SAGES Magazine

THE SOUTH AFRICAN GASTROENTEROLOGY REVIEW 2022 | VOLUME 20 | ISSUE 1 | 10 REVIEW Acute hepatitis A infection is caused by the hepatitis A virus (HAV), a single stranded RNA hepatovirus of the picornaviridae family 1 . Transmission is oro-faecal, either person-to-person contact or via the consumption of contaminated food or water. 1-3 Prevalence is higher in areas with poor sanitation or ablution facilities. Outbreaks have also been reported amongst men who have sex with men or institutions with people in close contact sharing bathrooms. 4,5 HAV infection is vaccine preventable but South Africa and most African countries do not have the vaccine in their expanded programs of immunization (EPI). Outbreaks occur worldwide with an estimated 1.4 million incident cases occurring annually 6 . These are sporadic and often cyclical, children <10 years often affected although the disease course is usually mild and self-limiting. HAV has an incubation period of 14-28 days, the presentation varying from asymptomatic to fulminant hepatitis. HAV replication initially begins in the epithelial cells of the small intestine crypts followed by viraemia and later exclusively within hepatocytes 1,7 . It is again shed into the colon via bile and maximal faecal shedding occurs during the latter 3-4 days of incubation and peaks just before the onset of liver injury 1 . This likely accounts for the GI symptoms of acute HAV. These levels drop with the onset of symptoms and with appearance of antibodies, but viral RNA particles can be found in faeces and within hepatocytes with RNA PCR for months 8 . Existing data suggests most of the symptomatic hepatitis A infections occur in the 7–40-year age group in Western Cape Province 9 . Fulminant liver failure is seen in less than 1% of patients infected with HAV and these are invariably in older patients with underlying liver disease 6 Jaundice develops in 40-70% of cases, typically peaking in about 2 weeks. Infected individuals are infectious from incubation period and remain highly infectious up to week after the appearance of jaundice. 1,10 We present 3 patients with acute hepatitis A infection – two from the same family. Patient 1 A 22-year-old male, with no prior medical history developed symptoms while holidaying with his family along the Southern Cape, that included nausea, vomiting, diarrhoea and extreme fatigue for about a week. He had a brief fever lasting 2 days. His mother (a medical doctor) noted jaundice and arranged blood tests. His initial blood demonstrated a significant hepatocellular injury (Table.1). Further history was non- contributory – he denied taking any herbals or toxins. Examination revealed an acutely unwell young man, lethargic and dehydrated. Except for tachycardia, he had normal vitals. He was jaundiced with no stigma of chronic liver disease. He had no hepatic fetor nor flap. Abdominal examination revealed right upper quadrant discomfort and mild hepatomegaly. Rest of examination was normal. A diagnosis of acute viral hepatitis was made, and likely aetiology given the prominent gastro symptoms was hepatitis A or E. SARS CoV-2 was amongst the differential, but his liver enzymes were out of keeping for SARS CoV-2. His COVID PCR was positive as was his hepatitis A IgM result. A diagnosis of acute HAV with simultaneous SARS CoV-2 co- infection was made. He remained in hospital for a week. Unfortunately, his immediate family could only be offered active hepatitis A vaccine as no passive immunoglobulin was available. A month following discharge he reported that his energy levels were low and repeat liver enzymes demonstrated an upward trend. He was advised to rest, and they slowly started settling 2 weeks later. The Complications of Hepatitis A Correspondence AT Murindagomo email: murindagomoa@yahoo.com AT Murindagomo 1 , SK Dlamini 1 , MW Sonderup 1,2 , NA Gogela 1,2 1 Department of Medicine, Groote Schuur Hospital, University of Cape Town ,Cape Town, South Africa 2 Division of Hepatology, Groote Schuur Hospital, University of Cape Town ,Cape Town, South Africa Table 1: Patient 1 Admission Follow up After resumption of exercise TP 64-83 (g/L) 68 Alb 35-52 (g/L) 40 T Bill <21 (umol/L) 98 19 11 10 10 6 C Bill <9 (umol/L) 79 11 5 6 3 ALT <35 (iu/L) 5380 172 169 158 317 381 AST <40 (iu/L) 3359 68 62 61 101 116 ALP 59-164 (iu/L) 203 88 90 88 GGT (iu/L) 215 35 28 21 25 INR 1.9 1.02 1.05 1.1 Hep A IgM Pos *For abbreviations refer to abbreviations section at the end TP 64-83 (g/L) Alb 35-52 (g/L T Bill <21 (umol/L) Bill <9 (umol/L) ALP 59-164 (iu/L) GGT <59 (iu/L) ALT <35 (iu/L) AST <40 (iu/L) INR AFP 0.9-8.8 (ug/L) Amm 8-72 (umol/L) Hep A IgM