What I Need to Know About Cirrhosis
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Evaluation of Abnormal Liver Chemistries
ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries Paul Y. Kwo, MD, FACG, FAASLD1, Stanley M. Cohen, MD, FACG, FAASLD2, and Joseph K. Lim, MD, FACG, FAASLD3 1Division of Gastroenterology/Hepatology, Department of Medicine, Stanford University School of Medicine, Palo Alto, California, USA; 2Digestive Health Institute, University Hospitals Cleveland Medical Center and Division of Gastroenterology and Liver Disease, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA; 3Yale Viral Hepatitis Program, Yale University School of Medicine, New Haven, Connecticut, USA. Am J Gastroenterol 2017; 112:18–35; doi:10.1038/ajg.2016.517; published online 20 December 2016 Abstract Clinicians are required to assess abnormal liver chemistries on a daily basis. The most common liver chemistries ordered are serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase and bilirubin. These tests should be termed liver chemistries or liver tests. Hepatocellular injury is defined as disproportionate elevation of AST and ALT levels compared with alkaline phosphatase levels. Cholestatic injury is defined as disproportionate elevation of alkaline phosphatase level as compared with AST and ALT levels. The majority of bilirubin circulates as unconjugated bilirubin and an elevated conjugated bilirubin implies hepatocellular disease or cholestasis. Multiple studies have demonstrated that the presence of an elevated ALT has been associated with increased liver-related mortality. A true healthy normal ALT level ranges from 29 to 33 IU/l for males, 19 to 25 IU/l for females and levels above this should be assessed. The degree of elevation of ALT and or AST in the clinical setting helps guide the evaluation. -
Acute Liver Failure J G O’Grady
148 Postgrad Med J: first published as 10.1136/pgmj.2004.026005 on 4 March 2005. Downloaded from REVIEW Acute liver failure J G O’Grady ............................................................................................................................... Postgrad Med J 2005;81:148–154. doi: 10.1136/pgmj.2004.026005 Acute liver failure is a complex multisystemic illness that account for most cases, but a significant number of patients have no definable cause and are evolves quickly after a catastrophic insult to the liver classified as seronegative or of being of indeter- leading to the development of encephalopathy. The minate aetiology. Paracetamol is the commonest underlying aetiology and the pace of progression strongly cause in the UK and USA.2 Idiosyncratic reac- tions comprise another important group. influence the clinical course. The commonest causes are paracetamol, idiosyncratic drug reactions, hepatitis B, and Viral seronegative hepatitis. The optimal care is multidisciplinary ALF is an uncommon complication of viral and up to half of the cases receive liver transplants, with hepatitis, occurring in 0.2%–4% of cases depend- ing on the underlying aetiology.3 The risk is survival rates around 75%–90%. Artificial liver support lowest with hepatitis A, but it increases with the devices remain unproven in efficacy in acute liver failure. age at time of exposure. Hepatitis B can be associated with ALF through a number of ........................................................................... scenarios (table 2). The commonest are de novo infection and spontaneous surges in viral repli- cation, while the incidence of the delta virus cute liver failure (ALF) is a complex infection seems to be decreasing rapidly. multisystemic illness that evolves after a Vaccination should reduce the incidence of Acatastrophic insult to the liver manifesting hepatitis A and B, while antiviral drugs should in the development of a coagulopathy and ameliorate replication of hepatitis B. -
Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease
