct disease; inherited diseases and cirrhosis; the symptoms and complications of cirrhosis; diagnostic tests that may be used to confirm cirrhosis; and treatment options. In the early stages of alcoholic cirrhosis, an effective treatment is abstaining from alcohol and following a nutritious diet. In advanced stages, cirrhosis is a life-threatening condition that can only be treated with liver transplantation. The back cover of the brochure lists facts about cirrhosis in a summarized format. Contact information for the American Liver Foundation is provided.
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Diagnosis and Long-Term Management of Wilson Disease. Gastroenterology and Hepatology. 3(1): 27-29. January 2007.
This article answers common questions that physicians may have regarding the diagnosis and long-term management of patients with Wilson disease. The article begins with a review of the pathophysiology of Wilson disease, an inherited disorder of copper metabolism. Dietary copper is absorbed by the gut and accumulates in the liver, leading to oxidative damage within the liver cells; this damage leads to the development of steatohepatitis, followed by fibrosis and cirrhosis. The author describes the natural course of the disease, the typical initial presentation of patients with Wilson disease, treatment options for these patients, salvage therapy other than transplantation for patients with advanced chronic Wilson disease, the prioritization of patients with Wilson disease for liver transplantation, the long-term prognosis of Wilson disease patients who respond to standard medical therapy, and associated conditions and complications in older patients with Wilson disease. 4 references.
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Hepatitis B: What You Need to Know About This Serious Liver Disease And How to Prevent it. New York, NY: American Liver Foundation. 2007. 2 p.
This brochure from the American Liver Foundation reviews hepatitis B, a disease of the liver that is caused by the hepatitis B virus (HBV). Written in a question-and-answer format, the brochure discusses the causes and transmission of HBV, the typical course of the disease, the symptoms of HBV infection, diagnostic tests that may be used to confirm the presence of HBV, risk factors for getting hepatitis B, chronic hepatitis B and its complications, treatment options, and prevention strategies. HCB is transmitted through body fluids such as blood, semen, and vaginal secretions. Many hepatitis B patients have no symptoms. In a small percentage of patients, hepatitis B persists as a chronic condition that can lead to more serious liver diseases, including cirrhosis, liver failure, and liver cancer. Vaccination is recommended as the best way to prevent hepatitis B. The back cover of the brochure lists facts about hepatitis B in a summarized format. Contact information for the American Liver Foundation is provided.
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Hepatitis C: What You Need to Know About This Serious Liver Disease And How to Manage it. New York, NY: American Liver Foundation. 2007. 2 p.
This brochure from the American Liver Foundation reviews hepatitis C, a disease of the liver that is caused by the hepatitis C virus (HCV). Written in a question-and-answer format, the brochure discusses the causes and transmission of HCV, the typical course of the disease, the symptoms of HCV infection, diagnostic tests that may be used to confirm the presence of HCV, risk factors for getting hepatitis C, treatment options including antiviral medications, prevention strategies, and the management of chronic HCV infections. HCV is transmitted through direct exposure to infected blood, often through sharing needles used to inject illegal drugs. Most hepatitis C patients have no symptoms, but a simple blood test can diagnose the disease. The HCV stays in the liver where it can cause continuous damage that can lead to cirrhosis and liver cancer. For some hepatitis C patients, antiviral medicines are helpful in fighting the virus and limiting liver damage. The back cover of the brochure lists facts about hepatitis C in a summarized format. Contact information for the American Liver Foundation is provided.
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Liver Cancer: What You Need to Know if You Have Liver Cancer or Are at Increased Risk. New York, NY: American Liver Foundation. 2007. 2 p.
This brochure from the American Liver Foundation reviews liver cancer. Written in a question-and-answer format, the brochure discusses the causes of liver cancer; the symptoms; the typical course of the disease; diagnostic tests that may be used to confirm the presence of liver cancer; treatment options, including transplantation, surgery, chemotherapy, and radiation therapy; prognosis; prevention strategies; and the management of patients who have liver cancer. The biggest risk factors for primary liver cancer are other liver diseases––mainly cirrhosis and chronic hepatitis B––and obesity. Treatment options are quite limited for liver cancers, except for those that are discovered early. Three websites and a reference book are suggested for readers who wish to obtain more information about liver cancer. The back cover of the brochure lists facts about liver cancer in a summarized format. Contact information for the American Liver Foundation is provided.
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Liver Diseases in Pregnancy. IN: Pregnancy in Gastrointestinal Diseases. 2nd ed. Bethesda, MD: American College of Gastroenterology. 2007. pp 32-53.
This chapter about liver diseases in pregnancy is from a monograph that presents updated information about pregnancy in women with gastrointestinal disorders. The authors stress that a complete understanding of the physiological changes that affect pregnancy and of the different liver diseases that occur during pregnancy is essential for early recognition and management of pregnancy-associated liver disorders. The chapter focuses on bringing readers up to date on the research in the area covered, the recommended treatments, and patient management concerns, notably issues of maternal and fetal safety. Separate sections discuss the physiological changes that affect pregnancy, diagnostic imaging tests used in pregnancy, liver disorders that are exclusive or unique to pregnancy, liver diseases that may occur during pregnancy or intercurrent liver diseases in pregnancy, and changes that occur when a woman with a pre-existing liver disease becomes pregnant. Specific conditions discussed include hepatic involvement in hyperemesis gravidarum, acute fatty liver of pregnancy (AFLP), intrahepatic cholestasis of pregnancy (IHCP), hemolysis, elevated liver enzymes and low platelets syndrome (HELLP syndrome), viral hepatitis, HIV infection, herpes simplex viral infections, cytomegalovirus infection (CMV), alcohol use, portal hypertension, autoimmune hepatitis (AIH), Wilson disease, primary biliary cirrhosis and primary sclerosing cholangitis, Budd-Chiari syndrome, gallstone disease in pregnancy, and liver transplant. The authors conclude that preventive measures, including early prenatal care, avoidance of risky behaviors that could increase a woman’s chance of acquiring infections, and cessation of smoking and drinking alcohol are vital in decreasing morbidity and mortality in pregnancy. Although liver disease in pregnancy is associated with an increased risk for morbidity and mortality, clinical outcomes have improved for both mother and baby, and pregnancy is not contraindicated in patients with liver disease or in patients who have had a liver transplant. 3 tables. 54 references.
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Prevention And Management of Gastroesophageal Varices And Variceal Hemorrhage in Cirrhosis. Hepatology. 46(3): 922-938. September 2007.
This article presents the practice guideline from the American Association for the Study of Liver Diseases (AASLD) on the prevention and management of gastroesophageal varices and variceal hemorrhage in people with cirrhosis. These recommendations are based on a formal review and analysis of recently published world literature on the topic; several consensus conferences among experts; the American College of Physicians' Manual for Assessing Health Practices and Designing Practice Guidelines; guideline policies produced by professional organizations, including the AASLD and the American Gastroenterological Association; and the authors' experience caring for patients with cirrhosis and varices. Topics include the pathophysiology of portal hypertension in cirrhosis, the evaluation of portal hypertension, the natural history of varices, gastric varices, the diagnosis of varices and variceal hemorrhage, and management recommendations. Twenty-four specific recommendations for patient care are provided. A combination of vasoconstrictive pharmacological therapy and variceal ligation is the preferred approach to the management of acute variceal hemorrhage. Prophylactic antibiotic therapy is considered standard of care as adjunctive treatment of the acute bleeding episode. For patients who fail medical therapy, transjugular intrahepatic portosystemic shunt (TIPS) or surgically created shunts are excellent salvage procedures. 3 tables. 135 references.
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Primary Biliary Cirrhosis. Bethesda, MD: National Digestive Diseases Information Clearinghouse. 2007. 2 p.
This fact sheet reviews primary biliary cirrhosis, a disease that slowly destroys the liver’s bile ducts. When the ducts are damaged, bile builds up in the liver and damages liver tissue. The fact sheet covers the symptoms, diagnosis, and treatment options for primary biliary cirrhosis (PBC). Initial treatment for PBC is usually aimed at relieving symptoms. Vitamin replacement therapy, calcium supplements, and drugs to treat itching are usually prescribed. The fact sheet concludes with the contact information for the American Liver Foundation and a brief description of the activities of the National Digestive Diseases Information Clearinghouse (NDDIC).
