PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “gout”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2024

Novel Genetic Loci in Early-Onset Gout Derived From Whole-Genome Sequencing of an Adolescent Gout Cohort.

OBJECTIVE: Mechanisms underlying the adolescent-onset and early-onset gout are unclear. This study aimed to discover variants associated with early-onset gout. METHODS: We conducted whole-genome sequencing in a discovery adolescent-onset gout cohort of 905 individuals (gout onset 12 to 19 years) to discover common and low-frequency single-nucleotide variants (SNVs) associated with gout. Candidate common SNVs were genotyped in an early-onset gout cohort of 2,834 individuals (gout onset &#x2264;30 years old), and meta-analysis was performed with the discovery and replication cohorts to identify loci associated with early-onset gout. Transcriptome and epigenomic analyses, quantitative real-time polymerase chain reaction and RNA sequencing in human peripheral blood leukocytes, and knock-down experiments in human THP-1 macrophage cells investigated the regulation and function of candidate gene RCOR1. RESULTS: In addition to ABCG2, a urate transporter previously linked to pediatric-onset and early-onset gout, we identified two novel loci (Pmeta < 5.0 &#xd7; 10-8): rs12887440 (RCOR1) and rs35213808 (FSTL5-MIR4454). Additionally, we found associations at ABCG2 and SLC22A12 that were driven by low-frequency SNVs. SNVs in RCOR1 were linked to elevated blood leukocyte messenger RNA levels. THP-1 macrophage culture studies revealed the potential of decreased RCOR1 to suppress gouty inflammation. CONCLUSION: This is the first comprehensive genetic characterization of adolescent-onset gout. The identified risk loci of early-onset gout mediate inflammatory responsiveness to crystals that could mediate gouty arthritis. This study will contribute to risk prediction and therapeutic interventions to prevent adolescent-onset gout.

Humans↗
PubMed2026

Gout and allopurinol adherence in newly diagnosed patients and the risk of fractures: a nationwide cohort study.

INTRODUCTION / OBJECTIVES: The association between gout and fractures remains controversial due to the competing effects of uric acid's antioxidant properties and gout-induced chronic inflammation. Our study aimed to evaluate the risk of fractures in newly diagnosed gout patients and to analyze the impact of Allopurinol medication adherence on this risk. METHODS: This nationwide cohort study utilized the National Health Insurance Service-National Health Screening Cohort (NHIS-HEALS) database (2002-2019). We identified 4,107 patients newly diagnosed with gout who remained on continuous allopurinol therapy during the 24-month medication assessment period and matched them 1:3 with 12,321 non-gout controls using propensity score matching. Allopurinol adherence was assessed via the Medication Possession Ratio (MPR) over a 24-month period and categorized into three groups: MPR&#x2009;<&#x2009;0.3, 0.3&#x2009;&#x2264;&#x2009;MPR&#x2009;<&#x2009;0.8, and MPR&#x2009;&#x2265;&#x2009;0.8. Multivariable Cox proportional hazards regression was used to calculate adjusted hazard ratios (aHR) and 95% confidence intervals (CI) for fractures (vertebral, hip, and distal radius). RESULTS: Gout patients demonstrated a significantly higher risk of overall fractures compared to the non-gout group (aHR 5.52; 95% CI 4.19-7.26). A significant inverse linear relationship was observed between allopurinol adherence and fracture risk (P for trend&#x2009;<&#x2009;.001). The risk was highest in the low-adherence group (MPR&#x2009;<&#x2009;0.3; aHR 5.91; 95% CI 4.40-7.93) and relatively lower in the high-adherence group (MPR&#x2009;&#x2265;&#x2009;0.8; aHR 4.77; 95% CI 2.94-7.72). Consistent trends were observed for vertebral (aHR 5.68) and hip (aHR 4.22) fractures. These associations remained consistent across all subgroups, including age, sex, and comorbidities. CONCLUSION: Newly diagnosed gout is associated with a substantially increased risk of fractures. Higher adherence to Allopurinol therapy is correlated with a significant reduction in this risk, suggesting that consistent urate-lowering therapy may mitigate gout-related bone fragility. Key Points &#x2022; Newly diagnosed gout patients have a significantly higher risk of major osteoporotic fractures compared to the non-gout population. &#x2022; A significant inverse linear relationship exists between Allopurinol adherence and fracture risk, with the highest adherence group (MPR &#x2265; 0.8) showing a relatively lower risk. &#x2022; Consistent urate-lowering therapy (ULT) may mitigate bone fragility in gout patients by reducing systemic inflammatory burden caused by urate crystal deposition.

