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Wilson Disease. Bethesda, MD: National Digestive Diseases Information Clearinghouse. 2008. 6 p.
Wilson disease is a genetic disorder that prevents the body from getting rid of extra copper. In this disorder, copper builds up in the liver, brain, eyes, and other organs and can cause life-threatening organ damage. This fact sheet, written in a question-and-answer format, provides basic information about Wilson disease. Topics include who gets Wilson disease, the causes of the disease, the signs and symptoms, diagnostic tests that can be used to confirm the presence of Wilson disease, who should be screened for Wilson disease, and treatment approaches. Wilson disease usually first attacks the liver, the central nervous system, or both. Symptoms can include swelling of the liver or spleen, jaundice, fluid buildup in the legs or abdomen, a tendency to bruise easily, and fatigue. Kayser-Fleischer rings result from a buildup of copper in the eyes and are the most unique sign of Wilson disease; they appear in each eye as a rusty-brown ring around the edge of the iris and in the rim of the cornea. Anyone with unexplained liver disease or neurologic symptoms with evidence of liver disease should be screened for Wilson disease. Wilson disease requires lifelong treatment to reduce and control the amount of copper in the body. However, if the disorder is detected early and treated effectively, people with Wilson disease can enjoy good health. The fact sheet concludes with a brief report of recent research in this area, a list of two organizations that can provide additional information, and the contact information and summary of the activities of the National Digestive Diseases Information Clearinghouse (NDDIC).
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Basic Research on Model Systems: Essential to Understanding the Causes And Treatments For Wilson's Disease And Disorders of Copper Metabolism. Copper Connection. p 10-11. September 2007.
This article, from a newsletter of the Wilson’s Disease Association, helps readers understand the basic physiology that underlies Wilson’s disease (WD) and other disorders of copper metabolism. The authors explain the reductionist approach to research, the use of model experimental systems such as microbes and mice to study copper homeostasis, other research model systems that are used for studies of Wilson’s disease, and the role of biochemistry. The authors note that using model systems such as the laboratory mouse, the zebrafish, and fruit flies has enabled the identification of genes and their encoded proteins that underlie Wilson’s disease and related disorders. These same model systems may be used to test the effectiveness of new drugs to treat Wilson’s disease or to uncover potential adverse effects of long-term treatment.
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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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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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Old School in Old Europe? D-Penicillamine Remains Important For the Treatment of Wilson's Disease. Copper Connection. p 8-9. September 2007.
This article, from a newsletter of the Wilson’s Disease Association, reports on the use of D-penicillamine to treat Wilson’s disease (WD). The authors first remind readers of the difficulties often encountered in the diagnosis of WD and then describe the initial approach to medical management, which should involve chelating agents such as D-penicillamine or Trientine. The article addresses concerns about the side effects of D-penicillamine, which include hypersensitivity reactions, particularly in the early treatment phase. Although Trientine is considered a gentler treatment option than D-penicillamine, the latter is still used widely throughout Europe. The authors report on the idiosyncrasies of the health insurance system in Germany that only pays for D-penicillamine, not Trientine, for this indication. The article concludes by encouraging patients to utilize support groups for information and comfort when dealing with this lifelong disease.
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Diagnosing and Misdiagnosing Patients with Hepatic Wilson's Disease. Copper Connection. p. 5. June 2006.
This brief newsletter article reports on the continuing difficulties of diagnosis for patients with hepatic Wilson’s disease (HWD). The author notes that the first barrier to diagnosis is failure to consider HWD in the differential diagnosis because it is rare. Misinformation about HWD may limit diagnostic testing and result in failure to diagnose. The author recommends testing for serum copper, serum ceruloplasmin, and 24 hour urine for total copper. Slip lamp evaluation for Kayser-Fleischer rings of the cornea is helpful when positive, but they are less often present in HWD, compared to their uniform presence in WD with neurological symptoms. Another barrier to an accurate diagnosis is a lack of familiarity with the spectrum of presentations of HWD and the wide age range of afflicted patients. The author provides guidelines for the testing of adults suspected of HWD, including the use of liver biopsy. 1 figure.
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Liver Biopsies in the Treatment of Wilson’s Disease. Copper Connection. p 7. March 2006.
This brief newsletter article considers the role of liver biopsies in the treatment of Wilson's disease, a condition characterized by copper accumulation in the body. Liver biopsies can provide information about the amount of copper in the liver, if the samples are properly collected and analyzed. The biopsy can also provide a snapshot of the extent of scar tissue and inflammation in the liver. The author outlines the use and indications of liver biopsy, situations where repeated biopsies may not be recommended, and the possibility of a secondary illness that may cause liver damage. A final section reminds readers that zinc acetate is the only form of zinc salt approved by the United States FDA for use in the treatment of Wilson's disease.
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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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Metabolic Liver Disease. IN: Lichtenstein, G.; Reddy, K.R.; Faust, T., eds. Clinician’s Guide to Liver Disease. Thorofare, NJ: Slack Incorporated. 2006. pp 139-160.
This chapter about metabolic liver disease is from a user-friendly reference book that provides gastroenterologists with an overview of the management of acute and chronic liver disease. The author notes that the metabolic liver diseases comprise a varied group of disorders, with differing modes of onset and clinical presentations. Most of these disorders are seen primarily in children. However, improved management has led to a greater longevity in those affected, with the patients making a transition to adult care with a gastroenterologist. The author’s discussion focuses on some of the more important disorders encountered in adult clinical practice, namely derangements of metal metabolism and the relatively uncommon disorder of alpha-1 antitrypsin deficiency. Disorders of metal metabolism covered include iron overload syndromes, hereditary hemochromatosis, Wilson disease, and Menke’s disease. The chapter includes patient care algorithms for Wilson disease and hereditary hemochromatosis. 2 figures. 1 table. 37 references.
