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.