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Prospective Evaluation of FIBROSpect II for Fibrosis Detection in Hepatitis C and B Patients Undergoing Laparoscopic Biopsy. Gastroenterology and Hepatology. 3(5): 367-376. May 2007.
This article reports on a study undertaken to validate a serum marker of liver fibrosis through the use of laparoscopic biopsy, which decreases sampling error and increases the reliability of histopathologic assessment. The authors prospectively evaluated the FIBROSpect II serum marker test for viral liver fibrosis against laparoscopic biopsies by studying 145 patients with chronic hepatitis B or C who underwent laparoscopy in a tertiary care setting. Results showed that the FIBROSpect II test was able to rule in significant fibrosis (stages 2 to 4) with a likelihood rate of 2.6. The test correctly indicated absence of diseases in 74 percent of stages 0 to 1 patients and correctly predicted significant disease in 67 percent of stages 2 to 4 patients. Multiple biopsies from 52 percent of patients differed by at least one stage. In 13 patients (9 percent), cirrhosis was detected by laparoscopy but not histologically. The authors conclude that FIBROSpect II provides valuable additional information for assessing fibrosis. 3 figures. 4 tables. 26 references.
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Terlipressin For The Treatment of Hepatorenal Syndrome. Gastroenterology and Hepatology. 3(10): 773-774. October 2007.
This article describes the use of terlipressin for the treatment of hepatorenal syndrome, a complication of the portal hypertension that occurs in patients with cirrhosis. The author answers common questions about hepatorenal syndrome and the use of terlipressin, including the rationale for the use of this drug, research studies on the use of terlipressin for hepatorenal syndrome, the difficulties of conducting clinical research on patients with a disease that has a rapid clinical course and a high mortality rate, new directions for future research, the use of terlipressin in patients undergoing liver transplantation, and how future monitoring of patients with cirrhosis could be improved to optimize terlipressin therapy. Terlipressin is an analog of the vasoconstrictor vasopressin, which is used to treat bleeding esophageal varices, another complication of portal hypertension. Terlipressin, a prodrug of vasopressin, is a much safer drug than vasopressin, with fewer side effects. Terlipressin is often given in combination with albumin, which expands the blood volume, resulting in improved renal function in patients with hepatorenal syndrome. 5 references.
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Autoimmune Hepatitis. IN: Lichtenstein, G.; Reddy, K.R.; Faust, T., eds. Clinician’s Guide to Liver Disease. Thorofare, NJ: Slack Incorporated. 2006. pp 105-120.
This chapter about autoimmune hepatitis is from a user-friendly reference book that provides gastroenterologists with an overview of the management of acute and chronic liver disease. The author describes autoimmune hepatitis as a condition of unresolving liver inflammation, which primarily affects young women. The condition is characterized by elevated liver enzymes, hypergammaglobulinemia, serum autoantibodies, interface hepatitis, plasma cell infiltrates on liver biopsy, extrahepatic manifestations, and steroid responsiveness. The chapter provides a brief historical perspective and discussion of epidemiology. It discusses pathogenesis, natural history and prognosis, clinical features, diagnosis and diagnostic tests, complications, and treatment options including medial therapy and liver transplantation. The author cautions that diagnosis of autoimmune hepatitis requires a high index of clinical suspicion because several liver conditions can mimic the disease. Most patients respond to immunosuppressive medications with improvement in clinical symptoms, biochemical liver tests, hepatic histology, and patient survival; however, relapse is common. Up to 40 percent of patients progress to cirrhosis despite therapy. The chapter includes tables and a patient care algorithm and concludes with a list of references. 1 figure. 6 tables. 19 references.
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Cirrhosis and Chronic Liver Failure: What You Should Know. American Family Physician. 74(5): 756. September 1, 2006.
This brief patient education fact sheet reviews the basics of cirrhosis and chronic liver failure. Written in a question-and-answer format, the fact sheet discusses the physiology and function of the liver, complications associated with cirrhosis, the causes of cirrhosis, symptoms that may be experienced by people with cirrhosis, and treatment options. The most common causes of liver cirrhosis are drinking too much alcohol and having hepatitis B or C infection. Symptoms can include lack of appetite, nausea, weight loss, jaundice, and pruritus. Treatment is based on the cause of the disease in each individual patient. The fact sheet concludes with contact information for the American Liver Foundation and the American Gastroenterological Association.
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Cirrhosis and Its Complications. IN: Lichtenstein, G.; Reddy, K.R.; Faust, T., eds. Clinician’s Guide to Liver Disease. Thorofare, NJ: Slack Incorporated. 2006. pp 31-56.
This chapter about cirrhosis and its complications is from a user-friendly reference book that provides gastroenterologists with an overview of the management of acute and chronic liver disease. The authors define cirrhosis as the marked disruption of hepatic structure with extensive fibrosis. Portal hypertension develops as a consequence of cirrhosis and is present at the time of diagnosis in 60 percent of patients with cirrhosis. The chapter discusses the etiology of cirrhosis and its diagnoses and considers complications including portal hypertension, variceal bleeding, ascites, hepatorenal syndrome, hepatic encephalopathy, and coagulopathy. For each complication, the authors discuss symptoms, prevention, diagnosis, risk factors, and treatment options. The chapter includes tables and patient care algorithms and concludes with a list of references. 4 figures. 8 tables. 34 references.
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Clinical Utility of Biomarkers of Liver Fibrosis. Gastroenterology and Hepatology. 2(1): 48-57. January 2006.
This article explores the clinical use of biomarkers of liver fibrosis. Liver fibrosis leads to impaired function, portal hypertension, and reduced survival. Thus an accurate evaluation of liver fibrosis in chronic liver disease is important to determine prognosis, therapy outcomes, and disease progression. The traditional method, needle liver biopsy, is an invasive procedure that is associated with small sample size and inaccurate staging, and provides only a semi-quantitative assessment of fibrosis. The authors review a number of simple and specific extracellular matrix biochemical markers that are predictive of fibrosis in patients with chronic liver disease. In patients with hepatitis C, serum HA has been shown to reflect virus response to therapy. Serum HA may also be predictive of severe complications in patients with compensated cirrhosis due to hepatitis C. Markers such as PIIINP and YKL-40 may also predict clinical outcomes in other chronic liver diseases such as primary biliary cirrhosis or alcoholic liver disease. The authors conclude by addressing concerns about overcoming the inherent issue of validation against a static and imperfect test such as liver biopsy; as with liver biopsy, noninvasive markers are imperfect. 4 tables. 78 references.
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Clinician’s Guide to Liver Disease. Thorofare, NJ: Slack Incorporated. 2006. 356 p.
This user-friendly reference book provides gastroenterologists with an overview of the management of acute and chronic liver disease. The book offers 16 chapters: evaluation of the liver patient, cirrhosis and its complications, acute and chronic viral hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis, autoimmune hepatitis, nonalcoholic fatty liver disease, metabolic liver disease, vascular diseases involving the liver, benign and malignant tumors of the liver, liver disease in pregnancy, postoperative jaundice, nonviral infections of the liver, hepatopulmonary syndrome, portopulmonary hypertension, liver transplantation, and drug hepatotoxicity. Each chapter presents an introduction, consideration of etiology, epidemiology, clinical presentation and symptoms, risk factors, complications, and treatment approaches. The chapters include charts and figures and conclude with a list of references. Most chapters include patient care algorithms. A subject index concludes the volume.
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Diagnostic Evaluation of Nonalcoholic Fatty Liver Disease. Journal of Clinical Gastroenterology. 40(Suppl 1): S34-S38. March 2006.
