MORE THAN ONE MILLION AMERICANS HAVE UNDETECTED IRON OVERLOAD (IODA) is a non-profit 501 (c) 3 organization and is the International Clearinghouse for information on iron overload conditions, including hereditary hemochromatosis. IOD Association is the one major repository of news from physicians, scientists and patients. To lead the search for millions of Americans and other nationals who have undiagnosed iron overload including hemochromatosis; to promote adequate treatment and to prevent the severe health problems, massively misspent medical money and avoidable deaths that result from neglect of iron overload. Iron Overload Books Available : THE IRON ELEPHANT and tick. READERS DIGEST/October 1995/"Is Iron Making You Sick?

Alagille syndrome is an inherited disorder that mimics other forms of prolonged liver disease seen in infants and young children. However, a group of unusual features in other organ systems distinguishes Alagille syndrome from other liver and bile duct diseases in infants. Children with Alagille Syndrome usually have a liver disease characterized by a progressive loss of the bile ducts within the liver over the first year of life and narrowing of bile ducts outside the liver. Narrowing of the blood vessel connecting the heart to the lungs (pulmonary artery) leads to extra heart sounds but rarely problems in heart function. The overall life expectancy for children with Alagille Syndrome is unknown, but depends on several factors: the severity of scarring in the liver, whether heart or lung problems develop because of the narrowing in the pulmonary artery, and the presence of infections or other problems related to poor nutrition. Diagnosis can be established by microscopic examination of liver biopsy specimens, a stethoscope examination of the child's heart and chest, a slip-lamp eye examination, an X-ray of the spinal column and an ultrasound (sonogram) examination of the abdomen.

The Liver Disease Center of Scripps Clinic provides comprehensive care by a highly specialized medical and surgical team for the full range of disorders affecting the liver and bile ducts. The Center is also in the vangard of efforts to advance the understanding and treatment of liver disease through its research and educational programs. Emerging Therapies for HCV updated 2/15/97 The Center's establishment reflects the major progress made over the past decade in the management of these often complicated patient conditions. Important breakthroughs include the prevention and improved treatment of chronic liver disease through vaccine development and new drug therapies, efforts to which Scripps Clinic has contributed through its basic and clinical research programs. Scripps Clinic and Research Foundation has regional medical facilities in Rancho Bernardo, Rancho San Diego, San Diego (Kearny Mesa), Escondido and San Marcos.

Gastroenterology is a division within the Department of Medicine of Columbia University's College of Physicians & Surgeons and The Presbyterian Hospital. The Division's faculty members are devoted to research and the clinical care of patients with gastrointestinal, liver and nutritional disorders. The Division is also responsible for the Gastroenterology Training Program at Columbia-Presbyterian and for teaching medical students, interns, residents, fellows and attending physicians aspects of gastrointestinal and liver diseases. Special interests include: Celiac Disease Diarrheal Diseases Endoscopy Research Esophageal Disorders Gallbladder and Bile Duct Disorders Inflammatory Bowel Diseases Irritable Bowel Syndrome Liver Diseases Molecular and Cell Biology Nutrition Pancreatic and Biliary Disorders Peptic Ulcer Disease Physiology of Intestinal Ion and Nutrient Transport Columbia Gastroenterology Manual [Under Construction] A manual for physicians and medical students prepared by the Columbia faculty covering gastrointestinal and liver diseases and nutrition. For information on kidney diseases, visit our colleagues at Columbia University Nephrology Web.

CENTER FOR LIVER DISEASES Liver, bile duct and gallbladder diseases afflict 25 million Americans, or one in every 10. Yet, even with recent developments, such as the development and availability of vaccines for certain types of hepatitis, liver disease continues to pose a threat to society, and its treatment remains a challenge to health care professionals. The Center for Liver Diseases at the University of Pittsburgh Medical Center (UPMC), which was established to develop better diagnostic methods and therapies to treat the full spectrum of liver diseases, complements the services already available at the UPMC through its renowned Transplantation Institute and Division of Transplantation Medicine. Patients seen at the center include those with complications from chronic liver disease, chronic viral hepatitis (B, C, D and others), genetic liver disease, cholestatic liver diseases, autoimmune liver disorders, biliary disorders and liver cancer. The center employs an integrated approach to the diagnosis and treatment of liver disorders, be it surgery for hepatobiliary disorders, chemotherapy for liver cancer, evaluation for transplantation or admission to a clinical trial. In general, the services provided by the Center for Liver Diseases include therapeutic endoscopy, biliary procedures, diagnostic procedures, medical and surgical therapies and 24-hour consultation.

GLOSSARY   ORGANIZATIONS   COMPUTER ACCESS   READING Liver diseases include cirrhosis, viral and other types of hepatitis, and more than 100 less common conditions. In about 5 percent of cases of hepatitis B, the individual develops a lifelong, chronic liver disease that can lead to cirrhosis. People who have contracted hepatitis C, the most common type of hepatitis transmitted through blood transfusions, run a 50 percent risk of developing chronic liver disease. FAX: 201-256-3214 Promotes understanding of the liver and its diseases, including hepatitis, cirrhosis, hereditary diseases such as Wilson's disease (abnormal accumulation of copper in the liver), hemochromatosis (iron overloading in the blood and endocrine system, which also affects the liver), and rare diseases. free information brochures, which include specific information on cirrhosis, hepatitis, and other liver diseases. FAX: 612-647-9131 Promotes awareness about hepatitis, especially hepatitis B. Sends information to callers and encourages immunization against and testing for the HBV (hepatitis B virus).

May be pylephlebitis due to ascending infection that enters the liver through the portal veins, or cholangitis, if the infection had reached the liver through the bile ducts. Greenish-yellow viscous fluid secreted by the liver, composed of bile sales, bilirubin and its derivatives (e.g. Biliverdin), cholesterol and mucus. Stagnation of bile in the liver, induced as bile plugs in the bile canaliculi or brown pigmentation of liver cells. Cirrhosis may be an outcome and or complication of viral hepatitis, alcohol abuse, drug toxicity, hereditary metabolic diseases (AAT deficiency, Wilson disease). Usually develops in cirrhotic liver especially often in cirrhosis caused by hepatitis B and C, AAT deficiency and hemochromatosis. Caused by hyperbilirubinemia which may be prehepatic (e.g. Hemolysis of red blood cells), hepatic (e.g. Viral hepatitis) or posthepatic (e.g. Obstruction of bile flow by carcinoma of pancreas).

Symptoms include jaundice, pale, loose stools and poor growth within the first three months of life. Alpha 1 - Antitrypsin Deficiency - a hereditary disease that may lead to hepatitis and cirrhosis. Cystic Disease of the Liver - These include choledochal cysts, Caroli's Syndrome, Congenital Hepatic Fibrosis, and Polycystic Liver Disease. Vomiting, liver enlargement, and jaundice are often the earliest signs of the disease, but bacterial infections, irritability, failure to gain weight, and diarrhea may also occur. While many individuals with this disease have no symptoms, injuries to the liver can slowly lead to cirrhosis if the illness is not treated. Hepatitis B - one of the most serious forms of hepatitis, this disease is more common and much more infectious than AIDS.

Hemochromatosis - What you don't know can hurt you April 1 1997 Hemochromatosis is a disorder that results when the intestinal tract absorbs too much iron from food. "We don't yet know what this gene is producing that causes hemochromatosis or the mechanism in the intestine that causes the excess iron absorption, but identifying the gene is an important first step," he says. Because these manifestations aren't specific for hemochromatosis and because it takes a long time for the disease to cause serious problems, years may elapse between the onset of the disease and its diagnosis. Since early diagnosis of hemochromatosis is critical to its successful treatment, many now advocate including the blood tests as part (including a test for serum iron-binding capacity) of routine exams. "It's also important for people with hemochromatosis to avoid taking iron in oral supplements or vitamins." If the disease has progressed to a point where serious organ damage has occurred, the outlook is less hopeful, according to Dr.

Alagille syndrome is an inherited disorder that mimics other forms of prolonged liver disease seen in infants and young children. However, a group of unusual features in other organ systems distinguishes Alagille syndrome from other liver and bile duct diseases in infants. Children with Alagille Syndrome usually have a liver disease characterized by a progressive loss of the bile ducts within the liver over the first year of life and narrowing of bile ducts outside the liver. Narrowing of the blood vessel connecting the heart to the lungs (pulmonary artery) leads to extra heart sounds but rarely problems in heart function. The overall life expectancy for children with Alagille Syndrome is unknown, but depends on several factors: the severity of scarring in the liver, whether heart or lung problems develop because of the narrowing in the pulmonary artery, and the presence of infections or other problems related to poor nutrition. Diagnosis can be established by microscopic examination of liver biopsy specimens, a stethoscope examination of the child's heart and chest, a special eye examination (slit-lamp exam), an x-ray of the spinal column and an ultrasound (sonogram) examination of the abdomen.

It removes toxins from the bloodstream, manufactures proteins that control blood clotting, stores energy, breaks down drugs, produces a fluid called bile that helps digestion, and rids the body of bilirubin a pigment produced during the breakup of old red blood cells. These tests include a physical examination of the patient to determine the size of the liver, blood tests that measure the level in the bloodstream of bilirubin and proteins produced by the liver, "imaging tests such as ultrasound and CT X-rays ("CAT scans") that provide a picture of the liver, its blood vessels and bile ducts, and liver biopsy. Jaundice (yellowing of skin and eyes) Tender or swollen liver Rapid weight gain Swelling in arms or legs Fluid accumulation in abdominal cavity High levels of bilirubin in the blood High levels of liver enzymes in the blood (SGOT, SGPT and alkaline phosphatase) Confusion These include minimizing or eliminating the use of certain drugs that can worsen the problem, relieving the buildup of fluids in tissues and organs with diuretics or dialysis restricting the intake of salt, carefully monitoring the volume of fluids in the body, and transfusing the patient with packed red blood cells to keep the circulating blood volume high until VOD has run its course. Several drugs administered to BMT patients to treat infections, GVHD, nausea, and high blood pressure as well as some sedatives and pain medications can cause or aggravate liver injury. Patients who have had acute GVHD of the liver are at greater risk for developing chronic GVHD of the liver than other allogeneic BMT patients.

NEW YORK (Feb 29, 1996 10:45 p.m. EST) -- A small number of healthy cells can multiply enough to take over a diseased liver, a finding that may open the door to gene therapy for liver diseases such as hepatitis, a study in mice found. A major barrier to gene therapy of the liver has been scientists' inability to deliver corrective genes that work long term in more than just a small percentage of liver cells. The healthy cells were able to take over the liver because they had the gene the other cells lacked. The approach might also be useful against several other genetic liver diseases in people, such as galactosemia, which strikes in about one in 20,000 live births and is treated with dietary restrictions, and a form of alpha-1-antitrypsin deficiency that occurs in about 1 in 10,000 births and can cause liver failure in childhood, Grompe said. With hepatitis B and C, which are caused by viruses, liver cells might be equipped with a gene to make them resist infection and so gain a growth advantage, he said. Liver cells could be given not only the gene needed to correct the disease but also a second gene, which would protect those cells as scientists administered a drug to make uncorrected liver cells die off.

Diagnosis: Necrotizing granulomatous hepatitis, associated with Bartonella (Rochalimaea) henselae infection. Discussion: Bartonella henselae, formerly called Rochalimaea henselae, is the main organism responsible for the recently described disorder, bacillary angiomatosis, which in immune-compromised patients most commonly causes a granulation tissue-like vascular proliferation in the skin, liver, and other organs. In the liver, this reaction results in a massive sinusoidal expansion, or peliosis. However, due either to antibiotic therapy or to some as yet undefinable aspect of the patient's immune status, in some cases there is no angiogenesis, and an entirely different pathologic appearance results, as seen in this case, where necrotizing granulomas predominate. This patient may have been taking antibiotics prior to his admission. (See also case 3) Reference: Slater NL, Pitha VJ, Herrera L, Hughson DM, Min KW, Reed AJ; Rochalimaea henselae infection in acquired immunodeficiency syndrome causing inflammatory disease without angiomatosis or peliosis.

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It is estimated that in the United States as many as 10 % of men and 3 % of women may suffer from persistent problems related to the use of alcohol. The Fourth Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) published by the American Psychiatric Association divides alcohol use disorders into "alcohol dependence" and "alcohol abuse. " Alcohol dependence is indicated by evidence of tolerance and/or symptoms of withdrawal such as delirium tremens (DTs) or alcohol withdrawal seizures (rum fits) upon cessation of drinking. Alcohol abuse is characterized by recurrent performance problems at school or on the job that result either from the after effects of drinking alcohol or from intoxication on the job or at school. In addition, patients with alcohol abuse disorders may use alcohol in physically adverse circumstances (e.g. while driving) and may miss work or school or neglect child care or household responsibilities because of alcohol use. In general, women who drink an equal amount of alcohol are at higher risk than men for the development of liver disease, possibly because of decreased metabolism of alcohol in the stomach prior to absorption.

The prevalent system is based on anatomy, i.e. , disease of hepatic parenchyma, disease of the hepatobiliary system, and disease of the hepatic vascular system. Mild-moderate disorder results in cell necrosis which is manifested as elevated transaminase levels (the enzymes AST and ALT present in hepatocytes leak into the serum as the cells die), transient decrease in protein synthesis, and decreased conjugation of bilirubin. Clinically, symptoms are due to loss of functional hepatocytes, i.e., jaundice ( decreased ability to metabolize bilirubin), edema (hepatorenal syndrome), coagulopathy (decreased ability to synthesize clotting factors), and portal hypertension (from fibrosis and regenerative nodules, which disrupt the portal venous blood flow). Portal Hypertension Portal hypertension is defined as portal vein pressures greater than 20 mm Hg and most commonly results from increased hepatic resistence to portal blood flow. The absence of valves in the portal venous system facilitates retrograde blood flow from the high pressure portal venous sytem to a lower pressure systemic circulation in cases of portal hypertension. Thus in patients with acute liver disease, bilirubin and ammonia levels in the blood may be high, but albumin may be normal because enough time hasn't elapsed for a defect in production to appear.

  Gilbert's syndrome is a common, often inherited disorder that affects processing by the liver of the greenish-brown pigments in bile (called bilirubin).     W hat causes it?     W hat are the signs and symptoms?     W hat investigations and treatment are necessary?     W hat should we do?   For these reasons the British Digestive Foundation suggests that all those with Gilbert's Syndrome carry with them at all times the message on this page - I am a Gilbert's Syndrome Sufferer  

The Canadian Liver Foundation is leading the fight against liver disease and to continue, we need your help. Provides research awards and grants to scientists, researchers and physicians involved in the study of liver disease. Wilson Disease In 1993, the defective gene responsible for Wilson disease, a hereditary disorder which causes copper poisoning of the liver and brain, was discovered by Dr. Identification of several different gene mutations in Wilson disease will help doctors recognize older and younger cases of the disease. Please make donations payable to: Canadian Liver Foundation 365 Bloor Street East, Suite 200 Toronto, Ontario M4W 3L4 demers@liver.ca ___ "I would like more information on becoming a CLF volunteer.