pathogens Article Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease Patients from Southern Italy: A Case-Control Study Giuseppe Losurdo 1,2 , Andrea Iannone 1, Antonella Contaldo 1, Michele Barone 1 , Enzo Ierardi 1 , Alfredo Di Leo 1,* and Mariabeatrice Principi 1 1 Section of Gastroenterology, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy; [email protected] (G.L.); [email protected] (A.I.); [email protected] (A.C.); [email protected] (M.B.); [email protected] (E.I.); [email protected] (M.P.) 2 Ph.D. Course in Organs and Tissues Transplantation and Cellular Therapies, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy * Correspondence: [email protected]; Tel.: +39-080-559-2925 Received: 14 September 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: We performed an epidemiologic study to assess the prevalence of chronic viral hepatitis in inflammatory bowel disease (IBD) and to detect their possible relationships. Methods: It was a single centre cohort cross-sectional study, during October 2016 and October 2017. Consecutive IBD adult patients and a control group of non-IBD subjects were recruited. All patients underwent laboratory investigations to detect chronic hepatitis B (HBV) and C (HCV) infection. Parameters of liver function, elastography and IBD features were collected. Univariate analysis was performed by Student’s t or chi-square test. Multivariate analysis was performed by binomial logistic regression and odds ratios (ORs) were calculated. We enrolled 807 IBD patients and 189 controls. Thirty-five (4.3%) had chronic viral hepatitis: 28 HCV (3.4%, versus 5.3% in controls, p = 0.24) and 7 HBV (0.9% versus 0.5% in controls, p = 0.64). -
Differential Metabolism of Alprazolam by Liver and Brain Cytochrome (P4503A) to Pharmacologically Active Metabolite
The Pharmacogenomics Journal (2002) 2, 243–258 2002 Nature Publishing Group All rights reserved 1470-269X/02 $25.00 www.nature.com/tpj ORIGINAL ARTICLE Differential metabolism of alprazolam by liver and brain cytochrome (P4503A) to pharmacologically active metabolite HV Pai1,2* ABSTRACT SC Upadhya1,2* Cytochrome P450 (P450) is a superfamily of enzymes which mediates metab- 1 olism of xenobiotics including drugs. Alprazolam, an anti-anxiety agent, is SJ Chinta * metabolized in rat and human liver by P4503A1 and P4503A4 respectively, SN Hegde1 to 4-hydroxy alprazolam (4-OHALP, pharmacologically less active) and ␣- V Ravindranath1,2 hydroxy alprazolam (␣-OHALP, pharmacologically more active). We exam- ined P450 mediated metabolism of alprazolam by rat and human brain 1Department of Neurochemistry, National microsomes and observed that the relative amount of ␣-OHALP formed in Institute of Mental Health & Neurosciences, brain was higher than liver. This biotransformation was mediated by a P450 Bangalore, India; 2National Brain Research Centre, ICGEB Campus, Aruna Asaf Ali Marg, isoform belonging to P4503A subfamily, which is constitutively expressed in New Delhi , India neuronal cells in rat and human brain. The formation of larger amounts of ␣-OHALP in neurons points to local modulation of pharmacological activity Correspondence: in brain, at the site of action of the anti-anxiety drug. Since hydroxy metab- V Ravindranath, National Brain Research olites of alprazolam are hydrophilic and not easily cleared through blood- Centre, ICGEB Campus, Aruna Asaf Ali ␣ Marg, New Delhi - 110 067, India CSF barrier, -OHALP would potentially have a longer half-life in brain. Tel: +91 124 630 8317 The Pharmacogenomics Journal (2002) 2, 243–258. -
Zoonotic Diseases Fact Sheet
ZOONOTIC DISEASES FACT SHEET s e ion ecie s n t n p is ms n e e s tio s g s m to a a o u t Rang s p t tme to e th n s n m c a s a ra y a re ho Di P Ge Ho T S Incub F T P Brucella (B. Infected animals Skin or mucous membrane High and protracted (extended) fever. 1-15 weeks Most commonly Antibiotic melitensis, B. (swine, cattle, goats, contact with infected Infection affects bone, heart, reported U.S. combination: abortus, B. suis, B. sheep, dogs) animals, their blood, tissue, gallbladder, kidney, spleen, and laboratory-associated streptomycina, Brucellosis* Bacteria canis ) and other body fluids causes highly disseminated lesions bacterial infection in tetracycline, and and abscess man sulfonamides Salmonella (S. Domestic (dogs, cats, Direct contact as well as Mild gastroenteritiis (diarrhea) to high 6 hours to 3 Fatality rate of 5-10% Antibiotic cholera-suis, S. monkeys, rodents, indirect consumption fever, severe headache, and spleen days combination: enteriditis, S. labor-atory rodents, (eggs, food vehicles using enlargement. May lead to focal chloramphenicol, typhymurium, S. rep-tiles [especially eggs, etc.). Human to infection in any organ or tissue of the neomycin, ampicillin Salmonellosis Bacteria typhi) turtles], chickens and human transmission also body) fish) and herd animals possible (cattle, chickens, pigs) All Shigella species Captive non-human Oral-fecal route Ranges from asymptomatic carrier to Varies by Highly infective. Low Intravenous fluids primates severe bacillary dysentery with high species. 