SAGES Magazine

THE SOUTH AFRICAN GASTROENTEROLOGY REVIEW 2022 | VOLUME 20 | ISSUE 1 | 11 Patient 2 A 54-year-old man, the father of patient 1, presented a month after his son’s admission with similar symptoms. Investigations revealed an acute hepatitis and confirmed HAV infection with a positive Hep A IgM. Despite bed and fluid support he continued to feel unwell and was subsequently admitted to hospital within 9 days of his initial symptoms. On admission he was lethargic, visibly jaundiced with grade 1 hepatic encephalopathy (mild fetor and a hepatic flap). His liver span was 14cm, with no splenomegaly or ascites. The rest of the examination was unremarkable. A diagnosis of hepatitis A infection with liver failure was made. He had cholestatic hepatitis with elevated ammonia levels and coagulopathy (see table 2). His bilirubin peaked at 143 umol/L and took a month to normalize. He remained in hospital for about 2 weeks and was advised to continue with bed rest. Two weeks post discharge a mild elevation was observed which subsequently reached a plateau then a downward trend again. Patient 3 An 18-year-old grade 12 scholar was referred by his GP with worsening jaundice. He had been unwell for a few weeks, complaining of anorexia, nausea and vomiting. In addition, he reported some intermittent loose non bloody stools that had since settled. His father noticed his yellow eyes and on further questioning he also noted that his urine had become dark coloured and stools pale. Of concern he had marked pruritis of his palms and feet. He had no travel history and none of his family members or immediate contacts reported similar symptoms. He denied any drugs or toxins. The clinical examination revealed a healthy young man with a normal body mass index. He was deeply jaundiced, no stigmata of chronic liver disease. He had extensive scratch marks over the trunk and upper limbs. Except for a mild hepatomegaly and tender liver, the rest of his examination was unremarkable. He was found to have a positive hep A IgM and a diagnosis of HAV infection was made. His liver profile initially demonstrated the typical hepatitis which rapidly settled in contrast to a rising and severe jaundice and cholestasis. Obstructive causes were appropriately excluded, and all his other viral and other serology was negative. Management was supportive. He was started on ursodeoxycholic acid but his pruritis proved to be severely debilitating and intractable. He required cholestyramine and ultraviolet light therapy for the pruritus to improve. It took 6 months to achieve a bilirubin of <50 umol/L, symptoms to resolve and he missed a significant portion of his matric year at school. Discussion Hepatitis A infection is usually self-limiting in otherwise healthy young adults. 1,7,11 However, it may have a protracted course in some with no long term sequalae. Mechanism of liver injury is a consequence of a robust T cell response with production of IFN- gamma by virus specific cytotoxic CD8+ T cells. Patients with a reduced regulatory T cell response tend to have markedly elevated ALT levels. 2 Presentations vary from mild to severe with most having gastrointestinal symptoms. Rare complications include rash, pancreatitis, Guillian- Barre syndrome and acute kidney injury in the form of glomerulonephritis. 12,15 Presentations are classified as i asymptomatic HAV infection seen in children less than 5 years, ii symptomatic infection with jaundice, iii cholestatic phase iv relapsing infection with clinical, biochemical and virological markers of acute hep A and v fulminant hepatitis sometimes requiring liver transplant. Mortality from fulminant HAV infection is infrequent. Most (99%) resolve completely with approximately 3% -20 % of clinical cases experiencing relapse. 13 Rarely HAV can unmask or induce autoimmune hepatitis, and this should be explored when patient REVIEW Table 2: Patient 2 TP 64-83 (g/L) 71 63 61 58 60 61 63 64 65 Alb 35-52 (g/L 42 34 33 32 32 31 31 31 32 32 TBill <21 (umol/L) 9 10 10 81 100 134 143 114 81 66 58 53 22 Bill <9 (umol/L) 5 5 5 61 75 103 110 90 62 48 39 32 14 ALP 59-164 (iu/L) 64 120 121 137 145 148 149 130 133 113 GGT <59 (iu/L) 63 73 89 279 231 204 219 221 206 176 139 111 ALT <35 (iu/L) 508 514 806 6003 5129 3003 2135 1522 1006 782 596 466 133 AST <40 (iu/L) 200 168 295 2188 1676 641 339 185 114 91 83 77 54 INR 1.23 1.09 1.06 1.53 1.36 1.16 1.13 1.08 1.04 AFP 0.9-8.8 (ug/L) 2.1 Amm 8-72 (umol/L) 108 84 56 52 50 33 HepAIgM Pos *For abbreviations refer to abbreviations section at the end Table 2: Patient 3 TP 64-83 (g/L) 67 74 Alb 35-52 (g/L 38 42 34 37 35 TBill <21 (umol/L) 250 388 735 776 867 698 643 437 221 69 CBill <9 (umol/L) 185 373 543 414 581 520 607 348 156 52 ALP 59-164 (iu/L) 206 221 790 811 836 894 668 536 341 167 GGT <59 (iu/L) 84 64 36 43 42 45 53 95 144 87 ALT <35 (iu/L) 3447 682 108 36 38 40 41 38 38 44 52 AST <40 (iu/L) 2068 159 39 57 51 50 53 37 27 INR HepAIgM Pos *For abbreviations refer to abbreviations section at the end