Microabscess^ Involved^ Heart disease, NOS^ Lung, NOS^ Kidney, NOS^ Splenic disorder, NOS^ Disease of liver, NOS^ Disease of pericardium, NOS^ Skin pH, NOS^ Lymph, NOS^ Lymph node, NOS^ . ###21504^31^W^F^1982^2^^ Infiltration, NOS^ Infiltrating duct carcinoma^ Right^ Right breast, NOS^ Right^ Altered^ Modified radical mastectomy, NOS^ Posterior axillary line^ Lymph, NOS^ Lymph node, NOS^ Positive^ Neoplasm, uncertain whether benign or malignant^ . Peritoneum, NOS^ Surface^ Soft^ Soft tissues, NOS^ Soft tissues of pelvis, NOS^ Retroperitoneum, NOS^ Inferior^ Kidney disease, NOS^ Aortic lymph node^ Mesentery, NOS^ Mesenteric lymph node, NOS^ Diaphragm, NOS^ Diaphragmatic pleura^ Disease of lung, NOS^ Disease of bone, NOS^ Bone marrow, NOS^ Rib syndrome^ Vertebra, NOS^ . Heart, NOS^ Cardiac catheterization, NOS^ Initial^ With^ Lung, NOS^ Stenosis, NOS^ Patent^ Right^ Shunt, NOS^ Increased size, NOS^ Left^ Atrium, NOS^ Following^ Atrium, NOS^ Common ventricle^ Regurgitation^ . Multiple^ Intermittent^ Including^ Right^ Right bundle branch block^ Immature^ Ventricle, NOS^ Contraction, NOS^ Complete^ Heart disease, NOS^ Heart block, NOS^ Pacing the floor^ . Autopsy examination, NOS^ Lung, NOS^ Splenic disorder, NOS^ Disease of liver, NOS^ Kidney disease, NOS^ Positive^ Candidiasis, NOS^ Candidiasis, NOS^ .

Hemochromatosis disease genetic disorder sickness fatigue Runner's child racing against clock to survive "I testify that the Lord Jesus Christ the son of God is.

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Back to previous level Hemochromatosis Med. of Wisconsin:Hemosiderosis / Hemochromatosis U. of Illinois, Urbana:Liver, cirrhosis, hemochromatosis U. of Pennsylvania:Hemochromatosis U. of Utah Webpath:Micronodular cirrhosis and fatty change of liver, gross Uniformed Services U. of the Health Sciences:Hemochromatosis Hepatolenticular Degeneration Hosp. of Wisconsin:Wormian bones Hypophosphatemia, Familial Kinky Hair Syndrome Med. of Wisconsin:Wormian bones Paralysis, Familial Periodic Hosp. of Wisconsin:Pseudohypoparathyroidism Last update: 04/25/97

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This page last modified Tuesday, 22-Apr-97 Hello 199.250.238.68 Student Web projects:  you think you're stressed out? Exploring the Possible Role of Vitamin C in the Regeneration of Vitamin E.  Jennifer Ellsworth, Susan Nelson, & Christine Swanson  The Role of Vitamin C in the Regeneration of Vitamin E   Jennifer Ruffing, Jennifer Rutman & Sandra Schouten  The Roles of Ascorbate and Carnitine in Scurvy   Heidi Brewer, Georgina Gomez & Justin Shimek  Response of Nuclear Regulatory Proteins in Riboflavin Deficiency   Director Animations of Reaction Mechanisms:  Niacin  Pyridoxine  Thiamin  Vitamin K  Iron 1  Iron 2  General lipoprotein structure  Triglyceride-rich lipoproteins  Cholesterol-rich lipoproteins  Exogenous lipoprotein pathway  Endogenous lipoprotein pathway  High density lipoprotein pathway  These and other projects may also be found by Searching the FScN Information Database 

No Title Type Organ Disease Quality 1763022 Hemochromatosis in liver Light microscopical Liver Degenerative disorders Good Liver hemosiderosis (1758003) Liver hemosiderosis (1758004) Liver hemosiderosis (1758005) Cholestasis (1758006) Cholestasis (1758007) Cholestasis (1758014) Extramedullary hemopoiesis in liver (1758037) Macronodular liver cirrhosis (1758062) Cirrhosis + fatty liver (1758066) Macronodular liver cirrhosis (1758067) Macronodular liver cirrhosis (CIBA) (1758075) Nutmeg liver (1763015) Nutmeg liver and purulent cholangitis (1763016) Hemochromatosis in liver (1763023) Mallory-body (1763025) Fatty liver and control liver (1763037) Fatty liver (1763038) Fatty liver (1763039) Fatty liver (1763040) Fatty liver (1763041) Fatty liver (1763042) Centrolobular fatty degeneration of the liver (1763043) Peripheral hepatic steatosis (1763044) Fatty degeneration of the liver (1763045) Fatty degeneration of the liver (1763046) Fatty degeneration of the liver (1763047) Fatty degeneration of the liver (1763048) Fatty degeneration of the liver (1763049) Fatty degeneartion of liver (oil-red o stain) (1763050) Central fatty degeneration of the liver (1763051) Extramedullary hemopoiesis (1811005)

Young patients without clinical evidence of cirrhosis should be told of the generally indolent nature of the infection and that they have many decades of productive life ahead: Patients should be advised of the different indications for treatment with interferon alfa and the physician should review details of the subcutaneous route of administration, duration of treatment, and factors that are believed to enhance or negate response; give a realistic appraisal of sustained response rates; and describe the side effects and clinical monitoring of treatment. Advantages Inhibits hepatitis C virus replication in some patients with chronic disease Sustained response in some patients Important component of combined antiviral treatment Can improve histological hepatitis Disadvantages Given by injection Low sustained response rates in many patients with type 1 hepatitis and higher levels of viraemia High relapse rates Side effects Neutralising antibodies in some patients Relative expense Serum aminotransferase activities usually relapse in patients who remain hepatitis C virus RNA positive at the end of treatment - but some patients may remain positive for a period despite normal serum aminotransferase values. There are inadequate data to indicate (a) whether patients with normal aminotransferase activities and negative for hepatitis C virus RNA at six months should continue treatment to prevent relapse (probably) and (b) whether patients with normal aminotransferase activities and posit* Several workers have suggested that patients with types 2 and 3 infection are more likely to have a sustained response to treatment than patients with type I (and possibly type 4). Though emerging evidence implies that genotyping or serotyping and measurement of viraemia may become a necessary part of the pretreatment assessment of patients, we are not yet at a point at which interferon can be proscribed for patients with type 1 infection, except possibly in older patients with advanced cirrhosis.

SILVIA FARGION,1 FRANCO BISSOLI,2 ANNA LUDOVICA FRACANZANI,1 ELENA SUIGO,2 CONSOLATO SERGI,2 EMANUELA TAIOLI,3 ROBERTO CERIANI,2 VALERIA DIMASI,3 ALBERTO PIPERNO,4 MAURIZIO SAMPIETRO,1 AND GEMINO FIORELLI1 Genetic hemochromatosis and 1-antitrypsin (AAT) deficiency are frequent in white populations. Conflicting data on the association of the two conditions and on the severity of the disease in those in whom these disorders coexist have emerged from analyses of small numbers of patients. To determine if the frequency of AAT deficiency is increased in genetic hemochromatosis, we characterized this protein by isoelectric focusing and DNA analysis in 115 Italian patients with the disease and 290 controls. The frequency of AAT deficiency in patients with genetic hemochromatosis was similar to that in controls (10% and 9%, respectively). The prevalence of cirrhosis in patients with genetic hemochromatosis with MM phenotype was 53%, compared with 58% in those with non-MM phenotype; that of hepatocellular carcinoma, occurring only in cirrhotic patients, was 22% and 28%, respectively. Patients in whom the two defects coexisted did not appear to have a more severe disease, but the limited number of subjects with non-MM phenotype does not allow a conclusive evaluation of clinical differences between them and patients with genetic hemochromatosis with MM phenotype.

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URL: http://www.emi.net/~iron_iod/ Summary: Currently known to be THE most common genetic disorder in which excess dietary iron is absorbed causing iron accumulation in, and damage to, vital organs and joints, and even premature death. Summary: HF works to increase national awareness that hemochromatosis is not only the most common genetic disorder but that it is probably the only genetic disorder which, if diagnosed early and treated adequately, is compatible with a healthy and full life-span. Summary: "We don't yet know what this gene is producing that causes hemochromatosis or the mechanism in the intestine that causes the excess iron absorption, but identifying the gene is an important first step," he says. URL: http://www.stepstn.com/nord/org_sum/245. Summary: Patients with hemochromatosis accumulate excessive amounts of iron in the liver and this eventually can lead to the development of cirrhosis, and in many cases, cancer of the liver.

Home Clinical Aspects Iron Metabolism Hepatic Pathology Other Organs Incidence of Hemochromatosis By Transferrin saturation 0.3% of the Caucasian population is homozygotic. In autopsy series only 1/100,000 cases is diagnosed as hemochromatosis To explain these discrepancies it is postulated that several factors, including the environment, must modulate full gene expression. Recently, the gene responsible for hemochromatosis has been isolated (although the function of the gene product remains unclear). It is expected that the use of molecular diagnostic technics will define the exact incidence of hemochromatosis. Currently there are discrepancies among the different methods used to estimate this incidence. Whatever the real number, it seems that hemochromatosis is often under diagnosed and even when diagnosed, all too often, is at a late stage.

) When chronic diseases cause the liver to become permanently injured and scarred, the condition is called cirrhosis. The scar tissue that forms in cirrhosis harms the structure of the liver, blocking the flow of blood through the organ. Other, less common, causes of cirrhosis are severe reactions to prescribed drugs, prolonged exposure to environmental toxins, and repeated bouts of heart failure with liver congestion. A serious problem for people with cirrhosis is pressure on blood vessels that flow through the liver. If the doctor suspects cirrhosis, you will be given blood tests. In some cases, cirrhosis is diagnosed during surgery when the doctor is able to see the entire liver.

- Clinical: The diagnosis of "asbestosis" requires both a history of asbestos exposure and evidence of interstitial lung disease. 2- Thickened subpleural lines occur due to interlobular septal (irregular thickening), and intralobular fibrosis in the lung periphery; 3- Parenchymal bands: Non-tapering linear densities measuring 2 to 5 cm in length that contact the pleural surface are probably most commonly identified in patients with asbestos related lung disease. Subpleural lines have been identified in up to 40% of patients with asbestosis (however, subpleural lines have been demonstrated in 15-20% of normal patients). Many of these patients may have a mixed disease (ie: concurrent silicosis) due to heavy exposure to silica in coal mines. - X-ray: CT: In addition to findings similar to silicosis, centrilobular emphysematous changes are common in patients with CWP. Silicosis is typically not a cause of emphysematous changes unless there is progressive massive fibrosis or an associated history of cigarette smoking. Clinical management of patients with hypersensitivity pneumonitis differs markedly from that of patients with idiopathic pulmonary fibrosis (desquamative interstitial pneumonitis [DIP]), however, the two may be indistinguishable on clinical examination.

Hemochromatosis is the most common genetic disorder in the USA, with one out of eight Caucasians being carriers, and one in 250 to one in 400 being affected homozygotes (over 1,000,000 affected homozygotes in the USA). Excessive accumulation of iron in bodily organs (e.g., heart, pancreas, skin, liver, joints, pituitary gland, testes) can result in congesticve heart failure, diabetes mellitus, "bronzed" skin, liver cirrhosis, liver cancer, joint pain and swelling (especially of the hands), impotence or premature menopause. Anyone with any of these condition needs to be tested for hemochromatosis, because if excess iron is the cause of the symptoms no improvement will be seen unless the hemochromatosis is treated. Hemochromatosis can be suspected if the percentage of transferrin, a protein in plasma, saturated with iron is greater than 62%. For most patients this treatment is needed several times a month to remove accumulated iron, then needed several times a year to prevent iron from accumulating again. For appointments contact the University of Pennsylvania Health Systems Penn Health line at (800) 789-PENN [(800) 789-7366] For questions contact penngen@www.med.upenn.edu Hemochromatosis Clinic page / penngen@www.med.upenn.edu / revised April 9, 1997

Hemochromatosis is a disease due to increased iron absorption that leads to accumulation of iron in diverse tissues. It can be hereditary (primary hemochromatosis) or secondary to chronic anemias as -thalassemias (ineffective erythropoiesis leading to increased erythrocitic destruction) or defects in hemoglobin synthesis ( as in porphyria cutanea tarda) ;multiple transfusion therapy ;or others less common conditions. In hemochromatosis this absortion reaches the rate of 4 to 5 mg/d and there is a progressive accumulation to 15 to 40 grams of body iron (normal ~ 2 to 3 g). The iron accumulates in every tissue of the body, but main clinical manifestations are secondary to iron deposition in: Liver, thyroid, hypothalamus, heart, pancreas, gonads and joints. Any patients presenting with unexplained hepatomegaly, cardiac insuficiency or arrhythimias, arthritis, diabetes mellitus, hyperpigmentation or hypogonadism hipo gonadothrofic should be investigated for hemochromatosis. Life expectancy rises from 33 to 89% if untreated patients are compared with patients treated with phlebotomy.

Your liver, the largest organ in your body, plays a vital role in regulating life processes. Some of these are: 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 that are easier for the body to use; and To detoxify and excrete substances that otherwise would be poisonous. Your liver helps you by: Producing quick energy when it is needed; Manufacturing new body proteins; Preventing shortages in body fuel by storing certain vitamins, minerals, and sugars; Regulating transport of fat stores; Regulating blood clotting; Aiding in the digestive process by producing bile; Controlling the production and excretion of cholesterol; Neutralizing and destroying poisonous substances; Metabolizing alcohol; Monitoring and maintaining the proper level of many chemicals and drugs in the blood; Cleansing the blood and discharging waste products into the bile; Maintaining hormone balance; Serving as the main organ of blood formation before birth; Helping the body resist infection by producing immune factors and by removing bacteria from the bloodstream; Regenerating its own damaged tissue; and Storing iron. Liver diseases There are many types of liver diseases, but among the most important are: Viral hepatitis; Cirrhosis; Liver disorders in children; Gallstones; Alcohol related liver disorders; and Cancer of the liver. Alcohol-related liver disorders There are three separate liver disorders related to alcohol: fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Each year more than 25 million Americans are afflicted with liver and gallbladder diseases and more than 43,000 die of liver disease each year.

