DOCSLIB.ORG

Autoimmune Hepatitis/ Autoimmune Pancreatitis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Autoimmune Hepatitis/ Autoimmune Pancreatitis Autoimmune Hepatitis/ Autoimmune Pancreatitis EdmundEdmund Krasinski,Krasinski, JrJr.,., D.O.D.O. F.A.C.G.F.A.C.G. Assessment of Liver Function WhichWhich ofof thethe followingfollowing isis notnot aa goodgood biochemicalbiochemical assessorassessor ofof hepatichepatic function?function? A)A) SerumSerum bilirubinbilirubin B)B) SerumSerum lactatelactate dehydrogenasedehydrogenase C)C) SerumSerum aspartateaspartate aminotransferaseaminotransferase (AST)(AST) D)D) SerumSerum alaninealanine aminotransferaseaminotransferase (ALT)(ALT) E)E) SerumSerum alkalinealkaline phosphatasephosphatase Assessment of Liver Function CorrectCorrect answeranswer :: BB MeasurementMeasurement ofof LDHLDH andand eveneven moremore specificspecific LDHLDH--55 addsadds littlelittle toto evaluationevaluation ofof suspectedsuspected hepatichepatic dysfunctiondysfunction HighHigh levelslevels ofof LDHLDH seenseen in:in: HepatocellularHepatocellular necrosis,necrosis, IschemicIschemic hepatopathyhepatopathy ““shockshock liverliver””,, Cancer,Cancer, HemolysisHemolysis Case Presentation AA 3535 yr.yr. OldOld femalefemale presentspresents forfor evaluation.evaluation. SheShe hashas notednoted jaundicejaundice manifestmanifest byby scleralscleral icterusicterus,, acholicacholic stools,stools,choluriacholuria.. SheShe alsoalso complainscomplains ofof undueundue fatigue.fatigue. SheShe tooktook aa recentrecent triptrip toto NewNew OrleansOrleans wherewhere sheshe ateate rawraw oysters.oysters. Case Presentation Meds:Meds: MacrodantinMacrodantin PhysicalPhysical examination:examination: GeneralizedGeneralized icterusicterus,,ScleralScleral icterusicterus,, TenderTender hepatomegalyhepatomegaly,, NoNo stigmatastigmata ofof chronicchronic liverliver diseasedisease Case presentation Labs:Labs: SerumSerum bilirubinbilirubin 15.015.0 SerumSerum ASTAST 15001500 SerumSerum ALTALT 17001700 SerumSerum AlkAlk phosphos 120120 Case Presentation WhichWhich ofof thethe followingfollowing diseasesdiseases areare consistentconsistent withwith thisthis clinicalclinical presentation?presentation? A)A) AutoimmuneAutoimmune hepatitishepatitis B)B) ViralViral hepatitishepatitis C)C) WilsonWilson’’ss DiseaseDisease D)D) DrugDrug--inducedinduced liverliver diseasedisease E)E) AllAll ofof thethe aboveabove Case Presentation CorrectCorrect answer:answer: E)E) AllAll ofof thethe above.above. AllAll ofof thethe diseasesdiseases inin thethe differentialdifferential diagnosisdiagnosis cancan presentpresent asas such.such. AllAll cancan presentpresent withwith acuteacute decompensationdecompensation withwith primarilyprimarily hepatocellularhepatocellular dysdysfunctionfunction Case Presentation AutoimmuneAutoimmune hepatitishepatitis-- ToTo bebe discusseddiscussed atat length.length. ViralViral hepatitis:hepatitis: HBsAgHBsAg,Anti,Anti--HBC,HBC,IgMIgM antianti-- HAV,HAV, AntiAnti--HCV.HCV. WilsonWilson’’ss Disease:Disease: SerumSerum ceruloplasminceruloplasmin,, 2424 hrhr urinaryurinary copper,copper, OpthoOptho evaleval forfor KayserKayser-- FleisherFleisher ringsrings DrugDrug inducedinduced liverliver dzdz..