Evidence map›Paper›PMID 31707543›Full record

ArticleClinical rheumatology2020

Anti-adalimumab antibodies kinetics: an early guide for juvenile idiopathic arthritis (JIA) switching.

Juliana Barbosa Brunelli, Clovis Almeida Silva, Sandra Gofinet Pasoto, Carla Gonçalves Schahin Saa, Katia Tomie Kozu, Claudia Goldenstein-Schainberg, Elaine Pires Leon, Margarete B G Vendramini, Nicole Fontoura, Eloisa Bonfa and 1 more

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In one paragraph

Article in Clinical rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 20% of its field
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Juliana Barbosa BrunelliPediatric Rheumatology Unit, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Clovis Almeida SilvaPediatric Rheumatology Unit, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Sandra Gofinet PasotoDivision of Rheumatology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, 3rd floor, room 3190 - Cerqueira Cesar, São Paulo, SP, 05403010, Brazil.
Carla Gonçalves Schahin SaaDivision of Rheumatology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, 3rd floor, room 3190 - Cerqueira Cesar, São Paulo, SP, 05403010, Brazil.
Katia Tomie KozuPediatric Rheumatology Unit, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Claudia Goldenstein-SchainbergDivision of Rheumatology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, 3rd floor, room 3190 - Cerqueira Cesar, São Paulo, SP, 05403010, Brazil.
Elaine Pires LeonDivision of Rheumatology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, 3rd floor, room 3190 - Cerqueira Cesar, São Paulo, SP, 05403010, Brazil.
Margarete B G VendraminiDivision of Rheumatology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, 3rd floor, room 3190 - Cerqueira Cesar, São Paulo, SP, 05403010, Brazil.
Nicole FontouraDivision of Rheumatology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, 3rd floor, room 3190 - Cerqueira Cesar, São Paulo, SP, 05403010, Brazil.
Eloisa BonfaDivision of Rheumatology, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Av. Dr. Arnaldo, 455, 3rd floor, room 3190 - Cerqueira Cesar, São Paulo, SP, 05403010, Brazil.
Nádia Emi AikawaPediatric Rheumatology Unit, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, São Paulo, SP, Brazil. nadia.aikawa@gmail.com.ORCID http://orcid.org/0000-0002-7585-4348
Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BR

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 303422/2015-7Conselho Nacional de Desenvolvimento Científico e Tecnológico 305068/2014-8Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/03756-4
6 · The paper itself

Abstract

objectiveTo assess the longitudinal production of anti-adalimumab antibody (AAA) and baseline risk factors for this antibody development in juvenile idiopathic arthritis (JIA) patients initiating adalimumab (ADA).

methodThirty consecutive JIA patients under ADA therapy were prospectively followed. JIA clinical/laboratorial/treatment data and sera for ADA and AAA assays (ELISA and bridging ELISA) were obtained at baseline (BL), 2 months (2M), 3 months (3M), 6 months (6M), 12 months (12M), and 24 months (24M). Patients with therapy failure requiring ADA withdrawn had their sera evaluated at their last medical visit prior to biologic switch (blinded to ADA and AAA levels).

resultsAAA was absent at BL, first detected at 2M after ADA initiation in 2/30 (7%) patients with a significant increase at 3M (10/29 (34%), p = 0.013) and no major change in 6M (11/30 (37%)) and 12M (9/26 (35%)). Of note, at 3M, AAA levels correlated negatively with ADA levels (r = - 0.781, p = 0.0001). Analysis of BL predictors revealed a significantly higher risk of developing AAA in patients with female gender (OR 21; 95% CI 1.08-406.57; p = 0.044), ESR > 30 mm/1st hour (OR 5.44; 95% CI 1.04-28.53; p = 0.045), and leflunomide use (OR 9.33; 95% CI 1.51-57.66; p = 0.016). In contrast, concomitant use of methotrexate was protective for AAA appearance (OR 0.08; 95% CI 0.01-0.53; p = 0.009). After 12M of ADA, 60% of AAA-positive patients required drug switch for drug failure compared with 15% in AAA-negative group (p = 0.03).

conclusionsThis study provides novel evidence of AAA production kinetics demonstrating a timely significant increase starting at 3M and stable throughout 24M. We also identified female gender, increased ESR, and leflunomide use as relevant risk factors for AAA production at BL, whereas methotrexate was protective. Early systematic monitoring of AAA at 3M may, therefore, guide drug switching in these patients.Key Points• Anti-adalimumab antibodies (AAA) production kinetics demonstrated a timely significant increase starting at 3M in juvenile idiopathic arthritis (JIA) patients under adalimumab therapy• Female gender, increased ESR, and leflunomide use were identified as relevant risk factors for AAA production in JIA, whereas methotrexate was protective.

Indexed as

Drug SubstitutionAdalimumabAdolescentAdultAntibodiesAntibody FormationAntirheumatic AgentsArthritis, JuvenileBlood SedimentationChildChild, PreschoolDrug Therapy, CombinationFemaleHumansKineticsLeflunomideAdalimumabAntibodiesAntirheumatic AgentsLeflunomideMethotrexateTumor Necrosis Factor InhibitorsAdalimumabAnti-adalimumab antibodyImmunogenicityJuvenile idiopathic arthritis

Identifiers

PMID31707543
OpenAlexW2985758722

What OpenQuestion holds

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Registered trials

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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.