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Monitoring People Taking Trientine and Zinc Acetate. Copper Connection. p 5. March 2006.
This brief newsletter article discusses the importance of monitoring people with Wilson's disease (a genetic disorder characterized by copper accumulation) who are taking Trientine and zinc acetate. This drug combination attacks copper on two fronts, lowering copper by raising the amount eliminated through the urine and blocking absorption of dietary copper through the gut. The author stresses that these two drugs need to be ingested at different times, as taking them together may lead to interactions in the stomach. Since both drugs need to be taken separately from food, this can lead to a challenging schedule for patients taking medications and eating carefully to be sure the drugs are given the opportunity to rid the body of the toxic copper. Monitoring for effectiveness of copper reduction involves carefully interpreting serum copper, ceruloplasmin, and twenty-four hour urinary copper and zinc levels. During initial therapy, testing should be performed at least once a year. Combination therapy is not used for maintenance treatment outside the period of initial diagnosis.
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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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Diagnosis and Current Therapy of Wilson's Disease. Alimentary Pharmacology and Therapeutics. 19(2): 157-165. January 2004.
Wilson's disease is an autosomal recessive inherited disorder of liver (hepatic) copper metabolism resulting in liver disease and or neuropsychiatric disease. This article reviews the diagnosis and current therapeutic recommendations for Wilson's disease. The diagnosis of neurological disease is straightforward if the following symptoms are present: Kayser-Fleischer rings, typical neurological symptoms, and low serum ceruloplasmin levels. The diagnosis is more complex in patients presenting with liver diseases. None of the commonly used parameters alone allows a diagnosis with certainty. A combination of various laboratory parameters is needed to firmly establish the diagnosis. Recently, a group of international experts has proposed a score based on a variety of tests and clinical symptoms. The validity of this score needs to be assessed prospectively. Treatment of Wilson's disease requires life-long administration of copper chelators (D-penicillamine, trientine, zinc). None of these treatments has been tested by prospective randomized controlled studies. Liver transplantation is reserved for severe or treatment-resistant cases with advanced liver disease, whilst experience with refractory neuropsychiatric disease is limited. 3 figures. 1 table. 57 references.
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Genetic 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. 109-118.
Genetic liver diseases include hereditary hemochromatosis, Wilson disease, the porphyries, cystic fibrosis, polycystic liver disease, alpha-1 antitrypsin deficiency, hereditary tyrosinemia, Alagille syndrome, and several neonatal cholestatic syndromes and inherited diseases of metabolism. This chapter on genetic 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, complications, etiology, and mechanisms of injury of genetic liver diseases that tend to present in adolescence or adulthood: hemochromatosis, Wilson disease, the porphyries, cystic fibrosis, polycystic liver disease, and congenital hepatic fibrosis. The chapter then outlines recent research advances in the areas of pathogenesis, diagnosis, monitoring, and therapy of these genetic liver diseases. The authors provide specific research goals for these same diseases. A final section considers the steps that would assist in achieving these research goals, noting that a major opportunity to help advance research in each of these genetic liver diseases is the pursuit of molecular diagnosis and studies of genotype-phenotype comparisons. 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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Pediatric 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. 101-109.
Pediatric liver diseases include biliary atresia, metabolic disorders, intrahepatic cholestatic disorders, alpha-1 antitrypsin deficiency liver disease, nonalcoholic steatohepatitis (NASH), autoimmune hepatitis, sclerosing cholangitis, parenteral nutrition-induced liver injury, drug-induced liver injury, Wilson disease, cystic fibrosis, and various forms of viral hepatitis. Although liver disease is uncommon in children, those liver diseases that occur tend to be severe and progressive. This chapter on pediatric 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 liver disease that occur in children and their symptoms, complications, etiology, and mechanisms of injury, then outline recent research advances in the areas of pathogenesis, and prevention and therapy. The authors then provide specific research goals in the areas of pathogenesis and management of biliary atresia, the molecular pathogenesis and treatment of neonatal cholestatic syndromes, the characterization and treatment of pediatric liver diseases beyond the neonatal period, and the optimization of liver transplantation in children. 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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Liver Transplantation for Hepatic and Neurological Wilson's Disease. Transplantation Proceedings. 35(4): 1445-1446. June 2003.
Wilson's disease (WD) is an autosomal recessive inherited disorder of copper metabolism characterized by excessive deposition of copper throughout the body. If medical treatment fails in cases of fulminant hepatic (liver) failure and progressive hepatic dysfunction due to advanced cirrhosis, liver transplantation (OLTx) has been demonstrated to be a valuable treatment option. This article reports on a subset from a series of 225 OLTxs in 198 patients that were performed in the authors' institution between 1993 and 2002. In this consecutive series, six patients ( 3 female, 3 male) were liver grafted for WD. The follow up ranged from 3 to 7 years. All patients are alive with well-functioning grafts at present. The ceruloplasmin levels increased after transplantation and remained normal. The Kayser-Fleischer ring disappeared in all patients, and urinary copper excretion normalized. The neurological manifestations in the 2 patients with severe neurological symptoms showed after 2 to 5 years a downward tendency; in one, the ataxic movements disappeared completely. The psychiatric disorder in one patient disappeared as did the mild neurological symptoms in the patient with CHILD A cirrhosis. These two patients are fully recovered and returned to work. The authors conclude that OLTx should be considered as a treatment option in patients with severe progressive neurological deficits, even in cases with stable liver function, since early liver grafting definitely cures the underlying biochemical defect. In such cases an early decision for liver transplantation is justified because neurological deficits may become irreversible. 4 references.