-- historyhistory ofof drugdrug POPO Autoimmune Hepatitis Definition:Definition: AA selfself--perpetuatingperpetuating hepatichepatic inflammationinflammation ofof unknownunknown cause,cause, characterizedcharacterized byby interfaceinterface hepatitis,hepatitis, hypergammaglobulinemiahypergammaglobulinemia,and,and liverliver associatedassociated antibodies.antibodies. Exclusion of other conditions WilsonWilson’’ss diseasedisease ChronicChronic viralviral hepatitishepatitis AlphaAlpha 11 antitrypsinantitrypsin deficiencydeficiency HereditaryHereditary hemochromotosishemochromotosis DrugDrug inducedinduced liverliver diseasedisease NonNon--alcoholicalcoholic steatohepatitissteatohepatitis ImmuneImmune cholangiopathiescholangiopathies:: PBC/PSCPBC/PSC Autoimmune Hepatitis Nomenclature:Nomenclature: AIHAIH replacesreplaces termsterms ofof lupoidlupoid hepatitis,hepatitis, autoimmuneautoimmune liverliver disease,disease, andand autoimmuneautoimmune chronicchronic activeactive hepatitis.hepatitis. Autoimmune Hepatitis NoNo subtypessubtypes formallyformally recognized,recognized, butbut descriptivedescriptive terms:terms: TypeType 11 TypeType 22 TypeType 33 Basic Diagnostic Tests AST,AST, ALT,ALT, BilirubinBilirubin,, alkalk phosphos,, gammagamma globulinglobulin levelslevels (( AssessAssess severityseverity ofof liverliver injuryinjury andand characterizecharacterize thethe patternpattern ofof injury)injury) SerumSerum albumin,albumin, PT/INRPT/INR (( EstimateEstimate levellevel ofof impairmentimpairment ofof hepatichepatic syntheticsynthetic function)function) ANAANA (( AntinuclearAntinuclear antibody)antibody) ASMAASMA (( AntiAnti-- smoothsmooth musclemuscle antibody)antibody) AntiAnti-- LKMLKM 11 (Anti(Anti--liverliver kidneykidney microsomalmicrosomal antibodyantibody SLASLA (( SolubleSoluble liverliver antigen)antigen) Autoimmune Hepatitis LiverLiver tissuetissue examinationexamination HistologicHistologic changeschanges confirmconfirm diagnosisdiagnosis InterfaceInterface hepatitishepatitis LobularLobular panacinarpanacinar hepatitishepatitis withwith interfaceinterface hepatitishepatitis Autoimmune Hepatitis ViralViral hepatitishepatitis exclusion:exclusion: HBsAgHBsAg// AntiAnti-- HBcHBc//IgMIgM AntiAnti--HAV/HAV/ AntiAnti--HCVHCV WilsonWilson’’ss diseasedisease exclusion:exclusion: SerumSerum ceruloplasminceruloplasmin HHCHHC exclusion:exclusion: SerumSerum Fe,Fe, TIBC/TIBC/ %% sat/sat/ FerritinFerritin// HFEHFE analysis(ifanalysis(if needed)needed) International Criteria for Diagnosis DiagnosticDiagnostic FeaturesFeatures DefinitiveDefinitive DiagnosisDiagnosis ExclusionExclusion ofof riskrisk DailyDaily ETOHETOH << 2525 factorsfactors forfor otherother gm/dgm/d diseasesdiseases NoNo hepatotoxichepatotoxic drugsdrugs NN AlphaAlpha 11 ATAT phenotypephenotype NormalNormal ceruloplasminceruloplasmin NormalNormal Fe/Fe/ ferritinferritin NoNo HAV/HBV/HCVHAV/HBV/HCV International Criteria for Diagnosis DiagnosticDiagnostic FeaturesFeatures Probable Diagnosis Daily ETOH < 50 gm/ d ExclusionExclusion ofof riskrisk No Hepatotoxic drugs factorsfactors forfor otherother Partial A1 AT deficiency diseasesdiseases Abnormal cu/ ceruloplasmin but Wilson’s excluded Non-specific Fe/ Ferritin abnls No HAV/HBV/HCV