(5.4)--viralhepatitis_casepresentations.pdf
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1、Case reportOpen AccessAcute hepatitis a virus infection presenting with multiorgandysfunction:a case reportAbdul Rasheed*and Shahzad SaeedAddress:Combined Military Hospital,Rawalpindi,PakistanEmail:AR*-;SS-saeed_*Corresponding authorReceived:2 June 2009Accepted:22 July 2009Published:30 July 2009Case
2、s Journal 2009,2:8124doi:10.4076/1757-1626-2-8124This article is available from:http:/ 2009 Rasheed et al.;licensee Cases Network Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License(http:/creativecommons.org/licenses/by/3.0),which permits unrest
3、ricted use,distribution,and reproduction in any medium,provided the original work is properly cited.AbstractIntroduction:Acute hepatitis due to hepatitis a virus is usually a benign self-limiting diseaseconferring lifelong immunity.However,few cases have been reported in literature with fulminanthep
4、atitis.We report this extremely rare case with multiorgan dysfunction including liver failure,hepatic encephalopathy,renal failure,pleural effusion,pericardial effusion and hematologicdysfunction as a sequale of this infection in an otherwise healthy male at the age of 18.Case presentation:An 18 yea
5、rs old Pakistani male presented with two days history of fever,cough,headache and vomiting.His condition gradually deteriorated and on day 7 developed multiorgandysfunction.Initially Immunoglobulin M anti hepatitis a virus was borderline 1.40 but repeated titersone week later confirmed the diagnosis
6、 of acute hepatitis a virus infection.Conclusion:This original case report highlights the importance of focusing first uncommonmanifestations of common illnesses while diagnosing difficult cases.Moreover this case also addsknowledge to the limited available data regarding complications and predictor
7、s of prognosis.IntroductionHepatitis A virus has plagued mankind for centuries bycausing acute hepatitis associated with significant morbi-dity and occasional mortality.HAV is a 7.5-kb positive-strand RNA virus of the Picornaviridae family and the onlymember of the genus Hepatovirus 1.All four genot
8、ypesbelong to a single serotype.HAV is spread via the fecal-oralroute.The incubation period averages 30 days(range 15 to49 days).The prevalence of HAV infection varies amongcountries in Asia 2.Countries with high endemicity forHAV infection include Pakistan,India,China,Nepal,Bangladesh,Myanmar and t
9、he Philippines.Most people inthese countries are exposed during childhood.HAVinfection usually results in an acute,self-limiting illnessand only rarely leads to fulminant hepatic failure 3.Inyoung children,the disease is often asymptomatic,whereas in older children and adults there might bea range o
10、f clinical manifestations from mild,anictericinfection to fulminant hepatic failure.The risk offulminant hepatitis is high in patients having an under-lying chronic liver disease and are aged more than 40 years4.This case report describes a young person from ahighly HAV endemic area with serological
11、ly confirmedacute HAV infection with multiorgan involvement.Page 1 of 3(page number not for citation purposes)Case presentationAn 18 years old Pakistani male presented with about twodays history of intermittent fever with chills,nonproduc-tive cough,generalized headache,nausea and nonbiliousvomiting
12、.He vomited thrice on day 1 and five times onthe next day.Vomitus contained food particles andwas devoid of blood.Clinical examination was unremark-able except raised temperature ranging from 37.22C(310.4 kelvin)to 39.44C(312.6 kelvin)with relativebradycardia(pulse ranging from 56/minute to 84/minut
13、e).Initial investigations revealed raised serum alanineaminotransferase(2043u/l),low normal platelet count(165 109/l)and total white cell count(4.2 109/l)withnormal differential count and morphology.Other investi-gations including haemoglobin,malarial parasite slides,bilirubin,alkalinephosphatase,as
14、partateaminotransferase,albumin,urea,creatinine,electrolytes,plasma glucose,widal test,DIC screening,urinalysis and chest radiographwere within normal limits.He was provisionally diagnosedas a case of anicteric hepatitis with differential diagnosesof malaria and enteric fever due to their high preva
15、lence inthe area.He was managed with antimalarial(artemether),third generation cephalosporin(Ceftriaxone)and suppor-tive parenteral fluids.Samples for blood cultures,viral(including hepatitis and dengue)screening,typhi dot,serology for brucella,leptospira,rickettsia and toxoplasmawere sent to labora
16、tory.On day 3,he developed dizziness and unsteadiness of gaitand asterixis while fever with relative bradycardia,head-ache and vomiting continued.CT scan head revealed noabnormality.IgM anti HAV was borderline 1.40(cut off1.20).Repeated investigations showed rising serumalanine aminotransferase 3690
17、u/l,prothrombin time30 seconds(control 12 seconds),PTTK 46 seconds(control 32 seconds),fibrinogen 130 mg/dl,D-dimers200400,serum albumin 28 g/l,urea 13 mmol/l,creatinine 266 umol/l,sodium 133 mmol/l potassium4.8 mmol/l,creatinine kinase 1112 u/l with CK-MB 6.1%,LDH 6130 u/l,AST 66 u/l,haemoglobin 12
18、.8 g/l,totalwhite cell count 11 109/l,platelets 116 109/l,pus cells(8-10/HPF)&red blood cells(5-7/HPF)seen onurinalysis.Other investigations including ECG,bilirubin,alkaline phosphatase,hepatitis B surface antigen,serologyfor hepatitis E,C,dengue,brucella,leptospira,rickettsia,toxoplasma and typhoid
19、 were normal.Antimalarial(artemether)was stopped when repeated malarial parasiteslides were found negative.Vitamin K was added totreatment but his clinical and laboratory parameterscontinued to deteriorate.On day 7,fever settled but his blood pressure rose to170/110 mmHgandbecame oliguric with 24hou
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