Alcohol and Liver Biliary Atresia Liver Biopsy Hepatitis B Hepatitis C Gallstones Gilbert's Syndrome Hemochromatosis Toxic Hepatitis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Liver Transplantation Wilson Disease WHERE IS THE LIVER LOCATED IN THE BODY? Viral hepatitis Viral hepatitis is an inflammation of the liver caused by one of several viruses: hepatitis A, B, C (formerly non-A, non-B), D and E. Most people who become infected with a hepatitis virus remain well and symptom-free, which means that this infectious disease may go unrecognized. Liver disease in children Thousands of Canadian children - from infants to adolescents - have liver disease, and many die from it each year. The following tests are performed: blood, urine and stool samples are analyzed; the liver and bile ducts are examined with ultrasound; a liver scan showing the liver and bile ducts is performed; a liver biopsy is obtained. In many cases, the specific cause of the chronic liver disease is highly suspected on the basis of blood tests, but a liver biopsy is used to confirm the diagnosis as well as determine the amount of damage to the liver. In some cases, blood testing is quite accurate in giving the doctor the information to diagnose chronic liver disease, while in other circumstances a liver biopsy is needed to assure an accurate diagnosis.

Summary: In addition to the X-linked dominant form of AS, autosomal dominant and autosomal receive varieties of disease are well documented. ] The disorder is inherited recessive in 85% of cases and primarily affect children and young adults and results in renal failure by age 4 in dominantly inherited disease and by age 13 in recessive inherited disease. Summary: Currently known to be THE most common genetic disorder in which excess dietary iron is absorbed causing iron accumulation in, and damage to, vital organs and joints, and even premature death. Summary: Medications, illicit drugs, alcohol, and tobacco smoke have also placed new stresses on this organ. Summary: The Liver Disease Center is one of a few centers nationwide participating in a multicenter trial of promising new drug therapys for chronic viral hepatitis, a persistent inflammation of the liver cells caused by the hepatitis B or C virus. Summary: Clues to Liver Disease by Cynthia Smith, D.V.M. reprinted from the ASTC Bulletin, Post National 1996 Issue Recent research has revealed the first firm evidence for what may cause chronic hepatitis, a progressive and potentially fatal condition that affects many dogs.

Target Audience: General Audience, Females, Contains: Causes, Signs & Symptoms, Diagnosis, Treatment, Medications, Patient Education, Keywords: primary biliary cirrhosis, liver disease, liver scarring, bile ducts, liver inflammation, mitochondrial antibodies, alkaline phosphate activity test, biliary tract disease, immune disorder, corticosteroids, thyroid hormone, liver transplant Primary Biliary Cirrhosis is a chronic liver disease which causes slow destruction of bile ducts in the liver. This American Liver Foundation (ALF) article, Primary Biliary Cirrhosis, details the causes of primary biliary cirrhosis, such as immune disorders or hormonal factors. There is also information on diagnosis and treatment. Primary biliary cirrhosis affects women 10 times more often than men. Pros: Information is clear and concise. Highlights: Check out the internal link to the ALF home page for more resources on liver disease.

An HTML version of this document is available at http://vm.cfsan.fda.gov/~dms/diabetes.html FDA Brochure: May 1993 IMPORTANT HEALTH INFORMATION FOR PEOPLE WITH DIABETES MELLITUS Protect Yourself: Only Eat Fish That's Been Thoroughly Cooked This brochure is to inform people with diabetes mellitus of the hazards they face if they eat raw molluscan shellfish-oysters, mussels, clams, and whole scallops. They're generally low in saturated fat and are excellent sources of protein, vitamins and minerals, although nutrition values differ depending on the type.Properly handled and thoroughly cooked, fish is tender, easy to digest, and safe to eat. Eating raw or undercooked shellfish can a be serious problem for persons with: - Liver disease, including cirrhosis, hemochromatosis, and chronic alcohol use - Diabetes mellitus - Immune disorders, including AIDS, cancer, and reduced immunity due to steroid or immunosuppressant therapy - Gastrointestinal disorders, including previous gastric surgery, and low gastric acid (for example, from antacid use or achlorhydria). The problem occurs because raw mollusks sometimes carry bacteria called Vibrios that may multiply after the shellfish are caught, even with refrigeration. These bacteria are completely killed when the shellfish are thoroughly cooked, removing all danger od the bacteria causing food poisoning. Mollusks feed by filtering water through their systems, so they are more likely to pick up and store bacteria or viruses from the water, including those that van cause illness in humans.

Target Audience: General Audience, Contains: Causes, Signs & Symptoms, Diagnosis, Treatment, Patient Education, Keywords: Gilbert's syndrome, liver disease, serum bilirubin, bile, hemoglobin, bone marrow, spleen, hepatic neurotics, nicotinic acid, radioactive bilirubin, American Liver Foundation, ALF Gilbert's Syndrome is a benign liver disorder characterized by an increase in the serum bilirubin enzyme excreted by the liver. This American Liver Foundation (ALF) site briefly details the nature of Gilbert's syndrome, and its non-specific symptoms, which tend to make diagnosis a problem. It is estimated that Gilbert's syndrome occurs in three to seven per cent of the population, more frequently in males than in females. Pros: Information is clear and concise. Highlights: Check out the internal link to the ALF home page for more resources on liver disease. Site presented by American Liver Foundation -

Target Audience: General Audience, Contains: Causes, Signs & Symptoms, Diagnosis, Treatment, Patient Education, Keywords: Gilbert's syndrome, liver disease, serum bilirubin, bile, hemoglobin, bone marrow, spleen, hepatic neurotics, nicotinic acid, radioactive bilirubin, American Liver Foundation, ALF Gilbert's Syndrome is a benign liver disorder characterized by an increase in the serum bilirubin enzyme excreted by the liver. This American Liver Foundation (ALF) site briefly details the nature of Gilbert's syndrome, and its non-specific symptoms, which tend to make diagnosis a problem. It is estimated that Gilbert's syndrome occurs in three to seven per cent of the population, more frequently in males than in females. Pros: Information is clear and concise. Highlights: Check out the internal link to the ALF home page for more resources on liver disease. Site presented by American Liver Foundation -

HEPATOMEGALY Enlargement of the liver indicates either primary or secondary liver disease, but absence of hepatomegaly does not exclude a serious disorder. Serial determinations of liver size may be of prognostic value; eg, a rapidly shrinking liver in fulminant hepatitis implies a poor outcome, as does an enlarging organ in metastatic carcinoma. Acute, tender enlargement may accompany hemorrhage into a cyst or the liver parenchyma. This consistency is often maintained in enlargement due to acute hepatitis, fatty infiltration, passive congestion, and early biliary obstruction. Hepatic tenderness is overdiagnosed, usually because of the patient's anxiety during palpation. Spontaneous right upper quadrant discomfort is usually minimal in these disorders, but occasionally severe pain and tenderness may mimic an acute surgical condition.

Sequential changes in insulin-like growth factor I (IGF-I) and IGF- binding proteins in children with end-stage liver disease before and after successful orthotopic liver transplantation. Doppler ultrasound and angiography of the vasculature of the liver in children after orthotopic liver transplantation: a prospective study. 0270-9139 The purpose of this study was to compare the incidence and severity of rejection episodes in a group of children receiving living related orthotopic liver transplants (LRLT) versus children receiving cadaveric liver transplants (CLT). Sequential changes in insulin-like growth factor I (IGF-I) and IGF- binding proteins in children with end-stage liver disease before and after successful orthotopic liver transplantation. An increased incidence of Epstein-Barr virus infection and lymphoproliferative disorder in young children on FK506 after liver transplantation. 0041-1337 The incidence of Epstein-Barr virus (EBV) infection and lymphoproliferative disorder (LPD) was determined in a pediatric liver transplant population consisting of 51 children treated with FK506 and 91 treated with cyclosporine.

48 y/o with signs of portal hypertension and skin discoloration. Marked decrease in signal is seen in the liver on the T2- and T2* Hemochromatosis is a disorder of iron metabolism resulting in excessive iron deposits in the liver, pancreas and skin. It is associated with diabetes, which this patient has recently developed. Send questions and comments with your email address to Ray Ballinger at ballingerr@xray1.xray.ufl.edu URL: http://www.xray.ufl.edu/~rball/teach/965.

Title: A 39-year-old man with chronic hepatitis, elevated serum ferritin values, and a family history of hemochromatosis. Author(s): Bacon BR; Fried MW; Di Bisceglie AM Address: Department of Internal Medicine, St. Source: Semin Liver Dis 1993 Feb;13(1):101-5 Abstract: The patient described is a heterozygote for hemochromatosis, and he has chronic hepatitis C. We have hypothesized that, because of chronic viral hepatitis, he could either have an increase in circulating NTBI or he could have up-regulation of hepatocyte TfR expression, perhaps caused by a viral effect on the IRE of TfR mRNA, or a combination of both. Either could result in an increase of his hepatocellular iron uptake, resulting in a redistribution of his total body iron burden (which is in the range seen for HHC heterozygotes) and, in effect, "concentrating" the iron in his liver, thus simulating homozygous HHC. It is likely that there are interrelationships between hepatic iron concentration, hepatocellular iron metabolism, and chronic viral hepatitis. Understanding of these interrelationships may be important in the understanding of some of the fundamental mechanisms of viral growth and replication and hepatocellular injury. A clearer understanding of these interactions is necessary to diagnose the cause of liver disease accurately in patients such as this one Major Indexes: Ferritin [blood] Hemochromatosis [genetics] Hepatitis C [diagnosis] Hepatitis, Chronic Active [diagnosis] Minor Indexes: Adult Biopsy Diagnosis, Differential Hemochromatosis [diagnosis] Hepatitis C [complications] Hepatitis, Chronic Active [complications] Heterozygote Liver [pathology] Substance Abuse, Intravenous Reagent Names: 9007-73-2 (Ferritin) Language: English

Hemochromatosis Hemochromatosis: an Elusive Disorder - an autosomal recessive genetic defect that results in excessive accumulation of iron in the body. is a trademark of Yahoo!

Complete medical dictionary Medmark Hematology Michael Loader Transplant Homepage Osteoporosis & Liver Disease Website Osteoporosis and Related Bone Diseases~National Resource Center Prednisone: Good Guy - Bad Guy Prescribing for patients with liver disease Preventing liver disease Stigma of liver disease & transplantation Pharminfonet Websites (Great websites with information on medications, articles on various diseases, clinical trials and other helpful links. Achlorhydria Autoimmune, Addison's Disease, Anti-phospholipid Syndrome, Antigen, Asthma & other allergies, Atopic Allergy, Autoimmune Atrophic Gastritis, Autoimmune Hepatitis, Autoimmune Thyroiditis, Celiac Disease, Chronic Fatigue Syndrome, Congenital Complete Heart Block, Dermatomyositis, Discoid Lupus Erythematosis, Goodpasture's Syndrome, Hashimoto's Thyroiditis, Idiopathic Adrenal Atrophy, Idiopathic Thrombocytopenia, Insulin-dependent Diabetes, Lambert-Eaton Syndrome, Lymphopenia (some cases), Male infertility (some), Mixed Connective Tissue Disease, Multiple Sclerosis, Myasthenia Gravis, Pemphigoid, Pemphigus Vulgaris, Phacogenic Uveitis, Premature onset of Menopause, Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis, Raynaud's Phenomenon, Rheumatoid Arthritis, Sarcoidosis , Scleroderma, Sjogrens Syndrome, Sympathetic Ophthalmia, Systemic Lupus Erythematosis, Thyrotoxicosis, Type B Insulin Resistance, Ulcerative Colitis, & Wegener's Granulomatosis. Allergies & Asthma Website Arthritis Foundation  (informative Arthritis Today articles) Ask the Physician (post a specific question) Autoimmune Disorders Autoimmunity Research Resources Chronic Fatigue Syndrome Columbia University Autoimmune Diseases Costochondritis and PBC Disorders of Immune Function Dry Eye Syndrome Fibromyalgia  Resource Pages Immune Response Immunity & Infection Immunologic Diseases Interesting Autoimmune Disease Article Is Mercury Toxicity an Autoimmune Disorder John Hopkins Patient Advocacy Site Lyme Disease Nat'l Jewish Center for Immunology & Respiratory National Sjogren's Syndrome Association Patient Consumer Health Information Patient Education and Materials Patient Guide Patient Health Autoimmune Diseases Patient's Network (most diseases) Raynaud's Phenomenon Rheumatoid Arthritis Sarcoidosis Website Transplant website (Ask your transplant questions)  Visit the Circle's Homepage or join the group Emotional Support Groups on the Internet Fritze's  homepage Healthcare & Support Newsgroups Immune System Group (e-mail support group) send to: immune-request @weber.ucsd.edu (in body of e-mail type subscribe and your name) Iron Overload Diseases Association: For current information send e-mail to StarLady11@emi.net or visit the IOD Website Internet BBS Listing. Transplant/Disease/Donor Support Page Transplant Newsgroup: bit.listserv.transplant Transplant Emotional Support (A fun group) Transplant Internet E-mail List (Send subscribe Transplant and your name) Same as Newsgroup. UNOS  United Network Organ Sharing Send the Autoimmune Liver Disease group your comments: E-mail Join Chronic Autoimmune Liver Disease  Support Group (CALD) or the Join Primary Biliary Cirrhosis  (PBCers) Support Group.

HF works to increase national awareness that hemochromatosis is not only the most common genetic disorder but that it is probably the only genetic disorder which, if diagnosed early and treated adequately, is compatible with a healthy and full life-span. HF promotes increased awareness of government agencies and the food industries of the potential harm from unneeded extra dietary iron. HF provides brochures for physicians and health care professionals concerning the most recent information about the diagnosis, treatment and prognosis of the hereditary form of hemochromatosis. There are also video teaching tapes available for purchase, and a quarterly newsletter, Hemochromatosis Awareness. The Iron Overload Diseases Association has a mission to lead the search for millions of Americans and other nationals who have undiagnosed hemochromatosis (iron overload) and to prevent the resulting severe health problems and avoidable deaths. NewsGroup: alt.health.hemochromatosis To read any newsgroup, the newsgroup must be available on your local news server.

