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Your search term(s) "hemochromatosis" returned 47 results.

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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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Hemochromatosis. Toronto, Ontario: Canadian Liver Foundation. 2000. 2 p.

This brochure describes hemochromatosis, a hereditary disease that causes excessive amounts of iron to accumulate in the body. The liver is the first organ to store iron and when its storage capacity is exhausted, the iron continues to accumulate in the heart, the pituitary gland, and elsewhere in the body. If untreated, damage to the liver, heart, and pancreas may eventually lead to death. Injury to the liver is reversible provided treatment is started before cirrhosis (liver scarring) has developed. Written in a question and answer format, the brochure discusses the causes of hemochromatosis, the symptoms of the condition, how hemochromatosis affects organs other than the liver, diagnostic strategies, screening guidelines, treatment options, and dietary considerations. The brochure concludes with the contact information for the Canadian Liver Foundation (www.liver.ca).

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Hereditary Hemochromatosis. Physician Assistant. p. 31-40, 43-44. February 1999.

This continuing education article familiarizes physician assistants with hereditary hemochromatosis (HHC), one of the most common genetic disorders in the United States. HHC is an autosomal recessive condition associated with primary overabsorption of iron from the gastrointestinal tract. It may cause lifelong excessive iron absorption and accumulation and serious health effects including arthritis, cirrhosis, diabetes, impotence, myocardial infarction, and death. HHC is often considered primarily a disease of European men. However, iron overloading occurs in all ethnic groups. HHC eventually causes serious illness and death if untreated. Complications can be avoided by routine screening before clinical symptoms develop. HHC is effectively treated by the early use of therapeutic phlebotomy. The cornerstone of screening is measurement of serum transferrin saturation and the serum ferritin level. A DNA based test for the hemochromatosis gene is commercially available, but its place in the diagnosis of HHC is still being evaluated. Appended to the article is a study guide and a posttest for earning continuing medical education (CME) credits. 4 figures. 1 table. 22 references.

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Update in Hepatology. Annals of Internal Medicine. 134(3): 216-223. February 6, 2001.

This article summarizes advances in hepatology (study of the liver and liver diseases) over the past 2 years. The author recounts some important aspects of the history of viral hepatitis and hemochromatosis and describes notable new reports that may help guide an internist's approach to patients with these liver diseases. The author offers nine abstracts of recent research studies on hepatitis A, hepatitis B, hepatitis C, and hemochromatosis. Hepatitis A is viewed as a rather benign condition. Certain groups are at increased risk, including travelers to the tropics or developing countries, children and caregivers in child care centers, and people who eat shellfish that is improperly handled or prepared. The author notes that now the viral genetic sequence of HAV is known, the Centers for Disease Control and Prevention can determine whether a single source caused an outbreak. Hepatitis B virus is a bloodborne, DNA virus that is transmitted sexually, parenterally, and perinatally. Hepatitis B has a tremendous potential for shortening life, but two established treatments are available: lamivudine and interferon. Hepatitis C is now the most common liver disease and is responsible for almost 40 percent of the liver transplantations done in the United States. The author cautions that although there has been a recent decline in the number of new cases per year, the slow but relentless progression of liver disease and the long natural history of hepatitis C will result in more patients coming into the health care system (with unexpected cirrhosis from hepatitis C and with complications of hepatitis C such as liver cancer). Advances in hereditary hemochromatosis have created a new screening dilemma for general internists. Genetic testing is expensive and not appropriate for general screening, but can be used as an adjunct to diagnosis, particularly in studying family members once a diagnosis has been made. Liver biopsy should be performed when the diagnosis is in doubt. The slow course of the disease underscores the importance of early detection when the disease is occult, and intervention with phlebotomy (therapeutic blood removal) can prevent cirrhosis. 2 tables. 9 references.

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Vibrio Vulnificus Fact Sheet for Health Care Providers. New York, NY: American Liver Foundation. 2006. 2 p.

