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showed that antibodies against the spike protein S1 of SARS-CoV-2 had high affinity against the following human tissue proteins: transglutaminase 3, transglutaminase 2, anti-extractable nuclear antigen, nuclear antigen, and myelin basic protein. As this is the same viral protein that the vaccine mRNA codes for, it is plausible that these vaccines may unmask autoimmune diseases in predisposed patients. Recently, several cases of immune thrombocytopenia (ITP) developing days after COVID-19 vaccination, have been reported to the Vaccine Adverse Event Reporting System (VAERS), reinforcing the possibility of vaccine-induced autoimmunity.
We have recently treated a 35-year-old Caucasian female in her third month postpartum, who developed autoimmune hepatitis after COVID-19 vaccination. During pregnancy, she was diagnosed with gestational hypertension and started on labetalol 100 mg bid. C-section was performed without any complications, and patient was discharged from the hospital on labetalol for blood pressure control. She resumed her job as a healthcare provider in mid-December, and received her first dose of Pfizer-BioNTech COVID-19 vaccine on January 4th. After 1 week, she started developing generalized pruritus, then choluria, and finally noticed jaundice, presenting to the emergency room on day +13 after COVID-19 vaccination.
She had a normal physical exam, except for scleral icterus, jaundice and palpable hepatomegaly. In the emergency room, laboratories were significant for: bilirubin 4.8 mg/dl, AST 754 U/L, ALT 2,001 U/L, alkaline phosphatase 170 U/L, and ammonium 61 mg/dl. Laboratory results were negative for hepatitis A, B, and C, Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex virus (HSV) type 1 and 2, and HIV. At the time of submission, HEV had not been tested. Antinuclear antibody (ANA) was positive (1:1,280; homogeneous pattern). Double-stranded DNA antibodies were also positive (1:80). Other antibodies (i.e. anti-mitochondrial, anti-smooth muscle, liver-kidney microsomal, antineutrophil cytoplasmic antibodies) were negative. Total IgG was 1,081 mg/dl (normal range: 694–1,618 mg/dl). Ceruloplasmin, transferrin saturation, alpha-1-antitrypsin, TSH, and serum protein electrophoresis were all normal. Abdominal ultrasound with Doppler reported hepatomegaly without cirrhotic morphology, and no intra- or extra-hepatic biliary dilation.
Endoscopic ultrasound showed no evidence of biliary lithiasis or biliary dilation, and transduodenal liver biopsies were obtained. In Fig. 1A–D we have included the slides of her liver biopsy and a full description of the histology. Liver biopsy was consistent with drug/toxin related liver injury, autoimmune hepatitis or infectious related etiologies. A PAS-D stain, CMV & HSV 1/2 immunohistochemical stains, EBV by in situ hybridization (EBER-ISH) and Grocott methenamine special stain for fungi were all negative. Other than the COVID-19 vaccine and labetalol, no other drugs, herbal supplements or toxins were reported by the patient. The Revised Original Score for autoimmune hepatitis pretreatment was 18 (results >15 suggest definite autoimmune hepatitis). Fig. 1E summarizes plasma ALT, AST, and total bilirubin over time, before and after treatment with prednisone 20 mg daily.
To our knowledge, this is the first reported episode of autoimmune hepatitis developing post-COVID-19 vaccination, raising concern regarding the possibility of vaccine-induced autoimmunity. As causality cannot be proven, it is possible that this association is just coincidental. However, severe cases of SARS-CoV-2 infection are characterized by an autoinflammatory dysregulation that contributes to tissue damage.
it is plausible that spike-directed antibodies induced by vaccination may also trigger autoimmune conditions in predisposed individuals. In support of this, several cases of ITP have been reported days after COVID-19 vaccination.
Several atypical features of her presentation deserve further discussion. First, immunoglobulin G levels were not elevated as typically reported for autoimmune hepatitis. However, Hartl et al. recently reported that ~10% of patients with autoimmune hepatitis had normal immunoglobulin G levels at presentation.
Finally, symptoms developed 6 days after vaccination, which instinctively appears as a short period of time. However, latency periods after vaccination of just days have been observed in prior reports.
In summary, autoimmune hepatitis developed in a healthy 35-year-old female in her third month postpartum. Whether there exists a causal relationship between COVID-19 vaccination and the development of autoimmune hepatitis remains to be determined. We are hopeful that this manuscript will not discourage healthcare providers from getting and prescribing COVID-19 vaccines, but that it will raise awareness about potential side effects that will likely emerge as we continue to vaccinate more people. Only long-term follow-up of large cohorts of patients receiving the vaccine will answer the question as to whether it increases the risk of autoimmune conditions. Until then, healthcare providers are encouraged to remain vigilant.
