DOCSLIB.ORG

The Role of Nutritional Therapy in Alcoholic Liver Disease

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Role of Nutritional Therapy in Alcoholic Liver Disease The Role of Nutritional Therapy in Alcoholic Liver Disease Christopher M. Griffith, M.D., and Steven Schenker, M.D. Alcoholic liver disease (ALD) evolves through various stages, and malnutrition correlates with the severity of ALD. Poor nutrition is caused both by the substitution of calories from alcohol for calories from food and by the malabsorption and maldigestion of various nutrients attributed to ALD. The only established therapy for ALD consists of abstinence from alcohol. Sufficient nutritional repletion coupled with appropriate supportive treatment modalities may be effective in reducing complications associated with ALD—particularly infection. Nutrition makes a significant positive contribution in the treatment of ALD, especially in selected malnourished patients. KEY WORDS: Ethanol metabolism; heavy alcohol use; alcoholic liver disease; alcoholic fatty liver; alcoholic hepatitis; fibrosis; alcoholic cirrhosis; gut; infection; anorexia; hepatic encephalopathy; nutrition; malnutrition; nutritional therapy; S-Adenosylmethionine (SAM); antioxidants; milk thistle; silymaryin; phosphatidylcholine; dietary fat; vitamins he study of malnutrition in alcoholic hepatitis) and only 20 percent Diversity of Liver Injury patients with alcoholic liver dis­ will progress to scarring of the liver (i.e., Tease (ALD) is based on several cirrhosis) (McCullough and O’Connor Alcoholic liver injury is known to general concepts and observations. 1998). Clearly, other risk factors, evolve through various stages. Patients Researchers and clinicians previously including genetic predisposition, obesity, exhibit a variety of clinical symptoms believed that malnutrition was the concomitant viral hepatitis infection, and signs in liver histology (as reviewed primary cause of liver injury in ALD and poor nutrition, may contribute in Dasarathy and McCullough 2003). rather than the consequence of excessive variably to the development of ALD. As previously mentioned, almost every­ alcohol consumption. This view was Indeed, in a large study of hospital­ one with heavy alcohol consumption based on the prevalence of malnutrition ized patients with varying severity of develops fatty liver. This often is a rather benign disorder and considered in alcoholics and those with clinical ALD, malnutrition (especially the type reversible upon cessation of alcohol evidence of liver (i.e., hepatic) dysfunction caused by deficient protein and calories) resulting from alcohol consumption intake. In some cases, continued drink­ was closely associated (although not ing may result in the development of (Mendenhall et al. 1984). It now is necessarily causal) with the severity of widely accepted that the quantity and alcoholic hepatitis, which may—and liver injury (Mendenhall et al. 1984). duration of alcohol consumption are the often does—end in severe clinical dis­ All patients with clinical evidence of principal agents in the development of ease. The severity of disease and liver alcoholic liver injury. This is based on ALD (regardless of severity) exhibited dysfunction correlates with an increas­ animal and human data showing that some features of malnutrition. With ing short-term mortality (as reviewed ALD can develop in well-nourished regard to the possible value of nutritional in Dasarathy and McCullough 2003). individuals who consume large amounts therapy, it would seem logical that It is in this acutely diseased group that of alcohol (Mezey 1991). However, a patients with more severe deficits would optimal nutritional therapy might have great deal of variability exists regarding benefit more, although convincing proof the most impact. Continued drinking the individual development of progres­ of this, to our knowledge, is not available. in this group of patients may lead to sive alcoholic liver injury. Although This article reviews the various forms more than 90 percent of people with of liver injury; the basis for and role of CHRISTOPHER M. GRIFFITH, M.D., is a excessive alcohol consumption will malnutrition in ALD, including the fellow of Gastroenterology and STEVEN develop fatty liver (defined as greater harmful effects of the products of alcohol SCHENKER, M.D., is professor of than 5 percent fat in the liver), only up metabolism; evidence for the benefits Medicine and Pharmacology, both at the to 35 percent will develop inflammation of nutrition; and special considerations University of Texas Health Science Center of the liver caused by alcohol (i.e., for nutritional therapy in ALD. at San Antonio, San Antonio, Texas. 