Evidence map›Paper›PMID 40993500›Full record

ArticleJournal of ophthalmic inflammation and infection2025

Characteristics of patients who developed transient anti-adalimumab antibodies.

Osama Elaraby, Dalia El Feky, Cigdem Yasar, Woong-Sun Yoo, Anadi Khatri, Dalia Abd Elmegid, Jia-Horung Hung, Battuya Ganbold, Zheng Xian Thng, Negin Yavari and 12 more

Abstract read
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In one paragraph

Article in Journal of ophthalmic inflammation and infection, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Osama ElarabyDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Dalia El FekyDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Cigdem YasarDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Woong-Sun YooDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Anadi KhatriDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Dalia Abd ElmegidDepartment of Public Health and Community Medicine, Tanta University, Tanta, Egypt.
Jia-Horung HungDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Battuya GanboldDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Zheng Xian ThngDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Negin YavariDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Aim-On SaengsirinavinDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Ngoc Trong Tuong ThanDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Frances Andrea AnoverDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Abdelrahman M HamoudaDepartment of Neurological Surgery, Mayo Clinic, Rochester, MN, USA.
S Saeed MohammadiDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Irmak KaracaDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Amir AkhavanrezayatDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Anh Tram Ngoc TranDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Jingli GuoDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Yue BaiDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Quan Dong NguyenDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA.
Christopher OrDepartment of Ophthalmology, Byers Eye Institute, Stanford University, 2452 Watson Court, Suite 200, Palo Alto, CA, 94303, USA. chrisor@stanford.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdalimumab is a monoclonal antibody approved for the treatment of autoimmune diseases and non-infectious uveitis (NIU). It targets tumor necrosis factor alpha, a key mediator in inflammation. However, the development of anti-adalimumab antibodies (AAA) can reduce therapeutic efficacy and prompt treatment modifications. This study aimed to describe the clinical characteristics of patients with transient AAA and compare them to patients with persistent AAA, testing whether serum antibody and drug levels differ between groups. MAIN BODY: We conducted a retrospective cohort study using the Stanford Research Repository (STARR) to identify patients treated with adalimumab for autoimmune conditions between June 2006 and May 2024 who developed AAA. Patients whose AAA became undetectable on follow-up testing were compared to an age-, sex-, and disease-matched cohort with persistent AAA. Demographics, diagnoses, treatment details, serum adalimumab and AAA levels, and concomitant immunomodulatory therapy (IMT) were analyzed. Among 190 AAA-positive patients, 18 (9.47%) demonstrated antibody resolution over a median follow-up of 6.5 months. These patients had lower median AAA levels (39.55 ng/mL vs. 92.35 ng/mL, p=0.020) and higher adalimumab levels (6.25 μg/mL vs. 1.55 μg/mL, p=0.018) than controls. AAA resolution was negatively correlated with AAA levels (p=0.018) and positively correlated with adalimumab levels (p=0.016).

conclusionsTherapeutic monitoring of AAA and drug levels may help guide personalized therapeutic strategies and support continued treatment in selected patients.

Indexed as

AdalimumabAnti-adalimumab antibodiesCrohn’s diseaseRheumatoid arthritisUveitis

Identifiers

PMID40993500
PMCPMC12460866

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.