Humans↗
PubMed2025

Metagenome-Based Characterization of the Gut Virome Signatures in Patients With Gout.

The gut microbiome has been implicated in the development of autoimmune diseases, including gout. However, the role of the gut virome in gout pathogenesis remains underexplored. We employed a reference-dependent virome approach to analyze fecal metagenomic data from 102 gout patients (77 in the discovery cohort and 25 in the validation cohort) and 86 healthy controls (HCs) (63 and 23 in each cohort). A subset of gout patients in the discovery cohort provided longitudinal samples at Weeks 2, 4, and 24. Our analysis revealed significant alterations in the gut virome of gout patients, including reduced viral richness and shifts in viral family composition. Notably, Siphoviridae, Myoviridae, and Podoviridae were depleted, while Quimbyviridae, Retroviridae, and Schitoviridae were enriched in gout patients. We identified 359 viral operational taxonomic units (vOTUs) associated with gout. Enriched vOTUs in gout patients predominantly consisted of Fusobacteriaceae, Bacteroidaceae, and Selenomonadaceae phages, while control-enriched vOTUs included Ruminococcaceae, Oscillospiraceae, and Enterobacteriaceae phages. Longitudinal analysis revealed that a substantial proportion of these virome signatures remained stable over 6 months. Functional profiling highlighted the enrichment of viral auxiliary metabolic genes, suggesting potential metabolic interactions between viruses and host bacteria. Notably, gut virome signatures effectively discriminated gout patients from HCs, with high classification performance in the validation cohort. This study provides the first comprehensive characterization of the gut virome in gout, revealing its potential role in disease pathogenesis and highlighting virome-based signatures as promising biomarkers for gout diagnosis and future therapeutic strategies.

Humans↗
PubMed1976

Occurrence of gout in Copenhagen males aged 40-59.

As part of a cardiovascular survey study on the relationships between physical fitness and coronary heart disease, 5249 Copenhagen males aged between 40 and 59 were interviewed to identify a history of gout. Subjects who had experienced attacks of painful swelling, with abrupt onset and remission in one to two weeks, diagnosed and treated as gout by their own physician, were regarded as having experienced gout. In an initial cross-sectional examination, 86 men fulfilled the criteria. At a one year follow-up examination it was discovered that 56 men had had gout during the year of observation. Among these 18 were new cases. At the end of the study a total of 104 men had experienced gout and these were compared, with respect to the continuously distributed variables, those 104 gout subjects were compared to 208 computer selected age-matched controls drawn at random from the entire sample. The gout cases were found to have higher relative weights, higher diastolic blood pressure and lower levels of physical fitness estimated by use of a bicycle ergometer test. Angina pectoris occurred more frequently among the gout cases than among controls. No significant differences in the occurrence of myocardial infarction, intermittent claudication or renal stones were found. The habits of smoking and coffee consumption were equal in gout cases and controls. Alcohol consumption and consumption of drugs were higher in gout cases than controls. Gout was the most frequent in the lowest social classes.

Adult↗
PubMed2026

The Progress of Gout Prediction Models Based on Multi-source Data.

INTRODUCTION: Gout, a highly serious inflammatory disease that is caused by monosodium urate crystals, is becoming an increasingly significant health concern. Artificial Intelligence and multi-omics-based research have made significant gains for the early detection and prevention of gout based on diverse approaches. This review intends to summarize current advances in forecasting gout susceptibility and gout-related symptoms, evaluate the predictive efficacy of different features, and ascertain which clinical and omics characteristics are most effective in these prediction models. METHODS: We explored the PubMed database after 2010 using keywords such as "gout", "predictive model", "risk prediction", and "machine learning", and confined our search to Englishlanguage articles. The original peer-reviewed research articles that developed gout models were selected. Research that was not original or lacked internal validation was excluded. RESULTS: Clinical features, genomics, microbiomics, radiomics, and metabolomics have been utilized to construct models related to gout and have demonstrated excellent predictive performance. Multisource data prediction models usually exhibit better effectiveness. DISCUSSION: Gout-oriented models performed excellently in predictive performance but present limitations in certain clinical and omics domains. However, if they are to affect actual patient care, they must overcome some external confirmation roadblocks and the fiscal and practical implications they will face ahead of time. CONCLUSION: This review indicates that clinical and multi-omics models of gout are significant instruments for clinical decision-making. The models constructed in these studies may be crucial for the treatment of gout and its practical benefits.

