Guest guest Posted May 26, 2006 Report Share Posted May 26, 2006 here are some facts on blood test ,Terry Paki HOME | MY PROFILE | LOGOUT ARTICLES What is the Hepatitis C Virus? Basic Information About Hepatitis C How is Hepatitis C Transmitted from Person to Person? Sex and HCV: Can You Infect Your Partner? Frequently Asked Questions About Hepatitis C Understanding Your Liver's Structure and Function Seniors and Hepatitis C Vaccination for Hepatitis A and B Understanding HCV / HIV Coinfection Self-Recovery of Hepatitis C: It May be About Genetics The Future of Liver Research ARTICLES Hepatitis C Tests Hepatitis C Viral Load Testing Common Liver Lab Tests Understanding Liver Biopsy Where To Get Tested for Hepatitis Infection Understanding the Complete Blood Count (CBC) with Differential Understanding the Basic Metabolic Profile (BMP) Understanding the Complete Metabolic Profile (CMP) ARTICLES General Hepatitis C Treatment Information Responding to Hepatitis Medications (or not) Viral Response as a Predictor of Treatment Outcome How Durable is the Sustained Viral Response? Is Retreatment an Option? Liver Transplant ARTICLES Inflammation of the Liver Liver Fibrosis Women May be Protected Against Fibrosis, Suggests Study Cirrhosis of the Liver End-Stage Liver Disease Liver Cancer Other Complications of HCV Infection Diseases and Conditions Associated with Hepatitis C Fibromylagia and Hepatitis C Infection Diabetes and Hepatitis C Infection Pain Management and Hepatitis C Infection Cryoglobulinemia and Hepatitis C Infection ARTICLES Symptoms of Acute HCV Infection Symptoms of Chronic HCV Infection Depression and Fatigue in HCV Infection Hepatitis C Symptom Emergencies ARTICLES Hepatitis A: What is it? Hepatitis A: How is it Transmitted? Hepatitis A: Prevention and Vaccination Hepatitis A: Diagnosis and Testing Hepatitis A: Symptoms and Course of Infection Hepatitis A: Treatment and Postexposure Prophylaxis Hepatitis A: Groups at Higher Risk of Infection Hepatitis B: What is it? Hepatitis B: How is it Transmitted? Hepatitis B: Prevention and Vaccination Hepatitis B: Diagnosis and Testing Hepatitis B: Symptoms and Course of Infection Hepatitis B: Treatment and Postexposure Prophylaxis Hepatitis D Hepatitis E Hepatitis G More articles... ARTICLES Testing and Diagnosis of Pediatric Hepatitis C Risk Factors for Pediatric HCV Infection Clinical Course of Pediatric Hepatitis C Infection Treatment of Pediatric Hepatitis C May. 30, 8PM ET Hepatitis Open Forum Emmet B. Keeffe, MD Common Liver Lab Tests Article Date: 9/24/2003 Below are brief explanations of some lab tests commonly used for patients with liver disease. Note that reference ranges (in parentheses) vary from lab to lab, your tests results may have slightly different reference ranges than those shown below. Albumin: 3.5 - 5 g/dl The liver makes albumin using amino acids that it gets from proteins. Low levels can cause swelling in the extremities (edema), and in the abdomen (ascites). Prealbumin: 16 - 40 mg/dl Prealbumin is a protein made by the liver. It is helpful in finding out if a person is malnourished. Globulin: 2 - 3 g/dl Testing for globulin is used to measure the total amount of immunoglobulins in the blood. These are also referred to as antibodies. If the test result is high, it is a sign of infection / inflammation. Total Protein: 5.5 - 9 g/dl Total protein is the combined amount of albumin and globulin. Prothrombin Time: 10 - 13 sec Prothrombin time measures the amount of time it takes blood to clot (coagulate). If the liver is injured, clotting is impaired, and the prothrombin time is prolonged. Alanine Aminotransferase (ALT): 3 - 30 IU/LAspartate Aminotransferase (AST): 8 - 42 IU/L Alanine aminotransferase (ALT) and aspartate transaminase (AST) are very sensitive indicators of inflammation and cell death (necrosis), which are released when liver cells are damaged or die, however, both ALT and AST may be elevated for reasons other than liver problems. Lactate Dehydrogenase (LDH): 100 - 225 IU/L LDH is less sensitive to liver disease than ALT / AST, but it can be elevated due to hepatitis. Gamma-glutamyl Transpeptidase (GGT): 8 - 38 U/L GGT (or GGTP) is sometimes elevated in people with cirrhosis or other forms of liver disease. Alkaline Phosphatase: 20 - 125 U/L Alkaline phosphatase is another liver enzyme that can be elevated in liver disease. Total Bilirubin: 0.3 - 1.0 mg/dl The appearance of yellow eye and skin color (jaundice) is the characteristic symptom of elevated bilirubin (hyperbilirubinemia). Ammonia: 30 - 70ug/dl A byproduct of protein metabolism, ammonia (NH4) is processed by the liver. In severe liver disease, ammonia can accumulate in the blood, causing neurological and mental deterioration (hepatic encephalopathy). SourceMosby's Diagnostic and Laboratory Test Reference, Second Edition. Mosby, St. Louis.Reviewed 7/13/05 by V. J. , RN, BSN, MA My Lab TrackerHepatitis C Tests Hepatitis C Viral Load TestingUnderstanding Liver BiopsyWhere To Get Tested for Hepatitis InfectionUnderstanding the Complete Blood Count with DifferentialUnderstanding the Basic Metabolic Profile (BMP)Understanding the Complete Metabolic Profile (CMP)How is Hepatitis C Transmitted from Person to Person? FAQ: Hepatitis Testing and Diagnosis (Word) NLM: CBC - Complete Blood Count NLM: WBC count NLM: CHEM-20 NLM: ELISA NLM: ALT NLM: AST NLM: Autoimmune liver disease panel NLM: Gallium Scan NLM: Hematocrit NLM: Hemoglobin NLM: Hepatitis virus test or panel NLM: Liver function tests NLM: Liver scan NLM: Platelet count NLM: RBC count NLM: Serum iron This link brought to you by Schering Corporation about us | contact us | privacy policy | terms of use | logout | news Hepatitis Neighborhood is a service of CuraScript www.curascript.com Copyright © 1999-2005 CuraScript, Inc. Return: Home / Understanding Hepatitis / Diagnosing Hepatitis C HOME | MY PROFILE | LOGOUT ARTICLES What is the Hepatitis C Virus? Basic Information About Hepatitis C How is Hepatitis C Transmitted from Person to Person? Sex and HCV: Can You Infect Your Partner? Frequently Asked Questions About Hepatitis C Understanding Your Liver's Structure and Function Seniors and Hepatitis C Vaccination for Hepatitis A and B Understanding HCV / HIV Coinfection Self-Recovery of Hepatitis C: It May be About Genetics The Future of Liver Research ARTICLES Hepatitis C Tests Hepatitis C Viral Load Testing Common Liver Lab Tests Understanding Liver Biopsy Where To Get Tested for Hepatitis Infection Understanding the Complete Blood Count (CBC) with Differential Understanding the Basic Metabolic Profile (BMP) Understanding the Complete Metabolic Profile (CMP) ARTICLES General Hepatitis C Treatment Information Responding to Hepatitis Medications (or not) Viral Response as a Predictor of Treatment Outcome How Durable is the Sustained Viral Response? Is Retreatment an Option? Liver Transplant ARTICLES Inflammation of the Liver Liver Fibrosis Women May be Protected Against Fibrosis, Suggests Study Cirrhosis of the Liver End-Stage Liver Disease Liver Cancer Other Complications of HCV Infection Diseases and Conditions Associated with Hepatitis C Fibromylagia and Hepatitis C Infection Diabetes and Hepatitis C Infection Pain Management and Hepatitis C Infection Cryoglobulinemia and Hepatitis C Infection ARTICLES Symptoms of Acute HCV Infection Symptoms of Chronic HCV Infection Depression and Fatigue in HCV Infection Hepatitis C Symptom Emergencies ARTICLES Hepatitis A: What is it? Hepatitis A: How is it Transmitted? Hepatitis A: Prevention and Vaccination Hepatitis A: Diagnosis and Testing Hepatitis A: Symptoms and Course of Infection Hepatitis A: Treatment and Postexposure Prophylaxis Hepatitis A: Groups at Higher Risk of Infection Hepatitis B: What is it? Hepatitis B: How is it Transmitted? Hepatitis B: Prevention and Vaccination Hepatitis B: Diagnosis and Testing Hepatitis B: Symptoms and Course of Infection Hepatitis B: Treatment and Postexposure Prophylaxis Hepatitis D Hepatitis E Hepatitis G More articles... ARTICLES Testing and Diagnosis of Pediatric Hepatitis C Risk Factors for Pediatric HCV Infection Clinical Course of Pediatric Hepatitis C Infection Treatment of Pediatric Hepatitis C May. 30, 8PM ET Hepatitis Open Forum Emmet B. Keeffe, MD Understanding the Complete Blood Count (CBC) with Differential Article Date: 4/9/2004 The Complete Blood Count (or CBC) is a measure of erythrocytes (red blood cells), leukocytes (white blood cells), and platelets. The "differential" part of the test divides the white blood cell count into the different kinds of white blood cells. Red Blood Cell Measures RBC Count. Red blood cell (RBC) count is a count of the actual number of red blood cells in a certain volume of blood. The normal RBC count is 4.7 to 6.1 million/mm3 for males and 4.2 to 5.4 million/mm3 for females. Hemoglobin. Hemoglobin measures the amount of oxygen-carrying protein in the blood. The normal range is 14 to 18 gms/Dl for males, and 12 to 16 gms/Dl for females. Hematocrit. Hematocrit measures the amount of space red blood cells take up in the blood. It is reported as a percentage. The normal range is 42 to 52 percent for males and 37 to 47 percent for females. Conditions that can cause increased RBC count, hemoglobin and hematocrit include: High altitudes Congenital heart disease Congestive heart failure Dehydration / hemoconcentration Lung diseases (COPD, fibrosis) Polycythemia vera Severe burns Diseases causing intravascular fluid loss (diarrhea, burns). Conditions that can cause decreased RBC count, hemoglobin and hematocrit include: Diseases causing anemia Bleeding / hemorrhage Destruction of cells (hemolysis) Hodgkin's disease Leukemia and other cancers Rheumatic diseases Autoimmune diseases, such as systemic lupus erythematosus Kidney disease / failure Enlarged spleen Cirrhosis Bone marrow failure. Mean corpuscular volume. Mean corpuscular volume (MCV) is a measurement of the average size of your red blood cells (RBC). The normal range is 80 to 95 