# A Case of Acetaminophen Toxicity in a Patient With an Unusual Alpha-1 Antitrypsin Phenotype

**Authors:** Ashwin Agrawal, Manar Chowdhury, Colin Winkie, Chickajajur Vijay

PMC · DOI: 10.7759/cureus.88224 · Cureus · 2025-07-18

## TL;DR

A teenager with a rare alpha-1 antitrypsin type and a history of liver issues developed liver damage from a normal dose of acetaminophen, highlighting the need for caution in similar patients.

## Contribution

This case report identifies a rare alpha-1 antitrypsin phenotype as a potential risk factor for acetaminophen-induced liver injury.

## Key findings

- A 16-year-old male with Pi*EM alpha-1 antitrypsin and liver history developed hepatotoxicity from a non-toxic acetaminophen dose.
- The patient's liver injury was likely due to intestinal failure-associated liver disease and the rare alpha-1 antitrypsin phenotype.
- The case emphasizes the need for caution with acetaminophen in patients with rare alpha-1 antitrypsin types and prior liver disease.

## Abstract

Acetaminophen is a commonly used over-the-counter analgesic and antipyretic that can be hepatotoxic if taken in excess. We present a case of acetaminophen-mediated hepatotoxicity following ingestion of a non-toxic dose of acetaminophen in a 16-year-old male with short bowel syndrome and a remote history of severe liver dysfunction with a rare alpha-1 antitrypsin phenotype Pi*EM. The patient initially presented with nonspecific symptoms of abdominal pain, nausea, vomiting, and diarrhea. N-acetylcysteine (NAC) therapy was initiated for acetaminophen toxicity. We suspect that the patient’s susceptibility to acetaminophen-induced liver injury was likely due to underlying intestinal failure-associated liver disease that occurred as a child, as well as the Pi*EM, making the liver more prone to insults. This case highlights the importance of prompt recognition and management of acetaminophen toxicity in patients with prior liver disease, even if the amount ingested is thought to be non-toxic. In addition, the case highlights that rare alpha-1 antitrypsin phenotypes should be treated with heightened caution for liver dysfunction, as there is limited literature indicating if these phenotypes are pathogenic or non-pathogenic.

## Linked entities

- **Proteins:** SPIA5 (serpin family A member 1)
- **Chemicals:** acetaminophen (PubChem CID 1983), N-acetylcysteine (PubChem CID 12035)
- **Diseases:** short bowel syndrome (MONDO:0015183), intestinal failure-associated liver disease (MONDO:0100615)

## Full-text entities

- **Genes:** SERPINA1 (serpin family A member 1) [NCBI Gene 5265] {aka A1A, A1AT, AAT, PI, PI1, PRO2275}
- **Diseases:** short bowel syndrome (MESH:D012778), nausea (MESH:D009325), liver dysfunction (MESH:D017093), liver disease (MESH:D008107), Toxicity (MESH:D064420), diarrhea (MESH:D003967), abdominal pain (MESH:D015746), vomiting (MESH:D014839), intestinal failure (MESH:D000090124)
- **Chemicals:** N-acetylcysteine (MESH:D000111), Acetaminophen (MESH:D000082)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12358055/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12358055/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12358055/full.md

---
Source: https://tomesphere.com/paper/PMC12358055