This article reviews the diagnostic evaluation of nonalcoholic fatty liver disease (NAFLD). The authors note that NAFLD should be considered in patients presenting with asymptomatic elevated amino-transaminases, patients with radiologic findings of hepatic fatty infiltration, or in patients with cryptogenic cirrhosis. The diagnosis of NAFLD requires evidence of fatty infiltration of the liver in the absence of excessive alcohol ingestion. Clinical evaluation should examine for metabolic risk factors, which include central obesity, glucose intolerance, hypertension, hypertriglyceridemia, and low HDL cholesterol. Secondary causes of NAFLD, such as medications and intestinal bypass surgery, must also be considered, as management of these conditions may differ. Confirmation of hepatic steatosis can usually be done by imaging studies, although occasionally liver biopsy is required. Liver biopsy is required to stage fibrosis and to distinguish between NAFLD and steatosis. This distinction is important to provide prognosis, to exclude other liver disease, and to monitor response to therapy and disease progression over time. The authors note that clinical features, particularly diabetes, obesity and older age, can aid in stratifying patients at risk for advanced fibrosis but are not sufficiently accurate to replace liver biopsy. 2 figures. 2 tables. 56 references.
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Diseases of the Gallbladder and Bile Ducts: Diagnosis and Treatment. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. 428 p.
This textbook provides a comprehensive and critical approach to both established and new diagnostic and therapeutic modalities for diseases of the gallbladder and bile ducts. The book was written by a multidisciplinary panel of international experts with extensive experience in this population of patients. The book offers 23 chapters in six sections: anatomy, pathophysiology, and epidemiology of the biliary system; diagnostic and therapeutic approaches for the biliary tree and gallbladder; specific conditions; the intrahepatic and extrahepatic bile ducts; intrahepatic cholestasis; and the pediatric population. Specific topics include noninvasive imaging, endoscopic diagnosis and treatment, percutaneous biliary imaging and intervention, radiation therapy, surgery, laparoscopic treatment, laparoscopic biliary injuries, treatment for biliary malignancies, the gallbladder, gallstones, acute cholangitis, cystic diseases of the biliary system, biliary complications of liver transplantation, primary sclerosing cholangitis, cholangiocarcinoma, primary biliary cirrhosis, and biliary disease in infants and children. Each chapter includes a summary of objectives, a list of suggested readings, extensive references, and a set of self-test questions that focus on the material covered in the chapter. The book is illustrated with black-and-white photographs and line drawings; one section of color plates is included. The book concludes with the answers to the self-test study questions and a detailed subject index.
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End-Stage Liver Disease. IN: Nilsson, K.R.; Piccini, J.P., eds. Osler Medical Handbook. Philadelphia, PA: Saunders. 2006. pp. 402-417.
Chronic liver disease includes a broad differential diagnosis of infectious, autoimmune, inherited, metabolic, toxic, and acquired origins. This chapter on end-stage liver disease is from a handbook that provides the essentials of diagnosis and treatment, as well as the latest in evidence-based medicine, for residents working bedside, in-patient care. The chapter begins with a presentation of essential Fast Facts and concludes with Pearls and Pitfalls useful to the practicing internist. The body of the chapter is divided into sections: Epidemiology, Clinical Presentation, Diagnosis, and Management. Specific topics covered include the most common causes of cirrhosis in the United States, notably alcoholic liver disease and chronic hepatitis C infection; nonalcoholic fatty liver disease (NAFLD); the causes of the clinical problems associated with cirrhosis; the risk factors for hepatic encephalopathy, including infection, dehydration, hypokalemia, alkalosis, and sedating medications; the risk of liver cancer in patients with cirrhosis; autoimmune hepatitis; the diagnostic tests used to confirm metabolic and inherited causes of chronic liver disease; and the use of the Model for End-Stage Liver Disease (MELD) score to predict mortality, particularly for those patients waiting for a liver transplantation. The chapter concludes with a list of references, each labeled with a 'strength of evidence' grade to help readers determine the type of research available in that reference source. 1 figure. 2 tables. 35 references.
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Epidemiology of Nonalcoholic Fatty Liver Disease in Adults. Journal of Clinical Gastroenterology. 40(Suppl 1): S5-S10. March 2006.
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease that has been shown to progress to cirrhosis and hepatocellular carcinoma. NAFLD includes a spectrum of liver pathology including simple steatosis, fibrosis, and cirrhosis. This article reviews the epidemiology of NAFLD in adults. The author focuses on the prevalence of NAFLD, the factors associated with this disorder, and the more advanced stages of NAFLD, which include nonalcoholic Steatohepatitis (NASH) and fibrosis. In the general population, the estimated prevalence ranges from 3 to 24 percent, with most estimates in the 6 to 14 percent range. In patients undergoing bariatric surgery, NAFLD is extremely common, ranging from 84 to 96 percent. NAFLD appears to be most strongly associated with obesity, and with insulin resistance states including diabetes, and with other features of the metabolic syndrome, such as high triglycerides and low HDL. More advanced stages of NAFLD are associated with older age, higher body mass index, diabetes, hypertension, high triglycerides, and insulin resistance. The author notes that although liver cancer can occur in the setting of NAFLD, the risk factors for liver cancer in these patients have not been established. 1 table. 68 references.
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Genetic Influences in Nonalcoholic Fatty Liver Disease. Journal of Clinical Gastroenterology. 40(Suppl 1): S30-S33. March 2006.
This article reviews the genetic influences in nonalcoholic fatty liver disease (NAFLD), a metabolic liver disease with widely variable phenotypes that extend from simple steatosis, through nonalcoholic Steatohepatitis (NASH), to cirrhosis and liver cancer. The authors stress that this variation reflects the interplay of well-recognized environmental factors and disease associations such as obesity and insulin resistance with host genetic factors, which are polygenic or complex in nature. The authors hypothesize that most of the observed phenotypic variability will probably be explained by variations in single nucleotide polymorphism frequency, although knowledge of the effect of most polymorphisms on biologic function is currently limited. Thus far, however, candidate gene association studies have had significant limitations such as small cohort sizes and poor reproducibility. Rapid technologic developments are increasing the capability of detecting genetic variation. This may result in better understanding of disease pathogenesis in NAFLD and thus improved patient care management. 1 figure. 1 table. 29 references.
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Helpful Tips for Carriers of HBV. Silver Spring, MD: Hepatitis Foundation International. 2006. 1 p.
Long-term infection with the hepatitis B virus (HBV) affects over one million people in the United States. This brief fact sheet offers a list of helpful tips for carriers of the HBV. The author notes that while a majority of infected people remain so-called healthy carriers, others develop more severe liver disease leading to cirrhosis, liver cancer, and liver failure. Tips include annual monitoring of liver function, periodic tests for liver cancer, regular review of all medications (even some over the counter medications can harm the liver), prevention of transmission to others, keep one's health care provider appraised of the HBV carrier status (particularly important for pregnant women), tell sexual partners about the HBV and make sure they get vaccinated, and stay informed about research developments. The contact information for the Hepatitis Foundation International is provided.
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Hepatitis B. Silver Spring, MD: Hepatitis Foundation International. 2006. 2 p.
Hepatitis B is a viral infection of the liver caused by the hepatitis B virus (HBV). About 95 percent of adults infected recover spontaneously within 6 months. However, 90 percent of children less than one year of age who get infected with HBV never clear the virus, remaining chronically infected, with an associated risk of scarring of the liver (cirrhosis) and liver cancer. This fact sheet reviews the epidemiology and transmission of hepatitis B, typical symptoms, diagnostic approaches, treatment options, and prevention strategies. Treatment is not warranted during the acute phase of hepatitis B, as the disease resolves in most patients within six months. Several drugs are available to treat those who are chronically infected with HBV. The best prevention for hepatitis B is the hepatitis B vaccine, which is recommended for people newborn through age 18 years. Health care workers are especially encouraged to get vaccinated against HBV and to follow universal precautions. Readers with HBV are cautioned against alcohol use, which can worsen any liver disease.
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Hepatitis C. Silver Spring, MD: Hepatitis Foundation International. 2006. 3 p.