femoliters. When the MCV is elevated, RBCs are larger than normal, or macrocytic. Causes of increased MCV include vitamin B12 or folic acid deficiency. When the MCV is decreased, RBCs are smaller than normal, or microcytic. Causes include iron deficient anemia or thalassemia. Mean corpuscular hemoglobin. Mean corpuscular hemoglobin (MCH) is a calculation of the amount of oxygen-carrying hemoglobin inside RBCs. The normal range is 27 to 31 picograms. This value is closely related to mean corpuscular volume, since RBCs with larger amounts of hemoglobin tend to be larger (macrocytic) and RBCs with less hemoglobin tend to be smaller (microcytic). Mean corpuscular hemoglobin concentration. Mean corpuscular hemoglobin concentration (MCHC) is a calculation of the percentage of hemoglobin in the RBCs. The normal range is 32 to 36 gm/DL. When the amount of hemoglobin inside the cell is low, cells are hypochromic. Causes of decreased MCH include iron deficient anemia or thalassemia. Red Cell Distribution Width. Red Cell Distribution Width (RDW) is a calculation of the variation in the size of RBCs.The normal range is 11 to 14.5 percent. The RDW is essentially an indicator of anisocytosis (variation in RBC size) and poikilocytosis (variation in RBC shape). This measure can be useful in identifying certain anemias. White Blood Cell Measures The white blood cell (WBC) count has two components: the leukocyte count and the differential. The Leukocyte Count. The first component is a simple count of the total number of leukocytes (WBCs) in a volume of blood. The normal range for the WBC count is 5,000 to 10,000 WBCs per mm3 of blood. Many diseases and some non-pathological situations can cause an increased WBC count. Conditions not directly related to illness that can increase the WBC count include: Eating, physical activity or stress Pregnancy and labor Patients who have had their spleen removed Many medications, including aspirin, heparin, steroids, quinine, and others. Illness and diseases associated with an increased WBC count include: Viral, bacterial and parasitic infections Inflammatory diseases, tissue inflammation and necrosis Autoimmune diseases Leukemias Metabolic disorders Exposure to radiation Physical trauma. A decreased WBC count can be associated with: Certain medications and medication toxicities Chemotherapy Bone marrow infiltration and failure Overwhelming infection Autoimmune disease. The DifferentialThe second component, the differential, breaks down the WBC count into each WBC subtype: neutrophils, lymphocytes, monocytes, eosinophils, and basophils. Differential WBC counts are reported as percentages of the WBC count. Neutrophils. Neutrophils (also called polymorphonuclear leukocytes or PMN's) are white blood cells that digest bacteria and cellular debris. The normal range for neutrophils is 55 to 70 percent. Neutrophils are further subdivided into "Band" and "Segmented" neutrophils. "Segs" are mature neutrophils. Although segmented neutrophils make up the majority of neutrophils, an abnormally high percentage of segmented neutrophils suggest the hepatic disease and pernicious anemia. The normal range for segmented neutrophils is 50 to 65 percent. "Bands" (also called "stabs") are immature neutrophils, and their presence indicates stimulation of neutrophil production and early release of neutrophils into circulation, characteristic of an ongoing, acute bacterial infection. The normal range for band neutrophils is 0 to 5 percent. Lymphocytes. There are two forms of lymphoctyes: B cells and T Cells. B lymphocytes produce antibodies, which are protein substances that bind with antigens (foreign particles), neutralizing their ability to cause infection, and providing a "handle" to which neutrophils can attach and then ingest the antigen. The normal range is 25 to 45 percent. T lymphocyes have the ability to recognize cells that are infected. They bind to and destroy infected cells by releasing chemicals onto the cell's surface. The differential WBC test does not differentiate between B and T cells, they are reported as a single, combined number. Increased lymphocyte percentages are found mainly in cases of viral infection, but can also be associated with: Bacterial infection, such as measles, mumps, rubella, infectious mononucleosis and infectious hepatitis Hormonal disorders, such as hypothyroidism and hypoadrenalism Cancers, including lymphocytic leukemia and lymphosarcome HIV / AIDS. Decreased lymphocyte counts are associated with: Hodgkin's disease Systemic Lupus Erythematosus Steroid use Burns and trauma. Monocytes. Monocytes are scavenger leukocytes that dispose of noninfectious foreign particles, so they are not as diagnostically significant as other leukocytes. The normal range for monocytes is 2 to 6 percent of the total leukocyte count. Monocyte percentages may be increased viral, bacterial and parasitic infections, as well as collagen diseases and some malignant blood disorders. Decreased monocyte counts are not associated with disease, but may be found in patients taking steroids.Eosinophils. Eosinophils are leukocytes that destroy parasites either by engulfing them or by attaching to them and releasing chemicals that destroy the parasites. The substances released by eosinophils have been implicated in allergic reactions, especially in the airway constriction seen in asthma.The normal range is 1 to 4 percent of the total leukocyte count. Elevated levels of eosinophils are found in hyperimmune or allergic reactions, parasitic infection, and some cancers. Decreased eosinophil counts are found in congestive heart failure, infectious mononucleoisis, hormonal disorders, some anemias, and increased degrees of physical stress. Interestingly, the number of eosinophils follows a circadian rhythm; that is, it fluctuates during the day. The count is lowest in the morning and increases throughout the day, peaking late in the evening. This trend is reversed in people who work at night. Basophils. The function of basophils is not as clear as other leukocytes. They appear to have a role in allergic reaction, and may have activity against parasites, but they do not phagocytize (ingest) foreign particles. The normal range for basophils is 0.5 to 1.0 percent of the total leukocyte count. Increased basophil numbers are associated with malignancies of the blood. Decreased counts are found in stress reactions associated with some disease states and in steroid therapy. Platelet Measures Platelets, also called thrombocytes, are the component of blood that control bleeding by clotting. At any one time, two-thirds of the platelets in the body are found in circulation, and one-third is found in the spleen. The normal range is for adults is 150,000 to 450,000 per mm3. Thus, diseases which affect the spleen (such as portal hypertension secondary to cirrhosis) will interfere with platelet activity and predispose the person to bleeding disorders. The platelet count is the number of platelets in a given volume of blood. Platelet counts below 20,000 are very serious and may cause spontaneous hemorrhage. Platelet counts above 40,000 rarely result in spontaneous bleeding, but the patient may experience prolonged bleeding secondary to injury. There are many non-pathological conditions that can cause variations in the platelet count, including: Onset of menses (decreases platelet count) Intense physical exercise (increases platelet count) Living at high altitude (increases platelet count). Additionally, platelets are usually increased in the winter and decreased in the summer. Pathological conditions that can decrease platelet counts include: Idiopathic thrombocytopenia purpura Bone marrow injury or failure Malignancies of the bone marrow (carcinoma, leukemia, lymphoma) Vitamin B12 or folic acid deficiency Infection Hemorrhage or massive transfusion Hemolytic anemias Systemic lupus erythematosus. Many drugs are also associated with decreased platelet counts. Elevated platelets can be found in: Hemorrhage Surgery, including surgical removal of the spleen Iron deficiency Chronic inflammatory disorders Certain cancers and Hodgkin's disease. Summary of Reference Ranges RBC count: 4.7 to 6.1 million/mm3 (male) and 4.2 to 5.4 million/mm3 (female) Hemoglobin: 14 to 18 gms/Dl (male) and 12 to 16 gms/Dl (female) Hematocrit: 42 to 52 percent (male) and 37 to 47 percent (female) MCV: 80 to 95 femoliters MCH: 27 to 31 picograms MCHC: 32 to 36 gm/DL RDW: 11 to 14.5 percent WBC count: 5,000 to 10,000 / mm3 Neutrophils: 55 to 70 percent Lymphocytes: 25 to 45 percent Moncytes: 2 to 6 percent Eosinophils: 1 to 4 percent Basophils: 0.5 to 1.0 percent Platelets: 150,000 to 450,000 / mm3 Source McFarland M, Grant M. Nursing Implications of Laboratory Tests, 3rd ed. Delmar Publishers Inc., 1994.Pagana K, Pagana T. Mosby's Diagnostic and Laboratory Test Reference. 