16 number of organisms and electrolytes, fevers, weakness, severe abdominal hours to 7 capable of causing Antibiotics: ampicillin, cramps, prostration, edema of the days. -
Fact Sheet - Symptoms of Pancreatic Cancer
Fact Sheet - Symptoms of Pancreatic Cancer Diagnosis Pancreatic cancer is often difficult to diagnose, because the pancreas lies deep in the abdomen, behind the stomach, so tumors are not felt during a physical exam. Pancreatic cancer is often called the “silent” cancer because the tumor can grow for many years before it causes pressure, pain, or other signs of illness. When symptoms do appear, they can vary depending on the size of the tumor and where it is located on the pancreas. For these reasons, the symptoms of pancreatic cancer are seldom recognized until the cancer has progressed to an advanced stage and often spread to other areas of the body. General Symptoms Pain The first symptom of pancreatic cancer is often pain, because the tumors invade nerve clusters. Pain can be felt in the stomach area and/or in the back. The pain is generally worse after eating and when lying down, and is sometimes relieved by bending forward. Pain is more common in cancers of the body and tail of the pancreas. The abdomen may also be generally tender or painful if the liver, pancreas or gall bladder are inflamed or enlarged. It is important to keep in mind that there are many other causes of abdominal and back pain! Jaundice More than half of pancreatic cancer sufferers have jaundice, a yellowing of the skin and whites of the eyes. Jaundice is caused by a build-up bilirubin, a substance which is made in the liver and a component of bile. Bilirubin contains a lot of yellow pigment, and gives bile it’s color. -
Hepatitis B? HEPATITIS B Hepatitis B Is a Contagious Liver Disease That Results from Infection with the Hepatitis B Virus
What is Hepatitis B? HEPATITIS B Hepatitis B is a contagious liver disease that results from infection with the Hepatitis B virus. When first infected, a person can develop Are you at risk? an “acute” infection, which can range in severity from a very mild illness with few or no symptoms to a serious condition requiring hospitalization. Acute Hepatitis B refers to the first 6 months after someone is exposed to the Hepatitis B virus. Some people are able to fight the infection and clear the virus. For others, the infection remains and leads to a “chronic,” or lifelong, illness. Chronic Hepatitis B refers to the illness that occurs when the Hepatitis B virus remains in a person’s body. Over time, the infection can cause serious health problems. How is Hepatitis B spread? Hepatitis B is usually spread when blood, semen, or other body fluids from a person infected with the Hepatitis B virus enter the body of someone who is not infected. This can happen through having sex with an infected partner; sharing needles, syringes, or other injection drug equipment; or from direct contact with the blood or open sores of an infected person. Hepatitis B can also be passed from an infected mother to her baby at birth. Who should be tested for Hepatitis B? Approximately 1.2 million people in the United States and 350 million people worldwide have Hepatitis B. Testing for Hepatitis B is recommended for certain groups of people, including: Most are unaware of their infection. ■ People born in Asia, Africa, and other regions with moderate or high rates Is Hepatitis B common? of Hepatitis B (see map) Yes. -
Primary Biliary Cholangitis: a Brief Overview Justin S