Nonalcoholic steatohepatitis (NASH) is described as inflammation of the liver associated with the accumulation of fat in the liver. It is not connected with other causes of chronic liver disease, including hepatitis B and C viruses, autoimmune disorders, alcohol, drug toxicity and the accumulation of copper (Wilson's disease) or iron (hemochromatosis). Since it was first recognized as a specific entity in 1980, NASH has also been called fatty liver hepatitis, nonalcoholic Laennec's, steatonecrosis and diabetic hepatitis. In addition the patient may have had excess fat (very low density lipoproteins, or lipids, a form of cholesterol) in the blood, and may have had other medical conditions, such as coronary artery disease, thyroid disease or hypertension (high blood pressure). Recent studies and the experience of physicians indicate that NASH can result in the development of fibrous tissue in the liver for up to 40% of patients or scarring of the liver (cirrhosis) in 5-10% of patients. Many patients with NASH will show an increase of certain iron proteins (ferritin) in their blood, but whether this relates to any injury to their liver is unknown.

Hemochromatosis Hemochromatosis: an Elusive Disorder - an autosomal recessive genetic defect that results in excessive accumulation of iron in the body. is a trademark of Yahoo!

Excessive accumulation of iron (both hemosiderin and ferritin granules) in parenchymal cells secondary to an in-born error of metablism effecting iron storage, transport or utilization. These patients often have progressive damage to organs because of the accumulation of iron. For example, these patients will eventually develop cirrhosis. There are two pictures below. Videodisc on left: Severe hemochromatosis of the liver, Prussian Blue stain. Digital shows H&E on left and prussian blue on right.

Diagnosis: Hemochromatosis / Hemosiderosis Discussion: These two terms define iron overload. Fe is stored in the body as hemosiderin or ferritin in the reticuloendothelial cells of liver, spleen and bone marrow (2-6gm). Reticuloendothelial cell deposition is seen with multiple transfusions, rhabdomyolysis, extravascular hemolysis; and associated changes are seen only in the organs with RE cells - including the liver, spleen, and the bone marrow, but not pancreas. With the parenchymal cell deposition, decreased signal can be seen within the liver, spleen, pancreas and myocardium. With the RE deposition, pancreas will appear normal, since RE cells are not present in the pancreas. Of note, however, following saturation of RE cells (estimated capacity = 10 gm, which corresponds with 40 units of blood), subsequent redistribution occurs to parenchymal cells.

Stone has been named the laboratory's first director Girl, 7, receives transplant for rare liver disorder Dad's gift saves son from mysterious illness 'Students' eager to learn at Mini-Medical School New pharmacy facilities point to hopes for future Telemedicine moves into home health care arena College of Surgeons verifies UIHC Burn Center Fast recovery from new heart bypass technique Roy Schmidt, a 48-year-old self-described "jack-of-all-trades" from Moline, Illinois, experienced a massive heart attack on August 1, 1996. At the UIHC, heart surgeons Ralph Delius, MD, and Kemp Kernstine, MD, offered Schmidt the opportunity to undergo a new procedure called minimally invasive direct coronary artery bypass (MIDCAB) that they believed offered him the best opportunity for recovery. In turn, their actions are coordinated with the gynecologic members of the IVF team, which include Craig Syrop, MD, Bradley J. Van Voorhis, MD, and Dale W. Stovall, MD. It was the second living-related liver transplant performed at the University of Iowa Hospitals and Clinics by transplant surgeons Maureen Martin, MD, and You Min Wu, MD, assisted by Claudia Corwin, MD, and Alfredo Fabrega, MD. Gibbs referred Johnathon to the University of Iowa Hospitals and Clinics, where he received follow-up care from pediatrician Linda Muir, MD, pediatric gastroenterologists Warren Bishop, MD, and Kathleen Sanders, MD, and Michael Voight, MD, medical director of liver transplantation. Welsh, Professor of Internal Medicine, and colleagues Edwin Stone, MD, Associate Professor of Ophthalmology, and Susan Johnson, MD, Professor of Obstetrics and Gynecology and Associate Dean in the College, presented the first session, "Genetic Engineering: Modern Miracle or Messing with Mother Nature," September 24.

Liverpool and Lancashire Autistic Society (LALAS) is a charitable organisation. It exists to meet the educational, personal and social needs of children and adults with Autism or Asperger Syndrome. var username = GetCookie('username'); if (username == null) { username = prompt('Please Enter The Name You Wish To Be Addressed By (or press cancel)',""); if (username == null) { alert('Its ok if you dont want to tell me your name'); username = 'WebSurfer'; } else { pathname = location.pathname; myDomain = pathname.substring(0,pathname.lastIndexOf('/')) +'/'; var largeExpDate = new Date (); largeExpDate.setTime(largeExpDate.getTime() + (365 * 1000)); SetCookie('username',username,largeExpDate,myDomain); } } // Cookie Functions - Second Helping (21-Jan-96) // Written by: Bill Dortch, hIdaho Design function getCookieVal (offset) { var endstr = document.cookie.indexOf (";", offset); if (endstr == -1) endstr = document.cookie.length; return unescape(document.cookie.substring(offset, endstr)); } function GetCookie (name) { var arg = name + "="; var alen = arg.length; var clen = document.cookie.length; var i = 0; while (i 2) ? "; // current message position var pos = 0; //flag to control message function ScrollMessage() { document.form1.text1.value = msg.substring(pos, msg.length) + spacer + msg.substring(0, pos); pos++; if (pos > msg.length) pos = 0; // set timeout for next update window.setTimeout("ScrollMessage()",300); } // Display a link help message function LinkMessage(text) { window.status = text; } Should you require any further information about any of the services we offer, please do not hesitate to contact our Email address and include as much information about your enquiry as possible.

A Prussian blue iron stain demonstrates the blue granules of hemosiderin in hepatocytes and Kupffer cells. Hemochromatosis can be primary (the cause is probably an autosomal recessive genetic disease) or secondary (excess iron intake or absorption, liver disease, or numerous transfusions). Hemochromatosis leads to bronze pigmentation of skin, diabetes mellitus (from pancreatic involvement), and cardiac arrhythmias (from myocardial involvement). Forward to the next image Back to the previous image Return to the index

Medullary sponge kidney is the disorder in this group which is not usually inherited but the name may be confused with Medullary cystic disease. Alport syndrome (AS) is defined as progressive hereditary hematuric non-immune nephritis characterized ultrastructurally by irregular thickening, thinning and lamellation of the glomerular basement membrane (GBM) associated in some patients with hearing losses, various ocular defects (15-30% of patients), abnormalities of platelets number and function, and esophageal, upper gastrointestinal and genital leiomyomatosis. There are at least three genotypes: ADPKD 1 (90-95%); ADPKD 2 and ADPKD 3 genotype has been also reported. The diagnosis of ADPKD is usually suspected in those with an affected family members, those with clinical complains compatible with ADPKD, and those in whom multiple cysts are found incidentally during renal or abdominal imaging. Hypertension is common in ADPKD (approximately 60% of patients), it starts before loss of renal function occurs, and most likely results from activation of rennin - AII-aldosterone axis due to cyst expansion resulting in stretch and attenuation of the intra-renal vessels. Thus it is not cost effective to screen all patients with ADPKD but it is indicated to screen families with ADPKD with positive history of IC.

Gilbert's Syndrome is a relatively common and benign congenital (probably hereditary) liver disorder, found more frequently in males. It is characterized by a mild, fluctuating increase in serum bilirubin, a yellow pigment excreted by the liver into bile. Bilirubin is produced from hemoglobin (the red pigment of red blood cells) in the bone marrow, the spleen and elsewhere and is carried to the liver in the blood. It undergoes chemical changes in the liver and then is excreted into bile and passes out of the body after further chemical changes in the intestines. However, when there is excessive breakdown of red blood cells or interference with bile excretion, the amount is increased and may produce jaundice. The onset of Gilbert's Syndrome usually occurs in the teens or early adulthood (20's and 30's); there are rarely significant symptoms, but occasionally mild jaundice may appear, and the white of the eye becomes yellow.

Source: Am J Hematol 1994 Apr;45(4):288-92 Abstract: The present investigation evaluated the serum transferrin receptor concentration in subjects with nontransfusional iron overload who were identified in two separate studies on the basis of a serum ferritin level above 400 micrograms/L. Subjects with preclinical hereditary hemochromatosis were evaluated in the first study and those with the African form of iron overload in the second. In the first study, hereditary hemochromatosis was identified in 14 white men on the basis of a persistent elevation in transferrin saturation above 55%. The serum receptor concentration was elevated above the upper cut-off of 8.5 mg/L in two of the subjects, but the mean receptor of 6.1 +/- 1.4 mg/L (mean +/- 2 SE) did not differ significantly from the normal mean for this assay of 5.6 +/- 0.3 mg/L. In the same study, 60 control subjects with secondary iron overload were identified on the basis of a serum ferritin persistently above 400 micrograms/L, with a normal serum C-reactive protein concentration but with a transferrin saturation 55%. Three of these subjects had an elevated serum receptor concentration but the mean value of 5.5 +/- 0.4 mg/L did not differ from normals nor from subjects with hemochromatosis. The mean serum receptor concentration of 5.0 +/- 0.8 mg/L and 4.5 +/- 0.4 mg/L, respectively, did not differ statistically. It was concluded that there is no evidence of generalized dysregulation of the transferrin receptor in hemochromatosis or African siderosis Major Indexes: Hemochromatosis [blood] [genetics] Receptors, Transferrin [analysis] Siderosis [blood] [genetics] Minor Indexes: Adult C-Reactive Protein [analysis] Hemochromatosis [epidemiology] Iron [metabolism] Middle Age Receptors, Transferrin [physiology] Siderosis [epidemiology] South Africa [epidemiology] Reagent Names: 0 (Receptors, Transferrin) 7439-89-6 (Iron) 9007-41-4 (C-Reactive Protein) Grant ID: DK39246-DK-NIDDK

The "Chronic Candida Syndrome" also known as the "Candida Related Complex" (CRC) is the result of intestinal Candida proliferation. Finally and most importantly, the disruption in IgE production in patients with allergies may suggest that these patients, as a result of allergies, have a comprimised IgE response to Candida. A comment from a 1988 report published in Digestion entitled Dead fecal yeasts and chronic diarrhea follows: "The authors report 20 patients in whom a large number of dead or severely damaged yeast cells, supposedly Candida albicans yeasts, were the possible cause of chronic recurrent diarrhea and abdominal cramps. On the other hand, recent clinical evidence and experimental data favor the role of intestinal candidiasis in seborrheic dermatits: a high quantity of Candida in the feces of the affected patients, elevated phospholipase activity of the Candida sp. Crook, president of the International Health Foundation, has tried to report all the possibilities behind the syndrome, as well as information he collects from physicians and patients who have dealt with the Candida problem. More Inability to concentrate Skin problems (hives, athlete's foot, fungous infection of the nails, jock itch, psoriasis (including of the scalp) or other chronic skin rashes) Gastrointestinal symptoms (constipation, abdominal pain, diarrhea, gas, or bloating) Symptoms involving your reproductive organs Muscular and nervous system symptoms (including aching or swelling in your muscles and joints, numbness, burning or tingling, muscle weakness or paralysis) Recurrent ear problems resulting in antibiotic therapy Respiratory symptoms Lupus Hyperactivity/Attention Deficit Disorder Recurrent yeast infections in women

To make comments, suggestions, or get more information about our homepage, send email to medlib@jaguar1.usouthal . edu or call (334)-414-8210. To get more information about the topic, please contact your physician or visit your local library.

GO-DRY^ Dry gangrene^ Left^ Left forearm^ Left^ Left hand^ Right^ Right foot^ . Left^ Left ventricle, NOS^ Hypertrophy, NOS^ Right and left^ Costophrenic angle^ . Disease of the aorta, NOS^ Left^ Anterior^ Descending^ Left^ Anterior^ Descending^ Circumflex branch of left coronary artery^ Marginal^ . Complete^ Remote^ Obstruction, NOS^ Right^ Right coronary artery, NOS^ Left^ Anterior^ Descending^ Transplantation, NOS^ Left^ Anterior^ Descending^ Left^ Anterior^ Descending^ Circumflex branch of left coronary artery^ Marginal^ Coronary artery, NOS^ Single coronary artery^ . Multiple^ Microscopic^ Focal^ Ischemia, NOS^ Fibrosis, NOS^ Right^ Right and left^ Common ventricle^ . Right^ Right and left^ Disease of liver, NOS^ .

Legends by Patricia J. O'Morchoe, M.D. Images from material collected by Donald R. Thursh, M.D. and Dr. Thursh collected these images during the 70's while he was Professor Pathology at New York Medical College, Valhalla, New York. The images were digitized and a hypertext version was initiated at the University of Illinois College of Medicine at Urbana-Champaign, by Dr. Volume 3 to 6 are in a format using frames. To view these volume, you will require a browser such as Netscape (V2 or above) that supports frames or Microsoft's Internet Explorer (for Windows 95 and Windows NT only). The Atlas is copyright 1994,95,96,97 by the Board of Trustees of the University of Illinois.

Gilbert's Syndrome is a relatively common and benign congenital (probably hereditary) liver disorder, found more frequently in males. It is characterized by a mild, fluctuating increase in serum bilirubin, a yellow pigment excreted by the liver into bile. Bilirubin is produced from hemoglobin (the red pigment of red blood cells) in the bone marrow, the spleen and elsewhere and is carried to the liver in the blood. It undergoes chemical changes in the liver and then is excreted into bile and passes out of the body after further chemical changes in the intestines. However, when there is excessive breakdown of red blood cells or interference with bile excretion, the amount is increased and may produce jaundice. Other diagnostic procedures that may be useful include: the effect of reduced caloric intake on plasma bilirubin concentration intravenous administration of nicotinic acid which appears to increase bilirubin formation in the spleen, or administration of radioactive bilirubin to estimate the percentage of the dose remaining in plasma after four hours Gilbert's Syndrome does not require treatment and will not interfere with a normal lifestyle.

Hereditary hemochromatosis (HHC) is a common inherited disorder of iron metabolism that results in increased amounts of iron being absorbed from the intestine. Studies have shown that about 1 in 250 to 400 Caucasians inherit both of the defective genes that cause hemochromatosis. Scientists believe that if the hemochromatosis gene can be precisely located, characterized, and differentiated from the thousands of other genes, then those at risk for developing hemochromatosis could be identified specifically and treated before they have any complications of the disease. Investigators at the conference also reported on other topics of iron metabolism including the relationship of hepatic iron concentration and responsiveness to treatment for hepatitis C, the use of iron supplements, liver transplantation for patients with hemochromatosis, and the role of iron in athletic performance. This has led to studies evaluating the efficacy of iron reduction by chronic phlebotomy therapy ("bloodletting") prior to interferon therapy in patients with chronic hepatitis C. Preliminary studies have shown favorable results and a multicenter study is currently ongoing to evaluate this phenomenon in a large series of patients. In developed countries, iron supplements are not necessary and can aggravate the expression of hemochromatosis, a common disorder of iron overload.

