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Journal of Clinical and Experimental Hepatology logoLink to Journal of Clinical and Experimental Hepatology
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. 2024 Feb 27;14(4):101389. doi: 10.1016/j.jceh.2024.101389

Acute Viral Hepatitis E Infection Complicating Postliving Liver Donor Hepatectomy Recovery

Kaleem Ullah 1, Sidhant Ochani 2,⁎, Hafiz B Ahmad 3
PMCID: PMC10950708  PMID: 38515503

Abstract

This study presents a case of a living liver donor who developed a hepatitis E virus (HEV) infection postdonation, complicating his recovery. The donor was a 28-year-old male with no prior health issues who underwent a right lobe hepatectomy. Initially, his postoperative course was uneventful, but on the third postoperative day, he became lethargic and icteric. Laboratory tests showed elevated liver function markers, with peak levels on the 5th day. The HEV infection was confirmed through serological and polymerase chain reaction (PCR) testing. The donor was managed supportively and recovered, with normal liver function at discharge. Unfortunately, the recipient of the liver graft died on the 5th postoperative day due to sepsis, and the impact of HEV infection on the recipient could not be fully assessed due to the complicating factors. This case highlights the importance of considering HEV infection in donors with abnormal postoperative liver functions, especially in regions with high HEV prevalence, and suggests the potential benefit of HEV vaccination for liver donors. Further research is needed to better understand and manage HEV infection in the context of liver donation.


Dear Editor,

Hepatitis E virus (HEV), an Orthohepevirus belongs to the family Hepeviridae.1 It has four major genotypes: 1 and 2 are found in humans, whereas 3 and 4 are zoonotic and infect humans through contaminated water and food consumption. Globally, estimated the annual HEV-infected population is approximately twenty million.2 HEV infection is an acute and self-limiting disease in most immunocompetent individuals.1 The incubation period varies from 2 to 8 weeks. The presenting symptoms are usually nonspecific and include generalized weakness, myalgia, abdominal pain, loss of appetite, and vomiting. Liver-related symptoms like jaundice and pruritus can occur only in severe diseases.3 Usually, mild elevations of aminotransferases are evident in minor illnesses. However, a deranged bilirubin level may also be present in severe illnesses. The disease usually subsides within a few days or weeks. However, very rarely, a patient may develop fulminant hepatic failure and might need liver transplantation.4

Live donor liver hepatectomy is a major surgical procedure with documented 15–30% morbidity. The postoperative recovery can get complicated secondary to surgical stress, peri-operative drugs, and various infections.5 We report a living liver donor who underwent donor right hepatectomy and whose postoperative recovery got complicated secondary to HEV infection.

The twenty-eight-year-old male donor, with no previous comorbidities and a body mass index (BMI) of 24.5 kg/m2, underwent a right lobe hepatectomy. The detailed history and physical examination were unremarkable. Basic lab investigations, including the liver function test, were within normal limits (total bilirubin: 0.9 mg/dl, ALT: 34 IU/ml, and AST: 29 IU/ml). Volumetric calculations on the computer tomography (CT) scan liver showed a liver attenuation index of 5.8, a total liver volume of 1292 g, in which the right lobe volume was 829 g, and a future liver remnant of 35%. Detailed screening for thrombophilia workup, hepatitis B/C viral serology, autoimmune profile, G6PD, copper, ceruloplasmin, and iron profile, and retic count did not show any abnormalities. Pan-cultures also showed no growth. Per routine, no liver biopsy was advised.

Graft without middle hepatic vein (MHV) was harvested. Operative blood loss was approximately 800 ml, and no blood transfusions were needed. Postoperatively, the patient was clinically fine. On the 2nd postoperative day (POD) his laboratory parameters showed a total bilirubin level of 1.9 mg/dl and mildly raised serum alanine aminotransferase (ALT) (276 IU/L) and aspartate aminotransferase (AST) (196 IU/L) levels as usual. On the 3rd POD, the donor was lethargic and slightly icteric on examination. His pulse was 90/minute, and he was afebrile. The LFTs report revealed a serum bilirubin level of 2.7 mg/dl, an ALT value of 604 IU/L, and an AST value of 486 IU/L. The ALT and AST attained peak values of 975 and 783 IU/L, respectively, on the 5th POD while the total bilirubin level progressively increased to 12.3 mg/dl on the 11th POD (with a direct bilirubin level of 9.1 mg/dl). However, alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) remained normal throughout this period. His international normalized ratio (INR) was slightly elevated (1.8, as usual with other donors) on the first POD. However, his INR remained below 1.5 later on. The drain output was also minimal. All the possible causes of deranged LFTs, including sepsis, biliary stricture, hemolysis, and drug-induced hepatotoxicity, were thoroughly ruled out. His ultrasound imaging and Magnetic resonance cholangiopancreatography (MRCP) showed normal studies. The serologies for Hepatitis A Virus (HAV) and HEV were also done. Hepatitis A serology was negative, while IgM for the hepatitis E virus turned out to be reactive. Qualitative HEV polymerase chain reaction (PCR) also turned out to be positive.

The donor was managed with supportive treatment. He recovered clinically over time. His bilirubin level started to settle down from the 12th POD onward. He was discharged on the 17th POD. Till the last follow-up, i.e. the donor is clinically stable and his LFTs are within the normal range.

Unfortunately, the recipient of this graft expired on the 5th POD due to sepsis secondary to a severe chest infection. He remained on a ventilator. His peak total bilirubin level was 4.4 mg/dl, and his peak ALT and AST were 296 IU/L and 275 IU/L, respectively. We were unable to determine the exact course of graft HEV illness in him secondary to severe sepsis.

The reported donor was an asymptomatic young male with normal liver function tests predonation. His HEV serology was not known predonation. Either due to the disease incubation period at the time of surgery or having a mild illness with normal clinical and biochemical parameters, which got worse postsurgery.

There should be a high index of suspicion of HEV illness in donors with deranged postoperative liver functions in highly prevalent areas. Also, vaccination may add protection against HEV infections in precious live liver donors. However, more observations and data are needed on this.

Credit authorship contribution statement

All author(s) contributed equally.

Conflicts of interest

The author(s) declared no potential conflicts of interest concerning the research, authorship, and/or publication of this article.

Acknowledgments

Not applicable.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Ethical approval and consent to participate

No ethical approval and consent to participate is needed, since we do not disclose any identifying patient information.

Consent for publication

All authors have read the final draft and have agreed for publication of the article.

References

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