REVIEW Primary Biliary Cholangitis: A Brief Overview Justin S. Louie,* Sirisha Grandhe,* Karen Matsukuma,† and Christopher L. Bowlus* Primary biliary cholangitis (PBC), previously referred to supported by the higher concordance of PBC in monozy- as primary biliary cirrhosis, is the most common chronic gotic compared with dizygotic twins.4 In addition, certain cholestatic autoimmune disease affecting adults in the human leukocyte antigen haplotypes have been associ- United States.1 It is characterized by a hallmark serologic ated with PBC, as well as variants at loci along the inter- signature, antimitochondrial antibody (AMA), and specific leukin-12 (IL-12) immunoregulatory pathway (IL-12A and bile duct pathology with progressive intrahepatic duct de- IL-12RB2 loci).5 struction leading to cholestasis. PBC is potentially fatal and can have both intrahepatic and extrahepatic complications. PATHOGENESIS EPIDEMIOLOGY The primary disease mechanism in PBC is thought to be T cell lymphocyte–mediated injury against intralobu- PBC affects all races and ethnicities; however, it is best lar biliary epithelial cells. This causes progressive destruc- studied in the Caucasian population. The condition pre- tion and eventual disappearance of the intralobular bile dominantly affects women older than 40 years, with a ducts. Molecular mimicry has been proposed as the ini- female/male ratio of 9:1.2 Although the incidence of PBC tiating event in the loss of tolerance primarily to mito- appears to be stable, the overall prevalence of the disease chondrial pyruvate dehydrogenase complex, E2, during is increasing.3 An individual’s genetic susceptibility, epige- which exogenous antigens evoke an immune response netic factors, and certain environmental triggers seem to that recognizes an endogenous (self) antigen inciting an play important roles. -
Hepatitis A, B, and C: Learn the Differences
Hepatitis A, B, and C: Learn the Differences Hepatitis A Hepatitis B Hepatitis C caused by the hepatitis A virus (HAV) caused by the hepatitis B virus (HBV) caused by the hepatitis C virus (HCV) HAV is found in the feces (poop) of people with hepa- HBV is found in blood and certain body fluids. The virus is spread HCV is found in blood and certain body fluids. The titis A and is usually spread by close personal contact when blood or body fluid from an infected person enters the body virus is spread when blood or body fluid from an HCV- (including sex or living in the same household). It of a person who is not immune. HBV is spread through having infected person enters another person’s body. HCV can also be spread by eating food or drinking water unprotected sex with an infected person, sharing needles or is spread through sharing needles or “works” when contaminated with HAV. “works” when shooting drugs, exposure to needlesticks or sharps shooting drugs, through exposure to needlesticks on the job, or from an infected mother to her baby during birth. or sharps on the job, or sometimes from an infected How is it spread? Exposure to infected blood in ANY situation can be a risk for mother to her baby during birth. It is possible to trans- transmission. mit HCV during sex, but it is not common. • People who wish to be protected from HAV infection • All infants, children, and teens ages 0 through 18 years There is no vaccine to prevent HCV. -
Active Peptic Ulcer Disease in Patients with Hepatitis C Virus-Related Cirrhosis: the Role of Helicobacter Pylori Infection and Portal Hypertensive Gastropathy
dore.qxd 7/19/2004 11:24 AM Page 521 View metadata, citation and similar papers at core.ac.uk ORIGINAL ARTICLE brought to you by CORE provided by Crossref Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: The role of Helicobacter pylori infection and portal hypertensive gastropathy Maria Pina Dore MD PhD, Daniela Mura MD, Stefania Deledda MD, Emmanouil Maragkoudakis MD, Antonella Pironti MD, Giuseppe Realdi MD MP Dore, D Mura, S Deledda, E Maragkoudakis, Ulcère gastroduodénal évolutif chez les A Pironti, G Realdi. Active peptic ulcer disease in patients patients atteints de cirrhose liée au HCV : Le with hepatitis C virus-related cirrhosis: The role of Helicobacter pylori infection and portal hypertensive rôle de l’infection à Helicobacter pylori et de la gastropathy. Can J Gastroenterol 2004;18(8):521-524. gastropathie liée à l’hypertension portale BACKGROUND & AIM: The relationship between Helicobacter