Report #2897558

Overview

Sex

Male

Age

Age unknown

State

NJ

Recovered

Recovered

Vaccinated

—

Onset

—

Days to onset

—

Hospital days

—

Symptoms (29)

Symptom narrative

diagnosis of AIH; This is a literature report for the following literature source(s). A 55-year-old male patient received BNT162b2 omicron (lp.8.1) (BNT162B2 OMICRON (LP.8.1)), as dose 1, single (Batch/Lot number: unknown) for covid-19 immunisation. The patient's relevant medical history included: "ulcerative colitis (UC)" (unspecified if ongoing), notes: 10 years history of UC. The patient's concomitant medications were not reported. Past drug history included: Sulfasalazine for ulcerative colitis, notes: oral. Vaccination history included: Covid-19 vaccine (DOSE 1; MANUFACTURER UNKNOWN), for COVID-19 immunisation. The following information was reported: AUTOIMMUNE HEPATITIS (medically significant), 21 days after the suspect product(s) administration, outcome "recovered", described as "diagnosis of AIH". The patient underwent the following laboratory tests and procedures: Alanine aminotransferase: 1476 IU/l; Antinuclear antibody: titer of 1:160; Aspartate aminotransferase: 1621 IU/l; Autoantibody test: Positive, notes: titer of 1 to 160; Biopsy liver: This revealed the classical features of AIH, notes: including a dense lymphoplasmacytic infiltrate in the portal tracts with prominent features, interface hepatitis, and evidence of emperipolesis; Blood bilirubin: 6.0 mg/dl; Blood immunoglobulin G: Negative; Blood immunoglobulin M: Negative; Body mass index: 30, notes: Unit: kg/m2; C-reactive protein: 45 mg/l; Endoscopic ultrasound: showed diffuse abnormal echotexture, notes: throughout the Liver; Hepatitis A antibody: Negative; Hepatitis B core antibody: Negative; Hepatitis B surface antigen: Negative; Hepatitis B virus test: Negative; Hepatitis C antibody: Negative; Hepatitis D virus test: Negative; Hepatitis E antibody: Negative; rule out infectious etiologies; Immunoassay: Positive, notes: titer of more than equals to 1 to 40; Inflammatory marker test: elevated; Examination: jaundiced with mild dull right upper quadrant, notes: RUQ tenderness; This revealed the classical features of AIH, notes: including a dense lymphoplasmacytic infiltrate in the portal tracts with prominent features, interface hepatitis, and evidence of emperipolesis; showed stage F0; laboratory investigations: revealed a significant hepato cellular injury; diagnosis of AIH; Liver function test: normalizing over 2 months; Magnetic resonance imaging: unremarkable; Red blood cell sedimentation rate: 65, notes: Unit: mm/h; Smooth muscle antibody: Positive, notes: titer of 1 to 80; titer of 1:80; Ultrasound abdomen: unremarkable; Vital signs measurement: stable. Therapeutic measures were taken as a result of autoimmune hepatitis. Clinical Course: Autoimmune hepatitis (AIH) following COVID-19 vaccination is a rare adverse event. The authors presented the case of a 55-year-old male with a history of ulcerative colitis (UC) who developed AIH 3 weeks after receiving his second dose of the Pfizer-BioNTech mRNA vaccine. He presented with jaundice and significantly elevated liver enzymes. A liver biopsy confirmed the diagnosis of AIH. The patient was successfully treated with corticosteroids and azathioprine, leading to complete clinical and biochemical remission. This case highlights the potential for vaccine-induced autoimmune phenomena, particularly in individuals with preexisting autoimmune conditions, and underscores the importance of prompt diagnosis and treatment. This case describes a patient with ulcerative colitis who developed acute autoimmune hepatitis (AIH) 3 weeks after a COVID-19 booster. While a causal link cannot be definitively proven, the temporal association highlights the importance of considering AIH in the differential diagnosis of postvaccination liver injury. Prompt diagnosis and treatment with standard immunosuppressive therapy led to complete remission. Patient with a 10-year history of UC, which had been well-controlled for the past 5 years on maintenance therapy with oral sulfasalazine alone and without any recent or chronic use of corticosteroids, presented to the emergency department with a three-week history of dull right upper quadrant (RUQ) abdominal pain and jaundice. His history was notable for receiving his second dose of the Pfizer-BioNTech SARS-CoV-2 vaccine 21 days prior to admission. He did not have liver function tests prior to presentation. He reported no recent travel, occupational exposures, or use of herbal supplements or acetaminophen. On examination, he was jaundiced with mild RUQ tenderness. His vital signs were stable, and his body mass index (BMI) was 30 kg/m2. The initial diagnostic workup included comprehensive laboratory testing, viral serologies, and imaging. Autoantibody testing for antinuclear antibody (ANA) and anti-smooth muscle antibody (ASMA) was performed using indirect immunofluorescence on HEp-2 cells, with a positive result defined as a titer of greater than or equal to 1:40. A comprehensive viral hepatitis panel was conducted to rule out infectious etiologies. Imaging included an abdominal ultrasound, MRI, and an endoscopic ultrasound. A liver biopsy was performed, and sections were stained with hematoxylin and eosin (H&E). Based on the clinical and histological findings, the patient was started on a 60 mg daily prednisone taper along with azathioprine for immunosuppressive therapy. Initial laboratory investigations revealed a significant hepatocellular injury, with an AST of 1621 U/L and ALT of 1476 U/L, accompanied by a total bilirubin of 6.0 mg/dL and elevated inflammatory markers (CRP 45 mg/L and ESR 65 mm/h). A com-prehensive viral hepatitis panel, including tests for Hepatitis A (IgM), Hepatitis B (sAg, core Ab, surface Ab), Hepatitis C (Ab), Hepatitis D (IgG), and Hepatitis E (IgG and IgM), was negative. Autoantibody testing was positive for ANA at a titer of 1:160 and ASMA at a titer of 1:80. While an abdominal ultrasound and MRI were unremarkable, an endoscopic ultrasound showed diffuse abnormal echotexture throughout the liver . A liver biopsy was performed, and