Hepatitis C is a viral infection of the liver caused by the hepatitis C virus (HCV), which has six genotypes. HCV is a major cause of chronic liver disease, including cirrhosis and liver cancer. This fact sheet reviews the epidemiology and transmission of hepatitis C, typical symptoms, diagnostic approaches, groups of people for whom hepatitis testing is recommended, medical evaluation and management for chronic HCV infection, treatment options, and prevention strategies. Hepatitis C is a slowly progressing liver disease, usually without symptoms, that can take 20 to 30 years to cause serious liver damage. Between 15 percent and 45 percent of infected individuals will clear the virus within six months and liver injury in these individuals resolves completely. The fact sheet notes that combination therapy with pegylated interferon and ribavirin is the treatment of choice, resulting in sustained response rates of 35 to 50 percent for patients infected with the most common genotype in the United States (genotype 1). Almost half of all liver transplants in the U.S. are performed for end-stage hepatitis C. Readers with HCV infections are cautioned against any alcohol use, which can accelerate the liver damage caused by the disease.
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Hepatobiliary Complications of Inflammatory Bowel Disease. Practical Gastroenterology. 30(8): 19-33. August 2006.
This article outlines the hepatobiliary complications that may be associated with inflammatory bowel disease (IBD, including Crohn’s disease and ulcerative colitis). The author notes that the prevalence of hepatobiliary abnormalities in IBD range from 5 percent to 15 percent. Common hepatobiliary manifestations of IBD can include chronic active hepatitis, cirrhosis, steatosis, and primary sclerosing cholangitis. The author outlines a recommended initial approach to the patient, then discusses primary sclerosing cholangitis (PSC), differential diagnosis, autoimmune hepatitis, cholelithiasis (gallstones), chronic viral hepatitis, and medication-induced hepatotoxicity (including that due to 5-ASA drugs, thiopurines, infliximab, and methotrexate). A final section considers some of the more rare hepatic complications of IBD, including liver abscess, and hepatic amyloidosis. The author concludes that PSC is the classic IBD-related liver disease and occurs most often in patients with ulcerative colitis. Readers are cautioned that patients with IBD are as likely as other patients to develop non-IBD-related liver disorders, so a diligent search for common causes of any hepatobiliary disease should be performed. 1 figure. 2 tables. 34 references.
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Liver Disease in Patients with Diabetes Mellitus. Journal of Clinical Gastroenterology. 40(1): 68-76. January 2006.
In addition to the well-known cardiovascular, renal, and ophthalmologic complications of diabetes, liver-related complications occur commonly and are often underrecognized. This article reviews the relationship between diabetes mellitus and two common liver diseases: chronic hepatitis C and nonalcoholic fatty liver disease. The author also discusses the association of diabetes and cirrhosis, acute liver failure, hepatocellular carcinoma, and outcomes following orthotopic liver transplantation. The liver plays a significant role in energy homeostasis and glucose metabolism; insulin enhances glycogen synthesis within the liver and prevents glucose production. These normal physiologic processes become dysregulated with insulin resistance and type 2 diabetes mellitus. Insulin resistance may work synergistically with hepatitis C infection to make changes in the liver, in the form of steatosis, inflammation, and fibrosis development. Once this occurs, progression to diabetes may occur in patients with underlying genetic susceptibility. Current treatment for preventing liver complications is focused on therapies that improve underlying insulin resistance, including weight loss or drug therapy. 1 figure. 2 tables. 158 references.
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Liver Disease in Patients with Diabetes Mellitus. Journal of Clinical Gastroenterology. 40(1): 68-76. January 2006.
In addition to the well-known cardiovascular, renal, and ophthalmologic complications of diabetes, liver-related complications occur commonly and are often underrecognized. This article reviews the relationship between diabetes mellitus and two common liver diseases: chronic hepatitis C and nonalcoholic fatty liver disease. The author also discusses the association of diabetes and cirrhosis, acute liver failure, hepatocellular carcinoma, and outcomes following orthotopic liver transplantation. The liver plays a significant role in energy homeostasis and glucose metabolism; insulin enhances glycogen synthesis within the liver and prevents glucose production. These normal physiologic processes become dysregulated with insulin resistance and type 2 diabetes mellitus. Insulin resistance may work synergistically with hepatitis C infection to make changes in the liver, in the form of steatosis, inflammation, and fibrosis development. Once this occurs, progression to diabetes may occur in patients with underlying genetic susceptibility. Current treatment for preventing liver complications is focused on therapies that improve underlying insulin resistance, including weight loss or drug therapy. 1 figure. 2 tables. 158 references.
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Liver Disease in Pregnancy. IN: Lichtenstein, G.; Reddy, K.R.; Faust, T., eds. Clinician’s Guide to Liver Disease. Thorofare, NJ: Slack Incorporated. 2006. pp 211-232.
This chapter about liver disease in pregnancy is from a user-friendly reference book that provides gastroenterologists with an overview of the management of acute and chronic liver disease. The authors stress that because early diagnosis and timely intervention can reduce perinatal and maternal morbidity and mortality, it is important to have a high index of suspicion for potential conditions affecting the liver. Gestational age is used to guide the differential diagnosis for hepatic biochemical test abnormalities during pregnancy. The chapter covers the liver in normal pregnancy, the use of imaging studies during pregnancy, intrahepatic cholestasis of pregnancy (ICP), acute fatty liver of pregnancy (AFLP), hyperemesis gravidarum, clampsia or eclampsia, the HELLP (hemolysis, elevated liver tests, low platelets) syndrome, and intercurrent liver disease in pregnancy, including cholelithiasis, Budd-Chiari syndrome, acute viral hepatitis, drug-induced liver damage, and metastases to the liver. The authors consider chronic liver disease in pregnancy, including cirrhosis, hepatitis C, autoimmune hepatitis, Wilson disease, inherited hyperbilirubinemia, and pregnancy in women who have received a liver transplant. Hyperemesis gravidarum is a first trimester condition, whereas ICP may present in the second trimester. Clampsia and the HELLP syndrome predominantly occur in the third trimester. 4 tables. 28 references.
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Management of the Cirrhotic Patient Before Liver Transplantation: The Role of the Referring Gastroenterologist. Gastroenterology and Hepatology. 2(5): 346-354. May 2006.
The referral of a patient with cirrhosis to a liver transplant center for evaluation is usually made by a local gastroenterologist. This article reviews the role of the referring gastroenterologist in the ongoing management of the patient with liver cirrhosis before liver transplantation. The role of the referring gastroenterologist begins with early identification and modification of high-risk behaviors, which may delay listing a patient for liver transplantation. The gastroenterologist must also understand what constitutes a timely referral of a patient to a liver transplant center and the consequences of late referral. Although patients experience the inevitable deterioration of their liver function, which in turn advances their priority on the liver transplant waiting list, the referring gastroenterologist must also anticipate medical complications of cirrhosis, and should initiate appropriate surveillance and prevention programs to detect and prevent these complications. Another important role of the referring gastroenterologist is as a link of information between the patient and the transplant center. The author concludes that adherence to these guidelines will increase the probability that a patient with chronic liver failure will undergo successful liver transplantation and will decrease post-transplant morbidity. 1 figure. 5 tables. 75 references.
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Medical Care of the Patient with Compensated Cirrhosis. Gastroenterology and Hepatology. 2(2): 124-133. February 2006.
This article reviews the surveillance and health maintenance recommendations that should be followed for every patient with compensated cirrhosis to delay or prevent the serious complications of cirrhosis. The authors note that although most gastroenterologists and hepatologists are comfortable managing the serious complications related to cirrhosis, many fail to provide the necessary education, prevention, and treatment for non-life-threatening problems associated with cirrhosis. Topics covered include the prognosis of compensated cirrhosis, patient education, alcohol use, acetaminophen use, Vibrio vulnificus infections, vitamin and mineral supplements, weight control, immunizations, dental hygiene, screening for osteoporosis, the primary prophylaxis of variceal hemorrhage, surveillance for hepatocellular carcinoma (liver cancer), medication use in patients with cirrhosis, screening and managing nonliver diseases in patients with cirrhosis, and when to refer for liver transplantation. The authors conclude that patient education, appropriate surveillance and preventive strategies, and regular monitoring of the patient’s condition can improve quality of life and can delay or prevent many of the serious complications associated with cirrhosis. 4 tables. 97 references.