Gout↗
PubMed2026

Timing of OMERACT core domain measurement in gout clinical trials: a systematic review of randomised trials.

AIMS: The Outcome Measures in Rheumatology (OMERACT) initiative has endorsed core domain sets for gout trials. The aims of this study were to evaluate the time points and frequencies at which the gout core domains are measured in existing gout urate-lowering therapy and gout flare trials, and whether all collected measurements were reported. METHODS: Urate-lowering therapy (n = 29) and gout flare randomised clinical trials (n = 14) from 2005 were identified from a prior systematic review of core domain reporting. Data were extracted for the time points and frequencies at which each core domain was measured, as well as whether all collected measurements were reported. RESULTS: In urate-lowering therapy trials, the core domains were measured at seven different frequencies. Serum urate and gout flares were most commonly measured monthly, and tophus burden was most commonly measured three monthly. Reporting of all collected measurements varied, from 24/29 (83%) trials for serum urate to 0/2 (0%) trials for activity limitation. In gout flare trials, core domains were measured at nine different frequencies. Pain, joint tenderness and joint swelling were most commonly measured monthly. Reporting of all collected measurements varied, from 13/14 (93%) trials for pain to 3/8 (37.5%) trials for joint tenderness. CONCLUSION: In both urate-lowering therapy and gout flare trials, there is substantial variability in when the core domains are measured, and reporting of collected measurements is inconsistent. This work provides the foundation for a consensus process to establish standardised time points and frequencies for measuring the OMERACT-endorsed gout core domains.

Gout↗
PubMed2026

Investigating the causal role of smoking in gout: A triangulation approach combining NHANES data, genetic correlation, and Mendelian randomization.

The relationship between smoking and the development of gout is not well understood. To address this, we adopted a triangulation framework that integrates observational analysis, genetic correlation estimation, and two-sample Mendelian randomization (MR) to examine whether smoking confers a causal risk for gout. We first performed a cross-sectional analysis using information for 13,626 participants from the National Health and Nutrition Examination Survey between 2013 and 2018. The association of smoking with gout was subsequently assessed through logistic regression models. We next investigated the extent of shared genetic factors between smoking phenotypes and gout. We were able to demonstrate this using the linkage disequilibrium score regression applied to genome-wide association study data of European ancestry. Finally, to verify the causality of our relationship, we carried out a two-sample MR analysis. We selected the inverse-variance weighted (IVW) method and confirmed the consistency of using the IVW method with other statistical methods, including weighted median, weighted mode, and simple mode, as well as MR-Egger regression. We performed sensitivity analyses to investigate the heterogeneity of the hypothesis and stability of the data. Our findings based on National Health and Nutrition Examination Survey data reveal that there is a strong positive association between smoking and the risk of gout (odds ratio [OR]&#x2005;=&#x2005;1.94, 95% confidence interval [CI]&#x2005;=&#x2005;1.48-2.55, P&#x2005;<&#x2005;.001). This association persisted after confounding adjustments (OR&#x2005;=&#x2005;1.41, 95% CI&#x2005;=&#x2005;1.04-1.91, P&#x2005;=&#x2005;.027). In the subgroup analyses, former smokers and current smokers of 10 to 20 cigarettes per day had a substantially increased risk. Post-linkage disequilibrium score regression analysis revealed that the significantly positive genetic correlations of smoking initiation and lifetime smoking index with gout risk were both significantly positive. Additional evidence for causality is presented by MR. Genetic prediction of smoking initiation statistically increases gout risk (IVW OR&#x2005;=&#x2005;1.55, 95% CI&#x2005;=&#x2005;1.26-1.90, P&#x2005;=&#x2005;3.17&#x2005;&#xd7;&#x2005;10-5). A much stronger association is evident for lifetime smoking index (IVW OR&#x2005;=&#x2005;1.99, 95% CI&#x2005;=&#x2005;1.44-2.76, P&#x2005;=&#x2005;3.24&#x2005;&#xd7;&#x2005;10-5). These findings are the same with or without heterogeneity by sensitivity analysis. In light of our integrated analysis, smoking is a causative factor for gout. This suggests that public health interventions like anti-smoking campaigns might reduce gout incidence.