International Criteria for Diagnosis Diagnostic Features Definitive Diagnosis Probable Diagnosis Inflammatory Indices Serum AST/ALT elev Serum AST/ALT elev Min chol. chng Min Chol. Chng Auotantibodies ANA/ASMA/ALKM ANA/ASMA/ALKM ≥ 1: 80 (adults) ≥ 1: 40 ≥ 1: 20 (peds) Immunoglobulins Glob, IgG ≥1.5 N Inc. IgG any degree Histologic features Interface hep. Mod- Same severe, no bile lesions, gran., other dz ∆ International Scoring System for Diagnosis Factor Score + AMA -4 Viral Markers + -3 - +3 Hepatotoxic drugs Yes -4 No +1 Pretreatment score > 15 Definite diagnosis 10-15 Probable Diagnosis International Scoring System for Diagnosis Factors Score ETOH < 25 gm +2 ETOH > 60 gm -2 HLA DR3 or DR4 +1 Concurrent AI Dz +2 Other liver Ab +2 Interface Hepatitis +3 Plasmacytic inflitrate +1 Rosettes +1 No Charact. Features -5 Biliary changes -3 Fat/ granulomas -3 International Scoring System for Diagnosis FactorsFactors ScoreScore TreatmentTreatment responseresponse +2+2 completecomplete RelapseRelapse +3+3 PostPost treatmenttreatment scorescore DefiniteDefinite DiagnosisDiagnosis >17>17 ProbableProbable diagnosisdiagnosis 1212--1717 Pathogenesis PrincipalPrincipal HypothesisHypothesis AutoantigenAutoantigen DrivenDriven cellcell--mediatedmediated AutoantibodyAutoantibody DependentDependent cellcell-- mediatedmediated cytotoxicitycytotoxicity Subclassifications TypeType 11-- ++ ANA/ASMAANA/ASMA MostMost commoncommon USAUSA FemaleFemale gendergender 78%78% ConcurrentConcurrent autoimmuneautoimmune diseasesdiseases 38%38% AutoimmuneAutoimmune thyroiditisthyroiditis 12%12% GravesGraves diseasedisease 6%6% UlcerativeUlcerative colitiscolitis 6%6% RheumatoidRheumatoid arthritisarthritis 11 %% PerniciousPernicious anemiaanemia 1%1% PSSPSS 1%1% Subclassifications TypeType 11 CoombCoomb’’ss positivepositive hemolytichemolytic anemiaanemia 1%1% ITPITP 1%1% LeucocytoclasticLeucocytoclastic vasculitisvasculitis 1%1% NephritisNephritis 1%1% ErythemaErythema nodosumnodosum 1%1% PyodermaPyoderma gangrenosagangrenosa (( II havehave seenseen oneone case)case) FibrosingFibrosing alveolitisalveolitis 1%1% Subclassifications TypeType 11 HLAHLA DR3DR3 andand DR4DR4 areare independentindependent riskrisk factorsfactors forfor susceptibilitysusceptibility andand suggestssuggests aa polygenicpolygenic disorder.disorder. Subclassifications TypeType 22 ++ AntiAnti LKMLKM antibodyantibody AffectsAffects mainlymainly childrenchildren (2(2--1414 yrs)yrs) AffectsAffects 20%20% EuropeanEuropean adultsadults AffectsAffects 44 %% USAUSA patientspatients CommonlyCommonly associatedassociated with:with: VitiligoVitiligo DMDM--11 AutoimmuneAutoimmune thyroiditisthyroiditis Subclassifications TypeType 33 ++ SolubleSoluble liverliver antigenantigen (SLA)(SLA) Newest,Newest, LeastLeast establishedestablished MaybeMaybe aa variantvariant ofof typetype 11 Variants OverlapOverlap withwith PBCPBC ++ AMAAMA ++ bilebile ductduct injuryinjury onon histologyhistology ++ responseresponse toto steroidssteroids ifif alkalk phosphos ≤≤ 22 XX NormalNormal Variants OverlapOverlap withwith
Load more

Recommended publications
  • Acute Pancreatitis Associated with Rotavirus Infection and Review Of