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Metabolic Diseases of the Liver. In: Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 2397-2415.
Hepatic (liver) involvement is a common feature in inborn errors of metabolism that are manifest in childhood and in adult life. In many of the genetic disorders affecting the liver, an environmental exposure to the specific substrate or toxin (galactose, fructose, copper, protein load) are important modifiers of the onset and severity of the disease phenotype. This chapter on metabolic diseases of the liver is from a comprehensive gastroenterology textbook that provides an encyclopedic discussion of virtually all the disease states encountered in a gastroenterology practice. In this chapter, the author discusses Wilson's disease, Reye's syndrome, alpha-1 antitrypsin deficiency, porphyria, and metabolic diseases of the neonate and of childhood. For each section, the author covers presentation, liver histology, genetics, pathogenesis and biochemistry, diagnostic criteria and tests, and treatment strategies. The chapter is illustrated with black-and-white graphs and drawings. 4 tables. 172 references.
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Practice Guideline on Wilson Disease Hepatology. 37(6): 1475-1492. June 2003.
Wilson's disease is a familial neurologic disease characterized by the accumulation of copper in the organs, including in the corneas. This article presents the practice guideline from the American Association for the Study of Liver Diseases (AASLD) on the management of patients with Wilson's disease. 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 experience of the authors in the specified topic. Wilson's disease was one of the first liver diseases for which effective drug treatment was identified. Topics in the practice guideline include clinical features, including hepatic, neurologic, and psychiatric symptoms; diagnostic testing, including biochemical liver tests, ceruloplasmin, uric acid, serum copper, urinary copper excretion, hepatic parenchymal copper concentration, radiocopper study, liver biopsy, radiologic imaging of the brain, and genetic studies; diagnostic considerations in specific target populations, including patients with fulminant liver disease; treatment approaches, including D-penicillamine, trientine, zinc, antioxidants, and diet; and treatment targets and monitoring of treatment. The article includes 20 specific recommendations for the management of the patient with Wilson's disease. 3 tables. 208 references.
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Acute Liver Failure. In: Sherlock, S.; Dooley, J. Diseases of the Liver and Biliary System. Malden, MA: Blackwell Science, Inc. 2002. p.111-126.
Acute liver failure describes the clinical syndrome of severe impairment of liver function (encephalopathy, coagulopathy and jaundice) within 6 months of the onset of symptoms. Although usually due to an acute insult (most frequently virus or drug) in a previously healthy person, acute liver failure may be the presenting feature of chronic liver disease, in particularly Wilson's disease, autoimmune chronic hepatitis, or delta superinfection in a patient with chronic hepatitis B. This chapter on acute liver failure is from a textbook that presents a comprehensive and up-to-date account of diseases of the liver and biliary system. Topics include a definition, causes, clinical features, investigations, associations, prognosis, and treatment. The authors conclude that liver transplantation cannot be accepted as the perfect and ideal treatment for fulminant hepatic failure, but it gives survival to many patients who otherwise would have died. Early referral of patients to a specialist center is crucial. 6 figures. 11 tables. 93 references.
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Cirrhosis of the Liver [Cirrosis del Higado]. Bethesda, MD: National Digestive Diseases Information Clearinghouse (NDDIC), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health. 2002. 3 p.
This fact sheet discusses cirrhosis of the liver, the eighth leading cause of death by disease. In the United States, chronic alcoholism and hepatitis C are the most common causes of cirrhosis. Other causes include chronic hepatitis B and D, autoimmune hepatitis, and a number of inherited diseases, including Alpha-1 antitrypsin deficiency, hemochromatosis, and Wilson's disease. The fact sheet covers topics including prevalence; causes; signs and symptoms; complications, diagnosis (including blood tests, liver scans, liver biopsy and laparoscopy); and treatment (including diet and drug therapies). A brief list of additional resources is included.
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Diseases of the Liver and Biliary System, Eleventh Edition. Malden, MA: Blackwell Science, Inc. 2002. 706 p.
Designed to serve practicing physicians, surgeons and pathologists, as well as clinical students, this textbook presents a comprehensive and up-to-date account of diseases of the liver and biliary system. The text offers 38 chapters: anatomy and function; the assessment of liver function; biopsy of the liver; the hematology of liver disease; ultrasound, computed tomography (CT scan) and magnetic resonance imaging (MRI); hepatocellular failure; hepatic encephalopathy; acute liver failure; ascites (fluid accumulation); the portal venous system and portal hypertension; the hepatic artery and hepatic vein, and the liver in circulatory failure; jaundice; cholestasis; primary biliary cirrhosis (PBC); sclerosing cholangitis; viral hepatitis, including general features, hepatitis A, hepatitis E, and other viruses; hepatitis B virus and hepatitis Delta virus; hepatitis C virus; chronic hepatitis, its general features and autoimmune chronic disease; drugs and the liver; hepatic cirrhosis (scarring); alcohol and the liver; iron overload states; Wilson's disease; nutritional and metabolic liver diseases; the liver in infancy and childhood; the liver in pregnancy; the liver is systemic disease, granulomas, and hepatic trauma; the liver in infections; nodules and benign liver lesions; malignant liver tumors; the role of interventional radiology and endoscopy in imaging of the biliary tract; cysts and congenital biliary abnormalities; gallstones and inflammatory gallbladder diseases; benign stricture of the bile ducts; diseases of the ampulla of Vater and the pancreas; tumors of the gallbladder and bile ducts; and hepatic transplantation. The text includes full-color and black-and-white illustrations and photographs. A detailed subject index concludes the volume.