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Mortality Difference by Dialysis Modaility Among New ESRD Patients with and Without Diabetes Mellitus. Dialysis and Transplantation. 35(4): 234-244. April 2006.
This article reports on a study that investigated mortality difference by dialysis modality (hemodialysis versus peritoneal dialysis) among new end stage renal disease (ESRD) patients with and without diabetes mellitus. The authors completed a retrospective analysis of data obtained from the China Medical University Hospital in Taiwan on all new ESRD patients undergoing hemodialysis (HD, n = 219) or peritoneal dialysis (PD, n = 226) for more than 3 months between January 2000 and December 2003. Of these patients, 102 HD patients and 96 PD patients also had diabetes. Their average age was 60 years (plus or minus 13 years) for the HD group and 57 years (plus or minus 16 years) for the PD patient group. Among these 445 patients, PD patients were associated with a significantly lower risk of death compared with the HD patients. Older age, diabetes mellitus as the cause of ESRD, co-morbidity of ischemic heart disease, congestive heart failure, cerebral vascular accident (CVA, stroke), peripheral artery occlusive disease, or liver cirrhosis, and HbA1c levels greater than 8 percent were associated with a significantly high risk of mortality. 4 figures. 4 tables. 20 references.
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Mortality Difference by Dialysis Modality Among New ESRD Patients With and Without Diabetes Mellitus. Dialysis and Transplantation. 35(4): 234-244, 266. April 2006.
This article reports on a study that investigated mortality difference by dialysis modality (hemodialysis versus peritoneal dialysis) among new end stage renal disease (ESRD) patients with and without diabetes mellitus. The authors completed a retrospective analysis of data obtained from the China Medical University Hospital in Taiwan on all new ESRD patients undergoing hemodialysis (HD, n = 219) or peritoneal dialysis (PD, n = 226) for more than 3 months between January 2000 and December 2003. Of these patients, 102 HD patients and 96 PD patients also had diabetes. Their average age was 60 years (plus or minus 13 years) for the HD group and 57 years (plus or minus 16 years) for the PD patient group. Among these 445 patients, PD patients were associated with a significantly lower risk of death compared with the HD patients. Older age, diabetes mellitus as the cause of ESRD, co-morbidity of ischemic heart disease, congestive heart failure, cerebral vascular accident (CVA, stroke), peripheral artery occlusive disease, or liver cirrhosis, and HbA1c levels greater than 8 percent were associated with a significantly high risk of mortality. 4 figures. 4 tables. 20 references.
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Natural History of Nonalcoholic Steatohepatitis. Journal of Clinical Gastroenterology. 40(Suppl 1): S11-S16. March 2006.
This review article covers the natural history of nonalcoholic steatohepatitis, a variation of nonalcoholic fatty liver disease (NAFLD). NAFLD is being increasingly recognized as one of the most common chronic liver diseases. The authors note that the natural history of this liver disease remains unclear due to its indolent nature, the paucity of prospective studies, and the lack of consensus regarding the various forms of this disorder. Patients with nonalcoholic steatohepatitis (NASH) appear to have a higher likelihood of progression to cirrhosis. Obesity and possibly type 2 diabetes appear to be associated with an increased risk of fibrosis. There is also an increased risk of liver cancer and end-stage liver disease among patients with NASH-related cirrhosis and those with cryptogenic cirrhosis, which likely represents a late stage of NAFLD. The authors also briefly review the recurrence of NASH in patients who have undergone liver transplantation for NASH-related end-stage liver disease. They conclude that long-term survival in patients with NAFLD may be slightly worse than survival from all-cause chronic liver disease, although survival appears to be higher than among patients with fatty liver from alcohol abuse, and is comparable to patients with chronic hepatitis C infection. 6 figures. 19 references.
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Nonalcoholic Fatty Liver Disease: A Clinic Approach and Review. Canadian Journal of Gastroenterology. 20(5): 345-349. May 2006.
This article reviews advances in nonalcoholic fatty liver disease (NAFLD), the most common cause of incidental elevation of liver enzymes in North America and Europe. Risk factors for NAFLD include a body mass index of 25 or greater, central obesity, and diabetes mellitus. The spectrum of disease is wide, ranging from simple steatosis with benign prognosis to nonalcoholic steatohepatitis and cirrhosis, with associated increases in morbidity and mortality. Topics covered include epidemiology and risk factors, diagnosis, pathogenesis, and patient care management, notably drug therapy in NAFLD, bariatric surgery, and the role of liver biopsy. The first abnormality in NAFLD is insulin resistance leading to hepatic steatosis. The second problem involves multiple proinflammatory cytokines, resulting in nonalcoholic steatohepatitis. Treatment is aimed at aggressive risk factor control and weight loss. 1 figure. 3 tables. 38 references.
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Nonalcoholic Steatohepatitis. Bethesda, MD: National Digestive Diseases Information Clearinghouse. 2006. 6 p.
Nonalcoholic steatohepatitis (NASH) is a common, often silent, liver disease. NASH resembles alcoholic liver disease but occurs in people who drink little or no alcohol. This fact sheet describes NASH and its management. The major feature of NASH is fat in the liver, along with inflammation and damage. If fat is suspected based on blood-test results or scans of the liver, this problem is called nonalcoholic fatty liver disease (NAFLD). Both NASH and NAFLD are becoming more common, possibly because of the greater number of Americans with obesity. NASH can be severe and can lead to cirrhosis, in which the liver is permanently damaged and scarred and no longer able to work properly. The fact sheet reviews diagnosis, symptoms, causes, and treatment of the disease, as well as current research studies on NASH. Although there are no specific treatments for NASH, people with this disease are counseled to achieve and maintain a healthy weight, follow a balanced and healthy diet, increase physical activity, and avoid alcohol and unnecessary medications. Experimental therapies being studied include antioxidants and anti-diabetes medications. Readers are referred to the American Liver Foundation at www.liverfoundation.org or 1–800–GO–LIVER and to two databases for additional information: the NIDDK Reference Collection at www.catalog.niddk.nih.gov/resources and Medline Plus at www.medlineplus.gov. A final section offers a brief description of the National Digestive Diseases Information Clearinghouse (NDDIC), a Federal Government agency that provides information about digestive diseases to people with digestive disorders and their families, health care professionals, and the public. 3 figures.
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Nutrition Concerns of the Patient with Primary Biliary Cirrhosis or Primary Sclerosing Cholangitis. Practical Gastroenterology. 30(4): 92-100. April 2006.
This article reviews the nutritional concerns of the patient with primary biliary cirrhosis (PBC) or primary sclerosing cholangitis (PSC), two cholestatic liver diseases that are characterized by impairment of the bile flow. The primary nutritional consequences of cholestasis are related to malabsorption caused by lack of sufficient bile acids in the intestinal lumen. Many digestive enzymatic reactions are affected by impaired bile flow into the small bowel. This decrease in biliary excretion of cholesterol and other lipids in cholestasis often lead to hyperlipidemia. The authors provide an overview of the nutritional assessment, diagnosis, and management of patients with chronic cholestatic liver disorders, notably PBC, PSC, and autoimmune cholangiopathy. The authors discuss protein-caloric malnutrition, fat malabsorption, hyperlipidemia (primarily high cholesterol levels), and fat-soluble vitamins deficiency. The authors caution that sodium and water retention and other factors may interfere with an accurate nutritional evaluation in this patient population. However, the nutritional complications of severe and progressive cholestasis should be addressed and treated in a systematic manner in these patients. 5 tables. 8 references.
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Pathology of the Intrahepatic and Extrahepatic Bile Ducts and Gallbladder. IN: Clavien, P.; Baillie, J., eds. Diseases of the Gallbladder and Bile Ducts: Diagnosis and Treatment. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 21-57.
