Evidence map›Paper›PMID 42579907›Full record

ArticleClinics (Sao Paulo, Brazil)2026

Clinical and inflammatory factors associated with prevalent gout in a Brazilian hospital population.

Jordana Dinorá de Lima, Leonel Witcoski Junior, André Guilherme Portela de Paula, Andressa Pacheco Czaikovski, Bruna Sadae Yuasa, Gabriela Yanaze Takamatsu, Caio Cesar Souza Smanioto, Maria Clara da Cruz Silva, Ederson Borges Francisco, Juliana Navarro Ueda Yaochite and 10 more

Abstract read
In one paragraph

Article in Clinics (Sao Paulo, Brazil), 2026. 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

20 authors.

Jordana Dinorá de LimaMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil. Electronic address: jordanabioufpr@gmail.com.
Leonel Witcoski JuniorMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
André Guilherme Portela de PaulaMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Andressa Pacheco CzaikovskiMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Bruna Sadae YuasaMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Gabriela Yanaze TakamatsuMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Caio Cesar Souza SmaniotoMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Maria Clara da Cruz SilvaMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Ederson Borges FranciscoMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Juliana Navarro Ueda YaochiteMedical Microbiology Graduate Program, Universidade Federal do Ceara (UFC), Fortaleza, CE, Brazil.
Marco Antonio de Freitas ClementinoMedical Microbiology Graduate Program, Universidade Federal do Ceara (UFC), Fortaleza, CE, Brazil.
Felipe Fortino VerdanComplexo Hospital de Clínicas, Universidade Federal do Parana (UFPR/EBSERH), Curitiba, PR, Brazil.
Valéria VidalComplexo Hospital de Clínicas, Universidade Federal do Parana (UFPR/EBSERH), Curitiba, PR, Brazil.
Cyntia Nancy WeçoskiComplexo Hospital de Clínicas, Universidade Federal do Parana (UFPR/EBSERH), Curitiba, PR, Brazil.
Niels Olsen Saraiva CâmaraBiomedical Sciences Institute IV, Universidade de São Paulo (USP), São Paulo, SP, Brazil.
Fellype BarretoDepartment of Internal Medicine, Rheumatology Unit, Universidade Federal do Parana (UFPR/EBSERH), Curitiba, PR, Brazil.
Eduardo S PaivaDepartment of Internal Medicine, Rheumatology Unit, Universidade Federal do Parana (UFPR/EBSERH), Curitiba, PR, Brazil.
Valderílio Feijó AzevedoDepartment of Internal Medicine, Rheumatology Unit, Universidade Federal do Parana (UFPR/EBSERH), Curitiba, PR, Brazil.
Bianca de Oliveira Cata-PretaDepartment of Public Health, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil.
Tárcio Teodoro BragaMicrobiology, Parasitology and Pathology Graduate Program, Universidade Federal do Parana (UFPR), Curitiba, PR, Brazil; Biosciences and Biotechnology Graduate Program, Instituto Carlos Chagas (ICC/Fiocruz), Curitiba, PR, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGout is a rheumatological disease characterized by the crystallization of uric acid (UA) in joints and tissues, which is believed to trigger inflammatory responses. This study aimed to characterize the inflammatory profile of gout patients in a Brazilian population and its potential influence on flare frequency.

methodsIn this observational cross-sectional study, we analyzed 193 patients from the Complex of Clinics Hospital in Curitiba, Brazil, categorized into two groups: gout (n = 102) and non-gout (n = 91). Data were obtained through in-person surveys, consultation of medical records, and serum analyses. We evaluated anthropometric measurements, lifestyle habits, medication use, serum UA levels, and cytokine profiles.

resultsMales were more prevalent in the gout group than in the non-gout group (p < 0.001). The gout group also showed higher consumption of uricogenic foods, including ethanol (p = 0.006), sugary drinks (p = 0.001), meat and seafood (p < 0.001), and processed meats (p = 0.034). UA levels were not correlated with cytokine presence and were not effective in distinguishing patients with low or high flare frequency (OR = 1.07; p = 0.6; AUC = 0.522). IL-6 levels alone modestly differentiated flare frequency (OR = 0.99; p = 0.8; AUC = 0.788), with improved discrimination when combined with monocyte counts (OR = 0.84; p = 0.029; AUC = 0.801).

conclusionsIL-6, particularly when combined with monocyte count, may be worth considering as a potential marker of gout flare frequency, enabling earlier identification of high-risk patients and supporting targeted interventions to improve disease management and outcomes.

Indexed as

AlcoholBrazilian populationGout flareIL-6MonocyteSex factor

Identifiers

PMID42579907
PMCPMC13487591

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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.