sections were stained with H&E. This revealed the classical features of AIH, including a dense lymphoplasmacytic infiltrate in the portal tracts with prominent features, interface hepatitis, and evidence of emperipolesis. In addition, there were clear foci of both macro vesicular and micro vesicular steatosis involving approximately 10% of hepatocytes. A trichrome stain for fibrosis showed stage F0. Based on the clinical picture, timing of vaccination, and exclusion of other causes, a diagnosis of probable vaccine-associated AIH was made. Following the initiation of immunosuppressive therapy, the patient experienced a complete clinical and biochemical recovery, with liver markers normalizing over 2 months. Although rare, AIH can follow COVID-19 vaccination, particularly in predisposed individuals such as those with UC. Early diagnostic consideration and prompt immunosuppressive therapy lead to favorable outcomes. Despite these isolated cases, the risk-benefit ratio overwhelmingly favors vaccination. Continuous reporting and research into these rare autoimmune phenomena will refine our understanding and guide clinical care. We report a 55-year-old REDACTED male with UC who developed AIH 21 days after the second dose of the Pfizer-BioNTech COVID-19 vaccine. The patient had markedly elevated AST (1621 U/L) and ALT (1476 U/L), positive ANA and ASMA, and experienced a full recovery following the initiation of high-dose prednisone and azathioprine. This presentation is rare, particularly because it involves UC as a predisposing autoimmune condition, which is an uncommon comorbidity among reported postvaccine AIH cases. While the close temporal association in our case is suggestive, it is critical to acknowledge that the presentation may be coincidental rather than causative. Millions of vaccine doses have been administered, and AIH can occur spontaneously. Establishing true causality is challenging and requires evidence that is often lacking in single case reports. When evaluating the likelihood of a true causal link, several factors can be considered. First, a rechallenge phenomenon, where hepatitis improves after the first dose and recurs more severely after the second, provides strong evidence. This was not observed in our patient, as he did not have documented liver enzyme monitoring after his first dose. Second, the absence of fibrosis on a liver biopsy would suggest a truly acute process rather than an acute exacerbation of a chronic condition; the trichrome stain showed fibrosis stage F0. Third, the strongest evidence for causality would be sustained remission after withdrawing immunosuppression, a point that requires a long-term follow-up beyond our current two-month window. Finally, while the background annual incidence of AIH in men is low (approximately 1-2 per 100,000), the sheer number of people vaccinated means that some cases of de novo AIH will inevitably occur in the post vaccination period by chance alone. Therefore, while we present a clinically significant case with a striking temporal relationship, we must remain circumspect and consider the association as possibly coincidental. Proposed mechanisms behind vaccine-related AIH, if a causal link exists, include molecular mimicry, epitope spreading, and bystander activation, where immune responses to SARS-CoV-2 antigens unintentionally target hepatic antigenic structures. An alternative hypothesis is that the vaccine-induced immune response unmasked a subclinical, undiagnosed mild chronic steatosis or an indolent form of AIH, rather than initiating de novo disease from a completely healthy baseline. The finding of micro vesicular steatosis on biopsy, while nonspecific, could be compatible with an acute exacerbation of an underlying predisposition. The patient's underlying UC may create a susceptible immunologic environment, predisposing to autoimmune sequelae following vaccination. Our case is distinctive for involving a male patient with UC, highlighting the need to monitor vaccine-triggered AIH not only in women but also in those with preexisting UC. The patient responded promptly to prednisone induction and azathioprine maintenance, consistent with traditional AIH management and outcomes reported in the literature. This suggests that even in vaccine-triggered cases, standard immunosuppressive regimens are effective. From a clinical standpoint, this case highlights several important implications. Physicians should maintain a high index of suspicion for AIH in patients presenting with liver dysfunction after vaccination, particularly those with autoimmune comorbidities. Prompt recognition and initiation of corticosteroids remain critical to favorable outcomes. Future research should prioritize systematic surveillance to determine the true incidence of vaccine-associated AIH, the role of genetic predisposition, and long-term outcomes across different vaccine platforms. Significantly, these findings should not deter vaccination. The overwhelming evidence continues to support the safety and efficacy of COVID-19 vaccines, with benefits far outweighing the rare risk of immune-mediated hepatitis. This case stands out for its detailed documentation and for highlighting UC as a possible susceptibility factor in vaccine-associated AIH. It underscores the need for heightened surveillance of liver injury in patients with preexisting autoimmune conditions postvaccination. From now on, prospective studies and registries should aim to clarify incidence, mechanisms, and long-term outcomes of vaccine-related AIH.; Sender's Comments: There is not a reasonable possibility that the reported event Autoimmune Hepatitis was related to the suspect product event most likely due to patient underlying contributory factors. The impact of this report on the benefit/risk profile of the Pfizer product is evaluated as part of Pfizer procedures for safety evaluation, including the review and analysis of aggregate data for adverse events. Any safety concern identified as part of this review, as well as any appropriate action in response, will be promptly notified to Regulatory Authorities, Ethics Committees, and Investigators as appropriate.