This chapter on pathology is from a textbook that provides a comprehensive and critical approach to both established and new diagnostic and therapeutic modalities for diseases of the gallbladder and bile ducts. The author focuses on the pathology of the intrahepatic and extrahepatic bile ducts and gallbladder. The chapter lists the characteristic morphologic features of primary biliary cirrhosis (PBC), with an emphasis on the florid duct lesion, and describes the histopathologic staging schemes for PBC and primary sclerosing cholangitis (PSC). Other topics include the morphologic features of acute cellular rejection in the hepatic allograft, use of grading schemas for rejection of a transplanted liver, the use of liver biopsy and the characteristic morphologic features of PSC, the secondary causes of sclerosing cholangitis, fibropolycystic diseases of the liver, the anatomic and gross features of cholangiocarcinoma, the staging systems used for gallbladder cancer, and the precursor lesions and etiologic factors in gallbladder cancer. The chapter includes a summary of objectives, a list of suggested readings, extensive references, and a set of self-test questions that focus on the material covered in the chapter. 25 figures. 10 tables. 122 references.
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Pathophysiology of Nonalcoholic Steatohepatitis. Journal of Clinical Gastroenterology. 40(Suppl 1): S17-S29. March 2006.
Nonalcoholic fatty liver disease (NAFLD) affects approximately 17 to 33 percent of adults in the United States and progresses to nonalcoholic steatohepatitis (NASH) in 6 to 17 percent of patients. NASH is the most severe histologic form of NAFLD and progresses to cirrhosis in 20 percent of these patients. This review article covers the pathophysiology of NASH, an important factor in preventing the liver-related deaths that are prevalent in this population. The author notes that non-liver mechanisms are largely responsible for the development of insulin resistance, which causes hepatic steatosis. Once developed, oxidative stress and diminished antioxidants within the liver initiate the progression from steatosis alone to NASH and ultimately to cirrhosis. However, not all patients progress to cirrhosis. The author hypothesizes that, as in other common complex metabolic disease, it is the interaction between the environment and genetics that will determine the phenotypic expression of NAFLD and NASH in each individual patients. Pathophysiologic factors discussed include lifestyle, fat mass, fat distribution, insulin resistance, bacterial overgrowth, and oxidative stress. 12 figures. 6 tables. 229 references.
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Primary Biliary Cirrhosis and Primary Sclerosing Cholangitis. IN: Lichtenstein, G.; Reddy, K.R.; Faust, T., eds. Clinician’s Guide to Liver Disease. Thorofare, NJ: Slack Incorporated. 2006. pp 87-104.
This chapter about primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) is from a user-friendly reference book that provides gastroenterologists with an overview of the management of acute and chronic liver disease. The authors define PBC as a chronic cholestatic, autoimmune liver disease that predominantly affects middle-aged women. Over time, fibrosis, cirrhosis, and complications of portal hypertension and cholestasis may develop in patients with PBC. Ursodeoxycholic acid has been shown to improve cholestatic liver-associated enzymes and to improve transplant-free survival, although the effect is not certain. Liver transplantation is the treatment of choice for patients with advanced PBC. Primary sclerosing cholangitis is a chronic cholestatic liver disease that primary affects young to middle-aged men, who typically have concurrent inflammatory bowel disease (IBD). PSC patients are at risk for bacterial cholangitis, cholangiocarcinoma, and complications of liver failure and cholestasis. Although there is no proven therapy specific for PSC, medical therapies should be directed toward managing the complications of portal hypertension and progressive cholestasis. Liver transplantation is the only option that has been clearly shown to improve patient survival. 5 tables. 20 references.
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Primary Biliary Cirrhosis. IN: Clavien, P.; Baillie, J., eds. Diseases of the Gallbladder and Bile Ducts: Diagnosis and Treatment. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 341-352.
This chapter on primary biliary cirrhosis (PBC) is from a textbook that provides a comprehensive and critical approach to both established and new diagnostic and therapeutic modalities for diseases of the gallbladder and bile ducts. The authors begin with a discussion of nomenclature, noting that health care providers must communicate clearly to patients the discrepancy between the name PBC and a patient’s actual clinical status. PBC is characterized by destruction of the interlobular bile ducts with duct invasion by chronic inflammatory cells and apoptosis of biliary epithelial cells, leading to progressive bile duct loss, fibrosis, and eventual cirrhosis. The authors describe the multifactorial etiology of PBC, the role of genetic factors in its development, the importance of early diagnosis even in asymptomatic patients, and the management of PBC and its complications. They note that no curative medical therapy for PBC exists; however, medications are available that slow down the progression of the disease and can relieve symptoms in the majority of patients. Some patients with PBC will develop end-stage liver failure and require liver transplantation. The chapter includes a summary of objectives, a list of suggested readings, extensive references, and a set of self-test questions that focus on the material covered in the chapter. 2 figures. 4 tables. 63 references.
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Therapy of NAFLD: Insulin Sensitizing Agents. Journal of Clinical Gastroenterology. 40(Suppl 1): S61-S66. March 2006.
Insulin resistance is an integral part of the underlying pathophysiology in most patients with nonalcoholic fatty liver disease (NAFLD), a chronic liver disease that can lead to cirrhosis and liver cancer. This article reviews the current literature on the use of insulin-sensitizing agents in the treatment of patients with NAFLD, particularly in those patients with the more severe form known as nonalcoholic steatohepatitis (NASH). The authors review the use of two major insulin-sensitizing agents: the thiazolidinediones and metformin (the only available biguanide). Thiazolidinedione administration in human NAFLD has been shown to decrease hepatic fat by several different measures and to decrease evidence of cellular injury, but it has also been associated with increased peripheral fat and weight gain. In contrast, metformin has been shown to improve biochemical markers without weight gain, but with more variable improvement in histology. Neither agent has current FDA approval for use in NAFLD, but existing studies provide hope for the benefits of incorporating these medications into NAFLD management strategies in selected patients. In addition, most of the studies do not determine the relative contribution of lifestyle changes compared with drug therapy, which can confound the results. 4 figures. 1 table. 61 references.
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Weight Loss as a Treatment for Nonalcoholic Fatty Liver Disease. Journal of Clinical Gastroenterology. 40(Suppl 1): S39-S43. March 2006.
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease that can lead to cirrhosis and liver cancer (hepatocellular carcinoma). NAFLD has been associated with obesity and other features of the metabolic syndrome, including insulin resistance, impaired glucose tolerance, and dyslipidemia. This article reviews the use of weight loss as a treatment for NAFLD. The author contends that there is very little empiric evidence to support the effectiveness of weight loss as a treatment for NAFLD. The author reviews the current literature on the effects of weight loss achieved through lifestyle modification or medications on NAFLD. Only three published trials (n = 89 subjects), which include a comparison group, have been published. These studies suggest that weight loss does result in improvement in liver enzymes or hepatic pathology, however, direct between-group comparisons are lacking. In addition, four small, nonrandomized studies (n = 59 subjects) have evaluated the effect of weight loss achieved with medications (orlistat and sibutramine) on NAFLD. These also suggest some improvement in liver enzymes and histopathology. A brief review of observational studies on the association between NAFLD pathology or liver enzymes and diet composition suggests a possible role for the manipulation of macronutrients or micronutrients in NAFLD treatment. The author concludes by calling for rigorously conducted, randomized controlled trials in this area. 2 tables. 49 references.
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Evaluation of the Patient for Liver Transplantation. Hepatology. 41(6): 1-26. June 2005.