Humans↗
PubMed1976

[Needle biopsy in gout and pseudogout (author's transl)].

INTRODUCTION: Radiological and morphological findings in advanced arthritis urica and pyrophosphate arthropathy are well known. In contrast, the early changes of synovial membrane in these disturbances of metabolism pose diagnostic problems. With the assistance of various cytological techniques and polarizing microscopical as well as electron microscopical investigation it was examined to what extent needle biopsies can be helpful in the differential diagnosis of gout and pseudogout. MATERIAL AND METHODS: In 8 patients with gout and 11 patients with pseudogout synovial fluid and small tissue specimens could be obtained with the aid of the Parker-Pearson needle. Both fluid and tissue specimens were investigated light and electron microscopically. Cell counts were evaluated in a Rosenthal chamber. The differentiation of the cells in stained smears was done by counting 200-600 cells per case. Crystals were identified by polarizing microscopy in wet preparations of freshly aspirated synovial fluid. RESULTS: Polarizing microscopy of synovial fluid detected intra- as well as extracellular urate and pyrophosphate crystals. The wedge-shaped urate crystals and the larger partly polygonal pyrophosphate crystals showed different polarizing microscopical properties and a negative birefringence. The absolute cell counts in gout were higher than those in pseudogout. The relative cell counts of the different cell types in synovial fluid showed more variation in gout than in pseudogout. Cases with acute gout developed a relative leukocytosis in contrast to a relative lymphocytosis in chronic gout. A relative leukocytosis was constant in all patients with pseudogout. Sclerosed areas with scarce and plump villi as well as sometimes hyperplastic and polymorphous synovial cell layers could be demonstrated histologically in the tissue specimens of the needle biopsies in cases with gout. Urate crystals were less frequent in specimens fixed in formalin. The histological alterations in pseudogout were uniform, 2-4 rows of slightly pleomorphic synovial cells lined the inner surface of the joint capsule, sclerosing alterations were less frequent. Pyrophosphate crystals and calcified particles were seen within the synovial lining cells, the connective tissue and the enodthelial cells of the blood vessels in pseudogout specimens. Intra- as well as extracellular crystals could also be demonstrated with the aid of scanning electron microscopy in sediments of synovial fluid in gout and pseudogout. Transmission electron microscopical investigations of synovial tissue specimens detected proliferated and pleomorphic synovial lining cells in gout in contrast to a more monomorphic appearance of these cells in pseudogout. The crystals were washed out during the preparation techniques for transmission electron microscopy so that needle-like empty spaces resulted within cytoplasm of the phagocytic cells. These clefts were surrounded by phagosomal structures and densified cytoplasmic ground substance; sometimes they were also lined by membranes...

Aged↗
PubMed2026

Spatial scaling of metagenomic diversity reveals ecological disruption in the gut microbiome of gout patients.

Gout, a painful inflammatory arthritis, is characterized by hyperuricemia and monosodium urate crystal deposition, with growing evidence linking its pathogenesis to gut microbiome dysbiosis. However, traditional diversity metrics fail to capture the complex spatial organization of microbial communities. This study addresses this gap by applying the novel metagenomic Diversity-Area Relationship (m-DAR) model to investigate scaling laws in the gout microbiome-quantifying how metagenomic diversity changes with the number of individuals sampled. Our analysis of gut microbiomes from gout patients and healthy controls revealed fundamental ecological disruptions. We found that gout microbiomes exhibited significantly altered scaling patterns: they showed greater inter-individual dissimilarity (higher z-values) at the level of rare genes (q&#x2009;=&#x2009;0), but weaker scaling of dominant genes (q&#x2009;=&#x2009;1-3) compared to healthy controls. Crucially, the maximal accrual diversity (MAD) was substantially lower in gout patients, indicating a severely constrained potential for total microbial gene diversity. Furthermore, profiling of metagenomic functional gene clusters (MFGCs) uncovered widespread functional perturbations, including increased diversity scaling for carbohydrate-active enzymes (CAZy) but decreased scaling in essential metabolic pathways (KEGG, KO). These results demonstrate that the gout gut microbiome is defined by a loss of ecological structure, featuring reduced homogeneity in dominant taxa, expanded rare biosphere variation, and an overall collapsed diversity capacity. This work introduces an ecological framework for characterizing dysbiosis in gout that complements traditional diversity metrics and may inform the development of microbiome-based therapeutic strategies. Further research is needed to translate these ecological patterns into clinical applications.