Hereditary hemochromatosis (HHC) is a common inherited disorder of iron metabolism that results in increased amounts of iron being absorbed from the intestine. Studies have shown that about 1 in 250 to 400 Caucasians inherit both of the defective genes that cause hemochromatosis. Scientists believe that if the hemochromatosis gene can be precisely located, characterized, and differentiated from the thousands of other genes, then those at risk for developing hemochromatosis could be identified specifically and treated before they have any complications of the disease. Investigators at the conference also reported on other topics of iron metabolism including the relationship of hepatic iron concentration and responsiveness to treatment for hepatitis C, the use of iron supplements, liver transplantation for patients with hemochromatosis, and the role of iron in athletic performance. This has led to studies evaluating the efficacy of iron reduction by chronic phlebotomy therapy ("bloodletting") prior to interferon therapy in patients with chronic hepatitis C. Preliminary studies have shown favorable results and a multicenter study is currently ongoing to evaluate this phenomenon in a large series of patients. In developed countries, iron supplements are not necessary and can aggravate the expression of hemochromatosis, a common disorder of iron overload.

The diagnostic acumen and treatent skills of the Liver Disease Center staff are particularly important for the care of complicated or unusual cases of liver and bile duct disorders. The Liver Disease Center is one of a few centers nationwide participating in a multicenter trial of promising new drug therapys for chronic viral hepatitis, a persistent inflammation of the liver cells caused by the hepatitis B or C virus. Several hepatitis studies are currently underway using the drugs CY-1899, Tucaresol, Famciclovir, and Intron-A with Ribavirin. Center specialists have extensive experience in the diagnosis and treatmentof rare liver disorders that are seen infrequently in routine practice. For example, the Center treats many patients with primary bilary cirrhosis, a disorder in which damage to the tiny bile ducts results in cirrhosis or scarring of the liver tissue. The Center evaluates a large number of potential liver transplant patients from throughout San Diego and Orange Counties in California as well as the western United States and Mexico.

Net Events - today's chats and programs on various diseases and conditions. Ebstein's Anomaly - case history of an Ebstein's Anomaly child along with informative links of procedures, and related sites including a detailed clinical, and pictoral history. Achromatopsia Network, The - information/support network for individuals and families concerned with the rare inherited vision disorder achromatopsia. Brief History of Tropical Disease Canadian Society for Mucopolysaccharide & Related Diseases Inc Cholesteatomas - experience of a surgical Cholesteatoma removal. Cholesteatoma is a formation in the inner ear. Communicable Diseases Dispepsia - oriented as an aid to gastroenterological patients, it also offers useful hints to physicians.

Prevalence of hemochromatosis among 11,065 presumably healthy blood donors. Prevalence of abnormal iron studies in heterozygotes for hereditary hemochromatosis: an analysis of 255 heterozygotes. Value of hepatic iron measurements in early hemochromatosis and determination of the critical iron level associated with fibrosis. Clinical and biochemical abnormalities in people heterozygous for hemochromatosis. Evidence that the ancestral haplotype in Australian hemochromatosis patients may be associated with a common mutation in the gene. Jouanolle AM, Gandon G, Jezequel P, et al.

Listed below are SOME of the adverse reactions/symptoms that have been reported and/or are associated with the use of Lupron. Conditions that were ATTRIBUTED to Lupron but were NOT REPORTED to the FDA, in the medical literature or in the package insert are NOT included. The package insert DOES NOT STATE THAT ALL MEDICAL PROBLEMS CAUSED BY LUPRON WILL GO AWAY WHEN YOU STOP TAKING THE DRUG Rash Petech(ia) + Sinusitis + Rash Pust(ular) + Skin Dis(order) + Rash Vesic(ular) Bull(ous) + Skin Discolor(ation) + React(ion) Aggr(avated) + Skin Dry + React(ion) Uneval(uated) + Skin Lesions * LUPRON: WHAT IS THE FDA's ROLE IN LUPRON? Copyright ©, 1994-1997 THE NATIONAL LUPRON VICTIMS NETWORK All rights reserved.

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Iron Overload Diseases Association is working with the CDC in Atlanta on a nation-wide survey of hemochromatosis patients; the survey project will begin during September 1996. National iron overload awareness week, is September 15-21, 1996. Alliance of Genetic Support Groups Current Directory Family Village Disability-Related Resources National organizations with information on genetic conditions or birth defects - variety of resources American Liver Foundation The National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health Directory of Digestive Diseases Organizations for Patients American Liver Foundation Hemochromatosis Pamphlet University of Minnesota Research Paper Professional Genetics Societies Genetic clinics, centers, departments

Urea cycle disorders are tragic illnesses that are characterized by excessive amounts of ammonia in the blood. The National Urea Cycle Disorders Foundation is a non-profit organization dedicated to the identification, treatment and cure of urea cycle disorders. A urea cycle disorder is a genetic disorder caused by a deficiency of one of the enzymes in the urea cycle. The urea cycle involves a series of biochemical steps that takes place in the liver, in which nitrogen, a component of protein, is removed from the blood and converted into urea. THE NEONATAL PERIOD: Children with severe urea cycle disorders typically show symptoms after the first 24 hours of life. CHILDHOOD: Children with mild or moderate urea cycle enzyme deficiencies may not show symptoms until early childhood.

Patients and laypersons looking for guidance among the target sources of this collection of links are strongly advised to review the information retrieved with their professional health care provider. Gaucher's Disease Gaucher Disease Home Page [W. Rosenfield] - (US) Gauchers Association Contents Page - (UK) Gaucher Disease: Current Issues in Diagnosis and Treatment - NLM Tech Ass Workshop Reports (US) Review Gaucher Disease [Neuroweb Forum] - MGH (US) Gaucher Treatment Program at MGH - Harvard (US) Leukodystrophy (not a MeSH term! ) United Leukodystrophy Foundation - Illinois (US) Hypoglycemia A Collection of Hypoglycemia Links & Some Information Hypoglycaemia - (AU) Reactive Hypoglycemia Home Page About Hypoglycemia - NIDDK (US) The Sugar Paradox - NutriMed (US) Hyperlipidemia Hyperlipidemia - Am Heart Assoc. Glucosephosphate Dehydrogenase Deficiency An Introduction to G6PD Deficiency Carbohydrate-Deficient Glycoprotein Syndrome The CDG Syndrome - What is it? ) A Case of Glutaric Acidemia [H Morton] - (US) Diabetes Insipidus The Diabetes Insipidus & Related Disorders Network - (US) About Diabetes Insipidus - The Merck Manual Fatty Acid Oxidation Disorder (not a MeSH term! Porphyria - MCS-Allergy About Porphyria - Am.

Canadian Hemochromatosis Society - Hemochromatosis, Iron overload, Arthritis, Liver Cancer, Diabetes. is a trademark of Yahoo!

Iron Overload Books Available : THE IRON ELEPHANT and tick. Airports: Do You Set Off The Metal Detectors? Patients: Do You Have A Story To Share? You Are Invited to the Annual IOD Association Medical Symposium! READERS DIGEST/October 1995/"Is Iron Making You Sick? ANN LANDERS PUBLISHES LETTER FROM SANDRA THOMAS/1991/"IRON OVERLOAD DISEASE CAN BE A SNEAKY KILLER"

(CSA/USA) ( Celiac Sprue) CSC (CSC) (Syndromes of the cerebellum Ataxia Joseph Disease Olivo-ponto-cerebelar atrophy) United Cerebral Palsy Association, Inc. (PPI) ( Cleft Lip/Palate) Cleft Palate Foundation (CPF) ( Cleft Palate) Share and Care Cockayne Syndrome Network (Cockayne Syndrome Xeroderma Pigmentosum) Coffin-Lowry Syndrome Foundation (CLSF) ( Coffin-Lowry Syndrome) Coalition for Heritable Disorders of Connective Tissue ((CHDCT) Connective Tissue Disorders Marfan Syndrome) Thalassemia Action Group (TAG) (Thalassemia Thalassemia minor Thalassemia major Thalassemia intermedia Beta - Thalassemia Cooley's Anemia) AHEPA Cooley's Anemia Foundation, Inc. (CdLS) ( Cornelia de Lange Syndrome) Agenesis of the Corpus Callosum Network (ACC Network) (Corpus Callosum Abnormalities, including Agenesis, Dysgenesis, Malformation, Underdevelopment of the Corpus Callosum; Agenesis of Commissura Magna Cerebri) About Face U.S.A. (Facial Anomalies Cleft Lip/palate Crouzon Apert Treacher-Collins Hemangioma Cystic Hygroma) Children's Craniofacial Association (CCA) (Craniofacial Anomalies Facial Disfigurement) FACES, National Association for the Craniofacially (Handicapped (FACES) Craniofacial Anomalies Facial Anomalies) Craniofacial Foundation of America (CFA) ( Craniofacial Anomalies) Let's Face It, Inc. (NPPSIS) Disabilities, general Rare disorders) National Self-Help Clearinghouse ( Any Disabilities) Association for Persons With Severe Handicaps ( Any Disabilities) National Center for Youth with Disabilities (NCYD) (Adolescents with Chronic IIlnesses Adolescents with Disabilities) Friends Health Connection (FHC) ( Any Disability) Parents Helping Parents (General Disability Children with Special Needs Tuberous Sclerosis) Association for Children with Down Syndrome, Inc. (FRAXA) ( Fragile X Syndrome) Freeman-Sheldon Parent Support Group (FSPSG) (Freeman-Sheldon Syndrome Whistling Face Syndrome Craniocarpotarsal Dysplasia) Parents of Galactosemic Children (PGC) ( Galactosemia) International Patient Advocacy Association (IPAA) (Gaucher Disease Rare Disorders) National Gaucher Foundation (NGF) ( Gaucher Disease) National Genealogical Society (NGS) ( Genealogical education & support) National Society of Genetic Counselors, Inc. (IOD) (Hemochromatosis Thalassemia Iron Overload Porphyria) International Joseph Diseases Foundation, INC (IJDF) (Joseph Disease Machado-Joseph Disease Spino Cerebellar Ataxia type 3 (SCA 3)) Joubert Synd Parents-In-Touch Network, Inc (JSPITN) ( Joubert Syndrome) American Association of Kidney Patients (AAKP) ( Kidney Disease) National Kidney Foundation ( Kidney Disease) Polycystic Kidney Research Foundation (PKR Foundation) ( Polycystic Kidney Disease) Klinefelter Syndrome and Associates, Inc.

Stanford University Medical Center's Pediatric Liver Transplant Program was launched in 1995, when the adult and pediatric liver transplant team at California Pacific Medical Center was recruited to join the Multi-Organ Transplant Center. Leading the nation with the highest success rate, the team performed more than 30 pediatric liver transplants annually. The team achieved a one-year patient survival rate of nearly 87 percent and a 36-month actuarial survival rate of 86 percent for recipients under 1 year of age and 83 percent for those older than 1 year old. These outcomes are particularly remarkable because two-thirds of the children transplanted weighed less than 10 kilograms. Among the factors influencing this success rate has been an "en-bloc" rapid harvesting technique, which greatly improves the function of the donor liver. Also, reduced-size liver transplants decrease waiting time for donors, especially for recipients under the age of one.

Please note: Full access to back issues is only available to registered subscribers. For demonstration purposes you may access the February and April 1997 issues by clicking on their heading in this list. Subscription Information Please note: You must have a browser capable of user-authentication to view the back issues and to access the database. For information on suitable software (Netscape and Microsoft) please have a look in our Software area. 6th Year Carnitine improves life for people with intermittent claudication Magnesium combats mitral valve prolapse syndrome Blood donors suffer fewer heart attacks Heart disease linked to vitamin C deficiency Iron deficiency common in the United States Do childhood infections protect against asthma? Probiotics combat eczema and food allergy Worrying is bad for your heart Adverse drug reactions are frequent and costly Digoxin controversy closer to resolution RESEARCH REPORT: Vitamin E: Your Heart

Hemochromatosis: When Your Blood Has Too Much Iron / AAFP Patient Information Handout Hemochromatosis: When Your Blood Has Too Much Iron Hemochromatosis is a blood disease that causes the body to absorb too much iron. If you have hemochromatosis, your blood tests show that you have too much iron in your blood. It's very important for people with hemochromatosis to have regular blood tests and to see their doctor regularly. You can contact the following organization to obtain more information about hemochromatosis: Hemochromatosis Foundation, Inc.

Michael's A friend of mine recently asked me what I thought I had gained, apart from the obvious liver disorder, during my time in CUSID, and what I would change about the nature of Canadian debating. Since I first walked into the Bickerstath room in Hart House four years ago, my love/hate relationship with the world of debating has left me with a few lasting impressions, not all of which do I expect to be popular, nor which I would present as fundamental truths. Though I enjoy grinding my opponents into the dust as much as the next man, I'm afraid I can't offer much advice as how to do this, except perhaps to quote a long haired Italian fellow who once told me to,"Talk about stuff that you know, and try to make sense." Despite my affection for that warm, fuzzy feeling that you get in the pit of your stomach when you see the carrion crows arrive to feast on the eyeballs of your opposition, I do not believe that winning rounds should be the primary reason to debate. As Yeats said, "Let them take it, there's more enterprise in walking naked." Be gracious in both victory and defeat, and if you want to question the judges after a round, do so in a manner which will give you some insight into how to better hone your skills. Don't exclude them because you don't feel they are your debating equal, nor should you exclude anyone by refusing to acknowledge their right to have an opinion because they can not get on the "net", don't go to the right parties, or go to the wrong school. Remember you have a right to express your opinion in the democracy, not technocracy, in which you find yourself, and that elected office is often a thankless job which you should not seek unless you are fully prepared to honour the commitments which you made in your campaign, and are prepared to be a leader in the true sense of the word.

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Forsyth, R., Bartlett, K. and Eyre, J. Dephosphorylation of 2-deoxyglucose 6-phosphate and 2-deoxyglucose export from cultured astrocytes Neurochemistry international 28, 243-250, 1996. Eaton, S., Pourfarzam, M. and Bartlett, K. The effect of respiratory chain impairment on beta-oxidation in rat heart mitochondria. Eaton S, Zaitoun AM, Record CO, & Bartlett K, Beta-oxidation in human alcoholic and non-alcoholic steatosis Clin Sci 90: 307-313 1996 Eaton, S and Bartlett, K, Tissue specific differences in intramitochondrial control of beta-oxidation. Hepatology 1993;17:1033-40 Eaton S, Turnbull DM, Bartlett K Redox control of beta-oxidation in rat liver mitochondria. Biochim Biophys Acta 1993 1141:81-9 Eaton S, Turnbull DM, Bartlett K Production of 3-enoyl-CoA esters from palmitate by rat liver mitochondria. Biochem Soc Trans 1993;21:804-7 Eaton S, Bhuiyan AK, Kler RS, Turnbull DM, Bartlett K. Intramitochondrial control of the oxidation of hexadecanoate in skeletal muscle.