Liver transplantation is the most effective treatment for many patients with acute or chronic liver failure resulting from a variety of causes. This article presents the practice guideline from the American Association for the Study of Liver Diseases (AASLD) on the evaluation of patients for liver transplantation. These recommendations are based on a formal review and analysis of the published literature on the topic; several consensus conferences among experts; the American College of Physicians' Manual for Assessing Health Practices and Designing Practice Guidelines; guideline policies produced by professional organizations, including the AASLD and the American Gastroenterological Association; and the authors’ experience in the specified topic. Topics include the indications of liver transplantation, when evaluation for transplantation should be considered, determining the need for liver transplantation, and recipient evaluation at the transplant center. The article offers recommendations for patients with the hepatopulmonary syndrome, portopulmonary hypertension, obesity, cigarette smoking, kidney failure, extrahepatic malignancies, osteoporosis, HIV infection, surgical contraindications, and psychosocial problems. The authors discuss specific indications for liver transplantation, including chronic noncholestatic liver disorders, chronic hepatitis C, chronic hepatitis B, autoimmune hepatitis, alcoholic cirrhosis, cholestatic liver disorders, primary biliary cirrhosis, primary sclerosing cholangitis, childhood cholestatic diseases, metabolic diseases, alpha-1-antitrypsin disease, Wilson disease, nonalcoholic steatohepatitis and cryptogenic cirrhosis, hereditary hemochromatosis, neonatal hemochromatosis, tyrosinemia and glycogen storage disease, metabolic diseases with severe extrahepatic manifestations, amyloidosis and hyperoxaluria, urea cycle and branched-chain amino acid disorders, hepatic malignancies, hepatocellular carcinoma, hepatoblastoma, fibrolamellar hepatocellular carcinoma and hemangioendothelioma, cholangiocarcinoma, and fulminant hepatic failure. The article includes 76 specific recommendations for the evaluation of the patient for liver transplantation. 3 tables. 328 references.
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Hepatitis and Liver Disease in the United States. New York, NY: American Liver Foundation. 2p.
This fact sheet offers basic information and statistics about hepatitis and liver disease in the United States. Twenty-five million Americans, or one in every 10, are or have been afflicted with a liver, biliary, or gallbladder disease. Alcoholic liver disease and chronic hepatitis C are the leading causes of cirrhosis (scarring of the liver that reduces or prevents proper functioning of the organ). The Centers for Disease Control and Prevention (CDC) estimate that the number of annual deaths from hepatitis C will triple in the next 10 to 20 years. Data for hepatitis B show that 78,000 people are infected with the virus each year; 1.25 million people are chronically infected. The estimated medical and work loss cost per year for hepatitis B is over $700 million' for hepatitis C it is over $600 million. Approximately 5,600 liver transplants were performed in 2003; however, because of the organ shortage, it is estimated that over 1,800 people died that year while waiting for a liver transplant. There are currently 17,700 people waiting for a liver transplant. The fact sheet concludes with listing the risk factors for hepatitis B and those for hepatitis C. A brief description of the American Liver Foundation (ALF) is also provided, along with the Foundation's contact information.
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Primary Biliary Cirrhosis. New England Journal of Medicine. 353(12): 1261-1273. September 22, 2005.
This article reviews advances in primary biliary cirrhosis (PBC), a slowly progressive, autoimmune disease of the liver that primarily affects women. The authors review the typical clinical findings in PBC, pathological findings, natural history and prognosis, causes, environmental factors, autoimmune responses, treatment of symptoms and complications, treatment of underlying disease, and ideas for future research. Common complications of PBC include pruritus, osteoporosis, hyperlipidemia, and portal hypertension. Treatment strategies reviewed include ursodeoxycholic acid (UDCA), colchicines and methotrexate, other drug therapies, and orthotopic liver transplantation. 4 figures. 2 tables. 98 references.
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Risk Factors and Comorbidities in Primary Biliary Cirrhosis: A Controlled Interview-Based Study of 1032 Patients. Hepatology. 42(5): 1194-1202. November 2005.
This article reports on a study of risk factors and comorbidities in primary biliary cirrhosis (PBC), an autoimmune disease of unknown etiology. The authors included patients with PBC (n =1,032) from 23 referral centers for liver diseases in the United States as well as random-dialed controls (n = 1,041) matched for sex, age, race, and geographical location. Data gathered showed that increased risk of PBC was associated with having a first-degree relative with PBC, a history of urinary tract infections, past smoking, or use of hormone replacement therapies. The frequent use of nail polish slightly increased the risk of having PBC. Other autoimmune diseases, including systemic lupus erythematosus, were found in 32 percent of cases and 13 percent of controls. This study did not confirm other previous reports, such as the increased prevalence of breast cancer in women with PBC. 1 figure. 6 tables. 38 references.
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Treatment for Hepatitis C. VetHep Update. 6: 3. Spring 2005.
This brief newsletter article describes the current recommended treatments for hepatitis C. The author notes that treatment is most often recommended for patients who have a greater risk of progressing to cirrhosis (scarring) of the liver. However, it can be difficult to determine which patients are most likely to have progressive liver disease. The most widely used treatment for hepatitis C is the combination of two medications: pegylated interferon, injected once a week, and ribavirin, taken in pill form twice a day. Treatment can last 6 to 12 months and is considered successful when the virus cannot be detected in the body, six months after the medication has been completed. The article outlines the six main phenotypes of hepatitis C virus (HCV). The article concludes with a list of tips for patients to maximize their chances of having a successful treatment. Readers are referred to the American Liver Foundation (800–465–4837) for more information.
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What I Need to Know About Cirrhosis of the Liver. Bethesda, MD: National Digestive Diseases Information Clearinghouse, 2005. 16 p.
Cirrhosis is scarring of the liver that happens because of injury or long-term disease. In cirrhosis, scar tissue replaces healthy tissue, but scar tissue cannot do what healthy liver tissue does: make protein, help fight infections, clean the blood, help digest food, and store energy. This brochure explains cirrhosis, its causes, and how it can be managed. Written in nontechnical language, the brochure covers a definition of liver cirrhosis, the typical symptoms of cirrhosis, the risk factors and causes of cirrhosis, how to know when to consult a health care provider, diagnostic tests to confirm the condition or determine the cause of the problem, treatment options, how to prevent cirrhosis in people who already have liver disease, and how to prevent cirrhosis from worsening. The booklet includes a list of resources where readers can get more information, and a list of acknowledgements. A final section briefly describes the goals and work of the National Digestive Diseases Information Clearinghouse (NDDIC). The brochure is illustrated with line drawings designed to clarify the concepts discussed in the text. 3 figures.
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Autoimmune Liver Disease. IN: U.S. Department of Health and Human Services. Action Plan for Liver Disease Research. Bethesda, MD: National Digestive Diseases Information Clearinghouse. 2004. pp. 95-100.
Autoimmune liver disease occurs when the body reacts inappropriately to its own cellular components. Autoimmune liver diseases include autoimmune hepatitis, primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC). All three of these diseases can be severe, progressive, and can lead to cirrhosis and death from end-stage liver disease. This chapter on autoimmune liver disease is from the Action Plan for Liver Disease Research that was developed to advance research on liver and biliary diseases. The Action Plan was undertaken to identify areas of scientific opportunity to help direct research resources at the National Institutes of Health (NIH) toward practical goals in the prevention, diagnosis, and management of liver and biliary diseases. In this chapter, the authors first review the symptoms, etiology, complications, and mechanisms of injury of autoimmune liver disease, then outline recent research advances in the areas of understanding general autoimmunity, causes of autoimmune liver disease, and therapies for autoimmune liver disease. The authors then provide specific research goals in the areas of basic research on pathogenesis, as well as clinical studies of pathogenesis, etiology, and therapy. A final section considers the steps that would assist in achieving these research goals. One chart summarizes the short (0 to 3 years), intermediate (4 to 6 years), and long-term (7 to 10 years) goals of research on these topics. 3 figures. 1 table.
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Complications of Liver Disease. IN: U.S. Department of Health and Human Services. Action Plan for Liver Disease Research. Bethesda, MD: National Digestive Diseases Information Clearinghouse. 2004. pp. 129-136.