Vibrio vulnificus is a gram-negative bacterium that is considered the most lethal of the vibrios inhabiting brackish and salt water. This bacterium occurs naturally in warm, coastal areas and is found in higher concentrations from April through October, when coastal waters are warm. This fact sheet helps health care providers understand the risks of V. vulnificus infection. Topics include the population most at risk of V. vulnificus infection; the clinical syndromes associated with V. vulnificus infections, including primary septicemia, gastroenteritis, and wound infection; diagnostic approaches; treatment, notably with antibiotics; long-term sequelae; case reporting, which is mandated at the state level; and strategies to reduce the risk of infection. Most healthy individuals are not at risk for V. vulnificus infection. Persons at high risk include those with liver disorders, including hepatitis, cirrhosis, and liver cancer; hemochromatosis; diabetes mellitus; and immunocompromising conditions such as HIV, AIDS, and cancer. The fact sheet includes the contact information for the Interstate Shellfish Sanitation Conference (www.issc.org; 803-788-7559). 3 references.

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What is Hemochromatosis?. Cedar Grove, NJ: American Liver Foundation. 2001. [4 p.].

This brochure reviews hemochromatosis, an inherited condition that causes the body to absorb and store too much iron. The brochure answers common questions about hemochromatosis, covering the risk factors for the disease, the symptoms, diagnostic tests for iron overload, treatment options, the prognosis for people with hemochromatosis, the presence of anemia with iron overload, the role of alcohol in accelerating liver damage, the relationship between diet and iron overload, and liver transplantation in patients with hemochromatosis. The brochure concludes with a brief description of the American Liver Foundation (ALF), a nonprofit, national voluntary health organization dedicated to the prevention, treatment, and cure of hepatitis and other liver diseases through research, education, and advocacy.

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Your Liver, Your Health. Toronto, Ontario: Canadian Liver Foundation. 2001. 4 p.

Virtually all the blood returning from the intestinal tract to the heart passes through the liver. This means that all foods and compounds that are swallowed that are absorbed into the bloodstream pass through the liver. This brochure describes the role of the liver and the common diseases that can affect the liver. Topics include the physiology of the liver; who is affected by liver disease; common liver diseases including gallstones, viral hepatitis, hepatitis A, hepatitis B, hepatitis C, cirrhosis (scarring of the liver), liver cancer, liver disease in children, autoimmune hepatitis, alcohol-related liver disease, hemochromatosis, and primary biliary cirrhosis (PBC); the symptoms and signs of liver disease; strategies for taking care of one's liver; and the use of liver transplantation. The brochure concludes with a brief description of the goals and activities of the Canadian Liver Foundation (www.liver.ca).

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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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Detecting Hereditary Hemochromatosis. Nurse Practitioner. 25(7): 64, 69, 73-74, 76. July 2000.

This article reviews the diagnosis of hereditary hemochromatosis (HH), the most commonly inherited autosomal recessive disorder. Hemochromatosis is a current or potential progression of abnormally high accumulations of iron in the liver. If left untreated, the condition can lead to chronic or irreversible hepatic (liver) fibrosis, cirrhosis (scarring), hepatocellular carcinoma (liver cancer), arthritis, and organ failure. Common signs and symptoms seen in the primary care setting include fatigue, weakness, abdominal pain, palpitations, skin pigmentation (coloring) changes, and arthropathy, but any symptom associated with organ damage may be reported. Because prompt intervention can cease or reverse the debilitating effects of iron overload, prompt disease diagnosis and treatments are imperative. The author notes that often an HH diagnosis is delayed in asymptomatic patients or patients with vague complaints of fatigue and arthropathy. The goal is to identify patients prior to symptom onset and organ damage; recent gene typing studies have made this a possibility. Early manifestations of HH include vague symptoms of weakness, fatigue, weight loss, skin pigmentation changes, abdominal pain, loss of libido, and diabetes mellitus symptoms. Advanced physical signs include liver and spleen enlargement, skin pigmentation changes, spider angiomas, arthropathy, ascites, cardiac arrhythmias, heart failure, testicular atrophy, and jaundice. Because HH is an inherited disorder, the family history should be specific and complete. Routine assays are the most commonly used testing. A definitive diagnosis is made via liver biopsy. Patients with HH should be instructed to increase their dietary protein, as hemoglobin is 96 percent protein; folic acid of 1 mg daily will assist in hemoglobin formation. Vitamin or mineral supplements that contain iron should be avoided. And because alcohol is a hepatotoxin and wine contains iron, alcohol should be avoided. 1 figure. 31 references.

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