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Albumin is a protein manufactured by the liver. What does albumin do? Albumin performs many functions including maintaining the "osmotic pressure" that causes fluid to remain within the blood stream instead of leaking out into the tissues. What diseases cause albumin to be too low? Liver disease, kidney disease, and malnutrition are the major causes of low albumin. If albumin gets very low swelling can occur in the ankles (edema) and fluid can begin to accumulte in the abdomen (ascites) and in the lungs (pulmonary edema).

Genetics of specific cognitive abilities. ), Methodology for genetic studies of twins and families (NATO ASI Series D: Vol. ), Methodology for genetic studies of twins and families (NATO ASI Series D: Vol. ), Methodology for genetic studies of twins and families (NATO ASI Series D: Vol. ), Methodology for genetic studies of twins and families (NATO ASI Series D: Vol. ), Methodology for genetic studies of twins and families (NATO ASI Series D: Vol.

(503) 639-6217 Purpose: Provides a support network for children, their parents, and others with Alagille syndrome. (800) 223-0179 or (201) 256-2550 Purpose: Creates awareness and supports research on liver disease; disseminates information about liver wellness, liver diseases and prevention of liver disease with audiovisual and printed materials, seminars, and training programs; promotes organ donation; encourages vaccination against hepatitis B; serves as trustee of transplant funds; and offers support groups through local chapters. (617) 935-9776 Purpose: Advocacy group that educates the public and medical community about the existence of chronic intestinal pseudo-obstruction (CIP); provides support for adults affected with the disease; serves as resource for physicians for information about CIP as it affects adults; supplies information about disability, social security, medical insurance, drug protocols, and practical strategies for dealing with the many components of CIP; maintains a reference library of pertinent articles from recognized medical journals for patients and physicians; maintains close contact with physicians at major medical institutions who treat adults with CIP; and provides referral lists of physicians willing to diagnose and treat adults with CIP. (818) 990-2354 Purpose: Non-profit corporation that provides services and support to persons with celiac disease and dermatitis herpetiformis, through programs of awareness, education, advocacy and research; telephone information and referral services; medical advisory board; and special educational seminars and quarterly meetings. (206) 325-6980 Purpose: Provides instructional and general information materials, as well as counseling and access to gluten-free products and ingredients to persons with celiac sprue and their families; operates telephone information and referral service; conducts educational seminars for health professionals; conducts and supports research; and offers leadership and assistance to 14 affiliates and local member contacts. (800) 776-OLEY or (518) 445-5079 Purpose: Promotes and advocates education and research in home parenteral and enteral nutrition; provides support and networking to patients through information clearinghouse and regional volunteer network; sponsors meetings and conferences, including annual patient/clinician conference; maintains consumers' representative speakers bureau; manages the North American Home Parenteral and Enteral Nutrition Patient Registry, formerly known as OASIS, which is a voluntary database of patient outcome information from across the United States and Canada, and publishes annual summaries of results and basic statistics.

Here are some photos of my husband, Richard, and me in Monterey, CA, and Munich, Germany. My husband has a genetic condition known as hemochromatosis which, simply put, means too much iron in the body. 5 in 1000 people have this condition, and 25 to 35 million people in the USA are carriers of it (carriers display symptoms although to a lesser degree than those who have it outright). Hemochromatosis is the #1 genetic killer in the USA. Most people who have hemochromatosis don't know it; many doctors don't know much about the condition, and because the symptoms of hemochromatosis are other diseases, it is often overlooked. It's quite easy to test for this condition (a simple blood test to check the level of iron in the blood) and, once identified, hemochromatosis is treatable.

Clues to Liver Disease by Cynthia Smith, D.V.M. reprinted from the ASTC Bulletin, Post National 1996 Issue Recent research has revealed the first firm evidence for what may cause chronic hepatitis, a progressive and potentially fatal condition that affects many dogs. The cause of chronic hepatitis, for example, an inherited defect, a drug-related reaction or an infection, is identified in relatively few cases. Most cases are idiopathic - the cause remains unknown. For years, researchers suspected an underlying autoimmune disorder, that is, the body's immune system attacks its own liver cells. A recent study identified a group of dogs with chronic hepatitis that has specific antibodies against the liver. hile this information is preliminary, further research is underway that may reveal whether a test can identify dogs with chronic hepatitis caused by an autoimmune disorder.

MORE THAN ONE MILLION AMERICANS HAVE UNDETECTED IRON OVERLOAD (IODA) is a non-profit 501 (c) 3 organization and is the International Clearinghouse for information on iron overload conditions, including hereditary hemochromatosis. IOD Association is the one major repository of news from physicians, scientists and patients. To lead the search for millions of Americans and other nationals who have undiagnosed iron overload including hemochromatosis; to promote adequate treatment and to prevent the severe health problems, massively misspent medical money and avoidable deaths that result from neglect of iron overload. Iron Overload Books Available : THE IRON ELEPHANT and tick. READERS DIGEST/October 1995/"Is Iron Making You Sick?

This list is updated regularly. Categories that are highlighted and underlined have trials that are actively seeking patients. Note: The trials listed here represent a fraction of the total studies being conducted. If you know of research centers in your area conducting clinical trials that are not listed here, please contact us and we will try to get those trials posted.

Hemochromatosis, a condition that causes the body to absorb and store too much iron, is a common inherited disorder. The American Liver Foundation is working to increase awareness of this iron overload disease, because hemochromatosis can be treated effectively if detected in time. How common is hemochromatosis? Blood tests for serum iron and either total iron binding capacity (TIBC) or transferrin are good screening devices. Anyone who has a blood relative with hemochromatosis should be testes with the various blood tests for iron mentioned above, even if there are no symptoms. Anyone with an iron overload problem should avoid taking tonics and medications with iron or eating large quantities of iron-containing foods, such as red meats.

Hemochromatosis, a condition that causes the body to absorb and store too much iron, is a common inherited disorder. The American Liver Foundation is working to increase awareness of this iron overload disease, because hemochromatosis can be treated effectively if detected in time. How common is hemochromatosis? Blood tests for serum iron and either total iron binding capacity (TIBC) or transferrin are good screening devices. Anyone who has a blood relative with hemochromatosis should be testes with the various blood tests for iron mentioned above, even if there are no symptoms. Anyone with an iron overload problem should avoid taking tonics and medications with iron or eating large quantities of iron-containing foods, such as red meats.

Thesis Statement (click here)Research Status: Officially Undertaken (click here)Personal Background (click here)Research History (click here)Family Medical History (click here)Telltale Symptoms (click here)Biochemistry of CNS Damage (click here)Relationship to Autoimmune MS (click here)How This Makes Sense of MS Epidemiology (click here)Treatment (click here)E-Mail Bobbie (click here)Links Page (frequently expanded) (click here)* CNS Damage and DisabilityOverall Pallor and Local Cyanosis (bluish nailbeds)Severe to Mild Abdominal Distress During Flares Constipation During Flares (can also be diarrhea instead)Weight Loss During FlaresFlare During Last Trimester of Pregnancy Dark, Reddish Urine During Flares Sun Induced Rash Following Flares Abnormally Strong Craving For Salt Tendency To Low Blood Pressure Bright Flashes of Light in the Peripheral Vision Regarding this last symptom, I have been told by a prominent Immunologist who specializes in MS that an immune system attack on the CNS cannot cause this symptom. I think this may be important to allowing CNS damage because it is the smaller of the 2 uroporphyrin isomer molecules, and is therefore the one more capable of crossing the blood-brain barrier and offering it's protection to the CNS. Without the protection offered by sufficient amounts of the Uroporphyrin 1 molecules, the CNS is left vulnerable to the neurotoxic ravages evoked by the precursors. It may be at that point that the immune system accidentally targets an inappropriate component of the CNS damage residue and autoimmune MS would thus become established. Also, one could expect an increased number of cases of MS in modern times because of: Discontinuance of cooking in iron pots Removal of iron from the water supply Increased environmental toxins If these principles stand up to testing, it may be prudent that virtually all victims of MS be kept on a regimen that ensures continuously adequate iron supplies.

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Albany, NY 12208 (518)489-0972 Materials: information kits that include a poster, educational booklets and a videotape for patients, the public, and professionals about the disorder and the organization Contact: Margit A. Krikker, M.D., Medical Director NRPA01@delphi.com (E-mail) Materials: posters, buttons, balloons, bumper stickers, promotional kit, and marketing guide Contact: Rikki S. Epstein

The body seems to know that iron is an important "food" for the cancer cell, and it reacts accordingly: it redirects iron to storage sites deep within certain organs, thus "starving" the cancer cells by decreasing the supply of available iron in the blood. Here are some common myths about iron that you may have heard: Iron deficiency is the number-one nutritional problem in the US Most women need more iron than they are getting from their diet People over fifty don't get enough iron You need meat in your diet to get enough iron Liver, a good source of iron, is one of the most nutritious and healthy meats Iron overload, wherein the body contains too much iron, is an extremely rare condition. Premenopausal women, who lose an average of 1.6 mitlligrams of iron per day, could go without iron for roughly three to seven months before depleting their iron stores of 200-300 milligrams. Liver - cirrhosis,liver cancer Heart - enlarged heart which causes retention of salt and water which backs fluid up into lungs 'congestive' Pancreas and Diabetes - damage to insulin producing cells in the pancreas has long been thought to be an important cause of diabetes in iron overload patients Joints - Arthritis caused by deposition of iron in the joints Pituitary Gland and Infertility - Iron damage to the brain's anterior pituitary gland causes greatly diminished secretion of the hormones necessary for sexual function This often occurs in younger patients. The diagnoses of iron overload in women has been somewhat lacking because doctors thought the chance of a young woman being iron overloaded was ludicrous because of their menstruation.The blood loss does not outweigh the intake of iron and younger women sometimes miss their periods completely and iron overload can actually cause the lack of menstruation. The popularity of anemia as a diagnosis and iron supplements as a cure-all for vague complaints, particularly in women, has done untold harm to thousands who are unaware that they are iron overload victims.

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Medline record 94189537 Title: Prevalence of abnormal iron studies in heterozygotes for hereditary hemochromatosis: an analysis of 255 heterozygotes. Source: Am J Hematol 1994 Feb;45(2):146-9 Abstract: Iron studies were compared in 434 patients from 80 hemochromatosis families classified as putative homozygotes, heterozygotes, and normal by HLA typing. 05, Mann Whitney test). Mean hepatic iron concentration was 54 +/- 6 mumol/g (n = 17), and the hepatic iron index was 2 in these patients. Heterozygotes with minor elevations in serum ferritin or transferrin saturation do not have significant iron overload as assessed by hepatic iron concentration Major Indexes: Hemochromatosis [blood] [genetics] Heterozygote Iron [blood] Minor Indexes: Ferritin [blood] HLA-A Antigens [analysis] HLA-B Antigens [analysis] Histocompatibility Testing Liver [chemistry] Middle Age Transferrin [metabolism] Reagent Names: 0 (HLA-A Antigens) 0 (HLA-B Antigens) 11096-37-0 (Transferrin) 7439-89-6 (Iron) 9007-73-2 (Ferritin) Language: English

Dave gets educated Okay, so it's not exactly true that I've no idea what Hemochromatosis is. A while after I added the links to the page on the Hemochromatosis Foundation, I got mail from the president of the foundation himself, saying, in part: To answer your question a little more simply than the prose supplied by our medical director, hemochromatosis is a genetic disorder which causes a person to absorb to much iron from the food they eat. Since iron is very toxic in even small amounts, it leads to all kinds of very unpleasant effects, including, eventualy, death. It is, in fact, the #1 genetic killer in the U.S., but most people (and unfortunately most doctors) don't know anything about it.

Runner's child racing against clock to survive Select a location Home Weather Archives About us Meet our staff How to contact us Advertising Subscription info -------- Cookbook Sports Welcome to Washington County Civil War inPHONEmation Runner's child racing against clock to survive By BOB PARASILITI Staff Writer Jared Stoner isn't old enough to have seen one of his father's races against the clock. "He had the chemotherapy and radiation treatments to help eliminate the tumor, but it caused the liver disease." Veno occlusive disease (VOD) is incurable and shuts down the veins in the liver. The Cumberland Valley Athletic Club has created the Jared Stoner Fund to help the Stoners defer the costs of treatments.

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Canadian Hemochromatosis Society - Hemochromatosis, Iron overload, Arthritis, Liver Cancer, Diabetes.

FIND US ONE PERSON AND WE HAVE HOPE OF SAVING A FAMILY! Click on the Heading to go to the information you need. More extensive information on HH) Who are we? The Canadian Hemochromatosis Society is an unfunded registered non profit society, run mostly by volunteers and supported entirely by donations. ) Care has been taken to ensure that this information is accurate at the time of publication. The Canadian Hemochromatosis Society disclaims for itself and for the author of this information, all responsibility for any mis-statements or for consequences of actions taken by any person while acting on information contained herin.

FIND US ONE PERSON AND WE HAVE HOPE OF SAVING A FAMILY! Click on the Heading to go to the information you need. More extensive information on HH) Who are we? The Canadian Hemochromatosis Society is an unfunded registered non profit society, run mostly by volunteers and supported entirely by donations. ) Care has been taken to ensure that this information is accurate at the time of publication. The Canadian Hemochromatosis Society disclaims for itself and for the author of this information, all responsibility for any mis-statements or for consequences of actions taken by any person while acting on information contained herin.