The authors received no financial support to produce this manuscript.
FB: Patient care, writing of the manuscript, and revision of the final version of the manuscript. SAD: Pathology reading, and revision of the final version of the manuscript. MD: Patient care, and revision of the final version of the manuscript. DMF: Patient care, and revision of the final version of the manuscript.
Conflict of interests
The authors declare no conflicts of interest that pertain to this work.
Please refer to the accompanying ICMJE disclosure forms for further details.
The following is the supplementary data to this article:
We read with interest the letter entitled “Autoimmune hepatitis developing after coronavirus disease 2019 (COVID-19) vaccine: Causality or casualty?” by Bril et al.1 recently published in Journal of Hepatology. We had a similar case which strengthens the message of SARS-CoV-2 vaccines as a potential trigger for autoimmune hepatitis (AIH).
We read with interest the comment by Capecchi et al.1 regarding our Letter to the Editor describing a case of autoimmune hepatitis (AIH) developing after COVID-19 vaccination.2 We thank the authors for their interest in our manuscript and for their thoughtful insight, which complemented our report.
We read with interest the letters “Autoimmune hepatitis developing after coronavirus disease 2019 (COVID-19) Vaccine: Causality or casualty?” by Bril et al.1 and “Autoimmune hepatitis following SARS-CoV-2 vaccine: May not be a casuality” by Rocco et al.2 which highlight the hypothesis that COVID-19 mRNA-based vaccines might increase the risk of developing autoimmune diseases. There are growing reports of autoimmune diseases developing after SARS-CoV-2 infection, including Guillain-Barré syndrome and primary biliary cholangitis.
We read with great interest the article by Bril F. et al. recently published in the Journal of Hepatology.1 In our opinion, several considerations increase the possibility that the described association is indeed coincidental, as also acknowledged by the authors.
We read with interest the article “Autoimmune hepatitis developing after coronavirus disease 2019 (COVID-19) vaccine: Causality or casualty?” by Bril et al. recently published in Journal of Hepatology.1 In this case, autoimmune hepatitis had some atypical features such as the absence of immunoglobulin G elevation and the presence of eosinophils on liver histology.
We read with interest the recent letter published by Bril et al. recently published in Journal of Hepatology.1 The authors describe a possible case of COVID-19 vaccine-associated autoimmune hepatitis (AIH) in a 35-year-old woman 3 months post-partum. The patient presented with pruritis and jaundice 13 days after receiving a BNT162b2 mRNA (Pfizer-BioNTech) COVID-19 vaccine, which may be the first report of COVID-19 vaccine-associated liver injury. As vaccination programs are being rolled out globally,2 many clinically significant side effects are starting to be identified, such as vaccine-induced immune thrombotic thrombocytopenia.
I read with interest the comments to our letter by Londoño et al.,1 Clayton-Chubb et al.,2 Tan et al.,3 McShane et al.,4 and Lodato et al.,5 and I appreciate their contribution. All these authors presented similar cases of autoimmune hepatitis (AIH) that developed after coronavirus disease 2019 (COVID-19) vaccine, with the exception of Lodato et al.,5 who actually described a case of acute liver injury with some features of autoimmunity.
The COVID-19 pandemic is still raging across the world and vaccination is expected to lead us out of this pandemic. Although the efficacy of the vaccines is beyond doubt, as many vaccines were granted expedited approval, safety still remains a concern.1 In light of this, we read with great interest a recent article by Bril et. al.2 They described a case of autoimmune hepatitis (AIH) possibly triggered by COVID-19 vaccination. However, as the patient was 3-months post-partum a true causal relationship is difficult to determine.
We have read with interest the recent cases suggesting the possibility of vaccine-induced immune-mediated hepatitis with Pfizer-BioNTech and Moderna mRNA-1273 mRNA vaccines for the SARS-CoV-2 virus. (1-7). However, as the cohort of vaccinated individuals against COVID-19 increases, the previously reported cases could not exclude a coincidental development of autoimmune hepatitis, which has an incidence of 3/100 000 population per year (8). Our case demonstrates conclusive evidence of vaccine-induced immune-mediated hepatitis with a rapid onset of liver injury after the first Moderna dose, which on re-exposure led to acute severe autoimmune hepatitis.
We read with interest the article: “Autoimmune hepatitis developing after coronavirus disease 2019 (COVID-19) Vaccine: Causality or casualty?ˮ by Bril F. et al.1 and the comment to the letter by Capecchi L. et al. recently published in J Hepatol.2