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Pregnancy-Related Hepatic and Gastrointestinal Disorders. In: Feldman, M.; Friedman, L.S.; Sleisenger, M.H. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 2002. p. 1448-1461.
Pregnancy is a state of altered, but normal, physiologic processes. Gastroenterologists and internists often are not well versed in the physiologic characteristics of pregnancy and may be uneasy when confronted with a pregnant patient who has a gastrointestinal or liver (hepatic) disorder. This chapter on pregnancy-related hepatic and gastrointestinal disorders is from a comprehensive and authoritative textbook that covers disorders of the gastrointestinal tract, biliary tree, pancreas, and liver, as well as the related topics of nutrition and peritoneal disorders. Topics include cholestasis of pregnancy; liver disease of preeclampsia; hemolysis, elevated liver enzymes, and low platelets syndrome; hepatic rupture, hematoma, and infarct; acute fatty liver of pregnancy; liver disorders complicating pregnancy, including viral hepatitis, portal hypertension caused by chronic liver disease, Wilson disease, autoimmune liver disease, hepatic neoplasia (liver cancer), Budd-Chiari syndrome, and liver transplant recipients; and gastrointestinal disorders complicating pregnancy, including nausea and vomiting of pregnancy, hyperemesis gravidarum, gastroesophageal reflux disease, constipation and diarrhea, hemorrhoidal disease, gallstone disease, pancreatitis, and inflammatory bowel disease (IBD). The chapter includes a mini-outline with page citations, full-color illustrations, and extensive references. 3 figures. 1 table. 172 references.
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Rare Case of Ulcerative Colitis Complicating Wilson's Disease: Possible Association Between the Two Diseases. Journal of Clinical Gastroenterology. 35(1): 43-45. July 2002.
This article describes a rare case of ulcerative colitis (UC, a type of inflammatory bowel disease, or IBD) complicated by Wilson's disease. Wilson's disease is a genetic disorder in which failure of copper excretion causes accumulation of copper in the liver and other organs. In this case, a 24 year old Japanese man, UC occurred 12 years after the diagnosis of Wilson's disease, and the colitis was intractable to prednisolone and salazosulfapyridine. Because copper is one of the trace elements necessary for antioxidant defenses during the inflammatory process, altered copper metabolism may have contributed to the intractability of the UC in this case. 2 figures. 31 references.
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What You Should Know About Wilson's Disease. Brookfield, CT: Wilson's Disease Association. 2002. 2 p.
This brochure familiarizes readers with Wilson's disease, a genetic disorder that is fatal unless detected and treated before serious illness develops from copper poisoning. Copper is present in most foods and most people get much more than they need; healthy people excrete copper they don't need, but people with Wilson's disease cannot. The brochure describes the symptoms of Wilson's disease, the complications it can cause, how the disease is diagnosed, the genetics involved in Wilson's disease, and treatment options. The brochure includes the address and telephone number of the Wilson's Disease Association.
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Wilson Disease. In: Feldman, M.; Friedman, L.S.; Sleisenger, M.H. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 2002. p. 1269-1277.
Copper, a component of several essential enzymes, is toxic to tissues when present in excess. Dietary intake of copper generally exceeds the trace amount required, and mechanisms to control the influx and efflux from cells must maintain an appropriate balance. Wilson disease is an autosomal recessive disorder of copper overload in which inadequate biliary copper excretion leads to cooper accumulation in the liver, brain, kidney, and cornea. This chapter on Wilson disease is from a comprehensive and authoritative textbook that covers disorders of the gastrointestinal tract, biliary tree, pancreas, and liver, as well as the related topics of nutrition and peritoneal disorders. Topics include the copper pathway in the body, the basic molecular defect in Wilson disease, clinical features (hepatic, neurologic, psychiatric, ocular signs, and involvement of other systems), pathology, diagnosis, treatment, and prognosis. Patients with Wilson disease are generally regarded as having a good prognosis if the disease is diagnosed promptly and treated consistently. The chapter includes a mini-outline with page citations, full-color illustrations, and extensive references. 3 figures. 2 tables. 49 references.
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Wilson Disease. In: Complete Directory for Pediatric Disorders. Millerton, NY: Grey House Publishing, Inc. 2002. p. 827-829.
This entry, from a directory of pediatric disorders, describes Wilson disease, a genetic disorder in which a defect in copper metabolism causes an abnormal accumulation of copper in the liver, brain, kidneys, corneas, and other tissues of the body. The entry describes the symptoms, pathology, genetics, and treatment of Wilson disease. The disorder is often characterized by progressive liver disease, degenerative changes of the brain, kidney failure, and the presence of characteristic rings at the outer margins of the corneas (Kayser-Fleischer rings). Wilson disease is a progressive disorder in which the age at onset may vary from patient to patient (some beginning in early childhood, more commonly beginning in mid-adolescence). The treatment of individuals with Wilson disease often consists of administration of penicillamine, a medication that binds with copper and enables it to be excreted from the body. The treatment is accompanied by supplementation of vitamin B6. The entry concludes with a reference to organizations that may be helpful (listed in the General Resources Section of the book), the addresses of related websites, national associations and support groups, and the citations for related printed materials.