Humans↗
PubMed1978

A prospective study of gout in New Zealand Maoris.

Results are reported from the first prospective study of gout in New Zealand Maoris based on a sample of 388 males and 378 females. At baseline, high mean levels of serum uric acid (SUA) were found, 0.422 +/- 0.092 mmol/1 (7.05 +/- 1.54 mg/100 ml) in males and 0.350 +/- 0.091 mmol/1 (5.85 +/- 1.52 mg/100 ml) in females. On the basis of traditional criteria (SUA above 0.42 mmol/1 (7.0 mg/100 ml) in males and above 0.36 mmol/1 (6.0 mg/100 ml) in females) the prevalence of hyperuricaemia was 49% in males and 42% in females. The baseline prevalence of gout (8.8% for males and 0.8% for females) and the subsequent 11-year incidence rates (10.3% for males and 4.3% for females) are discussed in relation to specified SUA classes. When traditional, sex-specific criteria for hyperuricaemia were used, no relationship was found between the prevalence of hyperuricaemia and the incidence of gout. There was, however, a sharp increase in the incidence rate of gout in both sexes when SUA levels were above 0.48 mmol/1 (8.0 mg/100 ml). In subjects with a baseline SUA above this level, the age-standardised 11-year incidence rate of gout was 29.1% for males and 37.2% for females. A previously unreported relationship linking muscle size to the incidence of gout in males is presented as a major finding of the study. Other risk factors associated with gout were body mass and blood pressure.

Adolescent↗
PubMed1977

Gout and hyperlipidaemia. Effect of overweight on the levels of circulating lipids.

A study of the serum lipids in 90 patients with gout and 90 controls matched for age and weight index demonstrated that in gout there was a significant elevation of the mean serum levels of cholesterol (282 +/- 55 mg/100 ml), triglycerides (183 +/- 161 mg/100 ml) and phospholipids (270 +/- 61 mg/100 ml) compared with the controls whose mean values were respectively 243 +/- 41 mg, 95 +/- 53 mg and 245 +/- 36 mg. Hyperlipidaemia of mixed type was the most common lipid defect in the patients with gout; there was no difference in the frequency of pure hypercholesterolaemia (without hypertriglyceridaemia) between gout and the controls. The frequency of anomalies of blood lipid levels in gout does not result from (or not solely from) obesity since patients with gout and controls were matched for their weight and height. There was a correlation between the serum lipid levels and obesity in the controls but this was not demonstrable in the patients with gout.

Adult↗
PubMed2026

Postoperative complications and outcomes after surgical treatment for tophaceous gout: A systematic review and meta-analysis.

