# Anti-tumor Necrosis Factor-Alpha (TNF-α)-Induced Hypertrophic Lichen Planus: A Case Report

**Authors:** Ahmed Alqefari, Ghaida B AlQefari, Sarah Alkhezzi, Sarah Mohammed

PMC · DOI: 10.7759/cureus.83491 · Cureus · 2025-05-05

## TL;DR

A 26-year-old man with inflammatory bowel disease developed a rare skin condition after switching anti-TNF-α therapy, highlighting the need for close monitoring of unusual skin reactions.

## Contribution

This is the second documented case of anti-TNF-α-induced hypertrophic lichen planus, emphasizing its rarity and potential complications.

## Key findings

- The patient developed hypertrophic lichen planus after switching from adalimumab to infliximab.
- Topical corticosteroids showed minimal effectiveness in treating the skin lesions.
- The case highlights the risk of paradoxical cutaneous reactions and possible increased cancer risk with anti-TNF-α therapies.

## Abstract

We report the case of a 26-year-old male patient with a six-year history of inflammatory bowel disease who developed pruritic, hyperpigmented, and hyperkeratotic nodules on his left abdomen three months after switching from adalimumab to infliximab therapy. Clinical examination and histopathological analysis confirmed the diagnosis of hypertrophic lichen planus (HLP), a rare variant of lichen planus characterized by thick, scaly plaques and intense pruritus. Notably, this adverse reaction represents only the second documented instance of anti-tumor necrosis factor-alpha (TNF-α)-induced HLP, highlighting the potential paradoxical cutaneous reactions associated with these therapies. Although the patient’s inflammatory bowel disease was well controlled with infliximab, the skin lesions responded only minimally to topical corticosteroids. This case underscores the importance of vigilant monitoring of unusual dermatologic manifestations in patients undergoing anti-TNF-α treatment, particularly because such adverse effects can lead to significant morbidity and may be associated with an increased risk of cutaneous squamous cell carcinoma. The mechanisms underlying this paradoxical reaction remain unclear but may involve a shift in cytokine balance following TNF-α inhibition. Increased clinician awareness and early detection are crucial for managing rare drug-induced eruptions and optimizing therapeutic outcomes.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor)
- **Diseases:** inflammatory bowel disease (MONDO:0005265), hypertrophic lichen planus (MONDO:0021377), cutaneous squamous cell carcinoma (MONDO:0002529)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** eruptions (MESH:D003875), inflammatory bowel disease (MESH:D015212), HLP (MESH:D008010), cutaneous squamous cell carcinoma (MESH:D002294), skin lesions (MESH:D012871), pruritus (MESH:D011537)
- **Chemicals:** infliximab (MESH:D000069285), adalimumab (MESH:D000068879)
- **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/PMC12136536/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12136536/full.md

## References

15 references — full list in the complete paper: https://tomesphere.com/paper/PMC12136536/full.md

---
Source: https://tomesphere.com/paper/PMC12136536