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Wilson's Disease. In: Sherlock, S.; Dooley, J. Diseases of the Liver and Biliary System. Malden, MA: Blackwell Science, Inc. 2002. p.413-422.
Wilson's disease is a rare autosomal recessive disorder of copper metabolism that is characterized by liver disease and neurological symptoms. This chapter on Wilson's disease is from a textbook that presents a comprehensive and up-to-date account of diseases of the liver and biliary system. The chapter covers molecular genetics, pathogenesis, pathology, the clinical picture (symptoms), hepatic (liver) forms, neuropsychiatric forms, renal (kidney) changes, other changes, laboratory tests, liver biopsy, scanning, diagnostic difficulties, treatment, and prognosis. 9 figures. 1 table. 51 references.
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Your Liver Lets You Live. Cedar Grove, NJ: American Liver Foundation. 2002. [4 p.].
The liver, the largest organ in the body, plays a vital role in regulating life processes. These processes include: to convert food into chemicals necessary for life and growth; to manufacture and export important substances used by the rest of the body; to process drugs absorbed from the digestive tract into forms tat are easier for the body to use; and to detoxify and excrete substances that otherwise would be toxic to the body. This brochure reviews the functions of the liver, the symptoms and signs of liver disease, prevention strategies, the problem of gallstones, alcohol related liver disorders (fatty liver, alcoholic hepatitis, alcoholic cirrhosis), cirrhosis (scarring of the liver), liver disorders in children (biliary atresia, chronic active hepatitis, galactosemia, Wilson's disease, Reye's syndrome), cancer of the liver, and research efforts in liver disease. The brochure concludes with a description of the work of the American Liver Foundation (ALF) and its contact information (www.liverfoundation.org). 1 figure.
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Autoimmune Liver Disease in Children. Journal of Gastroenterology and Hepatology. 16(6): 674-677. 2001.
Autoimmune liver disease (AILD) in children progresses to cirrhosis (liver scarring) and liver failure if not diagnosed and managed in time. In this article, the authors report on their prospective analysis of their patients with liver disease for autoimmune etiology and their outcome with treatment. All patients with liver disease were evaluated with liver function tests, abdominal ultrasonography, endoscopy, liver biopsy, viral markers, and investigations for Wilson's disease. Immunoglobulin (Ig) M hepatitis A virus, hepatitis E virus (HEV) and IgM hepatitis B core antibody were tested if acute viral hepatitis was suspected. Antinuclear antibody (ANA), antismooth muscle antibody (SMA), and liver kidney microsomal antibody (anti LKM1) were done in all cases. Autoimmune liver disease was diagnosed when one or more autoantibodies tested positive and no other etiology of liver disease was identified. Cases diagnosed to have AILD were treated with immunosuppressive drugs. AILD constituted 3.9 percent of chronic liver disease cases (6 of 153 patients; median age and duration of illness 8.5 years and 3 months, respectively). Four patients had acute hepatitis-like presentation. Three of the patients achieved remission with combination therapy of oral prednisolone (OP) and azathioprine (AZT), and one with only OP. The other two patients were not treated. Two of the patients in remission have been weaned off from immunosuppressive therapy, and one is in a withdrawal phase. Another patient, while in biochemical remission developed superimposed anicteric (without jaundice) acute HEV infection. The authors conclude that although AILD is uncommon in children, its search is rewarding, as remission is achieved with immunosuppressive therapy. Superimposed acute viral hepatitis can occur in endemic areas (the authors report from Lucknow, India). 1 figure. 2 tables. 14 references.
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Cirrhosis. In: Okuda, K., ed.,et al. Hepatobiliary Diseases: Pathophysiology and Imaging. Malden, MA: Blackwell Science, Inc. 2001. p. 119-151.
Cirrhosis (liver scarring) is an end stage of chronic diffuse liver disease. Cirrhosis is characterized by alteration of the normal liver architecture into structurally abnormal nodules of liver cells, surrounded by fibrosis (scar tissue). This chapter on cirrhosis is from a textbook that familiarizes the reader with various imaging modalities, the information they provide, and the merits of each, in order to facilitate the combined use of different imaging techniques in the diagnosis and management of hepatobiliary (liver and bile tract) diseases. Diseases that cause cirrhosis include alcoholic liver disease, chronic viral hepatitis, biliary obstruction, heart failure, metabolic disorders such as copper overload (Wilson's disease), and many others, but alcohol and hepatitis virus are by far the most common etiology. Clinical manifestations including wasting, ascites (fluid accumulation) and edema, splenomegaly (enlarged spleen), esophageal varices (enlarged veins or arteries in the esophagus), and encephalopathy (involvement of the brain tissue). The disease is progressive if it in not treated or if the offending agent is not removed, and for advanced cirrhosis, transplantation is the only cure. Most patients with uncomplicated cirrhosis die of variceal bleeding or hepatic (liver) failure. The author discusses epidemiology, pathophysiology, viral cirrhosis, clinical features, ascites and hepatic lymph, hepatic hydrothorax, portal-systemic encephalopathy, imaging features in cirrhosis, prognosis, and less common types of cirrhosis. 51 figures. 64 references.