    Case Report/Olgu Sunumu İstanbul Med J 2020; 21(1): 78-81 DO I: 10.4274/imj.galenos.2020.88319 Acute Pancreatitis Associated with Rotavirus Infection and Review of The Literature Rotavirüs Enfeksiyonuna Bağlı Akut Pankreatit Olguları ve Literatürün Gözden Geçirilmesi Kamil Şahin, Güzide Doğan University of Health Sciences, Haseki Training and Research Hospital, Department of Pediatrics, İstanbul, Turkey ABSTRACT ÖZ Agents causing acute gastroenteritis are not common causes of Çocuklarda pankreatit etiyolojisinde akut gastroenterit etkenleri pancreatitis etiology in children. Pancreatitis associated with sık görülen sebeplerden değildir. Rotavirüs enfeksiyonuna rotavirus infection is very rare. Cases with acute pancreatitis bağlı görülen pankreatit ise oldukça nadirdir. Rotavirüs during rotavirus gastroenteritis are reported due to rare gastroenteriti sırasında akut pankreatit gelişen olgular, associations. In this article, the causes of acute pancreatitis rotavirüs enfeksiyonuna bağlı akut pankreatitin nadir olması and cases of acute pancreatitis due to rotavirus infection were nedeniyle sunulmuştur. Bu yazıda, akut pankreatit sebepleri ve investigated. Clinical findings were mild, and complications rotavirüse bağlı gelişen akut pankreatit olguları incelenmiştir. were not observed in both of our patients, including a two- İki yaş kız ve üç yaşındaki erkek iki olgumuzda ve literatürde year-old female and a three-year-old male, and other cases değerlendirilen diğer olgularda klinik bulgular hafif seyretmiş, evaluated in the literature. The
    [Show full text]
  • Autoimmune Hepatitis
    Page 1 of 5 Autoimmune Hepatitis Autoimmune hepatitis is an uncommon cause of chronic hepatitis (persistent liver inflammation). The cause is not known. If left untreated, the inflammation causes cirrhosis (scarring of the liver). However, with treatment, the outlook for people with this condition is very good. Treatment is usually with steroids and other medicines which suppress inflammation. What does the liver do? The liver is in the upper right part of the abdomen. It has many functions which include: Storing glycogen (fuel for the body) which is made from sugars. When required, glycogen is broken down into glucose which is released into the bloodstream. Helping to process fats and proteins from digested food. Making proteins that are essential for blood to clot (clotting factors). Processing many medicines which you may take. Helping to remove or process alcohol, poisons and toxins from the body. Making bile which passes from the liver to the gut down the bile duct. Bile breaks down the fats in food so that they can be absorbed from the bowel. What is autoimmune hepatitis? Hepatitis means inflammation of the liver. There are many causes of hepatitis. For example, alcohol excess and infections with various viruses are the common causes of hepatitis. Autoimmune hepatitis is an uncommon cause of chronic hepatitis. Chronic means that the inflammation is persistent or long-term. The chronic inflammation gradually damages the liver cells, which can result in serious problems. What causes autoimmune hepatitis? Page 2 of 5 The cause is not clear. It is thought to be an autoimmune disease. Our immune system normally defends us against infection from bacteria, viruses and other germs.