Title: Differentiation between heterozygotes and homozygotes in genetic hemochromatosis by means of a histological hepatic iron index: a study of 192 cases. Source: Hepatology 1993 Jan;17(1):30-4 Abstract: The biochemical hepatic iron index, defined as the ratio of hepatic iron concentration (expressed as micromoles per gram dry weight) to age permits accurate prediction of genetic status in patients with genetic hemochromatosis. Therefore a histological hepatic iron index, defined as the ratio of total histological iron score (range = 0 to 60) to age, was evaluated in a total of 192 Australian and French patients with genetic hemochromatosis. These subjects had been classified previously as heterozygotes (n = 18) or homozygotes (n = 174) according to clinical and familial data only. Both were significantly (p 0.0001) increased in homozygotes (respectively, 6.7 +/- 3.8 [range = 1.2 to 22.6] and 0.62 +/- 0.28 [range = 0.14 to 1.5]) compared with heterozygotes (respectively, 1 +/- 0.4 [range = 0.45 to 1.6] and 0.08 +/- 0.05 [range = 0 to 0.14]). These data show that the age-dependent nature of iron accumulation can also be accommodated by calculating the histological hepatic iron index and that histological study is an accurate means of predicting the genetic status of hemochromatosis patients when hepatic iron concentration is not available Major Indexes: Hemochromatosis [genetics] Heterozygote Detection [methods] Iron [metabolism] Liver [metabolism] Minor Indexes: Adult Differential Threshold Hemochromatosis [metabolism] [pathology] Homozygote Liver [pathology] Reproducibility of Results Reagent Names: 7439-89-6 (Iron) Language: English

A substantial body of evidence has accumulated to show that mentally sick children and adults do, in fact, frequently suffer from markedly abnormal metabolism of such essential nutrients as vitamins, amino acids, and fatty acids. None of these statements will carry the dramatic impact of watching the process at work - seeing a quiet, normal patient turned into a depressed, suicidal, or violent psychotic after a test is done (under the tongue) of a food to which he is allergic - and the equal impact of reversal of the entire process by intravenous injections of Vitamin C and Vitamin B6. Fascinating fact is Vitamin C actually allows the body to effectively absorb more of the Heme Iron ( blood based ) but not the same effect on plant or organic iron based nutrient. The vascular cleansing formula must contain specific nutritional support to help the body (a) dissolve the fatty part of the plaque on the artery wall, (b) strengthen its processes, (c) keep the blood fats in solution so that they do not "clump up" downstream, (d) keep the blood "slippery" so that it flows past obstructions (e) dilate or enlarge blood vessels, (f) neutralize and destroy free radicals, (g) produce antioxidants to protect cellular membranes, (h) develop collateral circulation around blocked areas, (i) lower blood cholesterol and trygliceride levels, and (j) remove heavy metals Some of the key nutrients in this regard are the following: Vitamin A. Stimulates the thymus to grow in size, thus allowing more antibody production. Helps the body to utilize vitamin A Selenium. The daily intake of each supplementary nutrient necessary to produce the vascular cleansing response is the following: Vitamin A 33,000 - 40,000 I.U Vitamin D 200 - 670 I.U Vitamin E (d-alpha) 600 - 650 I.U Vitamin C 3,200 - 5,000 mg.

Liver iron quantification: studies in aqueous iron solutions, iron overloaded rats, and patients with hereditary hemochromatosis. Segmental iron deposition in the liver due to decreased intrahepatic portal perfusion: findings at MR imaging. Hemochromatosis: diagnosis and quantification of liver iron with gradient-echo MR imaging. Non-invasive assessment of tissue iron overload in the liver by magnetic resonance imaging. Comparison with a large perinatal control population, including cases with chronic liver disease. Magnetic resonance imaging and different levels of iron overload in chronic liver disease.

But, Patsy had to visit four doctors before one suggested a genetic test. She learned she has the gene for hemochromatosis. Judy Garber, Cancer Specialist at Dana Farber Cancer Institute in Boston says, "In the future, we'll be able to test for genes that are less powerful and still hopefully give us ways to reduce our risk of cancer and other diseases. Once she learned she had the gene, Patsy began a simple treatment to prevent hemochromotosis from developing. " Doctors and scientists say discrimination based on genetic traits is unfair because genetic information is inconclusive. Billings is one of many who say we won't be able to enjoy the full benefit of genetics until we have laws to keep genetic information private.

Wilson's disease is a rare genetic tissues, particularly in the liver, kidneys, brain and corneas It leads eventually to liver disease, abnormalities rusty-brown ring in the cornea of each eye known as a Kayser-Fleischer a non-profit advocacy group whose main purpose is to give aid This aid is given through the fostering of research,

Hemochromatosis disease genetic disorder sickness fatigue EARLY SYMPTOMS ARE ABSENT weakness/fatigue heart irregularities/failure Currently known to be THE most common genetic disorder in which excess dietary iron is absorbed causing iron accumulation in, and damage to, vital organs and joints, and even premature death. Information is available for your reference: Booklets: - for the public, patients and professionals

Hemochromatosis disease genetic disorder sickness fatigue EARLY SYMPTOMS ARE ABSENT weakness/fatigue heart irregularities/failure Currently known to be THE most common genetic disorder in which excess dietary iron is absorbed causing iron accumulation in, and damage to, vital organs and joints, and even premature death. Information is available for your reference: Booklets: - for the public, patients and professionals

Hemochromatosis disease genetic disorder sickness fatigue EARLY SYMPTOMS ARE ABSENT weakness/fatigue heart irregularities/failure Currently known to be THE most common genetic disorder in which excess dietary iron is absorbed causing iron accumulation in, and damage to, vital organs and joints, and even premature death. Information is available for your reference: Booklets: - for the public, patients and professionals

HEMOCHROMATOSIS: AN ELUSIVE DISORDER by Sherry Sanderson & Kimberly Schmidt This page last modified Wednesday, 06-Mar-96 Hello 199.250.238.68 Hereditary hemochromatosis (also called genetic or primary hemochromatosis) is an autosomal recessive genetic defect that results in excessive accumulation of iron in the body. However, although the genotype occurs with equal frequency between males and females, males are eight times more likely to show clinical signs from this disorder than females. In the "normal" adult, iron homeostasis exists in which the small amount of iron absorbed compensates for the equally small amount lost, while the majority of the iron pool is recycled. 1,4,6 Dietary nonheme iron absorption is generally thought to be the mechanism by which iron homeostasis is regulated, as heme iron absorption is not influenced by iron status. The actual absorption mechanism by which iron is taken up by the mucosal cells and how it goes on into the portal circulation is not clear, however, in normal iron metabolism the quantity of iron absorbed is dependent upon the body

Hemochromatosis disease genetic disorder sickness fatigue EARLY SYMPTOMS ARE ABSENT weakness/fatigue heart irregularities/failure Currently known to be THE most common genetic disorder in which excess dietary iron is absorbed causing iron accumulation in, and damage to, vital organs and joints, and even premature death. Information is available for your reference: Booklets: - for the public, patients and professionals

Your liver, the largest organ in your body, plays a vital role in regulating life processes. This complex organ performs many functions essential to life. The liver, located behind the lower ribs on the right side of your abdomen, weighs about 3 pounds and is roughly the size of a football. All of the blood that leaves the stomach and intestines must pass through the liver before reaching the rest of the body. The liver is thus strategically placed to process nutrients and drugs absorbed from the digestive tract into forms that are easier for the rest of the body to use. The liver converts them to substances that can be easily eliminated from the body.

Hemochromatosis is the accumulation of iron in the cells of the body. Hemochromatosis is often called pigment cirrhosis or bronze diabetes. The name bronze diabetes refers to the diabetes mellitus and pigmentation that occur with hemochromatosis.

URL: http://www.medaccess.com/diet_guide/food1.htm URL: http://diamond.mtk.nao.ac.jp/~bfr/McSpotkit/tok/media/reports/surgen_rep.html URL: http://www.icondata.com/health/pedbase/files/ANEMIA-I.HTM URL: http://worldmall.com/erf/lectures/NUTR.TXT URL: http://www.dietetics.com/groups/IADA.htm URL: http://www.cldc.howard.edu/~cotton/nutr.html

Source: Ann Gastroenterol Hepatol (Paris) 1993 Nov-Dec;29(6):292-8; discussion 298-9 Abstract: Haemochromatosis is an inherited disorder of iron metabolism characterized by a general iron over loading. Without diagnosis and early treatment, it is a serous and potentially fatal disease by cardiac failure or hepatocellular carcinoma in particular. Gene prevalence was estimated at 0.06 in Brittany, so that haemochromatosis may be the most common genetic disease in this area. The gene is also unknown but in 1975 it was located on the short arm of chromosome 6, closely linked to the HLA class I region, less than 1 cM from HLA-A. Characterization of new polymorphic markers and linkage disequilibrium analysis have led us to locate the gene within a 350 kb region around HLA-A. A structural analysis of these genes was undertaken to find an eventual abnormality in patients Major Indexes: Hemochromatosis [genetics] Minor Indexes: Chromosome Mapping Cloning, Molecular [methods] Gene Frequency Genetics, Biochemical HLA Antigens [genetics] HLA-A1 Antigen [genetics] Hemochromatosis [epidemiology] [metabolism] Heterozygote Detection Histocompatibility Antigens Class I [genetics] Inversion (Genetics) Linkage Disequilibrium Polymerase Chain Reaction Polymorphism (Genetics) Reagent Names: 0 (Histocompatibility Antigens Class I) 0 (HLA Antigens) 0 (HLA-A1 Antigen) 0 (HLA-E antigen) 0 (HLA-F antigen) Language: French

No matter hoe good your diet and digestion, The human liver has undergone a tremendous assault in the second half of the 20th century. Air- and water-borne pollutants have created new toxins for the liver to process. Take care of your health. Each Vegicaps supplies: Milk Thistle Extract Standardized to contain 80% Silymarin, including Silybinin, Silydianin and Silychristin. Citrus Bioflavonoid Complex Naturally derived from oranges, lemons, limes, tangerines and grapefruit.

Title: Liver iron quantification: studies in aqueous iron solutions, iron overloaded rats, and patients with hereditary hemochromatosis. Source: Magn Reson Imaging 1994;12(7):999-1007 Abstract: For the noninvasive liver iron quantification by MRI in human iron overload diseases, fundamental proton relaxation mechanisms were studied in aqueous solutions with ferritin and other iron compounds, in experimentally iron overloaded rats, and in patients with iron overload diseases. MR-relaxation rates as a function of iron concentrations in the range of 0-7.5 mg Fe/g aqueous iron solutions, 0-5.4 mg Fe/g rat liver in vivo, and 0.16-4.9 mg Fe/g human liver in vivo were determined from multi- and sets of single-spin echo sequences (1.5 T imager). As predicted by theory, transverse relaxation rates (1/T2) in aqueous iron solutions, in liver tissue of rats, and in human liver tissue increased linearly with the iron concentration. A preliminary calibration for the liver iron quantification by MRI was performed from in vivo measurements of liver 1/T2-relaxation rates and liver iron quantification by atomic absorption spectroscopy in biopsies from 13 patients. With the single spin-echo method, precise in vivo liver iron quantification in humans also above 2.0 mg Fe/g liver tissue (T2 15 ms) should be accomplished on any imager with shortest spin-echo time available, at least TE 20 ms Major Indexes: Hemochromatosis [genetics] [metabolism] Iron [chemistry] Liver [chemistry] Magnetic Resonance Imaging Minor Indexes: Adult Ammonium Compounds [chemistry] Calibration Ferric Compounds [chemistry] Ferritin [chemistry] Ferrous Compounds [administration & dosage] [chemistry] Image Enhancement Iron-Dextran Complex [chemistry] Iron [adverse effects] Magnetic Resonance Imaging [methods] Middle Age Models, Biological Models, Chemical Organometallic Compounds [administration & dosage] [chemistry] Rats, Wistar Rats Solutions Spectrophotometry, Atomic Absorption Reagent Names: 0 (Ammonium Compounds) 0 (Ferric Compounds) 0 (Ferrous Compounds) 0 (Organometallic Compounds) 0 (Solutions) 10028-22-5 (ferric sulfate) 19864-63-2 (ammonium ferrous sulfate) 67527-18-8 (HOE 117) 7439-89-6 (Iron) 79173-09-4 (teferrol) 9004-66-4 (Iron-Dextran Complex) 9007-73-2 (Ferritin) Language: English

Title: An autopsy case of pyruvate kinase deficiency anemia associated with severe hemochromatosis. Source: Intern Med 1994 Jan;33(1):56-9 Abstract: We report an autopsy case of pyruvate kinase deficiency anemia with severe hemochromatosis. This anemia is rarely associated with hemochromatosis. In this case, the autopsy findings showed hemochromatosis of the heart, pancreas, liver, kidneys, thyroid gland, adrenal glands, testes and skin. A family study showed negative data for iron overload and no known HLA type suggestive of idiopathic hemochromatosis. To explain this rare association, we suggest that this patient's iron overload was an acquired type, which might have mainly been caused by increased iron absorption due to the severe hemolytic anemia Major Indexes: Anemia, Hemolytic [complications] Hemochromatosis [complications] Pyruvate Kinase [deficiency] Minor Indexes: Adult Autopsy Fatal Outcome Heart Failure, Congestive [etiology] Hemochromatosis [pathology] Reagent Names: EC 2.7.1.40 (Pyruvate Kinase) Language: English

Medline record 94320881 Source: Hepatology 1994 Aug;20(2):404-10 Abstract: Recent preliminary reports suggest a poor outcome of orthotopic liver transplantation for patients with hemochromatosis. Between March 1988 and October 1992, nine of 249 adults (3.6%) undergoing orthotopic liver transplantation had hemochromatosis. Mean age was 53 yr (range, 42 to 62 yr), and eight of nine patients were men. The diagnosis of hemochromatosis was based on transferrin saturation 62% and hepatic iron index 2.0. (ABSTRACT TRUNCATED AT 250 WORDS) Major Indexes: Hemochromatosis [complications] Liver Transplantation Minor Indexes: Actuarial Analysis Adult Arrhythmia [etiology] Heart Failure, Congestive [etiology] Hemochromatosis [metabolism] [pathology] Iron [metabolism] Liver Transplantation [adverse effects] [mortality] Liver [metabolism] Middle Age Retrospective Studies Survival Rate Treatment Outcome Reagent Names: 7439-89-6 (Iron) Language: English

This resource is an alphabetical list of liver diseases and conditions with hypertext links to files at this site, or to other sites, that provide relevant information. It also has a link to "Current Papers in Liver Disease" and links to some other liver-related sites on the internet. Diseases of the Liver is maintained by: Last updated on May 24, 1997. Current Papers in Liver Disease: An annotated list of recently published papers that relate to diseases of the liver. This list contains papers that are either of outstanding significance or that may have an impact on the clinical care of patients with liver diseases.