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Copper Metabolism and the Liver. In: Arias, I.M., et al. Liver: Biology and Pathobiology, Fourth Edition. Philadelphia, PA: Lippincott Williams and Wilkins. 2001. p.331-343.
Copper is an essential trace element that plays a critical role in the biochemistry of all aerobic organisms. The inherited diseases of copper metabolism underscore both the essential need for copper as well as the toxicity of this metal. This chapter on copper metabolism and the liver is from a textbook on the pathobiology and biology of the liver. The authors note that elucidation of the molecular genetic basis of these diseases has revealed a remarkable conservation of the molecular mechanisms of copper metabolism. Wilson disease is an inherited disorder of copper metabolism resulting in hepatic cirrhosis (liver scarring) and basal ganglia degeneration. In humans, copper balance is entirely maintained by gastrointestinal absorption and biliary excretion, and this process is regulated at the stage of hepatocyte efflux of copper by the transport protein encoded at the Wilson locus. The authors cover physiology, cell biology, Wilson disease (genetics, pathogenesis, diagnosis and treatment), and copper associated cirrhosis in childhood. 6 figures. 100 references.
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Hepatobiliary Diseases: Pathophysiology and Imaging. Malden, MA: Blackwell Science, Inc. 2001. 764 p.
This textbook aims to familiarize the reader with various imaging modalities, the information they provide, and with the merits of each, in order to facilitate the combined use of different imaging techniques in the diagnosis and management of hepatobiliary (liver and bile tract) diseases. The book includes 47 chapters in seven sections: progress in imaging, anatomy and gross changes in the liver, diffuse liver diseases, vascular disease, space-occupying lesions, other liver diseases, and biliary tract disease. Specific topics include computed tomography (CT scan) and magnetic resonance imaging (MRI); harmonic ultrasound; anatomy of the liver; acute hepatitis and acute hepatic failure; chronic hepatitis; cirrhosis (liver scarring); fatty liver (steatosis); alcoholic liver disease; iron overload; Wilson's disease; amyloidosis, metabolic diseases, drug-induced and chemical-induced liver injuries; vascular anatomy of the liver and vascular anomalies; portal hypertension (high blood pressure); thrombosis (clotting) affecting the liver; Budd-Chiari syndrome; primary malignant tumors of the liver (liver cancer); benign liver lesions; cysts of the liver; liver abscess; blunt hepatic trauma; parasitic diseases; infections and the liver; transplantation; anatomy of the biliary tract; congenital anomalies and dilatation; Caroli's disease; stone disease (gallstones); biliary tract stenosis; primary sclerosing cholangitis; cholecystitis and Mirizzi syndrome; tumors of the gallbladder; adenomyomatosis and cholesterolosis; Hilar carcinoma; and tumors of the common bile duct and papilla of Vater. Each chapter includes black and white reproductions of imaging techniques and a list of references. The book includes a color plate section and a detailed subject index.
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Non-Viral Liver Disease. In: Farthing, M.J.G.; Ballinger, A.B., eds. Drug Therapy for Gastrointestinal and Liver Diseases. Florence, KY: Martin Dunitz. 2001. p. 259-288.
The last decade has seen important advances in the knowledge of the diagnosis, natural history, and treatment of non-viral-induced liver disease, including primary sclerosing cholangitis, primary biliary cirrhosis (PBC), autoimmune hepatitis, hemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency, alcoholic hepatitis, liver storage diseases, Budd-Chiari syndrome, and drug-induced liver disease. This chapter on non-viral liver disease is from a textbook that reviews the drug therapy for gastrointestinal and liver diseases. The chapter provides a brief summary of the pathophysiology of each disease, the rationale for drug intervention, and appropriate treatment regimens as indicated by current knowledge. The chapter concludes with a drug list that summarizes mode of action, and other aspects of clinical pharmacology where appropriate, drug doses, common adverse affects, and drug interactions. 3 tables. 113 references.
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Other Causes of Parenchymal Liver Disease. In: Beckingham, I.J., ed. ABC of Liver, Pancreas and Gallbladder. London, UK: BMJ Publishing Group. 2001. p.15-17.
This chapter on other causes of parenchymal (in the body of the organ) liver disease is from an atlas of the liver, pancreas and gallbladder. Topics covered include autoimmune hepatitis; metabolic causes of liver disease, including hemochromatosis (iron overload) and Wilson's disease (copper deposition); drug related hepatitis, including paracetamol and idiosyncratic drug reactions; and cholestatic nonobstructive jaundice, including primary biliary cirrhosis and primary sclerosing cholangitis. The author notes that most drugs have the potential to cause liver injury and 2 to 7 percent of admissions with nonobstructive jaundice are for drug related hepatitis. Herbal remedies and illegal drugs can also cause jaundice and liver damage. The chapter concludes with summary points of the concepts discussed. 6 figures. 3 tables.
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Wilson's Disease. In: Okuda, K., ed.,et al. Hepatobiliary Diseases: Pathophysiology and Imaging. Malden, MA: Blackwell Science, Inc. 2001. p. 191-196.