Chronic liver disease and cirrhosis account for approximately 27,000 deaths in the United States each year. The majority of patients who die of cirrhosis succumb ultimately to a complication of portal hypertension, such as variceal hemorrhage, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatopulmonary syndrome, or hepatorenal syndrome. These complications are also the most common proximal causes of death in patients awaiting liver transplantation. This chapter on the complications of liver disease is from the Action Plan for Liver Disease Research that was developed to advance research on liver and biliary diseases. The Action Plan was undertaken to identify areas of scientific opportunity to help direct research resources at the National Institutes of Health (NIH) toward practical goals in the prevention, diagnosis, and management of liver and biliary diseases. In this chapter, the authors first review the types of complications that patients with chronic liver disease encounter, including portal hypertension, ascites, esophageal varices, and kidney and pulmonary complications. Other complications of liver disease include symptoms such as fatigue, weakness, jaundice, and pruritus (itching). The chapter then outlines recent research advances in the areas of portal hypertension, the complications of portal hypertension, and the complications of cirrhosis. The authors provide specific research goals in these same areas, also focusing on patient care management and the prevention and therapy of acute liver failure. A final section considers the steps that would assist in achieving these research goals. One chart summarizes the short (0 to 3 years), intermediate (4 to 6 years), and long-term (7 to 10 years) goals of research on these topics. 1 figure. 1 table.
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Hepatitis Alert: The Low-Down from A to E. Digestive Health and Nutrition. p. 19-21. March/April 2004.
Hepatitis (liver inflammation) is spreading and its death toll is rising; the debilitating liver infection causes approximately 15,000 deaths every year in the United States. Most often caused by one of five hepatitis viruses (hepatitis A through E), the infection results in inflammation of the liver that can become severe enough to cause cirrhosis (scarring) of the liver, liver cancer, liver failure, or death. This article reviews each of the five most common types of hepatitis, focusing on etiology, transmission, epidemiology, symptoms, prevention, and treatment for each. The author stresses that all types of hepatitis are preventable. Hepatitis A, B, and D can be avoided through the vaccine Twinrix, which was recently approved by the Food and Drug Administration (FDA) for people over age 18. Vaccination against hepatitis C is not yet available, but one can protect against this infection by practicing safe sex and not sharing needles or personal hygiene items. The provision of clean water supplies and prudent hygiene practices when traveling to other countries can protect against hepatitis E. One sidebar defines the risk factors for the main types of hepatitis. 2 figures. 4 references.
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Hepatobiliary Disease in Type 2 Diabetes Mellitus. Annals of Internal Medicine. 141(12): 946-956. December 2004.
Liver disease is one of the leading causes of death in people with type 2 diabetes. This narrative review article discusses the spectrum of liver disease in type 2 diabetes, including nonalcoholic fatty liver disease, cirrhosis, hepatocellular carcinoma, hepatitis C, acute liver failure, and cholelithiasis. The authors also review the hepatotoxicity of antihyperglycemic medications and the treatment of diabetes in patients with liver disease. The article begins with a review of the metabolic effects of type 2 diabetes on the liver, including that of carbohydrate metabolism and lipid (fats) metabolism. The authors note that nonalcoholic fatty liver disease is now considered part of the metabolic syndrome and, with alcohol and hepatitis C, is the most common cause of chronic liver disease in the United States. Weight reduction and exercise are the basics of treatment for nonalcoholic fatty liver disease, but there are also promising results with the new thiazolidinediones (pioglitazone and rosiglitazone) as well as with metformin. In population studies, insulin use predisposes to the development of cirrhosis and hepatocellular carcinoma, but these disorders have not increased in clinical trials. In addition, patients with cirrhosis frequently need insulin treatment for metabolic control. The authors conclude that the presence of liver disease complicates the treatment of diabetes. 4 figures. 2 tables. References.
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Management of Adult Patients With Ascites Due to Cirrhosis. Hepatology. 39(3): 1-16. March 2004.
This article presents the practice guideline from the American Association for the Study of Liver Diseases (AASLD) on the management of adult patients with ascites due to cirrhosis. These recommendations are based on a formal review and analysis of the published literature on the topic; several consensus conferences among experts; the American College of Physicians' Manual for Assessing Health Practices and Designing Practice Guidelines; guideline policies produced by professional organizations, including the AASLD and the American Gastroenterological Association; and the authors’ experience in the specified topic. Ascites, the development of fluid retention, is the most common of the three major complications of cirrhosis; the other complications are hepatic encephalopathy and variceal hemorrhage. Topics include evaluation and diagnosis of cirrhosis and ascites, ascitic fluid analysis, differential diagnosis, treatment of ascites, managing refractory ascites, hepatorenal syndrome, spontaneous bacterial peritonitis (SBP), and the prevention of SBP. The article includes 27 specific recommendations for the management of the patient with ascites. 5 tables. 110 references.
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Screening for Hepatitis C Virus Infection in Adults: Recommendation Statement. Annals of Internal Medicine. 140(6): 462-464. March 2004.
This article summarizes the U.S. Preventive Services Task Force (USPSTF) recommendations on screening for hepatitis C virus (HCV) infection. These recommendations are based on the USPSTF's examination of evidence specific to asymptomatic persons for HCV testing and treatment. The complete information on which this summary is based, including evidence tables and references, is available in the accompanying article in this same issue, and in the summary of the evidence and systematic evidence review on this topic. These materials are also available on the USPSTF web site (www.preventiveservices.ahrq.gov). The USPSTF recommends against routine screening for HCV infection in asymptomatic adults who are not at increased risk (general population) for infection. The prevalence of HCV infection in the general population is low, and most who are infected do not develop cirrhosis (liver scarring) or other major negative health outcomes. There is no evidence that screening for HCV infection leads to improved long term health outcomes, such as decreased cirrhosis, hepatocellular cancer, or mortality. The current treatment regimen is long and costly and is associated with a high patient dropout rate due to adverse effects. 3 references.
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Screening for Hepatitis C Virus Infection: Recommendation from the U.S. Preventive Services Task Force. Annals of Internal Medicine. 140(6): I-62. March 2004.
This article summarizes for patients and lay readers the U.S. Preventive Services Task Force (USPSTF) recommendations on screening for hepatitis C virus (HCV) infection. These recommendations are based on the USPSTF's examination of evidence specific to asymptomatic persons for HCV testing and treatment. The complete information on which this summary is based, including evidence tables and references, is available in the accompanying article in this same issue, and in the summary of the evidence and systematic evidence review on this topic. These materials are also available on the USPSTF web site (www.preventiveservices.ahrq.gov). The USPSTF recommends against routine screening for HCV infection in asymptomatic adults who are not at increased risk (general population) for infection. The prevalence of HCV infection in the general population is low, and most who are infected do not develop cirrhosis (liver scarring) or other major negative health outcomes. There is no evidence that screening for HCV infection leads to improved long term health outcomes, such as decreased cirrhosis, hepatocellular cancer, or mortality. The current treatment regimen is long and costly and is associated with a high patient dropout rate due to adverse effects.
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Update on Current Standards of Care in the Diagnosis and Management of Non-Alcoholic Fatty Liver Disease (NAFLD) and Non-Alcoholic Steatohepatis (NASH): Diagnosis: Part 1. Practical Gastroenterology. 28(9): 70-88. September 2004.
Steatosis (fatty infiltration of the liver) also called non-alcoholic fatty liver disease (NAFLD), is increasingly recognized as a common cause of chronic liver disease. This disease ranges from the presence of fatty liver without inflammation to steatosis accompanied by inflammation and fibrosis. NAFLD is associated with obesity, hypertension (high blood pressure), hyperlipidemia (increased levels of blood fats), diabetes mellitus, and insulin resistance. These disorders are collectively known as the Metabolic Syndrome. This article reviews recommendations and the standard of care for the medical treatment of patients with NAFLD. The authors note that NAFLD is progressive and may lead to non-alcoholic steatohepatitis (NASH). NASH can, in turn, lead to cirrhosis (liver scarring) and end stage liver disease ultimately requiring liver transplantation. The authors review diagnostic tests, including liver chemistries, imaging studies, and the role of liver biopsy. NASH can be silent without any physical symptoms or lab abnormalities and may be associated with end stage 'cryptogenic' cirrhosis as well as hepatic (liver) cancer. For that reason, physicians must be alert in recognizing the clinical features of NASH so that earlier diagnosis, treatment, or at least monitoring, can be provided. The authors note that there is still no evidence-based definitive medical treatment of NASH. 5 tables. 125 references.
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