    [Show full text]
  • EASL Clinical Practice Guidelines: Autoimmune Hepatitisq
    Clinical Practice Guidelines EASL Clinical Practice Guidelines: Autoimmune hepatitisq ⇑ European Association for the Study of the Liver striking progress, and now patients in specialised centres have an Introduction excellent prognosis, both in respect to survival and to quality of life. Autoimmune hepatitis (AIH) was the first liver disease for which The aim of the present Clinical Practice Guideline (CPG) is to an effective therapeutic intervention, corticosteroid treatment, provide guidance to hepatologists and general physicians in the was convincingly demonstrated in controlled clinical trials. diagnosis and treatment of AIH in order to improve care for However, 50 years later AIH still remains a major diagnostic affected patients. In view of the limited data from large con- and therapeutic challenge. There are two major reasons for this trolled studies and trials, many recommendations are based on apparent contradiction: Firstly, AIH is a relatively rare disease. expert consensus. This is to some extent a limitation of this Secondly, AIH is a very heterogeneous disease. EASL-CPG, but at the same time it is its special strength: consen- Like other rare diseases, clinical studies are hampered by the sus in this guideline is based on intensive discussions of experts limited number of patients that can be included in trials. Possibly from large treatment centres. The core consensus group has and more importantly, the interest of the pharmaceutical indus- experience of over one thousand AIH patients managed person- try to develop effective specific therapies for rare diseases is lim- ally, and the recommendations have been reviewed by both the ited due to the very restricted market for such products.
    [Show full text]
  • Treatment Recommendations for Feline Pancreatitis
    Treatment recommendations for feline pancreatitis Background is recommended. Fentanyl transdermal patches have become Pancreatitis is an elusive disease in cats and consequently has popular for pain relief because they provide a longer duration of been underdiagnosed. This is owing to several factors. Cats with analgesia. It takes at least 6 hours to achieve adequate fentanyl pancreatitis present with vague signs of illness, including lethargy, levels for pain control; therefore, one recommended protocol is to decreased appetite, dehydration, and weight loss. Physical administer another analgesic, such as intravenous buprenorphine, examination and routine laboratory findings are nonspecific, and at the time the fentanyl patch is placed. The cat is then monitored until recently, there have been limited diagnostic tools available closely to see if additional pain medication is required. Cats with to the practitioner for noninvasively diagnosing pancreatitis. As a chronic pancreatitis may also benefit from pain management, and consequence of the difficulty in diagnosing the disease, therapy options for outpatient treatment include a fentanyl patch, sublingual options are not well understood. buprenorphine, oral butorphanol, or tramadol. Now available, the SNAP® fPL™ and Spec fPL® tests can help rule Antiemetic therapy in or rule out pancreatitis in cats presenting with nonspecific signs Vomiting, a hallmark of pancreatitis in dogs, may be absent or of illness. As our understanding of this disease improves, new intermittent in cats. When present, vomiting should be controlled; specific treatment modalities may emerge. For now, the focus is and if absent, treatment with an antiemetic should still be on managing cats with this disease, and we now have the tools considered to treat nausea.
    [Show full text]
  • AASLD PRACTICE GUIDELINES Diagnosis and Management of Autoimmune Hepatitis
    AASLD PRACTICE GUIDELINES Diagnosis and Management of Autoimmune Hepatitis Michael P. Manns,1 Albert J. Czaja,2 James D. Gorham,3 Edward L. Krawitt,4 Giorgina Mieli-Vergani,5 Diego Vergani,6 and John M. Vierling7 This guideline has been approved by the American ment on Guidelines;3 and (4) the experience of the Association for the Study of Liver Diseases (AASLD) authors in the specified topic. and represents the position of the Association. These recommendations, intended for use by physi- cians, suggest preferred approaches to the diagnostic, 1. Preamble therapeutic and preventive aspects of care. They are intended to be flexible, in contrast to standards of Clinical practice guidelines are defined as ‘‘systemati- care, which are inflexible policies to be followed in ev- cally developed statements to assist practitioner and ery case. Specific recommendations are based on rele- patient decisions about appropriate heath care for spe- vant published information. To more fully characterize 1 cific clinical circumstances.’’ These guidelines on the quality of evidence supporting the recommenda- autoimmune hepatitis provide a data-supported tions, the Practice Guidelines Committee of the approach to the diagnosis and management of this dis- AASLD requires a class (reflecting benefit versus risk) ease. They are based on the following: (1) formal and level (assessing strength or certainty) of evidence review and analysis of the recently-published world lit- to be assigned and reported with each recommenda- erature on the topic [Medline search]; (2) American tion.4 The grading system applied to the recommenda- College of Physicians Manual for Assessing Health tions has been adapted from the American College of 2 Practices and Designing Practice Guidelines; (3) Cardiology and the American Heart Association Prac- guideline policies, including the AASLD Policy on the tice Guidelines, and it is given below (Table 1).