Wilson's disease is a rare autosomal recessive disorder characterized by cirrhosis (liver scarring) and basal ganglia (islands of gray matter within each cerebral hemisphere of the brain) degeneration. This chapter on Wilson's disease is from a textbook that familiarizes the reader with various imaging modalities, the information they provide, and the merits of each, in order to facilitate the combined use of different imaging techniques in the diagnosis and management of hepatobiliary (liver and bile tract) diseases. Wilson's disease is caused by copper accumulation in the body, due to the absence or dysfunction of the copper transporting mechanism. The patient develops a greenish-brown pigment ring in the periphery of the cornea known as the Kayser-Fleischer ring. The disease usually presents in childhood, but the diagnosis is often delayed, leading to severe consequences. The disease may present with cirrhosis, aggressive hepatitis, a predominantly hemolytic illness, or acute liver failure with hemolysis (breakdown of red blood cells). In other cases, the disease course consists entirely of progressive disintegration of the motor centers of the brain. The authors discuss etiology, pathophysiology, clinical features, diagnosis, and treatment and prognosis. 5 figures. 13 references.
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Diagnosis of Wilson's Disease: An Experience Over Three Decades. Gut. 46(3): 415-419. March 2000.
Wilson's disease is a rare but treatable condition that often presents diagnostic dilemmas. These dilemmas, for the most part, have not been resolved by the identification and cloning of the Wilson's disease gene. This article reports on a study in which the clinical and laboratory findings of 30 patients with Wilson's disease were reviewed. The authors report their experience over three decades with patients with Wilson's disease in order to illustrate the diverse patterns of presentation and thereby broaden the approach to diagnosis. Twenty two of the patients presented with liver manifestations (8 with fulminant hepatic failure and 14 with chronic liver disease), three with neurological disease, and one with hemolysis; four were asymptomatic siblings of patients with Wilson's disease. Seventy percent were diagnosed within six months of the onset of symptoms, but diagnosis was delayed for up to nine years in some patients. Age range at diagnosis was wide (7 to 58 years of age) and five patients were over 40 years of age. In patients presenting with nonfulminant disease, 18 percent had neither Kayser Fleischer rings nor low ceruloplasmin concentrations. Increased liver copper concentrations were found in all but one patient who had undergone six years of penicillamine treatment. In fulminant hepatic failure (n = 8), additional features helpful in the diagnosis included evidence of hemolysis, increased urinary copper, and a high noncaeruloplasmin copper. The authors conclude that the diagnosis of Wilson's disease still depends primarily on the evaluation of clinical and laboratory evidence of abnormal copper metabolism. No one feature is reliable, but the diagnosis can usually be made provided that it is suspected. The authors remind readers that Wilson's disease should be considered in patients of any age with obscure hepatic or neurological abnormalities. 2 tables. 26 references.
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Genetic Liver Disease in Adults: Early Recognition of the Three Most Common Causes. Postgraduate Medicine. 107(2): 147-152, 155, 158-159. February 2000.
This article is the final entry in a four article symposium that provides a practical approach to the diagnosis and management of common hepatic disorders encountered by primary care physicians. In this article, the authors review the early recognition and diagnosis of the three most common causes of genetic liver disease in adults: Wilson's disease, hereditary hemochromatosis (HHC), and alpha1 antitrypsin deficiency. Although advances in molecular biology have led to the identification and characterization of the genetic defects in these disorders, gene testing has its strengths and limitations. The longstanding techniques of serum (blood) testing and histologic assessment can be combined with genetic evaluation to clarify the diagnosis. Genetic testing is probably most helpful in HHC because of the high frequency of the homozygous C282Y mutation among patients of northern European descent and the relatively high penetrance of the mutation with regard to clinical expression. Genetic testing is much less helpful in the other genetic liver diseases because of the high number of possible mutations and variable clinical expression. However, noninvasive phenotype based screening tests and specific treatments are available for most genetic liver diseases. A patient care algorithm is included. 1 figures. 4 tables. 19 references.
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Liver Disease. In: King, J.E., ed. Mayo Clinic on Digestive Health. Rochester, MN: Mayo Clinic. 2000. p. 151-166.
This chapter on liver disease is from a comprehensive guidebook from the Mayo Clinic that focuses on a variety of digestive symptoms, including heartburn, abdominal pain, constipation, and diarrhea, and the common conditions that are often responsible for these symptoms. Written in nontechnical language, the book includes practical information on how the digestive system works, factors that can interfere with its normal functioning, and how to prevent digestive problems. The first section of the chapter focuses on hepatitis, including the key signs and symptoms of hepatitis, notably fatigue, loss of appetite, nausea, unexplained weight loss, and yellowing of skin and eyes (jaundice). The authors describe the different types of hepatitis (alcohol or drug induced, hepatitis A, hepatitis B, hepatitis C, hepatitis D and E, autoimmune hepatitis, and nonalcoholic steatohepatitis); review the blood tests (liver function tests) that may be used to help diagnose or monitor hepatitis; and discuss treatment options, including corticosteroids, interferon, lamivudine, and liver transplantation. A final section reviews healthy lifestyle approaches for living with hepatitis, and strategies for preventing the disease. The next section of the chapter addresses hemochromatosis (a genetic abnormality that causes the intestines to absorb too much iron), noting that the symptoms can include fatigue, joint pain, impotence (erectile dysfunction) or loss of sex drive, increased skin pigmentation (bronzing), and increased thirst and urination. This section also reviews diagnosis, determining whether screening is necessary for family members of patients with hemochromatosis, and the use of diet therapy (reduced iron intake) to help treat the disease. One sidebar mentions Wilson's disease and alpha 1 antitrypsin deficiency as other inherited liver disease. The last section of the chapter addresses cirrhosis, a condition in which scar tissue forms in the liver and keeps it from functioning normally. 1 figure.
