46 Infectious Mononucleosis with clinical jaundice in 14 year old. (11th October 2021)

• Record Type: Journal Article
• Authors: Bhamkar, R; Davison, S; Selter, M; Sammons, H; Arend, A; Dalton, D
• Is Part Of: Archives of disease in childhood. Volume 106(2021)Supplement 2
• Page Start: A19
• Page End: A20
• Publication Date: 2021-10-11
• Subjects: Children -- Diseases -- Periodicals; Infants -- Diseases -- Periodicals; 618.920005
• DOI: 10.1136/archdischild-2021-europaediatrics.46
• Languages: English
• ISSNs: 0003-9888

Abstract

Abstract : Glandular fever or Infectious Mononucleosis (IMN) is caused by Ebstein-Bar Virus (EBV). It is characterised by fever, sore throat and lymphadenopathy. Mild elevation of liver enzymes or transaminitis is common in the illness, but is rarely associated with clinical jaundice. There are very few case reports of EBV with symptomatic hepatitis. We report a case of EBV infection with very high liver enzymes and clinical jaundice. A 14 year old girl presented with history of fever, sore throat and cervical lymphadenopathy. Her blood investigations showed white cell counts of 14000/mm3 with lymphocytic predominance and numerous atypical lymphocytes in the smear. Her IMN monospot test was positive. Her alanine aminotransferase (ALT) was 370 IU/L. She was discharged home with diagnosis of glandular fever on symptomatic treatment. A week later, she represented with jaundice, pruritus, nausea and anorexia. Her liver functions showed ALT: 1956 IU/L, aspartate aminotransferase (AST): 1007 IU/L, alkaline phosphatase (ALP): 162 IU/L, total bilirubin: 70 µmol/L, direct bilirubin: 47 µmol/L and albumin: 45 g/L. Her renal functions and clotting was normal. Her viral markers (hepatitis B virus surface antigen, anti-hepatitis C virus, hepatitis A virus immunoglobulin IgM) were negative. Hepatitis E IgG antibody was positive whereas IgM was negative. Antinuclear, anti-mitochondrial and anti-smooth antibody profile was negative. Ultrasound abdomen showed mild splenomegaly (14cm). Her copper level was 35.8 µmol/L (N: 11-22 µmol/L) and ceruloplasmin level was 0.52 g/L (0.16-0.45 g/L). EBV viral capsid antigen IgM and IgG were positive and EBV nuclear antigen IgG was negative. Cytomegalovirus IgM was negative and IgG were positive. Her IgA and IgM antibody levels were mildly elevated 3.36 g/L (N: 0.8-2.8 g/L) and 2.8 g/L (N: 0.5-1.9 g/L) respectively. She was treated with ursodeoxycholic acid and fat soluble vitamins. Her liver functions improved but were still deranged 4 weeks later. Symptomatic hepatitis in IMN is rare, more so in paediatric population compared to elderly. The elevation in aminotransferases levels are usually less than fivefold and hyperbilirubinaemia is seen in up to 5% of patients. In our patient ALT increased more than 30 times and she became clinically jaundiced and symptomatic. Fulminant hepatitis is very rare. Possible mechanisms are lymphocytic infiltration of hepatocytes, cholestasis and auto-immune hepatitis. Treatment is mainly symptomatic and supportive. Conclusion: Patients with IMN should be observed for jaundice and subsequently monitored for liver function in case of hepatitis. EBV should be considered in patients presenting with clinical jaundice.