C. Pastecchia

F. Caredda

M. Moroni

S. Antinori

T. Re

Caredda F.

Antinori S.

Re T.

Pastecchia C.

Moroni M.

AIR Universita degli studi di Milano

BRITISH MEDICAL JOURNAL VOLUME 292 31 MAy 1986 1429blood pressure later is not known, but circumstantial evidence in man anddirect evidence in some animals suggest that it may. ' We think that the highintake of salt, as well as other aspects of the diet of young children in theUnited Kingdom, should be a cause for concern and further research.This study was part of a paediatric project on the paediatric firm, and wegratefully acknowledge the help ofDr David Murdoch and Dr Michael Latter.1 MacGregor GA. Sodium is more important than calcium in essential hypertension. Hypertnsion1985;7:628-40.2 Knudsen KD, Dahi LK. Essential hypertension: inbornerrorofsodiummetabolism. PossgradMedJ 1966;42:148-52.3 Hofman A, Hazebroek A, ValkenburgHA. A randomized trial ofsodium intake and blood pressurein newborn infants.JAMA 1983;250:370-3.(Accepted 28Febraay 1986)Charing Cross and Westminster Medical School, London W6 8RFSALLY DE COURCY, MB, Bs, house surgeonHILARY MITCHELL, MB, Bs, house surgeonDAVID SIMMONS, BA, MB, house physicianGRAHAM A MAcGREGOR, FRcp, senior lecturer and honorary consultantphysicianCorrespondence to: Dr G A MacGregor, Blood Pressure Unit, Department ofMedicine, Charing Cross and Westminster Medical School, London W6 8RF.Acute non-A non-B hepatitis aftertyphoid feverTen years after its initial description non-A non-B hepatitis remains adiagnosis of exclusion. Nevertheless, non-A non-B hepatitis includesinfections of the liver caused by at least three viruses provisionallydesignated "blood transmitted," "coagulation factor transmitted," and"epidemic waterborne."' Furthermore, there is some evidence of anassociation between shellfish consumption and some cases of non-A non-Bhepatitis,2 3 and it has been suggested that these cases reported in Westerncountries may be sporadic cases of epidemic waterborne non-A non-Bhepatitis,' a hypothesis supported by an analysis of the clinical andbiochemiical features in 20 cases.4 Here we describe two patients admitted toour infectious diseases clinic for typhoid fever who then developed acutenon-A non-B hepatitis.Case 1A 25 year old man experienced an abrupt onset of fever (39°C), headache, andmalaise. He was given acetylsalicylic acid (500 mg every 4 hours). Five days later,because ofpersisting fever, constipation, abdominal pain, and discomfort, he wasadmitted to hospital. Because ofa history of shellfish consumption 15 days beforethe onset of symptoms blood and stool cultures were performed and Widalreaction was tested. Salmonella typhi was isolated from the blood, and anincreased titre of 0 agglutinins was recorded during the second week of illness.Chloramphenicol was started and continued according to the standard therapeuticregimen.Routine alanine aminotransferase determinations showed a nineteenfoldincrease over the normal values during the second week of illness (four weeksafter shellfish consumption), but without any symptoms. Acute non-A non-Bhepatitis was diagnosed by exclusion: he was negative for hepatitis B surfaceantigen, IgM antibody to hepatitis B core antigen, cytomegalovirus, anti-hepatitis A virus, and heterophile antibody to Epstein-Barr virus, In particular,the assay for IgM anti-hepatitis A virus was repeatedly negative. HBsAg and IgManti-hepatitis A were assayed by Abbott radioimmunoassays, IgM anti-coreantigen by enzyme linked immunosorbent assay Corzyme-M (Abbott), IgM anti-cytomegalovirus by Enzygnost-Cytomegalie (Behringwerke), and antibodies toEpstein-Barr virus by Monosticon (Organon).The patient recovered completely from both typhoid fever and non-A non-Bhepatitis: his serum