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Liver Disorders Sourcebook. Detroit, MI: Omnigraphics. 2000. 591 p.
This Sourcebook provides basic health care information about liver functions, guidelines for liver health, and tests that assess liver distress. The book also presents the symptoms, treatments, and preventive measures available for liver cancer; hepatitis A, B, C, D and E; genetically based liver diseases; and other liver diseases. The liver transplantation process is explained. Specific topics include strategies for protecting the liver, risk factors, common laboratory tests in liver disease, liver biopsy, cancer tumor markers, cirrhosis (scarring of the liver), infectious agents and parasites, pregnancy and the liver, jaundice in the healthy newborn, the liver's response to drugs, alcohol and the liver, acetaminophen, herbs and alternative medicine, galactosemia, Gaucher disease, hereditary hemochromatosis, Niemann-Pick disease, Wilson's disease, biliary atresia, cystic disease of the liver, fatty liver, gallstones, primary biliary cirrhosis, primary sclerosing cholangitis, organ donation, and the bioartificial liver. A glossary, a directory of organizations and support groups with up to date contact information (including websites and email addresses), a listing of transplant centers, and a subject index conclude the volume.
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Resources on Hepatitis. Postgraduate Medicine. 107(2): 163-166. February 2000.
This listing of resources on hepatitis accompanies a four article symposium that provides a practical approach to the diagnosis and management of common hepatic disorders encountered by primary care physicians. The listing is divided into four categories: resources for physicians, resources for patients, publications about hepatitis, and resources on other liver disease topics. Organizations included are the American Association for the Study of Liver Diseases, the American Liver Foundation, the Centers for Disease Control and Prevention (CDC), CliniWeb International, TransWeb, CenterWatch, the C. Everett Koop Institute at Dartmouth, Children's Liver Association for Support Services, Hepatitis B Foundation, HIV and Hepatitis.com, Immunization Action Coalition, National Hepatitis C Coalition, the National Task Force on Hepatitis B Immunization (Focus on Asians and Pacific Islanders), National Cancer Institute, National Center for the Study of Wilson's Disease, Alpha1 Association, Iron Disorders Institute, and the Wilson's Disease Association. The entry for each organization includes the address and telephone numbers, Internet addresses and websites as available, and a short description of the activities and services offered.
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Wilson's Disease. Birmingham, England: Children's Liver Disease Foundation. 2000. 8 p.
Wilson’s disease is an inherited condition in which copper is not excreted properly from the body. The excess copper can build up in the liver, the brain, or collect in other parts of the body including the eyes and the kidneys. This brochure helps parents and caregivers of children with Wilson’s disease understand the disease and the care needed for these children. The brochure explains how copper is used in the body; the signs and symptoms of Wilson’s disease; the kinds of liver disease that are caused; neurological problems that can be caused; diagnostic approaches; treatment options, such as drug therapy and liver transplantation; administration and dosage considerations; dietary therapy; lifestyle modifications; the indications for a liver transplant; genetic tests, indications for screening family members; and pregnancy in women with Wilson’s disease. The brochure also explains the work of the England-based Children’s Liver Disease Foundation, and reports on current advances in the prevention and understanding of hepatitis A. A form with which readers can donate to the Children’s Liver Disease Foundation is provided.
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Wilson's Disease. Birmingham, England: Children's Liver Disease Foundation. 2000. 8 p.
Wilson’s disease is an inherited condition in which copper is not excreted properly from the body. The excess copper can build up in the liver, the brain, or other parts of the body including the eyes and the kidneys. This brochure helps parents and caregivers of children with Wilson’s disease to understand the disease and the care for these children. The brochure explains how copper is used in the body, the signs and symptoms of Wilson’s disease, the kinds of liver disease that are caused by Wilson’s disease, neurological problems that can be caused by Wilson’s disease, diagnostic approaches, treatment options (drug therapy and liver transplantation), administration and dosage considerations, dietary therapy, lifestyle modifications, the indications for a liver transplant, genetic tests for Wilson’s disease, indications for screening family members for Wilson’s disease, and pregnancy in women with Wilson’s disease. The brochure also explains the work of the England-based Children’s Liver Disease Foundation, and reports on current advances in the prevention and understanding of hepatitis A. A form with which readers can donate to the Children’s Liver Disease Foundation is provided.
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Wilson's Disease. Birmingham, England: Children's Liver Disease Foundation. 2000. 8 p.
Wilson’s disease is an inherited condition in which copper is not excreted properly from the body. The excess copper can build up in the liver, the brain, or other parts of the body including the eyes and the kidneys. This brochure helps parents and caregivers of children with Wilson’s disease to understand the disease and the care for these children. The brochure explains how copper is used in the body, the signs and symptoms of Wilson’s disease, the kinds of liver disease that are caused by Wilson’s disease, neurological problems that can be caused by Wilson’s disease, diagnostic approaches, treatment options (drug therapy and liver transplantation), administration and dosage considerations, dietary therapy, lifestyle modifications, the indications for a liver transplant, genetic tests for Wilson’s disease, indications for screening family members for Wilson’s disease, and pregnancy in women with Wilson’s disease. The brochure also explains the work of the England-based Children’s Liver Disease Foundation, and reports on current advances in the prevention and understanding of hepatitis A. A form with which readers can donate to the Children’s Liver Disease Foundation is provided.
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