HISTORIQUE ET BUT : Le lien entre l’infection à Helicobacter pylori pylori infection and peptic ulcer disease in cirrhosis remains contro- et l’ulcère gastroduodénal dans la cirrhose reste controversé. Le but de la versial. The purpose of the present study was to investigate the role of présente étude est de vérifier le rôle de l’infection à H. pylori et de la gas- H pylori infection and portal hypertension gastropathy in the preva- tropathie liée à l’hypertension portale dans la prévalence de l’ulcère gas- lence of active peptic ulcer among dyspeptic patients with compen- troduodénal évolutif chez les patients dyspeptiques souffrant d’une sated hepatitis C virus (HCV)-related cirrhosis. -
Medical History and Primary Liver Cancer1
[CANCER RESEARCH 50, 6274-6277. October I. 1990] Medical History and Primary Liver Cancer1 Carlo La Vecchia, Eva Negri, Barbara D'Avanzo, Peter Boyle, and Silvia Franceschi Istituto di Ricerche Farmaco/logiche "Mario Negri," 20157 Milan, Italy [C. L. V., E. N., B. D.]; Institute of Social and Preventive Medicine, University of Lausanne, Lausanne, Switzerland ¡C.L. V.¡;Unitof Analytical Epidemiology, The International Agency for Research on Cancer, Lyon, France ¡P.B.f;and Servizio di Epidemiologia, Centro di Riferimento Oncologico, 33081 Ariano (PN), Italy [S. F.] ABSTRACT The general structure of this investigation has already been described (12). Briefly, trained interviewers identified and questioned cases and The relationship between selected aspects of medical history and the controls in the major teaching and general hospitals of the Greater risk of primary liver cancer was analyzed in a hospital-based case-control Milan area. The structured questionnaire included information on study conducted in Northern Italy on 242 patients with histologically or sociodemographic characteristics, smoking habits, alcohol drinking, serologically confirmed hepatocellular carcinoma and 1169 controls in intake of coffee and 14 selected indicator foods, and a problem-oriented hospital for acute, nonneoplastic, or digestive diseases. Significant asso medical history including 12 selected diseases or interventions. By ciations were observed for clinical history of hepatitis (odds ratio (OR), definition, the diseases or interventions considered had to anticipate by 3.7; 95% confidence interval (CI), 2.3-5.9], cirrhosis (OR, 16.8; 95% CI, at least 1 year the onset of the symptoms of the disease which led to 9.8-28.8), and three or more episodes of transfusion in the past (OR, admission. -
Inherited Thrombophilia Protein S Deficiency
Inherited Thrombophilia Protein S Deficiency What is inherited thrombophilia? If other family members suffered blood clots, you are more likely to have inherited thrombophilia. “Inherited thrombophilia” is a condition that can cause The gene mutation can be passed on to your children. blood clots in veins. Inherited thrombophilia is a genetic condition you were born with. There are five common inherited thrombophilia types. How do I find out if I have an They are: inherited thrombophilia? • Factor V Leiden. Blood tests are performed to find inherited • Prothrombin gene mutation. thrombophilia. • Protein S deficiency. The blood tests can either: • Protein C deficiency. • Look at your genes (this is DNA testing). • Antithrombin deficiency. • Measure protein levels. About 35% of people with blood clots in veins have an inherited thrombophilia.1 Blood clots can be caused What is protein S deficiency? by many things, like being immobile. Genes make proteins in your body. The function of Not everyone with an inherited thrombophilia will protein S is to reduce blood clotting. People with get a blood clot. the protein S deficiency gene mutation do not make enough protein S. This results in excessive clotting. How did I get an inherited Sometimes people produce enough protein S but the thrombophilia? mutation they have results in protein S that does not Inherited thrombophilia is a gene mutation you were work properly. born with. The gene mutation affects coagulation, or Inherited protein S deficiency is different from low blood clotting. The gene mutation can come from one protein S levels seen during pregnancy. Protein S levels or both of your parents.