2nd ed. Mosby, 1995. Traub S. Basic Skills in Interpreting Laboratory Data, 2nd ed. American Society of Health-System Pharmacists, 1996.Reviewed 7/14/05 by V. J. , RN, BSN, MA Hepatitis C Tests Hepatitis C Viral Load TestingCommon Liver Lab TestsUnderstanding Liver BiopsyWhere To Get Tested for Hepatitis InfectionUnderstanding the Basic Metabolic Profile (BMP)Understanding the Complete Metabolic Profile (CMP)My Lab Tracker NLM: CBC - Complete Blood Count NLM: WBC count NLM: CHEM-20 NLM: ELISA NLM: ALT NLM: AST NLM: Autoimmune liver disease panel NLM: Gallium Scan NLM: Hematocrit NLM: Hemoglobin NLM: Hepatitis virus test or panel NLM: Liver function tests NLM: Liver scan NLM: Platelet count NLM: RBC count NLM: Serum iron This link brought to you by Schering Corporation about us | contact us | privacy policy | terms of use | logout | news Hepatitis Neighborhood is a service of CuraScript www.curascript.com Copyright © 1999-2005 CuraScript, Inc. Return: Home / Understanding Hepatitis / Diagnosing Hepatitis C HOME | MY PROFILE | LOGOUT ARTICLES What is the Hepatitis C Virus? Basic Information About Hepatitis C How is Hepatitis C Transmitted from Person to Person? Sex and HCV: Can You Infect Your Partner? Frequently Asked Questions About Hepatitis C Understanding Your Liver's Structure and Function Seniors and Hepatitis C Vaccination for Hepatitis A and B Understanding HCV / HIV Coinfection Self-Recovery of Hepatitis C: It May be About Genetics The Future of Liver Research ARTICLES Hepatitis C Tests Hepatitis C Viral Load Testing Common Liver Lab Tests Understanding Liver Biopsy Where To Get Tested for Hepatitis Infection Understanding the Complete Blood Count (CBC) with Differential Understanding the Basic Metabolic Profile (BMP) Understanding the Complete Metabolic Profile (CMP) ARTICLES General Hepatitis C Treatment Information Responding to Hepatitis Medications (or not) Viral Response as a Predictor of Treatment Outcome How Durable is the Sustained Viral Response? Is Retreatment an Option? Liver Transplant ARTICLES Inflammation of the Liver Liver Fibrosis Women May be Protected Against Fibrosis, Suggests Study Cirrhosis of the Liver End-Stage Liver Disease Liver Cancer Other Complications of HCV Infection Diseases and Conditions Associated with Hepatitis C Fibromylagia and Hepatitis C Infection Diabetes and Hepatitis C Infection Pain Management and Hepatitis C Infection Cryoglobulinemia and Hepatitis C Infection ARTICLES Symptoms of Acute HCV Infection Symptoms of Chronic HCV Infection Depression and Fatigue in HCV Infection Hepatitis C Symptom Emergencies ARTICLES Hepatitis A: What is it? Hepatitis A: How is it Transmitted? Hepatitis A: Prevention and Vaccination Hepatitis A: Diagnosis and Testing Hepatitis A: Symptoms and Course of Infection Hepatitis A: Treatment and Postexposure Prophylaxis Hepatitis A: Groups at Higher Risk of Infection Hepatitis B: What is it? Hepatitis B: How is it Transmitted? Hepatitis B: Prevention and Vaccination Hepatitis B: Diagnosis and Testing Hepatitis B: Symptoms and Course of Infection Hepatitis B: Treatment and Postexposure Prophylaxis Hepatitis D Hepatitis E Hepatitis G More articles... ARTICLES Testing and Diagnosis of Pediatric Hepatitis C Risk Factors for Pediatric HCV Infection Clinical Course of Pediatric Hepatitis C Infection Treatment of Pediatric Hepatitis C May. 30, 8PM ET Hepatitis Open Forum Emmet B. Keeffe, MD Understanding the Basic Metabolic Profile (BMP) Article Date: 4/13/2004 The Basic Metabolic Profile (BMP) is a group of tests that examine blood chemistry, that is, the components of blood excluding red and white blood cells and platelets. The tests which make up a BMP may vary slightly between labs or institutions, but generally they will provide the physician with information about serum electrolytes, blood sugar and kidney function. The tests described in this article include: Sodium Potassium Chloride Carbon Dioxide Calcium Glucose Blood Urea Nitrogen (BUN) Creatinine Anion Gap SodiumThe normal range for serum sodium in the adult is 135 to 148 mEq/L. Sodium (Na) aids in the regulation of the body's fluid balance, and along with potassium, maintains the electrical potential in the body that allows nerves to operate properly. The fluids containing sodium are found almost entirely in extracellular (outside the cell) spaces, such as blood vessels. Sodium levels are maintained by the ingestion of sodium in food, and it is excreted through sweat, urine and feces. Common causes of decreased serum sodium (hyponatremia) include: Decreased sodium intake / increased sodium loss Excess water ingestion Diarrhea Vomiting Administration of diuretics Kidney disease ’s disease Edema and/or ascites. Common causes of increased sodium (hypernatremia) include: Increased sodium intake / decreased sodium loss Excessive free water loss, such as sweating, burns Diabetes insipidus Osmotic diuresis. PotassiumThe normal range for serum potassium in the adult is 3.5 to 5.5 mEq/L. Potassium (K), as opposed to sodium, is found almost entirely inside the cells of the body. Proper levels of potassium are critical to the normal function of muscles, including the heart.Abnormal levels of potassium can cause severe irregularities in the heart's rhythm and ability to contract. Potassium is ingested in the diet and is excreted in urine. Common causes of decreased potassium (hypokalemia) include: Diuretic use without potassium replacement Administration of IV fluids without potassium Alcoholic cirrhosis Diarrhea Crohn's disease Cushing's syndrome. Common causes of increased potassium (hyperkalemia) include: Kidney disease or failure Rapid administration of IV fluids containing potassium Burns and crushing injuries, trauma Myocardial infarction (heart attack) 's disease. ChlorideThe normal range for serum chloride in the adult is 95 to 105 mEq/L. Chloride (Cl) works with sodium to maintain the balance of fluids in the body, and aids in the regulation of the acid / base balance. It is an anion (negatively charged particle) found mainly in extracellular spaces. Chloride abnormalities can cause increased nervous system irritability, exaggerated reflex responses, decreased respiration, weakness, stupor and coma. Alterations in chloride levels are unusual, but are found in association with other electrolyte imbalances. Common causes of deceased chloride (hypochloremia) include: Vomiting, diarrhea, or gastrointestinal suctioning Administration of diuretics Administration of IV fluids without electrolyte replacement. Common causes in increased chloride (hyperchloriemia) include: Dehydration Acid/base imbalances Administration of medications containing chloride. Carbon DioxideThe normal range for serum carbon dioxide in the adult is 23 to 30 mEq/L or 23 to 30 mmol/L. Carbon dioxide (CO2) is an anion (negatively charged ion) that assists in acid / base balance and helps maintain the electrical neutrality of fluids both inside and outside cells. In solution, carbon dioxide (CO2) combines with water (H2O) to form carbonic acid (H 2CO3). Higher levels of CO2 in the blood create an acidic condition (acidosis), and low levels create an alkaline condition (alkalosis). Levels of CO2 are regulated by the kidneys and CO2 is expelled by the lungs during respiration. Alterations in the concentration of this electrolyte do not occur in isolation; that is, abnormalities in CO2 are always related to a co-existing disease or condition. Common causes of increased serum carbon dioxide (acidosis) include: Diseases / conditions that decrease respiration Burns Congestive heart failure Uncontrolled diabetes Starvation Kidney disease / failure Diarrhea Certain medications and poisons. Common causes of decreased serum carbon dioxide (alkalosis) include: Diseases / conditions that increase respiration (hyperventilation) Fluid losses from the GI tract (vomiting, suctioning) Administration of diuretics Administration of steroids Cushing's disease Salicylate intoxication Excessive administration of medications containing bicarbonate. CalciumThe normal range for serum calcium in the adult is 9 to 10.5 mg/dL, or 2.25 to 2.75 mmol/L. Calcium (Ca) is found primarily in the body in the form of bones and teeth; however, about 10% is found in the blood, in the form of a cation (positively charged ion) that plays an important role in the function of nerves and coagulation of blood. When levels of serum calcium are low, the body produces hormones that remove calcium from bone to supplement serum calcium. Because serum calcium plays an important role in nerve function, alterations in calcium levels can cause serious symptoms. These include decreased or exaggerated muscle tone, abnormal reflexes, severe gastrointestinal problems, such as nausea, vomiting, cramping and constipation, and disorders of the central nervous system, like lethargy, depression, convulsions and coma. In extreme cases, pathological bone fractures can occur as a result of prolonged calcium loss. Common causes of decreased serum calcium (hypocalcemia) include: Diseases of the small intestine, interfering with calcium absorption Excessive protein intake Administration of blood with citrate Hypoparathyroidism. Common causes of increased serum calcium (hypercalcemia) include: Prolonged immobilization Hyperparathyroidism Diseases involving the breakdown of bone Excessive ingestion of vitamin D Kidney diseases / failure. GlucoseThe normal range for serum glucose in the adult is 70 to 110 mg/dL. Glucose (Glu) is a form of sugar that circulates in the blood to provide metabolic fuel for all body processes. Carbohydrates and sugars are ingested through food, broken down and absorbed in the small intestine, and are stored in the liver in the form of glucose. The most common cause of abnormal blood sugar levels is Diabetes Mellitus, a disease in which serum glucose is consistently elevated as a result of decreased or absent insulin production, insulin resistance, or both. The physical consequences of persistently elevated serum glucose / diabetes are many, and affect almost every body system. The symptoms of decreased levels of serum glucose (hypoglycemia) can include sweating, anxiety, rapid pulse, and headache. If serum glucose drops to below 50 mg/dL, the patient may have loss of consciousness, and perhaps convulsions. Common causes of increased serum glucose (hyperglycemia) include: Diabetes Mellitus Administration of certain steroids and hormones Administration of total parenteral nutrition Administration of diuretics Diseases of the pancreas. Decreased serum glucose (hypoglycemia) is not common, but causes may include: Administration of insulin or other hypoglycemic medication Exercise Exposure to severe cold Malnutrition Prolonged fever Diseases of the pancreas Decreases in pituitary or adrenocortical function. Blood Urea NitrogenThe normal range for blood urea nitrogen in the adult is 4 to 22 mg/dL. Blood urea nitrogen (BUN) is a waste product of protein metabolism. It is produced by the liver and excreted in the urine. Abnormal elevations of BUN are most commonly caused by diseases of the kidney, prostate, and urinary tract, and the patient may