transaminase activity returned to normal within five weeksand remained normal for more than six months (figure).Case 2A 23 year old man was admitted to hospital with a one week history of highfever (40°C), continuous headache confined to the frontal region, and constipationfollowed by diarrhoea. He had eaten oysters and mussels 10 days before the onsetof symptoms. Salmonella typh was isolated from stools, and treatment withchloramphenicol was started.At the end of the fourth week of illness (five weeks after shellfish ingestion)there was a sharp rise in his serum transaminase activity with a decrease ofprothrombin activity (<70% of normal). The patient was symptom free andanicteric. In this case too acute non-A nQn-B hepatitis was diagnosed byexclusion. The hepatitis ran an uneventful course with liver function valuesreturning to normal and remaiing so over 12 months after the onset of thedisease.CommentTyphoid fever occurs sporadically in Italy, and shellfish ingestion is oftenresponsible. Occasionally it is associated with acute hepatitis A, which isprimarily transmitted by the faecal-oral route. Although faecal-oral non-Anon-B hepatitis has been suggested to occur in some patients with biphasichepatitis A,' we are not aware ofreports ofnon-A non-B hepatitis in patientswith other stool borne transmitted diseases.HBsAgIgM anti-HBcIgM arti -HAYIgM arti-CMVAnti-EBV - 6002.3003 i00Pos tivestool cultureP-olq 200 239 0~~38 SheIfish 100&~~~~~4~ ~~ 0--- flo y.Weeks MonthsCase 1. Non-A non-B hepatitis after typhoid fever.The observation of two cases ofnon-A non-B hepatitis after typhoid feveris intriguing. Although there is no direct evidence that the source ofSalmonella typhi and non-A non-B virus was the same, the absence in thesepatients of a history of blood transfusion or admission to hospital within thepreceding six months or a history of drug addiction or any other possibleparenteral exposure suggests that food contaminated with human excretamight have been the source. In Western countries non-A non-B hepatitisoccurs as sporadic cases and such contaminated food could be the source insome of these. This may be a rare event. On the other hand, given thefrequent asymptomatic course of the disease, such a source may not be thatuncommon since it may not be looked for in a patient with a normalconvalescence.1 Tabor E. The three viruses of non-A, non-B hepatitis. Lancet 1985;i:743-5.2 BamberM, Thomas HC, Bannister'B, Sherlock S. Acute type A, B, and non-A, non-B hepatitis in ahospital population in London: clinical and epidemiological features. Gui 1983;24:561-4.3 Caredda F, d'Arminio Monforte A, Rossi E, Lopez S, Moroni M. non-A, non-B hepatitis inMilan. Lancet 1981;ii:48.4 Caredda F, Antinori S, Re T. Pastecchia C, Zavaglia C, Moroni M. Clinical features of sporadicnon-A, non-B hepatitis possibly associated with faecal-oral spread. Lancet 1985;ii:444-5.5 Caredda F, d'Arminio Monforte A, Rossi E, Zampini L, Lazzarin A, Moroni M. Prolonged courseand relapses of acute type A hepatitis. Boll Ist SieroterMilan 1984;63:34-6.(Accepted 21 March 1986)Infectious Diseases Clinic, University of Milan, L Sacco Hospital, 20157Milan, ItalyF CAREDDA, MD, clinical research assistantS ANTINORI, MD, residentT RE, MD, residentC PASTECCHIA, MD, residentM MORONI, MD, directorCorrespondence to: Dr Caredda. on 2 August 2019 by guest. Protected by copyright.http://www.bmj.com/Br Med J (Clin Res Ed): first published as 10.1136/bmj.292.6533.1429 on 31 May 1986. Downloaded from 

Acute non-A non-B hepatitis after typhoid fever

https://air.unimi.it/retrieve/handle/2434/660252/1289672/1429.full.pdf

Acute non-A non-B hepatitis after typhoid fever

Abstract

Similar works

Full text

Available Versions

AIR Universita degli studi di Milano