296 Alcohol Research & Health Nutritional Therapy in ALD the development of excess scar tissue in Decreased Food Intake decreased intestinal enzyme activity the liver (i.e., fibrosis) and the subse­ (i.e., lactase) required for carbohydrate People with ALD will substitute calories quent anatomical changes of cirrhosis. digestion and absorption, and/or from food with calories from alcohol. It Cirrhosis is considered a late stage of decreased absorption from increased has been shown in patients with ALD swelling of the gut. The latter is attrib­ the disease, clinically manifested by that calories from alcohol may con­ progressive liver dysfunction with asso­ uted to increased pressure in the drain­ tribute more than 50 percent of their ing vein (i.e., portal vein) and lym­ ciated yellowing of skin and whites total calories, with calories from pro­ of the eyes (i.e., jaundice)—caused by phatic vessels connecting the intestines tein comprising only 6 to 10 percent with the liver. The changes in intestinal decreased liver clearance of bilirubin, (Mendenhall et al. 1984). In addition, fluid accumulation in the abdomen digestion and absorption appear to the proportion of calories from alcohol reverse once the patient ceases drinking (i.e., ascites), and impaired brain func­ appears to increase, whereas those from tion caused by the accumulation of and starts to follow a normal diet, sug­ food decrease with escalating liver dys­ gesting that nutritional replacement ammonia in the brain tissues (i.e., function (Mezey 1991). This increase encephalopathy) (as reviewed in may be of special benefit (Mezey 1991). in alcohol calories and decrease in food Finally, the preferential metabolism Dasarathy and McCullough 2003). calories may be partially explained by These three disorders may occur of alcohol by the liver alters the meta­ the diversion of funds from the pur­ bolism of sugars (i.e., carbohydrates), separately or often in association with chase of food to that of alcohol; how­ each other. In many instances, these fats (i.e., lipids), and proteins (i.e., ever, hospitalized patients with ALD amino acids/nitrogen) (Mezey 1991). stages of liver injury may be difficult to given adequate access to nutrition still distinguish either clinically or by labo­ Abnormal breakdown of fat results in demonstrate decreased ingestion of the formation of triglycerides that are ratory measures of liver dysfunction (as nonalcohol calories (Schenker and reviewed in Dasarathy and McCullough deposited in the liver, manifesting as Halff 1993). This decreased desire for fatty liver (Schenker and Halff 1993). 2003). Prior studies regarding nutri­ food (i.e., anorexia) also correlates with tional therapy in ALD often did not Altered fat metabolism also may propa­ the severity of liver injury (Hirsh et al. gate fibrosis by increasing collagen for­ differentiate between these various types 1999; Mendenhall et al. 1995). Anorexia of liver disease, complicating researchers’ mation (Schenker and Halff 1993). is pervasive in ALD and is a key reason The altered functional mass of the liver abilities to assess the true benefit of for decreased dietary intake of nonalcohol from these increased deposits of fat and nutritional therapy. This has been a prob­ calories (Mezey 1991). collagen may result in decreased stores lem in the assessment of such data in the of vitamins and carbohydrates. Glycogen, past as well as for the present authors. Poor Absorption and Digestion of the storage form of carbohydrates in Nutrients the liver, serves as an energy reserve for periods of increased energy need. Basis for Malnutrition in Another factor contributing to poor Inadequate glycogen reserves cause the ALD nutrition in patients with ALD is the body to make use of other metabolic malabsorption and maldigestion of var­ pathways for energy, such as the break­ The signs and symptoms of nutritional ious nutrients from the gut (Mezey down of muscle (Schenker and Halff deficits in ALD patients have been well 1991; Schenker and Halff 1993). This 1993). This may explain the increased characterized (Mendenhall et al. 1984; may