have symptoms characteristic of fluid overload: decreased urine output, weight gain, edema, and distended neck veins. The skin may be yellowed and easily bruised, and the patient's mental state may be affected. Decreased BUN is uncommon, but common causes may include: Liver failure, inhibiting protein metabolism Negative nitrogen balance (when protein breakdown exceeds protein intake) Anorexia Malnutrition Prolonged IV therapy in patients receiving inadequate oral nutrition Overhydration. Common causes of increased blood urea nitrogen (azotemia) include: Kidney diseases / failure Diseases decreasing the ability to excrete urine Increased protein metabolism Breakdown of muscle tissue (starvation, anorexia nervosa) Infection Trauma Surgery Gastrointestinal bleeding Administration of corticosteroids Administration of tetracyclines Dehydration. CreatinineThe normal range for serum creatinine in the adult is 0.6 to 1.2 mg/dL. The ideal BUN:creatinine ratio is 20:1. Creatinine (Cr) is a nitrogen-based waste product that is produced as a result of protein metabolism in muscle tissue. Creatinine is produced at a very steady rate and is not subject to rapid fluctuations. It is excreted by the kidneys. Creatinine and BUN both measure kidney function, but in slightly different ways. It is clinically useful to evaluate the ratio of BUN to creatinine when conducting a diagnostic assessment. Dehydration and protein breakdown can cause elevation in BUN, but may affect serum creatinine only slightly or not at all. However, if both BUN and serum creatinine are elevated, this strongly suggests the presence of primary kidney disease. Common causes of increased serum creatinine include: Kidney diseases / failure Administration of diuretics, sulfonamides, chloramphenicol, ascorbic acid Use of marijuana Diet high in red meat. Decreased serum creatinine is rare, but has been associated with muscular dystrophy. Anion GapThe normal range for anion gap is 12 to 18 mmol/L; however, newer, more sensitive test equipment may have a reference range of -4 to 7 mmol/L. The anion gap is a figure calculated by subtracting the number of anions (chloride and bicarbonate, the negatively charged electrolytes) from the cations (sodium and potassium, the positively charged electrolytes). The remainder, the "gap," is composed of unmeasured electrolytes, organic ions, and plasma proteins. An increased anion gap indicates that presence of an excess of the unmeasured anions which can occur when surplus hydrogen ions have been introduced into the body. Surplus hydrogen ions can shift the pH (the measure of acid / base balance) of the body towards an acid state, or acidosis. Common causes of an increased anion gap include condition or diseases that induce acidosis, such as: Diabetic ketoacidosis Lactic acidosis Kidney failure associated with increased BUN Various drug or chemical toxicities. Summary of Normal Ranges (Adult) Sodium: 135 to 148 mEq/L Potassium: 3.5 to 5.5 mEq/L Chloride: 95 to 105 mEq/L Carbon Dioxide: 23 to 30 mEq/L or 23 to 30 mmol/L Calcium: 9 to 10.5 mg/dL, or 2.25 to 2.75 mmol/L Glucose: 70 to 110 mg/dL BUN: 4 to 22 mg/dL Creatinine: 0.6 to 1.2 mg/dL BUN / Creatinine ratio: 20:1 Anion Gap: 12 to 18 mmol/L (older equipment) Anion Gap: -4 to 7 mmol/L (newer equipment) SourceMcFarland M, Grant M. Nursing Implications of Laboratory Tests, 3rd ed. Delmar Publishers Inc., 1994.Pagana K, Pagana T. Mosby's Diagnostic and Laboratory Test Reference. 2nd ed. Mosby, 1995. Traub S. Basic Skills in Interpreting Laboratory Data, 2nd ed. American Society of Health-System Pharmacists, 1996.Reviewed 7/14/05 by V. J. , RN, BSN, MA Hepatitis C Tests Hepatitis C Viral Load TestingCommon Liver Lab TestsUnderstanding Liver BiopsyWhere To Get Tested for Hepatitis InfectionUnderstanding the Complete Blood Count with DifferentialUnderstanding the Complete Metabolic Profile (CMP)My Lab Tracker NLM: CBC - Complete Blood Count NLM: WBC count NLM: CHEM-20 NLM: ELISA NLM: ALT NLM: AST NLM: Autoimmune liver disease panel NLM: Gallium Scan NLM: Hematocrit NLM: Hemoglobin NLM: Hepatitis virus test or panel NLM: Liver function tests NLM: Liver scan NLM: Platelet count NLM: RBC count NLM: Serum iron This link brought to you by Schering Corporation about us | contact us | privacy policy | terms of use | logout | news Hepatitis Neighborhood is a service of CuraScript www.curascript.com Copyright © 1999-2005 CuraScript, Inc. Return: Home / Understanding Hepatitis / Diagnosing Hepatitis C HOME | MY PROFILE | LOGOUT ARTICLES What is the Hepatitis C Virus? Basic Information About Hepatitis C How is Hepatitis C Transmitted from Person to Person? Sex and HCV: Can You Infect Your Partner? Frequently Asked Questions About Hepatitis C Understanding Your Liver's Structure and Function Seniors and Hepatitis C Vaccination for Hepatitis A and B Understanding HCV / HIV Coinfection Self-Recovery of Hepatitis C: It May be About Genetics The Future of Liver Research ARTICLES Hepatitis C Tests Hepatitis C Viral Load Testing Common Liver Lab Tests Understanding Liver Biopsy Where To Get Tested for Hepatitis Infection Understanding the Complete Blood Count (CBC) with Differential Understanding the Basic Metabolic Profile (BMP) Understanding the Complete Metabolic Profile (CMP) ARTICLES General Hepatitis C Treatment Information Responding to Hepatitis Medications (or not) Viral Response as a Predictor of Treatment Outcome How Durable is the Sustained Viral Response? Is Retreatment an Option? Liver Transplant ARTICLES Inflammation of the Liver Liver Fibrosis Women May be Protected Against Fibrosis, Suggests Study Cirrhosis of the Liver End-Stage Liver Disease Liver Cancer Other Complications of HCV Infection Diseases and Conditions Associated with Hepatitis C Fibromylagia and Hepatitis C Infection Diabetes and Hepatitis C Infection Pain Management and Hepatitis C Infection Cryoglobulinemia and Hepatitis C Infection ARTICLES Symptoms of Acute HCV Infection Symptoms of Chronic HCV Infection Depression and Fatigue in HCV Infection Hepatitis C Symptom Emergencies ARTICLES Hepatitis A: What is it? Hepatitis A: How is it Transmitted? Hepatitis A: Prevention and Vaccination Hepatitis A: Diagnosis and Testing Hepatitis A: Symptoms and Course of Infection Hepatitis A: Treatment and Postexposure Prophylaxis Hepatitis A: Groups at Higher Risk of Infection Hepatitis B: What is it? Hepatitis B: How is it Transmitted? Hepatitis B: Prevention and Vaccination Hepatitis B: Diagnosis and Testing Hepatitis B: Symptoms and Course of Infection Hepatitis B: Treatment and Postexposure Prophylaxis Hepatitis D Hepatitis E Hepatitis G More articles... ARTICLES Testing and Diagnosis of Pediatric Hepatitis C Risk Factors for Pediatric HCV Infection Clinical Course of Pediatric Hepatitis C Infection Treatment of Pediatric Hepatitis C May. 30, 8PM ET Hepatitis Open Forum Emmet B. Keeffe, MD Understanding the Complete Metabolic Profile (CMP) Article Date: 4/21/2004 The Complete Metabolic Profile (CMP) includes all of the lab tests that comprise the Basic Metabolic Profile, plus additional tests of electrolytes, fats, enzymes and serum proteins, including: Magnesium Phosphorus Tyiglycerides Total Bilirubin Alkaline Phosphatase ALT (alanine aminotransferase) AST (aspartate aminotransferase) Albumin Globulin Total Protein In this article we will review these tests, their normal ranges and common causes of deviations from normal. Different labs and institutions use slightly different reference ranges for normal ranges, so the ranges given below may not exactly match those printed on lab results. Magnesium The normal range of serum magnesium in the adult is 1.2 to 2.0 mEq/L. Magnesium is a cation (positively charged ion) that is found predominantly in the fluid inside cells. It plays a very important role in energy metabolism and nearly all metabolic processes. Magnesium is critical to the metabolism of carbohydrates, proteins and nucleic acids, and it facilitates the function of muscles and nerves. Magnesium is ingested through food, and is found in highest concentrations in dark green vegetables and fruit. The absorption of magnesium can be impaired by the presence of excess fat, phosphates and calcium. Shifts in the acid/base balance towards alkalosis can also impair magnesium absorption. Decreased levels of magnesium can cause weakness, irritability, changes in the heart's electrical activity, delirium and convulsions. Increased levels of magnesium can slow the electrical conduction of the heart, retard reflexes and depress respiration. Common causes of decreased magnesium levels (hypomagnesemia) include: Malnourishment due to malabsorption Alcohol use Chronic kidney disease Diabetes Thyroid disease Hyperaldosteronism. Common causes of increased magnesium levels (hypermagnesemia) include: Ingestion of magnesium-containing antacids Ingestions of medications containing magnesium Chronic kidney disease / failure. Phosphorus The normal range for serum phosphorus in the adult is 2.5 to 4.5 mg/dL or 1.7 to 2.6 mEq/dL. Phosphorus is the major intracellular anion (negatively charged ion). In combination with calcium, it is a major component of bones and teeth, and plays a major role in maintaining the acid/base balance. Phosphorus is present in most foods, and dietary deficiencies are uncommon. Decreased levels of serum phosphorus are associated with a range of neurological, musculo-skeletal, renal (kidney), hepatic (liver) and hematological (blood) symptoms. These symptoms may include changes in consciousness, weakness, joint stiffness, bone pain, excessive excretion of calcium in the urine, and hepatic coma. Increased levels of serum phosphorus are usually associated with specific disease states, and symptoms vary accordingly. Common causes of decreased phosphorus (hypophosphatemia) include: Abnormally high levels of parathyroid hormone IV administration of carbohydrates, diuretics and hyperalimentation (IV feeding) Alcoholism Dialysis Vomiting Ingestion of phosphate-binding