Medline record 94314125 Title: Screening for hemochromatosis: a cost-effectiveness study based on 12,258 patients. Source: Gastroenterology 1994 Aug;107(2):453-9 Abstract: BACKGROUND/AIMS: Current emphasis in hemochromatosis has focused on early detection and treatment to prevent permanent liver damage and hepatocellular carcinoma. RESULTS: One hundred twenty-seven patients had an initial serum iron concentration or = 180 micrograms/dL. Eight patients (age, 38-71 years; 7 men and 1 woman) had transferrin saturation or = 62% (range, 84-99) and serum ferritin value or = 400 micrograms/L (range, 457-4004) with no other explanation for the abnormal iron test results. Even at this yield, screening appears cost-effective Major Indexes: Hemochromatosis [prevention & control] Mass Screening [economics] Minor Indexes: Adolescence Adult Aged Child Cost-Benefit Analysis Feasibility Studies Hemochromatosis [genetics] [metabolism] Heterozygote Homozygote Iron [blood] [metabolism] Liver [metabolism] Middle Age Pilot Projects Prospective Studies Reagent Names: 7439-89-6 (Iron) Language: English

Medline record 94056654 Title: Hepatic morphology and iron quantitation in perinatal hemochromatosis. Source: Am J Pathol 1993 Nov;143(5):1312-25 Abstract: We compared hepatic morphology, hepatocellular siderosis, extrahepatic parenchymal siderosis, and (by chemical assay of liver and spleen) the amount of elemental iron and copper in 12 cases of perinatal hemochromatosis (PH) with 119 perinatal controls. Controls were subgrouped according to diagnoses based on clinical and autopsy findings; 37 had chronic liver disease, either hepatic fibrosis (17) or cirrhosis (20). By chemical assay, total hepatic iron in PH cases was not significantly greater than in any control group except the preterm. Its distinctive hepatic morphology seems related to onset of liver disease during fetal life, when periportal hepatocytes normally contain hemosiderin (as in 71 of 82 controls without chronic liver disease).

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Hemochromatosis Foundation P.O. Box 8569 Albany, NY 12208 (518)489-0972 Materials: information kits that include a poster, educational booklets and a videotape for patients, the public, and professionals about the disorder and the organization Contact: Margit A. Krikker, M.D., President National Therapeutic Recreation Society National Recreation and Park Association 2775 South Quincy Street, Suite 300 Arlington, VA 22206-2204 (703)578-5548; (703)578-5559 (TDD); (703)671-6772 (Fax) NRPA01@Delphi.Com (E-mail) Materials: posters, buttons, balloons, bumper stickers, promotional kit, and marketing guide Contact: Rikki S. Epstein, M.Ed.

Hemochromatosis is usually caused by B. Autosomal recessive inherited trait 2. Clinical manifestations of hemochromatosis include all of the following EXCEPT: D. Chronic interstitial nephritis leading to renal failure 3. The best laboratory test to screen for hemochromatosis is: E. Transferrin saturation 4. The best laboratory test to confirm a suspected diagnosis of hemochromatosis is: A. Liver biopsy with quantitative iron and "iron index" 5. Phlebotomy in a patient with hemochromatosis appears to improve which of the following clinical manifestations?

The generalist physician should also remember that primary biliary cirrhosis is curable by liver transplantation, so patients with moderately advanced disease should be assessed at some point for possible referral to a specialist or transplant centre. (C), The University of Calgary, Foothills Hospital Primary Biliary Cirrhosis (PBC) is an uncommon chronic liver disease manifested by the gradual destruction of the small bile ducts within the liver resulting in chronic cholestasis and ultimately biliary cirrhosis. The clinical presentation may also be related to a number of diseases which are associated with PBC. In fact non-hepatic disorders are found in up to 70% of patients with PBC. Diseases and disorders associated with PBC include a number of connective tissue diseases including scleroderma and the CREST syndrome, Sjogren's syndrome, autoimmune thyroiditis (occurring in up to 20% of patients with PBC), autoimmune thrombocytopenia, renal tubular acidosis, and asymptomatic bacteriuria. A number of mathematical formulas including one developed at the Mayo Clinic (the Mayo Model) have been developed for prognostication of patients with PBC and has applicability for referral of patients to liver transplantation centres. At present there is no known cure for PBC. The treatment falls into three main categories: (1) general measures for patients with cholestasis, (2) specific treatment for PBC and (3) treatment of symptoms. Pruritus is a common complaint in patients with PBC and can be very difficult to treat in some patients.

Source: J Vet Intern Med 1994 Mar-Apr;8(2):105-11 Abstract: Two 2-year-old Salers cattle from different herds raised on pasture were evaluated for retarded growth and diarrhea. Increase of liver enzyme activities and prolonged sulfobromophothalein (BSP) half life (T1/2) indicated liver disease with impaired liver function. Transferrin saturation (TS) and liver iron content were markedly increased, consistent with a diagnosis of hemochromatosis. Continued surveillance of the second herd (serum iron, total iron binding capacity [TIBC], unsaturated iron binding capacity [UIBC], and TS), identified a heifer as a hemochromatosis suspect in a subsequent generation. The absence of dietary iron loading in conjunction with the histopathologic and metabolic findings were consistent with a diagnosis of primary hemochromatosis. The reported disease is similar to idiopathic hemochromatosis in human beings in which there is a hereditary defect in iron metabolism Major Indexes: Cattle Diseases [diagnosis] Hemochromatosis [veterinary] Minor Indexes: Cattle Diseases [genetics] Cattle Hemochromatosis [diagnosis] Hemosiderin [metabolism] Iron [blood] Liver Cirrhosis [pathology] Pedigree Transferrin [metabolism] Reagent Names: 11096-37-0 (Transferrin) 7439-89-6 (Iron) 9011-92-1 (Hemosiderin) Language: English

David, spread the word about iron overload. I bought a book called "The Iron Elephant". The iron overload has caused cirrhosis of my liver, I have an enlarged heart due to muscle damage, I'm taking testosterone shots every two weeks due to hypogonadism caused by the high iron, I have osteoporosis in my hips due to the storage iron. was diagnosed in 1984 for the diabetes but I suspect the iron overload was causing it back then.

Medline record 95100174 Source: Am J Gastroenterol 1995 Jan;90(1):152-3 Major Indexes: Anemia [etiology] Bloodletting Hemochromatosis [complications] [therapy] Hypogonadism [complications] Iron [blood] Minor Indexes: Anemia [blood] Hemochromatosis [blood] [genetics] Hypogonadism [blood] Middle Age Reagent Names: 7439-89-6 (Iron) Grant ID: T32DK07218-17-DK-NIDDK

The black population group in South Africa often suffer from iron overload problems but this is usually a result of eating acidic foods cooked in iron pots. The blood test: Measure Serum Iron (SI) and Total Iron Binding Capacity (TIBC) Divide TIBC into SI to get a percentage iron saturation. If you have been diagnosed with iron deficiency anaemia without having blood tests done you may have iron overload. Nearly 10% of all diabetics have undiagnosed iron induced diabetes from iron storage in the pancreas. When their iron levels tested higher than normal he was 100% convinced I had hemochromatosis and put me on treatment to reduce the iron. Hemochromatosis: An Elusive Disorder An article by Sherry Sanderson & Kimberly Schmidt NetBiochem Medical Biochemistry Center Information on heme and iron metabolism Hemochromatosis: Not So Rare Pamphlet by the American Liver Foundation Hemochromatosis: A Deadly & Undiagnosed Condition Pamphlet by the Environmental and Preventive Health Center of Atlanta [Index]  If you are a hemochromatosis sufferer and live in Southern Africa please contact me.

Title: Does rapidly progressive iron overload in a young girl with sideroblastic anemia also signify the presence of hereditary hemochromatosis? Source: Pediatr Hematol Oncol 1994 Jan-Feb;11(1):99-104 Abstract: A severely anemic 3-year-old girl with refractory sideroblastic anemia and fulminant, fatal hemochromatosis is described. The patient had transfusion-dependent anemia with clinical cardiac, liver, and endocrine dysfunction that resulted from iron loading. The patient was minimally transfused, and deferoxamine chelation was started at age 34 months. Despite treatment, the patient died at age 46 months as a result of severe iron overload. Sideroblastic anemia and iron overload in childhood are reviewed, and a pathophysiologic mechanism for the patient's clinical course is postulated Major Indexes: Anemia, Sideroblastic [therapy] Hemochromatosis [genetics] Iron [blood] Minor Indexes: Anemia, Sideroblastic [blood] [complications] [pathology] Child, Preschool Fatal Outcome Hemochromatosis [blood] [complications] [therapy] Time Factors Reagent Names: 7439-89-6 (Iron) Language: English

People don't rust like the Tin Man, but iron can be dangerous to us, too. If you have hemochromatosis (HC), a defect in your intestine causes it to soak up iron like a sponge. ) Early menopause or impotence Liver disease or cancer Not everyone with HC has all these symptoms, nor does having some of these always mean you have HC. ) Early detection and treatment of HC will prevent the damage caused by iron excess. Your tax-deductible donations make it possible for us to provide this free information about iron, and supports the research needed to better understand how iron affects your health. Stay informed, ask your doctor about cutting back on your iron intake, and have your iron status checked soon.

"the three C's" Cation disease hyperparathyroidism (Ca++) hemochromatosis (Fe++) Wilson disease (Cu++) Crystal deposition disease gout (sodium monourate) calcium pyrophosphate deposition (CPPD, pseudogout) Cartilage degeneration of unknown cause Also: ochronosis acromegaly hypophosphatasia osteoarthritis

Medline record 94056467 Title: Essential hypertension genetics, HLA associations, and heterozygous hemochromatosis [letter; comment] Author(s): Sullivan JL Source: Am J Med 1993 Nov;95(5):552 Major Indexes: HLA Antigens [genetics] Hemochromatosis [genetics] Hypertension [genetics] Minor Indexes: Hemochromatosis [complications] Heterozygote Hypertension [complications] Reagent Names: 0 (HLA Antigens) Language: English

Hemochromatosis is the #1 genetic killer in the U.S., affecting nearly two million Americans, yet most victims are unaware that they have it. If left undetected and untreated, hemochromatosis is fatal in most cases. Hemochromatosis is an inherited disorder of the small intestine that causes a person to absorb too much iron from their food. Although hemochromatosis is widespread, the blood test for it, called a "fasting Percent TIBC Saturation" (% TIBC SAT), is rarely included in general screenings. The Hemochromatosis Foundation is a nonprofit organization that has worked for nearly twenty years to improve the lives of people with hemochromatosis. For more information about the disease, screening events in your area, or how you can help in finding the cure for hemochromatosis, contact your local chapter, or write to:

Hemochromatosis - A Deadly & Undiagnosed Condition The information that follows is © June, 1994 Leslie N. Johnston, D.V.M. Used with permission. Heredity Hemochromatosis (HH) was once thought to be rare, and if you consider 5 out of 1,000 people who have the double recessive genes to develop the diseases that this condition will lead to, then you can say that it is still a rare condition. Let us think of HH as a condition rather than a disease, for it HH is not properly managed, it will lead to all kinds of diseases. Like the wind on the ocean, just enough is needed to keep the waves choppy enough to keep the water aerated for the sea animals and just strong enough to gracefully make our ships sail across the water. What we don

Hemochromatosis is the #1 genetic killer in the U.S., affecting nearly two million Americans, yet most victims are unaware that they have it. If left undetected and untreated, hemochromatosis is fatal in most cases. Hemochromatosis is an inherited disorder of the small intestine that causes a person to absorb too much iron from their food. Although hemochromatosis is widespread, the blood test for it, called a "fasting Percent TIBC Saturation" (% TIBC SAT), is rarely included in general screenings. The Hemochromatosis Foundation is a nonprofit organization that has worked for nearly twenty years to improve the lives of people with hemochromatosis. For more information about the disease, screening events in your area, or how you can help in finding the cure for hemochromatosis, contact your local chapter, or write to:

NORD does not promote or endorse participation in any specific organization. The information is subject to change without notice. The Hemochromatosis Foundation is a national not-for-profit organization dedicated to finding a cure for Hemochromatosis. It seeks to increase general awareness of Hemochromatosis so more people will receive the correct early diagnosis and fewer people will experience avoidable health problems associated with Hemochromatosis. In addition, the Foundation works to improve the quality of life for people with Hemochromatosis and their families. The Foundation seeks to establish local chapters; sponsor discussion groups where people can share their experiences with others who understand Hemochromatosis; and provide physician referrals, general information, and local contacts.

In studies in which patients received a single 30-mg oral dose of dexfenfluramine, mean peak plasma concentrations of dexfenfluramine ranged between 11 and 41 ng/mL in individual patients after 1.5 to 8.0 hours. Following administration of single 30-mg, 40-mg, and 60-mg doses of dexfenfluramine to healthy volunteers, dexfenfluramine Cmax values of 25 ng/mL, 33 ng/mL, and 51 ng/mL and area-under-the-curve values of 144 ng-hr/mL, 191 ng-hr/mL, and 275 ng-hr/mL, respectively, were found. In a dose response study of Dexfenfluramine involving obese patients treated for 12 weeks, dexfenfluramine C min values of 24 ng/mL at a dose of 15 mg twice daily and 58 ng/mL at a dose of 30 mg twice daily were observed. Mean (+/-SD) steady-state plasma concentrations of dexfenfluramine and d-norfenfluramine after six months of treatment (15 mg twice daily) in 18 obese patients over 60 years old were 27.3 (+/- 16.3) ng/mL and 14.0 (+/- 7.4) ng/mL, respectively, compared to values of 24.1 (+/-15.9) and l5.6 (+/-1 1.2), respectively, in 268 patients under 60 years old. In a cohort of these patients followed through 12 months of treatment (15 mg twice daily) mean (+/-SD) steady-state plasma concentrations of dexfenfluramine and d-norfenfluramine in 17 obese patients over 60 years old were 32.9 (+/-16.8) ng/mL and 18.0 (+/-8.0) ng/mL, respectively, compared to values of 23.9 (+/-12.9) and 14.4 (+/-8.2), respectively, in 186 obese patients under 60 years old. Some short-term studies have suggested that weight loss with Dexfenfluramine may be associated with a reduction in hyperglycemia in obese diabetic patients, a reduction in blood pressure in obese hypertensive patients, and improvement in the lipid profile in obese hyperlipidemic patients.

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Have you taken our email survey yet? The goals of the Hemochromatosis Foundation include: (1) increasing the awareness of the public, professionals, and government agencies about the disorder; (2) encouraging routine screenings; (3) promoting research aimed at identifying the defect(s) causing the increased iron absorption and at understanding the toxic effects of iron; and (4) cautioning against extra-dietary iron supplements and vitamin C which increases iron absorption, and iron-fortified foods. The Foundation sponsors periodic teaching conferences for families and for professionals, and supports biennial international conferences on hemochromatosis. The Foundation distributes several general brochures concerning information about the diagnosis, treatment, and prognosis of the hereditary form of hemochromatosis intended for health care professionals, patients, and the general public. A videotape is available for purchase.

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