relate to the impaired output of muscle wasting, increased nitrogen Mezey 1991; Schenker and Halff 1993; bile from the liver, resulting in decreased excretion in the stool, and negative Nompleggi and Bonkovsky 1994; absorption of fat and fat-soluble vita­ nitrogen balance seen in patients with Hirsh et al. 1999) and include muscle mins. The possibility of concomitant ALD. It is important to note that in wasting, decreased lean body mass, var­ pancreatitis causing decreased output healthy individuals these alternate ious vitamin deficiencies, and decreased of enzymes necessary for absorption of pathways of energy usually are found measurable serum proteins. A complete fats and proteins also can occur with only after periods of prolonged fasting description of specific nutritional deficits alcohol abuse. Moreover, there may or starvation. Patients with ALD, how­ is beyond the scope
Load more

Recommended publications
  • Adult Tube Feeding
    Guide to ADULT TUBE FEEDING Parents’ Practical Guide to Pediatric Tube Feeding | XX Contents Introduction 3 Finding Community Support 4 Understanding the Tube Feeding System 6 Monitoring Your Response to Tube Feeding 8 Taking Charge of Your Doctor Visits 18 Tube Feeding Monitoring Checklist 20 Medication Record 28 Notes 30 Glossary 32 Guide to Adult Tube Feeding | 1 Introduction We know that tube feeding brings major changes to your life. But you don’t have to face them alone. We hope you find this guide a useful, practical resource that can help you tube feed successfully at home. You’ll find step-by-step instructions on handling issues you face every day, from coping with infections to preparing for a doctor’s appointment. The guide includes worksheets (P. 20-31) that make it simple to record important information about your progress. We’ve also added a helpful glossary (P. 32-34) that you can refer to if you come across any unfamiliar terms. While technical and medical support form the foundation of tube-feeding success, we believe that emotional support is just as important. Hopefully, you’ll find resources in this guide that make your journey easier. Guide to Adult Tube Feeding | 3 Finding Community Support With support and guidance, you can take control of the tube-feeding process and adjust successfully to this new lifestyle change. Visit the link below to find educational resources, support groups and the opportunity to connect with others in your situation. The Oley Foundation The Oley Foundation is a nonprofit organization for people who depend on home enteral (tube) feeding or parenteral (intravenous) feeding.
    [Show full text]
  • Nutrition Department This Booklet Has Been Developed by the Nutrition and Gastroenterology Department’S at Alfred Health, Melbourne
    Nutrition Department This booklet has been developed by the Nutrition and Gastroenterology Department’s at Alfred Health, Melbourne. Inside you will find information on tube feeding at home CONTENTS 1. Your tube & feeding regime Tube details page 1 Feeding regime page 1 2. Important contact phone numbers page 1 3. Introduction What is tube feeding? page 2 Who receives tube feeding? page 2 4. The feeding tube Nasogastric tube page 3 Nasojejunal tube page 3 Gastrostomy tubes page 3—7 Jejunostomy tubes page 8 Trans-gastric jejunostomy tubes page 8 5. The formula Formula selection & feeding plan page 9 - 10 Formula storage & preparation page 10 6. Feeding methods Continuous OR Intermittent feeding using a pump page 11 - 12 Continuous OR Intermittent feeding using gravity drip page 13 - 14 Bolus feeding page 15 - 16 Oral feeding page 16 7. Medication Administration of medication page 17 8. Care during tube feeding Gastrostomy feeding tube care: Care immediately post tube insertion page 18 Daily tube & stoma care page 19 Jejunostomy, trans-gastric jejunostomy & PEG—J page 20 Nasogastric tube care page 20 Care of the tube feeding equipment page 21 Mouth care page 21 9. Possible problems & solutions Blocked Tube page 22 Constipation page 22 - 23 Diarrhoea page 23 - 24 Irritation, skin redness &/or oozing page 24 Leaking around tube page 24 Nausea & vomiting page 25 Reflux page 25 Tube dislodged or falls out page 25 Tube deteriorated or damaged page 25 What to do if your feeding tube has fallen out page 26 10. The Alfred Home Enteral Nutrition (HEN) program Requirements of the HEN Program page 27 The PEG/HEN Clinic page 28 Ordering formula & equipment pager 28 11.