antacids Infection of the blood with gram-negative bacteria. Common causes of increased phosphorus (hyperphosphatemia) include: Chronic kidney disease, associated with increased Blood Urea Nitrogen (BUN) and Creatinine Abnormally low levels of parathyroid hormone Bone diseases, such as multiple myeloma, Paget's disease and osteolytic metastatic tumor Healing bone fractures. TriglyceridesFor adult males, the normal range is 40 to 160 mg/dL or 0.45 to 1.81 mmol/L. For adult females, the normal range is 35 to 135 mg/dl or 0.40 to 1.52 mmol/L. Triglycerides, cholesterol and lipoproteins make up the group of plasma lipids, or fats, that are found in the blood. Triglycerides comprise the largest proportion of lipids in the diet, adipose (fatty) tissue and blood. They are formed in the intestine from glycerides present in foods, and are stored in adipose tissue and gradually released and metabolized between meals according to the energy needs of the body. Triglycerides are often measured as a reflection of lipid ingestion and metabolism, or as part of an evaluation of coronary risk factors. Unlike most tests in the Basic or Complete Metabolic Profiles, accurate testing of triglycerides requires the patient not to eat for 12 hours before the test. Additionally, many medications may affect the results of this test and the patient may be instructed by the physician to discontinue taking medications for 24 hours before the test. The normal range for serum triglycerides varies by age group and sex. Common causes of decreased serum triglyceride levels include: Malabsorption syndrome (inadequate absorption of nutrients in the intestinal tract) Malnutrition Hyperthyroidism Low fat diet Medications, including ascorbic acid, asparginase, clofibrate and cholestipol may cause decreased serum triglycerides. Common causes of increased serum triglyceride levels include: Ingestion of fatty meals or alcohol Glycogen storage diseases Hyperlipidemias Hypothyroidism High-carbohydrate diets Poorly controlled diabetes Kidney disease Hypertension Alcoholic cirrhosis Pregnancy Myocardial infarction Medications, including cholestyramine, estrogens and oral contraceptives may cause elevated serum triglycerides. Total Bilirubin The normal range for total bilirubin in the adult is 0.1 to 1.0 mg/dL or5.1 to 17.0 micromol/L.Bilirubin is a yellow-orange bile pigment that is formed when old or damaged red blood cells are broken down and removed for circulation. Normally, bilirubin is converted by the liver into direct (or conjugated) bilirubin, and excreted in feces. When the breakdown of red blood cells (hemolysis) occurs at a faster rate than the liver can handle, bilirubin levels increase and can the substance can be deposited in skin, resulting in jaundice. Also, in hepatitis cases, the liver may be unable to convert bilirubin to a form that can be excreted rapidly enough, resulting in elevated serum bilirubin levels and jaundice. In severe cases of jaundice, bile salts can be deposited in the skin, resulting in severe itching (pruritis). In extreme cases, bile salts can accumulate on the surface of the skin, causing a white scale (uremic frost). Total bilirubin is calculated by adding the direct (conjugated) and indirect (unconjugated) bilirubin. The metabolic pathway for bilirubin, from creation to excretion is very complex, and many diseases and conditions can cause elevated levels (hyperbilirubinemia). Some of the more common causes include: Blood disorders, including sickle cell anemia, hereditary spherocytosis, transfusion incompatibility, autoimmune hemolytic disease Lymphomas Bone marrow disease, such as thalassemia or pernicious anemia Physiological defects, including Gilbert's syndrome and Crigler-Najjar syndrome Liver diseases, including viral and alcoholic hepatitis Diseases of the bile ducts, such as gallstones, cancerous compression of the pancreatic head, carcinoma of the ampulla of Vater. Alkaline Phosphatase The normal range for alkaline phosphatase in the adult is: 25 to 97 U/L 1.4 to 4.5 Bodansky Units/dL 0.8 to 2.3 Bessey-lowry units/ml Alkaline Phosphatase is an enzyme found in many tissues, including the liver, biliary tract, bone, kidneys, intestine and placenta. It is called alkaline because it is more active in alkaline environments, and is released into the blood when tissues are damaged. Alkaline Phosphatase has several isoenzymes, or varieties, that vary depending on the type of tissue they are released from. The assay of individual alkaline phosphatase isoenzymes is not part of a standard complete metabolic profile. Because there are so many possible sources of this enzyme, elevated serum levels of alkaline phosphatase have little clinical meaning without a complete history and physical examination. Of relevance to liver disease patients is the fact that alkaline phosphatase levels generally will be elevated in cases of jaundice due to obstructive disease of the biliary tree, but will be normal or near-normal when jaundice is caused by diseases of the liver tissue. Common causes of increased serum alkaline phosphatase include: Cirrhosis Paget's disease Rheumatoid arthritis Primary or metastatic liver tumors Normal pregnancy Normal bones of growing children Interrupted blood flow to the intestines Metastatic bone tumor Healing bone fractures Hyperparatyroidism Medication, including various antibiotics, estrogen, methyldopa, oral contraceptives and others. Common causes of decreased serum alkaline phosphatase include: Hypothyroidism Malnutrition Milk-alkali syndrome Pernicious anemia Hypophosphatemia Scurvy (chronic vitamin C deficiency) Celiac disease Excessive ingestion of vitamin B. Alanine Aminotransferase (ALT) The normal range for serum alanine aminotransferase in adults is: 4 to 36 IU/L 5 to 35 el Units/ml 5 to 25 Wroblewski Units/ml 8 to 50 Karmen Units/ml Alanine Aminotransferase is an enzyme that participates in protein metabolism. It is found in highest concentration in the liver, but also in the heart and other tissues. Well known to most hepatitis patients, this enzyme is an indicator of damage to liver tissue. In general, hepatic disease is indicated if lab tests reveal elevated ALT with mild to moderated AST elevation. However, if ALT is normal and AST and Lactic Dehydrogenase (not described in this article) are elevated, liver disease is not indicated. Common causes of elevated serum alanine aminotransferase include: Viral or non-viral hepatitis Cirrhosis Hepatic necrosis Cholestasis Interrupted blood flow to the liver Liver tumor Medications, such as acetaminophen, many antibiotic and anti-infective drugs, oral contraceptives, pain medications and others. Aspartate Aminotransferase (AST) The normal range for serum AST is 8 to 46 U/l (male) and 7 to 34 U/l (female). Like alanine aminotransferase (ALT), aspartate aminotransferase (AST) is also an enzyme that participates in protein metabolism. It is found in heart muscle tissue, in the liver, and in skeletal muscle, kidney and brain tissue. Generally, elevations in AST can be attributed to either myocardial infarction (heart attack) or liver disease. Comparing the ratio of AST to ALT can be revealing. When the AST:ALT ratio exceeds 1.0, alcoholic cirrhosis, and tumors of the liver may be suspected. An AST:ALT ratio of less than 1.0 may be seen in acute hepatitis, viral hepatitis or infectious mononucleosis. Common causes of elevated aspartate aminotransferase include: Myocardial infarction Cardiac surgery / catheterization Hepatitis, cirrhosis, and/or hepatic necrosis Hepatic tumor Pancreatitis Skeletal muscle trauma Severe burns Hemolytic anemia Muscular dystrophy Infectious mononucleosis Recent convulsion Acute kidney disease Many medications, such as blood pressure medications, anticoagulants, antibiotics, oral contraceptives, opiates and others. Common causes of decreased aspartate aminotransferase include: Beriberi (vitamin B-1 deficiency) Diabetic ketoacidosis Pregnancy. Albumin The normal range for serum albumin in the adult is 3.5 to 5.5 g/dL or 35 to 50 g/L. Albumin is the most common of many proteins found in the blood, and has a critical role in the distribution of fluids in the body. Albumin is a colloid, an extremely minute particle that remains suspended in solution. Albumin's colloidal effect helps "hold" fluid (plasma) in circulation, preventing it from leaking out into surrounding tissues. It also assists in distributing substances such as medications, hormones and enzymes that require a protein carrier molecule. Albumin is formed in the liver and is negatively affected by diseases of the liver. Common causes of decreased levels of serum albumin include: Liver diseases (viral and non-viral hepatitis, liver cancer) Diseases of protein malabsorption Malnourishment Protein-wasting diseases, such as kidney diseases Massive fluid imbalances, as in ascites or burns Excessive administration of IV fluids Diseases causing increased permeability of blood vessels, such as autoimmune diseases. There are no known disease states associated with increased albumin levels. Globulin The normal range for serum globulin in the adult is 1.5 to 3.3 g/dL. The globulins are a family of serum proteins, functioning primarily as agents of the immune system but also assisting in the transport of protein dependent substances throughout the body. They also play a role in the regulation of fluid balance. Globulins are produced in the reticuloendothelial system, a major component of the body's system of protection against infection. Globulin levels are not affected by many disease states, but can be elevated in liver diseases, including liver cancer. Common causes of increased serum globulin levels include: Acute and chronic liver disease with hepatic necrosis Metastatic liver cancer Fatty liver disease Cancers of the immune system, such as multiple myeloma Medications, including steroids, hormones and insulin. Common causes of decreased serum globulin levels include: Malnutrition Deficiencies of the immune