Dermatology: Practical and Conceptual


Research Letter | Dermatol Pract Concept. 2025;15(3):5320 1

Hepatotoxicity Associated with Adalimumab  
in Hidradenitis Suppurativa: A Report of Two Cases 

of Drug-Induced Liver Injury
Cristian Fernando Caballero-Linares1, Bianca Cei2, Fernando Alfageme1

1 Dermatology Department, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain

2 Dermatology Department, University of Pisa, Italy

Key words: Hidradenitis suppurativa, Adalimumab, Drug-induced liver injury (DILI), Hepatotoxicity, Liver toxicity

Citation: Caballero-Linares CF, Bianca C, Alfageme F. Hepatotoxicity Associated with Adalimumab in Hidradenitis Suppurativa: A Report 
of Two Cases of Drug-Induced Liver Injury.  Dermatol Pract Concept. 2025;15(3):5320. DOI: https://doi.org/10.5826/dpc.1503a5320 

Accepted: January 27, 2025; Published: July 2025

Copyright: ©2025 Caballero-Linares et al. This is an open-access article distributed under the terms of the Creative Commons Attribution-
NonCommercial License (BY-NC-4.0), https://creativecommons.org/licenses/by-nc/4.0/, which permits unrestricted noncommercial use, 
distribution, and reproduction in any medium, provided the original authors and source are credited.

Funding: None.

Competing Interests: None.

Authorship: All authors have contributed significantly to this publication. 

Corresponding Author: Cristian Fernando Caballero-Linares, MD, Dermatology Department; Hospital Universitario Puerta de Hierro 
Majadahonda; Calle Joaquín Rodrigo, 1, 28222, Majadahonda, Madrid, Spain. ORCID: 0009-0005-5652-7754. E-mail address: 
cristianfernando.caballero@salud.madrid.org.

Introduction

Adalimumab, a TNF-α inhibitor, is widely used in hidradeni-

tis suppurativa (HS). While generally considered safe, hepa-

totoxicity has been documented as a potential adverse effect. 

We present two cases of drug-induced liver injury (DILI) as-

sociated with adalimumab in patients with HS, highlighting 

the variability in onset and severity of hepatic damage.

Case Presentation

The first case involves a 47-year-old female diagnosed with 

HS Hurley III in 2019, with a medical history of endome-

triosis managed with oral contraceptives, no known drug 

allergies, no hypertension, diabetes, or dyslipidemia, and no 

personal or family history of liver disease. She was initially 

treated with rifampicin and clindamycin for two months 

while undergoing pre-biological screening. Subsequently, she 

started adalimumab 80 mg every two weeks. In 2021, her 

therapy was switched to a biosimilar at the same dosage. 

In July 2024, after more than two years of treatment, she 

developed right upper quadrant discomfort with transami-

nases elevated fivefold. Liver elastography, previously nor-

mal, revealed severe steatosis; antinuclear and liver-specific 

antibodies were negative. Adalimumab was discontinued, 

and she received a tapering course of oral corticosteroids, 

with progressive improvement in liver enzymes. 

The second case describes a 56-year-old female, smoker 

(eight cigarettes/day), with a history of anxiety managed in-

termittenly with lorazepam, no drug allergies or chronic co-

morbidities, and no personal or family history of liver disease. 

Diagnosed with HS Hurley III in February 2022, she initially 

received clindamycin for one month during her pre-biological  

screening. Then, adalimumab was initiated in April 2022 



2 Research Letter | Dermatol Pract Concept. 2025;15(3):5320

with an induction dose of 160 mg. Within just three days of 

this first and only dose, she developed severe epigastric pain. 

Laboratory tests revealed elevated ALT (1595 U/L), AST  

(587 U/L), and GGT (556 U/L). Liver elastography was nor-

mal; antinuclear and liver-related antibodies were negative. 

Adalimumab was immediately discontinued, and liver en-

zymes gradually normalized during follow-up. The final di-

agnosis was DILI, attributed to recent adalimumab initiation.

Hepatotoxicity occurred at different stages- delayed in 

the first case and acute in the second- highlighting the un-

predictable latency of DILI. As noted by Frider et al. [1], 

adalimumab-related liver injury is often idiosyncratic, likely 

driven by an abnormal immune response rather than a direct 

dose-dependent toxicity. Elevated transaminases were the 

main laboratory finding in both cases, reflecting the degree 

of hepatocellular injury. In the second case, the rapid onset 

with transaminase elevation within days of starting treat-

ment suggests a more severe inflammatory response, indicat-

ing acute liver damage.

The underlying mechanism of adalimumab-induced hepa-

totoxicity is not entirely understood. It may involve aberrant 

immune activation due to TNF-α blockade, potentially resulting 

in eosinophilic infiltration and hepatic inflammation, as seen in 

liver biopsies from affected patients [2]. The resolution of liver 

enzyme abnormalities following drug discontinuation, as ob-

served in our patients, supports the idea that prompt cessation 

of therapy is crucial to preventing severe liver damage [3].

Conclusion

We present two cases of DILI associated with adalimumab 

in patients with HS, an occurrence not previously described 

in the literature. While adalimumab remains a cornerstone 

of HS treatment, these cases underscore the need for rou-

tine hepatic monitoring, especially at early stages of ther-

apy. Clinicians should be aware of the possibility of severe 

hepatotoxicity and act promptly when clinical or bio-

chemical abnormalities appear. Further research is needed 

to better understand the risk factors and mechanisms of 

 adalimumab-induced liver injury, ensuring safer use of this 

treatment.

References

1. Frider B, Bruno A, Ponte M, Amante M. Drug-induced liver 

injury caused by adalimumab: a case report and review of 

the bibliography. Case Reports Hepatol. 2013;2013:406901. 

DOI:10.1155/2013/406901. PMID: 25431703.

2. Kok B, Lester ELW, Lee WM, et al. Acute Liver Failure from 

Tumor Necrosis Factor-α Antagonists: Report of Four Cases 

and Literature Review. Dig Dis Sci. 2018;63(6):1654-1666. 

DOI:10.1007/s10620-018-5023-6. PMID: 29564668.

3. French JB, Bonacini M, Ghabril M, Foureau D, Bonkovsky HL. 

Hepatotoxicity Associated with the Use of Anti-TNF-α Agents. 

Drug Saf. 2016;39(3):199-208. DOI:10.1007/s40264-015-

0366-9. PMID: 26692395