    [Show full text]
  • JEJUNOSTOMY Feeding Tube PASSPORT (JEJ)
    Hull University Teaching Hospitals NHS Trust JEJUNOSTOMY Feeding Tube PASSPORT (JEJ) Tube INFORMATION ABOUT MY JEJUNOSTOMY FEEDING TUBE Affix Addressograph Has a tube How inserted? Site of bowel insertion: e.g. Jejunum, Terminal Ileum (Circle) Date inserted: Skin Suture Removal Date Yes / No Weekly Balloon change (If required) Abdominal measurement (If required) cm Type of feed: Continuous/mls per hour mls Flush with of sterile water pre & post feed & medication. 30mls Additional flushes can be given as indicated by your dietitian. Long term plan If during the first 7 days following your tube insertion, you notice any leak of fluid around the tube, pain on feeding, flushing or if there is fresh bleeding, STOP the feed immediately and contact Ward 14 Castle Hill Hospital - see contact numbers on page 16 2 CONTENTS Page Going home with a jejunostomy tube 4 What is a feeding jejunostomy tube 4 How long will I need it? 5 Surgically placed jejunostomy tube with stitches 5 & 6 Jejunostomy tube with balloon 6 General care / stoma care 7 Flushing 8 Pump feeding/Key Points 9 My Feed regime 10 & 11 Tube blockage 12 Tube fallen out 12 Mouth care 13 Medicine 13 Feed storage and disposal 13 Training prior to going home 14 Going home 14 Equipment for discharge 15 When discharged from hospital 15 Contact numbers between 9am-5pm 16 Emergency contact details after 5pm 16 This booklet contains useful information and advice for patients leaving hospital with a Jejunostomy feeding tube. How it works and how to maintain it. It also lists specific interventions of what to do should you encounter any problems.
    [Show full text]
  • Tube Feeding Protocol: Supporting an Individual with a Feeding Tube
    Tube Feeding Protocol: Supporting an Individual with a Feeding Tube Introduction Some people may be unable to take foods or fluids by mouth due to dysphagia. Others may require supplementation because they are unable to take sufficient foods or fluids by mouth, and formula delivered through a feeding tube may provide them with much needed additional nutrients. It is helpful if guidelines (A Tube Feeding Protocol) are in place prior to the need for this intervention. Below are some suggested guidelines for supporting an Individual with a feeding tube. Information to be documented by the physician The reason (medical diagnosis) requiring feeding tube insertion Type of feeding tube inserted Types of feeding tubes The Nasogastric Tube (NG tube): Passed into either nostril, down the esophagus and into the stomach. This is used for short term feedings. The Gastrostomy tube (G - tube or PEG): Surgically placed through the abdominal wall into the stomach. The tube will be located below the rib cage and to the left. The Jejunostomy tube (J - tube or PEJ): Surgically implanted in the upper portion of the jejunum (Part of the small intestine.) The tube will be located lower in the abdomen and more toward the center than the G – tube. Feedings through a J – tube must always be by pump. The Gastrostomy-Jejunostomy (GJ - tube): Surgically placed in the stomach, like the G – tube, but the tubing is longer, the end is in the jejunum, and there are two ports. Feeding technique Feeding techniques Bolus: A set amount of formula is given over a short period of time via syringe.