BACKGROUND: Surgical treatment remains necessary for selected patients with tophaceous gout, particularly when mechanical limitation, nerve compression, ulceration, infection, deformity, or failure of conservative treatment is present. However, postoperative outcomes after surgery for tophaceous gout have not been comprehensively quantified. This systematic review and meta-analysis evaluated postoperative complication profiles and recurrence burden after surgical treatment for tophaceous gout. METHODS: A systematic search of PubMed, Embase, Web of Science, and the Cochrane Library was conducted from database inception to March 25, 2026. Original studies reporting postoperative outcomes after surgical treatment for tophaceous gout were included. Pooled event rates with 95% confidence intervals (CIs) were calculated using a random-effects single-arm meta-analytic approach. Primary outcomes were postoperative infection, delayed wound healing, and recurrence. Secondary outcomes were reoperation, amputation, and overall complications. Functional outcomes were summarized descriptively. RESULTS: 18 retrospective studies were included. The pooled postoperative infection rate was 11.3% (95% CI 8.0%-15.7%), delayed wound healing 9.9% (95% CI 5.1%-18.2%), and recurrence 8.5% (95% CI 4.7%-14.9%). Secondary pooled rates were 9.7% (95% CI 5.5%-16.7%) for reoperation, 3.7% (95% CI 2.0%-6.8%) for amputation, and 24.0% (95% CI 14.0%-38.1%) for overall complications. Significant subgroup differences were identified only for infection according to anatomic site and intervention type. Sensitivity analyses showed that pooled estimates were robust. The certainty of evidence was very low for all outcomes. CONCLUSIONS: Surgical treatment for tophaceous gout is associated with measurable postoperative risks, particularly infection and overall complications. These findings support careful perioperative counseling, structured postoperative surveillance, integrated long-term urate-lowering management, and more standardized reporting of perioperative risk factors and postoperative outcomes in future surgical studies of tophaceous gout.

Humans↗
PubMed2026

Causal determinants of gout in 614,000 adults: A two-sample Mendelian randomization study of dietary, lifestyle, and metabolic traits.

Gout affects over 55 million people worldwide, with prevalence projected to rise by 70% by 2050. Although observational studies have implicated several dietary, lifestyle, and metabolic risk factors, causal relationships remain uncertain because of confounding and reverse causation. Univariable and multivariable two-sample Mendelian randomization (MR) analyses were performed using genome-wide association data from 2 European cohorts: UK Biobank (6543 self-reported gout cases and 456,390 controls) and FinnGen (3576 cases and 147,221 controls). Genetic instruments for 12 exposures, including dried fruit, salad, and cheese intake; smoking initiation; physical activity; body mass index (BMI); and lipid traits, were derived from established genome-wide association study datasets. Inverse-variance weighted regression with multiplicative random effects was the primary analysis, complemented by weighted median, weighted mode, MR-Egger, MR-Pleiotropy RESidual Sum and Outlier, and 3 predefined multivariable models. Benjamini-Hochberg correction was applied across all 24 tests. BMI showed the strongest and most consistent causal effect on gout (FinnGen: odds ratio [OR]&#x2005;=&#x2005;1.97, 95% confidence interval [CI]&#x2005;=&#x2005;1.51-2.57; UK Biobank: OR&#x2005;=&#x2005;1.006, 95% CI&#x2005;=&#x2005;1.003-1.009; both P&#x2005;<&#x2005;.001) and remained significant in 5 of 6 multivariable models. Triglycerides increased risk in both cohorts (FinnGen: OR&#x2005;=&#x2005;1.34, 95% CI&#x2005;=&#x2005;1.08-1.66; UK Biobank: OR&#x2005;=&#x2005;1.008, 95% CI&#x2005;=&#x2005;1.004-1.012). These associations survived Benjamini-Hochberg correction, as did high-density lipoprotein cholesterol in UK Biobank (OR&#x2005;=&#x2005;0.997, 95% CI&#x2005;=&#x2005;0.994-0.999). Dried fruit intake was inversely associated with gout in FinnGen (OR&#x2005;=&#x2005;0.34, 95% CI&#x2005;=&#x2005;0.13-0.92, P&#x2005;=&#x2005;.034) but not in UK Biobank, and did not survive correction for multiple testing. No other exposure reached significance in either cohort. This study provides genetic evidence that BMI is the dominant modifiable causal determinant of gout, with triglycerides contributing independently. Dietary associations were weaker and did not withstand correction for multiple testing, and should be regarded as hypothesis-generating. These findings support prioritizing weight management and metabolic health in gout prevention.

Gout↗
PubMed1979

Coexistent gout and rheumatoid arthritis. Case report and literature review.

A 73-year-old woman with Felty's syndrome and arthritis mutilans of long duration presented with tophaceous gout. The 7 previously reported cases of coexistent gout and rheumatoid arthritis (RA) are critically reviewed. Possible explanations for the rare coexistence of RA and gout are discussed: if uric acid is an inhibitor of the immune response, then hyperuricemia and gout could protect against development of RA. Conversely, crystalline protein binding may be a critical factor in the pathogenesis of gout, and the presence of abnormal proteins in RA could protect against gout.

Aged↗