system Medications, including estrogens, hepatotoxic drugs and oral contraceptives. The Albumin/Globulin (A/G) Ratio The A/G ratio has limited clinical utility and is being replaced by a process called protein electrophoresis, a test that identifies the various quantities of the different proteins present in serum. However, the test may aid in identifying diseases in which the ratio of albumin to globulin is deranged. Disease states that result in a decreased albumin level, but normal or elevated globulin level include: Collagen vascular diseases Chronic liver diseases. Total Protein The normal range for serum total protein in the adult is 6.0 to 8.0 g/dL. Like the A/G ration, the total protein count is of limited utility unless it is accompanied by protein electrophoresis. The total protein count is made up of many different proteins, which may be individually elevated or decreased, but collectively yield a normal test result. Common causes of increased serum total protein include: Dehydration causing hemoconcentration Severe fluid loss secondary to burns Multiple myeloma Typhus Parasitic diseases. Common causes of decreased serum total protein include: Malnutrition Protein deprivation Hemorrhage Kidney disease resulting in protein loss in the urine Diseases of protein malabsorption Burns Open wounds Chronic liver disease. Summary of Normal Ranges (Adult) Magnesium: 1.2 to 2.0 mEq/L Phosphorus: 2.5 to 4.5 mg/dL or 1.7 to 2.6 mEq/dL Triglycerides (male): 40 to 160 mg/dL or 0.45 to 1.81 mmol/L Triglycerides (female): 35 to 135 mg/dl or 0.40 to 1.52 mmol/L Total Bilirubin: 0.1 to 1.0 mg/dL or 5.1 to 17.0 micromol/L Allkaline Phosphatase: 25 to 97 U/L (ALT) Alanine Aminotransferase: 4 to 36 IU/L (AST) Aspartate Aminotransferase (male): 8 to 46 U/l (AST) Aspartate Aminotransferase (female):7 to 34 U/l Albumin: 3.5 to 5.5 g/dL or 35 to 50 g/L Globulin: 1.5 to 3.3 g/dL Total Protein: 6.0 to 8.0 g/dL Source McFarland M, Grant M. Nursing Implications of Laboratory Tests, 3rd ed. Delmar Publishers Inc., 1994. Pagana K, Pagana T. Mosby's Diagnostic and Laboratory Test Reference. 2nd ed. Mosby, 1995. Traub S. Basic Skills in Interpreting Laboratory Data, 2nd ed. American Society of Health-System Pharmacists, 1996.Reviewed 7/14/05 by V. J. , RN, BSN, MA My Lab TrackerHepatitis C Tests Hepatitis C Viral Load TestingCommon Liver Lab TestsUnderstanding Liver BiopsyWhere To Get Tested for Hepatitis InfectionUnderstanding the Complete Blood Count with DifferentialUnderstanding the Basic Metabolic Profile (BMP) NLM: CBC - Complete Blood Count NLM: WBC count NLM: CHEM-20 NLM: ELISA NLM: ALT NLM: AST NLM: Autoimmune liver disease panel NLM: Gallium Scan NLM: Hematocrit NLM: Hemoglobin NLM: Hepatitis virus test or panel NLM: Liver function tests NLM: Liver scan NLM: Platelet count NLM: RBC count NLM: Serum iron This link brought to you by Schering Corporation about us | contact us | privacy policy | terms of use | logout | news Hepatitis Neighborhood is a service of CuraScript www.curascript.com Copyright © 1999-2005 CuraScript, Inc. Return: Home / Understanding Hepatitis / Diagnosing Hepatitis C HOME | MY PROFILE | LOGOUT ARTICLES PEG-Intron, Pegasys and Infergen: Understanding Interferon and Pegylated Interferon Rebetol and Copegus: Understanding Ribavirin Experimental Medications for HCV A Warning about Pregnancy and Ribavirin Combo Therapy: Interferons plus Ribavirins Vaccines for Hepatitis A and B HBV Medications: Intron-A, Epivir HBV, Hepsera, Baraclude & Pegasys Hepatitis Medication Table Dual Hepatitis Meds to Face-Off Complementary and Alternative Medicine and Hepatitis C Infection Asian Herbal Medicine and Hepatitis My Treatment Diary / My Lab Tracker ARTICLES Interferons / Pegylated Interferons Side Effects Ribavirin Side Effects Hepatitis A and B Vaccine Side Effects Hepatitis B Medication Side Effects: Epivir HBV, Baraclude, Hepsera and Intron-A ARTICLES The Role of the Liver in Normal Digestion Nutritional Concerns in Hepatitis Infection Hepatitis C and Weight Management Food & Drug Interactions Carbohydrates in the Diet Protein in the Diet Fat in the Diet Fat-Soluble Vitamins: A, D, E and K Water-Soluble Vitamins: The B Family and Vitamin C Understanding Mineral Supplements Herbs to Avoid ARTICLES Understanding Social Security Disability Federal Law and Employment Discrimination Discussing Disability with the Potential Employer The Americans with Disabilities Act (ADA): Disability Defined The ADA: Your Employment Rights as an Individual With a Disability Facts About the Family and Medical Leave Act (FMLA) FAQ about the Family and Medical Leave Act (FMLA) Stress in the Workplace Understanding Stress and Anxiety Anxiety Disorders: Panic Disorder Anxiety Disorders: Social Anxiety Disorder Anxiety Disorders: Post-Traumatic Stress Disorder Anxiety Disorders: Obsessive Compulsive Disorder Anxiety Disorders: Phobias Anxiety Disorders: Generalized Anxiety Disorder Anxiety Disorders: Options for Treatment More articles... ARTICLES An Introduction to Clinical Trials Participating in a Clinical Trial Questions to Ask before Joining a Clinical Trial Patient Care Costs in Clinical Trials Glossary of Clinical Trials Terms Locating Current Clinical Trials Finding Recent Studies in Liver Disease ARTICLES CuraScript Pharmacy Works for You May. 30, 8PM ET Hepatitis Open Forum Emmet B. Keeffe, MD Herbs to Avoid Article Date: 7/7/2004 Dietary supplements, including herbs, routinely enter the marketplace without undergoing a safety review by the Food and Drug Administration (FDA). Although there is no established system for gaining information about the risks of dietary supplements, an increased number of reports of adverse reactions to dietary supplement products has recently been recognized. Many sites on the internet offer lists of "bad herbs," but very few cite references, so the consumer is left to question the validity of the information. In this article, we will identify some herbs known to cause health problems, including liver disease. Additionally, we will provide references to clinical studies of each herb and brief excerpts from the studies' abstracts. The following herbs are presented: Aristolochia (Guang Fang Ji) Atractylis gummifera (African Herbal Remedy) Calliepsis laureola (Impila) Cassia species (Senna) Chelidonium majus (Greater Celandine) Crotalaria species Ephedra (Ma huang) Heliotropium species Larrea tridetata (Chapparal, Creosote) Lobelia (Lobelia inflata) Lycopodium serratum (Jin Bu ) Mentha pulegium (Pennyroyal) Pausinystalia yohimbe (Yohimbe) Piper methysticum (Kava-kava) Salix species (Willow Bark) Sassafras albidum (Sassafras) Senecio (Gordolobo yerba) Symphytum species (Comfrey) Teucrium chamaedrys (Germander) Tusilago farfara (Coltsfoot) Valeriana officinalis (Valerian) The data presented below was obtained from the National Center for Biotechnology Information database, a service of the United States National Library of Medicine. Note that some studies are on animal subjects. Additional information was obtained from the article "Illnesses and Injuries Associated With the Use of Selected Dietary Supplements" from the Center for Food Safety and Applied Nutrition, part of the U. S. Food and Drug Administration. Adenostyles alliariae (Alpendost) Reversible hepatic veno-occlusive disease in an infant after consumption of pyrrolizidine-containing herbal tea.Sperl W, Stuppner H, Gassner I, Judmaier W, Dietze O, Vogel W.Eur J Pediatr. 1995 Feb;154(2):112-6. "Veno-occlusive disease was diagnosed in an 18-month-old boy who had regularly consumed a herbal tea mixture since the 3rd month of life. The boy developed portal hypertension with severe ascites. Histology of the liver showed centrilobular sinusoidal congestion with perivenular bleeding and parenchymal necrosis without cirrhosis." Aristolochia (Guang Fang Ji) Renal interstitial fibrosis and urothelial carcinoma associated with the use of a Chinese herb (Aristolochia fangchi).Nortier JL, Vanherweghem JL. Toxicology. 2002 Dec 27;181-182:577-80. "Exposure to Aristolochia species (spp.) is associated with the development of renal interstitial fibrosis (CHN) and urothelial cancer in humans. Health professionals should be aware that in traditional Chinese medicine, Aristolochia spp. are considered interchangeable with certain other herbal ingredients and are also sometimes mistaken for ST, Akebia, Asarum, Clematis spp. and Cocculus spp. in herbal remedies." Atractylis gummifera (African Herbal Remedy) A review of acute poisoning from Atractylis gummifera L.Hamouda C, Hedhili A, Ben Salah N, Zhioua M, Amamou M.Vet Hum Toxicol. 2004 Jun;46(3):144-6. "Atractylis gummifera glucosides cause a severe hepatitis with fatal liver failure common. Clinical manifestations are related to an induced hypoglycemia and neurovegetative disorders or subsequent renal failure. Liver transplantation or immunotherapy may improve the often fatal prognosis." Hepatotoxicity due to Atractylis gummifera-L.Georgiou M, Sianidou L, Hatzis T, Papadatos J, Koutselinis A.J Toxicol Clin Toxicol. 