Abstract
The common side effects of COVID-19 vaccination were mostly self-restricted local reactions that quickly resolved. Nevertheless, rare autoimmune hepatitis cases have been reported in some vaccinated with mRNA COVID-19 vaccines. This article presents a young man who developed fulminant hepatitis a few days after vaccination with the first dose of the AstraZeneca COVID-19 vaccine.
Keywords: COVID-19; SARS-CoV-2; AstraZeneca; Vaccine, Fulminant; Hepatitis
Introduction
The common side effects of COVID-19 vaccination were mostly self-restricted local reactions that quickly resolved (1). Nevertheless, rare autoimmune hepatitis cases have been reported in some vaccinated with mRNA COVID-19 vaccines (2,3). This article presents a young man who developed fulminant hepatitis a few days after vaccination with the first dose of the AstraZeneca COVID-19 vaccine.
Case presentation
A 35-year-old man was admitted to our hospital with generalized weakness, abdominal pain, and jaundice. He received the first dose of the AstraZeneca COVID-19 vaccine 8 days earlier. Five days after vaccination, the patient experienced fever and headache. Despite the improvement of fever, his abdominal pain was exacerbated, and loss of appetite, jaundice, and vomiting was also manifested. Thus, he was admitted to our center. He had a history of psychological problems under control with paroxetine and sodium valproate. His laboratory results on admission are summarized in Table 1. According to the high D-dimers, low platelet count, and low Fibrinogen level, vaccine-induced immune thrombosis thrombocytopenia (VITT) was suspected. Therefore, high-dose dexamethasone 40 daily, IVIG 1 mg/kg for 2 days, and rivaroxaban 15 mg daily, was started for the patient. Abdominal ultrasonography showed a grade I fatty liver disease, normal gall bladder, and pancreas with mild effusion in subdiaphragmatic space. Also, no intra- or extra-hepatic biliary dilatation was observed. Color Doppler ultrasonography revealed normal portal and hepatic vein and inferior vena cava. The laboratory results of his second hospitalization day were indicative of a surge in his hepatic enzymes, decreasing platelet, prolonged PTT, and increased INR (Table 1) (Fig. 1A).
Furthermore, laboratory results were negative for hepatitis A, B, C, and E viruses, HIV, EBV, HSV-1, and HSV-2. Anti-nuclear antibody (ANA), anti-smooth muscle antibody (ASMA), and SARS-CoV-2 reverse transcriptase-polymerase chain reaction (RT-PCR) were also negative. Hence, fulminant hepatitis was suspected for the patient. Due to a lack of clinical improvement, he became a liver transplant candidate. Unfortunately, after 3 days of hospitalization, he was expired as of disseminated intravascular coagulation (DIC), after which a liver necropsy was performed, indicating drug/toxin-induced hepatitis (Fig. 1B-D).
Discussion
Vaccines have been shown to trigger an immune response leading to a broad spectrum of autoimmune diseases (4). The spike glycoprotein of SARS-CoV-2 or adenoviral vector spike protein vaccines share genetic similarities with a large heptapeptide human protein, so this is an additional factor that can trigger autoimmune disease after vaccination due to molecular mimicry (5). In our patient viral markers were negative, and there was no history of drug or toxin exposure. Unfortunately, our patient died quickly after hospitalization, making our laboratory tests incomplete to determine the etiology of his fulminant hepatitis. On the other hand, the patient was being treated with paroxetine and sodium valproate for his psychological illnesses that might have increased the chance of fulminant hepatitis following vaccination. Since these side effects are infrequent, such cases should not discourage people from being vaccinated against COVID-19, yet physicians must be vigilant for such potential adverse events.