    [Show full text]
  • Quick Guide to Gastrostomy Feeding Tubes and Devices
    QUICK GUIDE TO GASTROSTOMY FEEDING TUBES AND DEVICES A gastrostomy feeding tube or device is one which has been inserted directly through the abdominal wall into the stomach. It is secured by an internal retention device (either a balloon or a soft disc known as a “bumper”) on the inside and a firm external retention device (known as a “flange”) on the outside.11 Placement of a ballooned gastrostomy tube Cross-section: non-ballooned tube Oesophagus Stomach Clamp External Flange Gastrostomy tube Skin Fat Muscle Skin Internal Bumper Stomach Photo: APhoto: Kennedy Photo: MPhoto: Sutherland Patient with a ballooned gastrostomy Patient lying down with a non-ballooned tube insitu gastrostomy tube in situ See page 8 and 9 for a summary of the different types of tubes and devices you might see. A Clinician’s Guide: Caring for people with gastrostomy tubes and devices 7 Common features of gastrostomy feeding tubes and devices include, but are not limited to: Refer to manufacturer’s guidelines for advice on brand specific tube and device features Ballooned Gastrostomy Tube Ballooned Gastrostomy Tube With side port Without side port Feeding Port Feeding Port (Enteral Dispenser (Enteral Dispenser and Feed Bag and Feed Bag connect here) connect here) ml/cc Balloon Port Balloon Port ml/cc Side Port (X ml/cc) (X ml/cc) French (size) [For example:16/18/20] French (size) [For example:16/18/20] FR FR cm markings cm markings External External Flange Flange Balloon Balloon Non-ballooned Gastrostomy Tube Non-ballooned Gastrostomy Tube with collapsible internal
    [Show full text]
  • Mic Gastrostomy Feeding Tubes Care Booklet.Pdf
    GASTROSTOMY CARE GUIDE GASTROSTOMY CARE GUIDE Universal INDICATIONS FOR Adapter TUBE FEEDING Medication PATIENT INFORMATION Complete nutrition supports Port development, growth, and heal- ing. If the ability to eat or Replaceable Date of tube insertion swallow is lost, or the patient is unable to tolerate food, enteral Feeding feeding can sustain life, nour- Patient name Phone ish, and even increase body Adapter weight. Tube feeding is also Physician Phone used to supplement a deficient food and fluid intake. The feed- Type 0100 0110 0150 0160 (circle one) Fr Size ing procedure can be managed safely and economically at Manufacturer's lot number (printed on package) home, away from the hospital setting. A surgical gastrostomy Mark above the SECUR-LOK® Ring in cm provides access to the stomach if long term nutritional support (this means the mark after the initial placement) is necessary. Balloon volume if 0100, or 0110 type G Tube Pure medical grade silicone (the volume should be between 7 and 10 cc) construction makes MIC Feeding Tubes durable, yet soft and comfortable to wear. They SECUR-LOK® Formula are also translucent, allowing Ring visualization of the inside of Brand name the tube above the skin line. All MIC Enteral Feeding Tubes Method of delivery are latex free. Volume, rate and time the feeding should take MIC PEG Total amount of daily water PEG stands for Percutan- eous (through the skin) Additional ingredients Endoscopic (use of a flexible lighted tube to visualize tube Irrigate the tube with water before and after feeding and medication placement) Gastrostomy administration. (surgical opening into the stomach).
    [Show full text]
  • 2Nd Quarter 2001 Medicare Part a Bulletin
    In This Issue... From the Intermediary Medical Director Medical Review Progressive Corrective Action ......................................................................... 3 General Information Medical Review Process Revision to Medical Record Requests ................................................ 5 General Coverage New CLIA Waived Tests ............................................................................................................. 8 Outpatient Hospital Services Correction to the Outpatient Services Fee Schedule ................................................................. 9 Skilled Nursing Facility Services Fee Schedule and Consolidated Billing for Skilled Nursing Facility (SNF) Services ............. 12 Fraud and Abuse Justice Recovers Record $1.5 Billion in Fraud Payments - Highest Ever for One Year Period ........................................................................................... 20 Bulletin Medical Policies Use of the American Medical Association’s (AMA’s) Current Procedural Terminology (CPT) Codes on Contractors’ Web Sites ................................................................................. 21 Outpatient Prospective Payment System January 2001 Update: Coding Information for Hospital Outpatient Prospective Payment System (OPPS) ......................................................................................................................... 93 he Medicare A Bulletin Providers Will Be Asked to Register Tshould be shared with all to Receive Medicare Bulletins and health care
    [Show full text]
  • 6.14 Alcohol Use Disorders and Alcoholic Liver Disease
    6. Priority diseases and reasons for inclusion 6.14 Alcohol use disorders and alcoholic liver disease See Background Paper 6.14 (BP6_14Alcohol.pdf) Background The WHO estimates that alcohol is now the third highest risk factor for premature mortality, disability and loss of health worldwide.1 Between 2004 to 2006, alcohol use accounted for about 3.8% of all deaths (2.5 million) and about 4.5% (69.4 million) of Disability Adjusted Life Years (DALYS).2 Europe is the largest consumer of alcohol in the world and alcohol consumption in this region emerges as the third leading risk factor for disease and mortality.3 In European countries in 2004, an estimated one in seven male deaths (95 000) and one in 13 female deaths (over 25 000) in the 15 to 64 age group were due to alcohol-related causes.3 Alcohol is a causal factor in 60 types of diseases and injuries and a contributing factor in 200 others, and accounts for 20% to 50% of the prevalence of cirrhosis of the liver. Alcohol Use Disorders (AUD) account for a major part of neuropsychiatric disorders and contribute substantially to the global burden of disease. Alcohol dependence accounts for 71% of all alcohol-related deaths and for about 60% of social costs attributable to alcohol.4 The acute effects of alcohol consumption on the risk of both unintentional and intentional injuries also have a sizeable impact on the global burden of disease.2 Alcoholic liver disease (ALD) is the commonest cause of cirrhosis in the western world, and is currently one of the ten most common causes of death.5 Liver fibrosis caused by alcohol abuse and its end stage, cirrhosis, present enormous problems for health care worldwide.