1988;26(7):487-93. "The authors describe an intoxication by Atractylis gummifera in a 7-year old boy who drunk an extract made from the plant's root as traditional medicine. Laboratory findings showed severe hepatocellular damage and acute renal failure. In spite of all treatment and therapeutic efforts, the boy died 8 days after admission." Calliepsis laureola (Impila) The clinical syndrome of Impila (Callilepis laureola) poisoning in children. AR, Coovadia HM, Bhoola KD.S Afr Med J. 1979 Feb 24;55(8):290-2. "The administration of herbal medicines made from Callilepis laureola... can and does cause poisoning, which has only been diagnosed with any confidence at postmortem examination, where the characteristic hepatic and renal tubular necrosis is obvious." Toxicity of Callilepis laureola.Wainwright J, Schonland MM, Candy HA.S Afr Med J. 1977 Aug 13;52(8):313-5. "Chemical extraction has yielded a product, identified as atractyloside, which is responsible for the nephrotoxic and hypoglycaemic effects of Callilepis laureola. The hepatotoxic principle has not yet been isolated." Toxic hepatitis in black patients in natal.Wainwright J, Schonland MM.S Afr Med J. 1977 Apr 23;51(17):571-3. "The clinical and pathological features of toxic centrilobular zonal necrosis in Natal Blacks are described. It is suggested that this condition may be caused by the toxic action of Callilepis laureola (known to the Zulu as 'impila')." Cassia species (Senna) Finger clubbing and aspartylglucosamine excretion in a laxative-abusing patient.Malmquist J, sson B, Hulten-Nosslin MB, Jeppsson JO, Ljungberg O.Postgrad Med J. 1980 Dec;56(662):862-4. "A young woman with a previous history of anorexia nervosa presented with severe finger clubbing. Urine samples intermittently contained significant amounts of aspartylglucosamine. Liver biopsy showed abnormal cytoplasmic inclusions in phagocytic cells." Acute hepatitis associated with Barakol.Hongsirinirachorn M, Threeprasertsuk S, Chutaputti A.J Med Assoc Thai. 2003 Jun;86 Suppl 2:S484-9. "Barakol is a natural anxiolytic extracted from Cassia siamea, known as "Khi-lek" in Thailand. The authors studied the adverse effects of Barakol in 12 healthy Thai patients... Liver biopsy was done in 3 cases and the histopathological findings were compatible with interface hepatitis." Chelidonium majus (Greater Celandine) Acute hepatitis induced by Greater Celandine (Chelidonium majus).Stickel F, Poschl G, Seitz HK, Waldherr R, Hahn EG, Schuppan D.Scand J Gastroenterol. 2003 May;38(5):565-8. "We report on two cases of acute liver injury along with the intake of Greater Celandine (Chelidonium majus), a well-known herbal remedy frequently used for irritable bowel syndrome." Acute hepatitis after use of a herbal preparation with greater celandine (Chelidonium majus). Crijns AP, de Smet PA, van den Heuvel M, Schot BW, Haagsma EB.Ned Tijdschr Geneeskd. 2002 Jan 19;146(3):100-2. "A 42-year-old woman developed jaundice due to acute hepatitis several weeks after ingestion of a herbal preparation containing greater celandine (Chelidonium majus) and curcuma root, which had been prescribed by an alternative therapist due to a skin complaint. The hepatitis was ascribed to the known hepatotoxic effects of C. majus." Acute hepatitis induced by greater celandine (Chelidonium majus).Benninger J, Schneider HT, Schuppan D, Kirchner T, Hahn EG.Gastroenterology. 1999 Nov;117(5):1234-7. "In the last 2 years, we have observed 10 cases of acute hepatitis induced by preparations of greater celandine (Chelidonium majus), which are frequently prescribed to treat gastric and biliary disorders. The course of hepatitis was mild to severe." Crotalaria species Crotalaria juncea intoxication in horses.Nobre D, Dagli ML, Haraguchi M.Vet Hum Toxicol. 1994 Oct;36(5):445-8. "Twenty horses died 30 d after being fed a diet containing 40% of tritured Crotalaria juncea seeds. At necropsy the most evident lesions were areas of lung parenchyma consolidation and enlarged and congested livers." Toxic effects of Crotalaria saltiana in mice.Barri ME, Adam SE, Omer OH.Vet Hum Toxicol. 1988 Oct;30(5):429-31. "Dry Crotalaria saltiana shoots were fed to strain ASL mice... [producing] toxicity and death after 7 to 29 days. The main lesions were necrosis, portal fibroplasia and hemorrhage in the liver, pulmonary congestion and emphysema, focal catarrhal enteritis, and degeneration of the cells of the renal tubules." Toxicological studies on the ethanolic extract of Crotalaria juncea seeds in rats.Prakash AO, Dehadrai S, S.J Ethnopharmacol. 1995 Mar;45(3):167-76. "The effect of the ethanolic extract of Crotalaria juncea Linn. (Leguminosae) seeds has been assessed on liver, kidney, spleen and adrenals of adult rats. Histology revealed remarkable disintegration necrosis and degeneration in the liver (and) other vital organs too were also affected." Ephedra (Ma huang) Ephedra-associated cardiomyopathy.Naik SD, Freudenberger RS.Ann Pharmacother. 2004 Mar;38(3):400-3. Epub 2004 Jan 23. "It is well documented that ephedra, through its sympathomimetic effects, can cause a range of cardiovascular toxicities including myocarditis, arrhythmias, myocardial infarction, cardiac arrest, and sudden death." Ischemic stroke after using over the counter products containing ephedra.Chen C, Biller J, Willing SJ, AM.J Neurol Sci. 2004 Jan 15;217(1):55-60. "Ephedrine, like other sympathomimetic agents, predisposes patients to both ischemic and hemorrhagic strokes." Final rule declaring dietary supplements containing ephedrine alkaloids adulterated because they present an unreasonable risk. Food and Drug Administration, HHS.Fed Regist. 2004 Feb 11;69(28):6787-854. "The Food and Drug Administration is issuing a final regulation declaring dietary supplements containing ephedrine alkaloids adulterated under the Federal Food, Drug, and Cosmetic Act because they present an unreasonable risk of illness or injury under the conditions of use recommended or suggested in labeling, or if no conditions of use are suggested or recommended in labeling, under ordinary conditions of use." Heliotropium species Herbal medicines and veno-occlusive disease in India.Datta DV, Khuroo MS, Mattocks AR, Aikat BK, Chhuttani PN.Postgrad Med J. 1978 Aug;54(634):511-5."Six cases are described of veno-occlusive disease (VOD) after medicinal herb ingestion. Two patients presented with fulminant hepatic failure while the other four patients had a clinical picture suggestive of decompensated cirrhosis." An outbreak of hepatic veno-occlusive disease in north-western Afghanistan.Mohabbat O, Younos MS, Merzad AA, Srivastava RN, Sediq GG, Aram GN.Lancet. 1976 Aug 7;2(7980):269-71. "Following a 2-year period of severe drought a very large number of patients with massive ascites and emaciation were observed in north-western Afghanistan. The outbreak was caused by consumption of bread made from wheat contiminated with seeds of Heliotropium plants, which were shown to contain pyrrolizidine alkaloids." An epidemic of veno-occlusive disease of the liver in Afghanistan. Pathologic features.Tandon HD, Tandon BN, Mattocks AR.Am J Gastroenterol. 1978 Dec;70(6):607-13. "A large outbreak of veno-occlusive disease occurred in Afghanistan... caused by consumption of wheat flour heavily contaminated with seeds of a plant of the heliotropium species. Centrilobular hemorrhagic necrosis was followed by occlusive changes in the hepatic veins, finally resulting in nonportal cirrhosis." Larrea tridetata (Chapparal, Creosote) The safety of low-dose Larrea tridentata (DC) Coville (creosote bush or chaparral): a retrospective clinical study.Heron S, Yarnell E.J Altern Complement Med. 2001 Apr;7(2):175-85. "Larrea should be used with caution in persons with a history of previous, or current, liver disease. It may be preferable to avoid the use of Larrea capsules because they have been associated with potentially dangerous overdosing." Chaparral-associated hepatotoxicity.Sheikh NM, Philen RM, Love LA.Arch Intern Med. 1997 Apr 28;157(8):913-9. "Of 18 reports of illnesses associated with the ingestion of chaparral, there was evidence of hepatotoxicity in 13 cases. These data indicate that the use of chaparral may be associated with acute to chronic irreversible liver damage with fulminant hepatic failure..." Lobelia (Lobelia inflata) Use of alternative and complementary therapies for pediatric asthma.Mazur LJ, De Ybarrondo L, J, Colasurdo G.Tex Med. 2001 Jun;97(6):64-8. "This survey of 48 multicultural parents of children with asthma identifies and compares alternative and complementary treatments used for asthma, and compares any potentially effective or harmful effects. Three herbal remedies were potentially toxic: lobelia, possible pennyroyal mint, and tree tea oil." Lycopodium serratum (Jin Bu ) Acute hepatitis associated with the Chinese herbal product jin bu huan.Woolf GM, Petrovic LM, Rojter SE, Wainwright S, Villamil FG, Katkov WN, Michieletti P, Wanless IR, Stermitz FR, Beck JJ, et al.Ann Intern Med. 1995 Apr 15;122(8):636. "Hepatitis was associated with symptoms of fever, fatigue, nausea, pruritus, and abdominal pain and with signs of jaundice and hepatomegaly. Although the hepatotoxic mechanisms are not defined, they may include hypersensitive or idiosyncratic reactions or direct toxicity to active metabolites." Chronic hepatitis induced by Jin Bu Huan.Picciotto A, Campo N, Brizzolara R, Giusto R, Guido G, Sinelli N, Lapertosa G, Celle G.J Hepatol. 1998 Jan;28(1):165-7."We report a case of chronic hepatic damage following administration of Jin Bu Huan Anodyne tablets. This case reinforces the already known hepatotoxicity of this product and should make us think more about the uncontrolled use of alternative products." Jin bu huan toxicity in adults--Los Angeles, 1993.[No authors listed]MMWR Morb Mortal Wkly Rep. 1993 Dec 3;42(47):920-2. "Jin Bu Huan (JBH) is a traditional Chinese herbal product used as a sedative and analgesic... the first cases of acute hepatitis attributed to use of JBH were diagnosed in three women in Los Angeles during July and August 1993." Hepatitis associated with Chinese herbs.McRae CA, Agarwal K, Mutimer D, Bassendine MF.Eur J Gastroenterol Hepatol. 2002 May;14(5):559-62. "We describe two patients who suffered severe hepatitis, one of whom died, after taking Chinese herbal remedies for minor complaints. Two products appear to be implicated frequently: Jin bu huan was taken by 11 patients, and Dictamnus dasycarpus was taken by six patients, including both fatal cases." The clinical spectrum of Jin Bu Huan toxicity.Horowitz RS, Feldhaus K, Dart RC, Stermitz FR, Beck JJ.Arch Intern Med. 1996 Apr 22;156(8):899-903. "A single, acute ingestion (of Jin Bu Huan) in children rapidly produced life-threatening neurologic and cardiovascular manifestations, while long-term jin bu huan use in adults was associated with hepatitis." Mentha pulegium (Pennyroyal) Mitigation of pennyroyal oil hepatotoxicity in the mouse.Sztajnkrycer MD, Otten EJ, Bond GR, Lindsell CJ, Goetz RJ.Acad Emerg Med. 2003 Oct;10(10):1024-8. "Pennyroyal oil ingestion has been associated with severe hepatotoxicity and death. The primary constituent, R-(+)-pulegone, is metabolized via hepatic cytochrome P450 to toxic intermediates." Multiple organ failure after ingestion of pennyroyal oil from herbal tea in two infants.Bakerink JA, Gospe SM Jr, Dimand RJ, Eldridge MW.Pediatrics. 