    [Show full text]
  • 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).
    [Show full text]
  • Case Report: a Patient with Severe Peritonitis
    Malawi Medical Journal; 25(3): 86-87 September 2013 Severe Peritonitis 86 Case Report: A patient with severe peritonitis J C Samuel1*, E K Ludzu2, B A Cairns1, What is the likely diagnosis? 2 1 What may explain the small white nodules on the C Varela , and A G Charles transverse mesocolon? 1 Department of Surgery, University of North Carolina, Chapel Hill NC USA 2 Department of Surgery, Kamuzu Central Hospital, Lilongwe Malawi Corresponding author: [email protected] 4011 Burnett Womack Figure1. Intraoperative photograph showing the transverse mesolon Bldg CB 7228, Chapel Hill NC 27599 (1a) and the pancreas (1b). Presentation of the case A 42 year-old male presented to Kamuzu Central Hospital for evaluation of worsening abdominal pain, nausea and vomiting starting 3 days prior to presentation. On admission, his history was remarkable for four similar prior episodes over the previous five years that lasted between 3 and 5 days. He denied any constipation, obstipation or associated hematemesis, fevers, chills or urinary symptoms. During the first episode five years ago, he was evaluated at an outlying health centre and diagnosed with peptic ulcer disease and was managed with omeprazole intermittently . His past medical and surgical history was non contributory and he had no allergies and he denied alcohol intake or tobacco use. His HIV serostatus was negative approximately one year prior to presentation. On examination he was afebrile, with a heart rate of 120 (Fig 1B) beats/min, blood pressure 135/78 mmHg and respiratory rate of 22/min. Abdominal examination revealed mild distension with generalized guarding and marked rebound tenderness in the epigastrium.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Pancreatic Resection: Nutritional Implications and Long Term Follow Up
    NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #150 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #150 Carol Rees Parrish, M.S., R.D., Series Editor Pancreatic Resection: Nutritional Implications and Long Term Follow Up Mary E. Phillips Pancreatic resection is carried out for benign and malignant diseases of the pancreas, duodenum and distal common bile duct. These operations contribute significantly to both macro-nutrient and micro-nutrient malabsorption. Pancreatic enzyme supplements are underused and should be administered routinely to all patients who have had a pancreatic head resection. Patients suffer both short term and long term deficiencies and are prone to other gastro-intestinal conditions with similar symptoms. Thus, identifying the cause of their symptoms is challenging and requires careful follow up in a multi-professional setting. Vitamin and mineral deficiencies are common and weight loss, abdominal symptoms and diabetes have a significant impact on quality of life and survival. Patients should have access to specialist dietetic support and endocrine function should be assessed routinely following all pancreatic resection. Assessment of vitamin and mineral status should be carried out in patients who have undergone curative resection or who have benign disease. INTRODUCTION ypes of pancreatic resections vary considerably; poor, but some pancreatic resections are carried out each having a different impact on the digestive for benign disease, and long term implications must Tsystem and therefore on the patient’s nutritional be considered in all patients with benign disease, and status. Poor nutritional status is associated with poor those who have had surgery with curative intent. quality of life,1 and reduced survival.2 Pancreatic Fat, carbohydrate and protein malabsorption all exocrine insufficiency (PEI) is common and occur in PEI;5-7 yet historical treatment has focused on fat undertreated3 and there is a lack of funding for dietetic malabsorption.
    [Show full text]