    [Show full text]
  • Alcoholic Liver Disease and Its Relationship with Metabolic Syndrome
    Research and Reviews Alcoholic Liver Disease and Its Relationship with Metabolic Syndrome JMAJ 53(4): 236–242, 2010 Hiromasa ISHII,*1 Yoshinori HORIE,*2 Yoshiyuki YAMAGISHI,*3 Hirotoshi EBINUMA*3 Abstract Alcoholic liver disease (ALD), which occurs from chronic excessive drinking, progresses from initial alcoholic fatty liver to more advanced type such as alcoholic hepatitis, liver fibrosis, or liver cirrhosis when habitual drinking continues. In general, chance of liver cirrhosis increases after 20 years of chronic heavy drinking, but liver cirrhosis can occur in women after a shorter period of habitual drinking at a lower amount of alcohol. Alcoholic liver cirrhosis accounts for approximately 20% of all liver cirrhosis cases. The key treatment is abstinence or substantial cutting down on drinking; the prognosis is poor if the patient continues drinking after being diagnosed with liver cirrhosis. Factors that exert adverse effects on the progression of ALD include gender difference, presence of hepatitis virus, immunologic abnormality, genetic polymorphism of alcohol-metabolizing enzymes, and complication of obesity or overweight. Recently, particular attention has been paid to obesity and overweight as risk factors in the progression of ALD. Conditions such as visceral fat accumulation, obesity, and diabetes mellitus underlie the pathologic factor of metabolic syndrome (MetS). In liver, MetS may accompany fatty liver or steatohepatitis, with possible progression to liver cirrhosis in some cases. Caution is required for patients with MetS who have a high alcohol intake because alcohol consumption further accelerates the progression of liver lesions. Key words Alcoholic liver disease, Metabolic syndrome, Obesity, NAFLD/NASH Introduction following hypertension and smoking, as a global disease burden.
    [Show full text]
  • Expert Mark H
    Ask the expert Mark H. DeLegge, Enteral nutrition MD, FASGE 1. Q: How do you code for percutaneous endoscopic jejunostomy (PEJ)? A: For direct (D) PEJ, I use code 44372, with a Relative Value Unit (RVU) of 6.72. Ask the expert features questions submitted 2. Q: In the severely ill patient, is there any role for amino acid supplementation? by members, with A: Arginine and glutamine are two very important amino acids for the critically ill patient, who is often in the intensive care unit (ICU) on a ventilator. Arginine is a conditionally essential amino acid, meaning answers provided by that in critical situations, it should be supplemented. Multiple studies have determined that arginine is an ASGE physician experts. immuno-enhancing supplement that has been shown to improve rates of morbidity and mortality and days ASGE’s Publications on a ventilator in an ICU in some very ill patients. There have been concerns about the use of arginine in septic patients, because arginine is metabolized to nitrous oxide – a vasodilator. However, these concerns Committee identifies are unfounded. authors and topics for Glutamine is an immune-stimulating amino acid that is also trophic for the small bowel mucosa. Although oral the column. In this or enteral administration of glutamine has not been shown to improve clinical outcomes in critically ill patients, issue, Mark H. DeLegge, intravenous administration of glutamine has been shown to be beneficial. Intravenous glutamine is currently available internationally but not in the United States. Therefore, oral arginine supplementation or use of an MD, FASGE, responds arginine-fortified enteral formula should be considered in critically ill patients.