Medical history

Medical History/Concurrent Conditions: Ulcerative colitis (10 years history of UC)

Lab data

Test Name: ALT; Result Unstructured Data: Test Result:1476 IU/l; Test Name: Antinuclear antibody (ANA); Result Unstructured Data: Test Result:titer of 1:160; Test Name: AST; Result Unstructured Data: Test Result:1621 IU/l; Test Name: Autoantibody test; Test Result: Positive ; Comments: titer of 1 to 160; Test Name: liver biopsy; Result Unstructured Data: Test Result:This revealed the classical features of AIH; Comments: including a dense lymphoplasmacytic infiltrate in the portal tracts with prominent features, interface hepatitis, and evidence of emperipolesis.; Test Name: total bilirubin; Test Result: 6.0 mg/dl; Test Name: IgG; Test Result: Negative ; Test Name: IgM; Test Result: Negative ; Test Name: body mass index; Result Unstructured Data: Test Result:30; Comments: Unit: kg/m2; Test Name: CRP; Result Unstructured Data: Test Result:45 mg/l; Test Name: endoscopic ultrasound; Result Unstructured Data: Test Result:showed diffuse abnormal echotexture; Comments: throughout the Liver; Test Name: Hepatitis A test (IgM); Test Result: Negative ; Test Name: Hepatitis B core Ab; Test Result: Negative ; Test Name: Hepatitis B sAg surface; Test Result: Negative ; Test Name: Hepatitis B sAg; Test Result: Negative ; Test Name: Hepatitis C test Ab; Test Result: Negative ; Test Name: Hepatitis D test (IgG); Test Result: Negative ; Test Name: Hepatitis E test IgG; Test Result: Negative ; Test Name: Hepatitis E test IgM; Result Unstructured Data: Test Result:rule out infectious etiologies; Test Name: indirect immunofluorescence on HEp- 2 cells; Test Result: Positive ; Comments: titer of more than equals to 1 to 40; Test Name: inflammatory markers; Result Unstructured Data: Test Result:elevated; Test Name: Examination; Result Unstructured Data: Test Result:jaundiced with mild dull right upper quadrant; Comments: RUQ tenderness; Test Name: hematoxylin and eosin (H&E) Stain; Result Unstructured Data: Test Result:This revealed the classical features of AIH; Comments: including a dense lymphoplasmacytic infiltrate in the portal tracts with prominent features, interface hepatitis, and evidence of emperipolesis.; Test Name: trichrome stain for fibrosis; Result Unstructured Data: Test Result:showed stage F0; Test Name: laboratory investigations; Result Unstructured Data: Test Result:revealed a significant hepato cellular injury; Test Name: Liver biopsy; Result Unstructured Data: Test Result:diagnosis of AIH; Test Name: liver markers; Result Unstructured Data: Test Result:normalizing over 2 months; Test Name: MRI; Result Unstructured Data: Test Result:unremarkable; Test Name: ESR; Result Unstructured Data: Test Result:65; Comments: Unit: mm/h; Test Name: anti- smooth muscle antibody (ASMA); Test Result: Positive ; Comments: titer of 1 to 80; Test Name: anti-smooth muscle antibody; Result Unstructured Data: Test Result:titer of 1:80; Test Name: abdominal ultrasound; Result Unstructured Data: Test Result:unremarkable; Test Name: vital signs; Result Unstructured Data: Test Result:stable