1996 Nov;98(5):944-7. "Pennyroyal oil is a highly toxic agent that may cause both hepatic and neurologic injury if ingested." Pennyroyal toxicity: measurement of toxic metabolite levels in two cases and review of the literature. IB, Mullen WH, Meeker JE, Khojasteh-BakhtSC, Oishi S, SD, Blanc PD.Ann Intern Med. 1996 Apr 15;124(8):726-34. "Pennyroyal is a widely available herb that has long been used as an abortifacient despite its potentially lethal hepatotoxic effects." Pausinystalia yohimbe (Yohimbe) Yohimbine-induced cutaneous drug eruption, progressive renal failure, and lupus-like syndrome.Sandler B, Aronson P.Urology. 1993 Apr;41(4):343-5. "We describe a forty-two-year black man in whom a generalized erythrodermic skin eruption, progressive renal failure, and lupus-like syndrome developed following treatment with the drug, yohimbine." Piper methysticum (Kava-kava) Kava kava: examining new reports of toxicity.Clouatre DL.Toxicol Lett. 2004 Apr 15;150(1):85-96. "A total of 78 cases of hepatotoxicity reputedly linked to kava ingestion are available for review from various databases. Of these adverse events, four probably are linked to kavalactones taken alone and another 23 are potentially linked to kava intake, but also involve the concomitant ingestion of other compounds with potential hepatotoxicity." Hepatitis induced by Kava (Piper methysticum rhizoma).Stickel F, Baumuller HM, Seitz K, Vasilakis D, Seitz G, Seitz HK, Schuppan D.J Hepatol. 2003 Jul;39(1):62-7. "We analyzed 29 novel cases of hepatitis along with Kava ingestion... Nine patients developed fulminant liver failure, of which eight patients underwent liver transplantation. Three patients died, two following unsuccessful liver transplantation and one without." Hepatic toxicity possibly associated with kava-containing products--United States, Germany, and Switzerland, 1999-2002.MMWR Morb Mortal Wkly Rep. 2002 Nov 29;51(47):1065-7. "A total of 11 patients who used kava products had liver failure and underwent subsequent liver transplantation. FDA continues to advise consumers and health-care providers about the potential risk associated with the use of kava-containing products." Acute hepatitis induced by kava kava.Humberston CL, Akhtar J, Krenzelok EP.J Toxicol Clin Toxicol. 2003;41(2):109-13. "A previously healthy 14-year-old female was admitted to the hospital with hepatic failure. The liver biopsy showed hepatocellular necrosis consistent with chemical hepatitis. The patient gave a history of taking a kava kava-containing product for four months." Salix species (Willow Bark) Salicylate hepatitis.O'Gorman T, Koff RS.Gastroenterology. 1977 Apr;72(4 Pt 1):726-8. "Two patients developed acute hepatic injury as a result of salicylate therapy. Salicylate-induced liver injury should be considered in the differential diagnosis of hepatic disease occurring in patients receiving high dose salicylate therapy, regardless of serum salicylate levels." Hepatotoxicity of mild analgesics.Prescott LF.Br J Clin Pharmacol. 1980 Oct;10 Suppl 2:373S-379S."Salicylate hepatitis is often asymptomatic, and may only be revealed by finding elevated levels of aminotransferases. Most cases have occurred in children or young adults with connective tissue diseases, who take high doses of salicylates for long periods." Effects of non-narcotic analgesics on the liver.Prescott LF.Drugs. 1986;32 Suppl 4:129-47. "About 50% of patients given aspirin regularly in anti-inflammatory doses develop mild, dose-dependent reversible liver damage as shown by elevation of the plasma aminotransferase activity." Hepatic toxicity of nonsteroidal anti-inflammatory drugs. JH.Clin Pharm. 1984 Mar-Apr;3(2):128-38. "Intrinsic hepatotoxins, such as salicylates, produce injury in a large percentage of exposed individuals that is often dose related and occurs after a short, fixed latent period. In most cases of hepatocellular injury, the prognosis of those patients who survive the acute phase of injury is good." Sassafras albidum (Sassafras) Carcinogenicity of some folk medicinal herbs in rats.Kapadia GJ, Chung EB, Ghosh B, Shukla YN, Basak SP, Morton JF, Pradhan SN.J Natl Cancer Inst. 1978 Mar;60(3):683-6. "Twelve medicinal herbs were bioassayed to correlate a high incidence of esophageal carcinoma in natives of different places with their habitual consumption of these products. Diospyros and extracts of Sassafras albidum and Chenopodium ambrosiodes were tumorigenic in over 50% of the treated animals." Senecio (Gordolobo yerba) Hepatic veno-occlusive disease due to pyrrolizidine (Senecio) poisoning in Arizona.Stillman AS, Huxtable R, Consroe P, Kohnen P, S.Gastroenterology. 1977 Aug;73(2):349-52. "An infant with documented hepatic veno-occlusive disease due to ingestion of pyrrolizidine alkaloids is presented. Among these people, this herb is known as gordolobo yerba. The patient presented with acute hepatocellular disease and portal hypertension which progressed over 2 months to extensive hepatic fibrosis." Herb use and necrodegenerative hepatitis.Mokhobo KP.S Afr Med J. 1976 Jul 3;50(28):1096-9. "Twelve patients with herbally-induced hepatitis are described and the clinicopathological features of their illness, which seem to present a recognisable spectrum, are discussed. Senecio species are the principal source of hepatotoxic alkoloids, especially pyrrolizidines." Symphytum species (Comfrey) The efficacy and safety of comfrey.Stickel F, Seitz HK.Public Health Nutr. 2000 Dec;3(4A):501-8. "The main liver injury caused by comfrey (Symphytum officinale) is veno-occlusive disease, a non-thrombotic obliteration of small hepatic veins leading to cirrhosis and eventually liver failure. Patients may present with either acute or chronic clinical signs with portal hypertension, hepatomegaly and abdominal pain as the main features." Carcinogenic activity of Symphytum officinale.Hirono I, Mori H, Haga M.J Natl Cancer Inst. 1978 Sep;61(3):865-9. "The carcinogenicity of Symphytum officinale L., Russian comfrey, used as a green vegetable or tonic, was studied in inbred ACI rats. Hepatocellular adenomas were induced in all experimental groups that received the diets containing comfrey roots and leaves. Hemangioendothelial sarcoma of the liver was infrequently induced." Teucrium chamaedrys (Germander) Hepatitis after germander (Teucrium chamaedrys) administration: another instance of herbal medicine hepatotoxicity.Larrey D, Vial T, Pauwels A, Castot A, Biour M, M, Michel H.Ann Intern Med. 1992 Jul 15;117(2):165-6. "Hepatitis characterized by jaundice and a marked increase in serum aminotransferase levels occurred 3 to 18 weeks after germander administration. Liver biopsy specimens in three patients showed hepatocyte necrosis. Germander may be hepatotoxic, which supports the view that herbal medicines are not always as safe as generally assumed." Acute hepatitis due to ingestion of Teucrium chamaedrys infusions. Alvarez J, Saez-Royuela F, Gento Pena E, Morante A, Velasco Oses A, Lorente J.Gastroenterol Hepatol. 2001 May;24(5):240-3. "We present two cases of acute hepatitis after ingestion of herbal infusions over a period of several months. One patient presented acute, cholestatic hepatitis and another presented mixed (hepatocellular and cholestatic) hepatitis." Acute hepatitis caused by wild germander. Hepatotoxicity of herbal remedies. Two cases. Pauwels A, Thierman-Duffaud D, Azanowsky JM, Loiseau D, Biour M, Levy VG.Gastroenterol Clin Biol. 1992;16(1):92-5. "We report on two women who had severe acute hepatocellular liver injury occurring within one to two months of treatment with Wild Germander (Teucrium chamaedrys L.), a herbal medicine for losing weight." Tusilago farfara (Coltsfoot) Carcinogenic activity of coltsfoot, Tussilago farfara l.Hirono I, Mori H, Culvenor CC.Gann. 1976 Feb;67(1):125-9. "Rats were divided into 4 groups. Group I received 32% coltsfoot diet for 4 days... and 8 out of 12 rats developed hemangioendothelial sarcoma in the liver... Chemical studies on the dried, young flowers used in this experiment suggested that the carcinogenicity of coltsfoot is most probably due to senkirkine, a hepatotoxic pyrrolizidine alkaloid." Valeriana officinalis (Valerian) Poisoning due to an over-the-counter hypnotic, Sleep-Qik (hyoscine, cyproheptadine, valerian).Chan TY, Tang CH, Critchley JA.Postgrad Med J. 1995 Apr;71(834):227-8. "The main clinical problems were central nervous system depression and anticholinergic poisoning. ...subclinical liver dysfunction in the acute stage (onset after 12-24 hours) and in the intervening period after discharge from hospital could not be excluded." Reviewed October 4, 2005 by V. J. , RN, BSN, MA. The Role of the Liver in Normal Digestion Nutritional Concerns in Hepatitis Infection Hepatitis C and Weight Management Food & Drug Interactions Carbohydrates in the Diet Protein in the Diet Fat in the Diet Fat-Soluble Vitamins: A, D, E and K Water-Soluble Vitamins: The B Family and Vitamin C Understanding Mineral Supplements AHRQ: Milk Thistle: Effects on Liver Disease and Cirrhosis and Clinical Adverse Effects NCCAM: Are You Considering Using Complementary and Alternative Medicine (CAM)? NCCAM: Herb Clinical Trials NCCAM: Kava Linked to Liver Damage This link brought to you by Schering Corporation about us | contact us | privacy policy | terms of use | logout | news Hepatitis Neighborhood is a service of CuraScript www.curascript.com Copyright © 1999-2005 CuraScript, Inc. Return: Home / Treatment Options / Food & Nutrition Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.