    [Show full text]
  • Diagnosis and Management of Autoimmune Hemolytic Anemia in Patients with Liver and Bowel Disorders
    Journal of Clinical Medicine Review Diagnosis and Management of Autoimmune Hemolytic Anemia in Patients with Liver and Bowel Disorders Cristiana Bianco 1 , Elena Coluccio 1, Daniele Prati 1 and Luca Valenti 1,2,* 1 Department of Transfusion Medicine and Hematology, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; [email protected] (C.B.); [email protected] (E.C.); [email protected] (D.P.) 2 Department of Pathophysiology and Transplantation, Università degli Studi di Milano, 20122 Milan, Italy * Correspondence: [email protected]; Tel.: +39-02-50320278; Fax: +39-02-50320296 Abstract: Anemia is a common feature of liver and bowel diseases. Although the main causes of anemia in these conditions are represented by gastrointestinal bleeding and iron deficiency, autoimmune hemolytic anemia should be considered in the differential diagnosis. Due to the epidemiological association, autoimmune hemolytic anemia should particularly be suspected in patients affected by inflammatory and autoimmune diseases, such as autoimmune or acute viral hepatitis, primary biliary cholangitis, and inflammatory bowel disease. In the presence of biochemical indices of hemolysis, the direct antiglobulin test can detect the presence of warm or cold reacting antibodies, allowing for a prompt treatment. Drug-induced, immune-mediated hemolytic anemia should be ruled out. On the other hand, the choice of treatment should consider possible adverse events related to the underlying conditions. Given the adverse impact of anemia on clinical outcomes, maintaining a high clinical suspicion to reach a prompt diagnosis is the key to establishing an adequate treatment. Keywords: autoimmune hemolytic anemia; chronic liver disease; inflammatory bowel disease; Citation: Bianco, C.; Coluccio, E.; autoimmune disease; autoimmune hepatitis; primary biliary cholangitis; treatment; diagnosis Prati, D.; Valenti, L.
    [Show full text]
  • Hepatitis C and Alcohol
    Hepatitis C and Alcohol Eugene R. Schiff, M.D., and Nuri Ozden, M.D. Patients infected with the hepatitis C virus (HCV) who drink heavily are likely to suffer more severe liver injury, promoting disease progression to cirrhosis and increasing their risk for liver cancer. Some research, although not conclusive, suggests that even moderate drinking may spur liver damage in HCV-infected patients. Research areas that have the greatest potential for developing more effective treatment options include HCV virology, immunology, animal models, and the mechanisms of liver injury. KEY WORDS: hepatitis C virus; alcoholic beverage; chronic AODE (alcohol and other drug effects); amount of AOD use; epidemiology; risk factors; disease course; alcoholic liver cirrhosis; gender differences; biochemical mechanism; RNA; mutation; apoptosis; inflammation; hepatocellular carcinoma; regulatory proteins; immune response; alcoholic fatty liver; treatment issues; treatment outcome; interferon epatitis C is an infectious liver the time of infection, male gender, are considerably more likely to test disease caused by the hepatitis obesity, abnormal accumulation of fat positive for HCV infection than those HC virus (HCV). The virus, in the liver (a condition known as fatty with less severe liver disease (Takase et which causes inflammation in the liver liver, or steatosis), and excessive alco­ al. 1993). and can lead to more serious illness, hol consumption (Poynard et al. 2001). primarily is spread by intravenous This article discusses the mechanisms contact with the blood of an infected by which alcohol may exacerbate Levels of Alcohol person. About 4 million people in the HCV-infected patients’ risk of disease Consumption in HCV United States have been infected, progression, reviews issues in the Patients and the Risk of making it the Nation’s most common treatment of alcoholic patients with Further Liver Disease blood-borne disease, resulting in the HCV infection, and addresses impor­ deaths of between 10,000 and 12,000 tant areas of future research.
    [Show full text]