Carlos Pineda

Background: Hyperuricemia and gout are closely associated with alterations in gut microbiota function. Short-chain fatty acids (SCFAs) produced by intestinal microorganisms may modulate immune responses and inflammation relevant to gout pathophysiology. This study evaluated fecal SCFA concentrations, their associations with dietary purine intake, and the relationship between Akkermansia spp. and Prevotella spp. abundance and fecal SCFA profiles across the clinical spectrum of hyperuricemia. Methods: This cross-sectional study included 380 Mexican adults: normouricemic controls (n = 141), individuals with asymptomatic hyperuricemia (AH; n = 98), and patients with gout (n = 141). Fecal SCFAs were quantified by GC-FID and bacterial abundance by qPCR. Dietary intake was assessed by semi-quantitative food frequency questionnaire and classified by purine content. Between-group differences were evaluated by the Kruskal–Wallis test (Benjamini–Hochberg correction); multivariable linear regression adjusted for age, sex, and BMI was used to assess associations, including a pre-specified dietary purine intake per clinical group interaction term. Results: Fecal acetate and propionate were significantly higher in gout patients than controls, whereas AH individuals had significantly higher butyrate. Moderate-purine food intake showed opposing associations with fecal acetate in controls (β = +3.61, p = 0.019) and gout patients (β = −4.59, p = 0.036), with a significant interaction (p = 0.004). Exploratory analyses revealed a positive association between Prevotella spp. abundance and fecal acetate exclusively in the gout group (β = 0.085, p = 0.020). Conclusion: These findings suggest distinct fecal SCFA profiles across stages of urate-related disease, with a disease-specific gut metabolic response to dietary purine intake potentially contributing to the inflammatory environment of established gout. Longitudinal studies with whole-microbiome profiling are needed to establish causality.

Takayasu arteritis (TA) is a chronic, immune-mediated vasculitis that primarily affects the large arteries, particularly the aorta and its main branches, leading to stenosis, occlusion, dilation, or aneurysms. Traditional imaging modalities, including computed tomography angiography (CTA), magnetic resonance angiography (MRA), and positron emission tomography/computed tomography (PET-CT), offer valuable diagnostic information; however, their clinical applicability has limitations, including high costs, radiation exposure, and reduced availability. In recent years, contrast-enhanced ultrasound (CEUS) has emerged as a minimally invasive, radiation-free technique capable of detecting vascular wall neovascularization as a potential surrogate imaging marker of TA inflammatory activity. Objective: This scoping review, conducted in accordance with the Joanna Briggs Institute (JBI) methodology and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) checklist, aims to synthesize current evidence on the diagnostic and monitoring utility of CEUS in patients with TA and carotid involvement. Methods: We systematically searched MEDLINE/PubMed, Scopus, Web of Science, LILACS and EBSCO from inception to May 2025 for original studies of adult patients with TA in whom CEUS was used to assess disease activity. Results: Eighteen studies (8 cross-sectional, 3 cohort, 7 case reports; 631 patients) met the eligibility criteria. Across these studies, CEUS detected arterial wall neovascularization compatible with active inflammation, particularly in the carotid arteries, and demonstrated moderate-to-strong correlations with inflammatory biomarkers, PET-CT findings, and clinical activity scores such as the Indian Takayasu Activity Score (ITAS) and the National Institutes of Health (NIH) criteria. Importantly, CEUS can reveal subclinical or residual inflammation even when clinical symptoms or laboratory markers are absent. Its ability to detect early relapses and monitor therapeutic response has been demonstrated in both observational cohorts and individual case reports. Despite this, substantial heterogeneity in imaging protocols and activity definitions limits comparability across studies and restricts integration into clinical practice. Conclusion: CEUS is a minimally invasive, reproducible, and effective technique for both detecting and monitoring disease activity in TA with carotid vessel involvement, thereby facilitating early and accurate therapeutic decisions. Its future incorporation into clinical practice will require validated scoring systems, harmonized acquisition protocols, and demonstration of added value in treatment decision-making and long-term outcomes.

» Dual mobility cup (DMC) implants reduce dislocation rates in both primary and revision total hip arthroplasty (THA), particularly in high-risk patients with neuromuscular disorders, cognitive impairment, or obesity. » The dual articulation mechanism enhances joint stability by increasing jump distance and the head-to-neck ratio, without compromising range of motion. » Incorporation of highly cross-linked polyethylene and vitamin E–infused liners improves wear resistance, supporting broader use in younger, more active patients. » Long-term survivorship of modern DMCs is comparable or superior to fixed-bearing implants, with a lower revision burden and durable fixation when appropriately selected and implanted. » Systemic metal ion levels remain low in well-functioning modular DMCs, though continued monitoring is recommended in younger patients and those with reproductive potential.

The human gut microbiota plays a critical role in maintaining immune homeostasis and modulating inflammatory processes. The review article by Maciel-Fiuza et al.(2023) entitled "Role of Gut Microbiota in Infectious and Inflammatory Diseases"(1) provides a valuable overview of the current knowledge in this field, with a focus on autoimmune and infectious diseases. While the article presents a broad and detailed analysis, we noticed that gout, one of the most common forms of inflammatory arthritis, was not discussed. Given the growing body of evidence linking the gut microbiota to gout pathogenesis, we believe its inclusion could further enhance the review and provide a more complete overview on microbiotaassociated inflammatory diseases.Gout is preceded by a prolonged period of hyperuricemia, which triggers the formation and deposition of monosodium urate (MSU) crystals in joints and soft tissues. TheseMSU crystals elicit a potent acute inflammatory response that, over time, leadsleading to chronic joint damage. Gout affects millions of individuals worldwide, and is associated with a significant morbidity (12). Despite its high prevalence, it is often frequently underrepresented in discussions concerning inflammatory diseases related to the microbiome.A central component of the inflammatory cascade during gout attacks is the NLRP3 inflammasome, which senses MSU crystals through its LRR domain.NLRP3 inflammasome activation, initiatesing the production of the proinflammatory cytokine IL-1β. The ultimate result of this cascade is and ultimately promoting neutrophil recruitment and the formation of neutrophil extracellular traps (NETs). This process ; all of which results in joint damage (32,43).Beyond innate immunity, adaptive responses involving T helper 17 (Th17) and regulatory T cells (Tregs) are also implicated in the disease. Th17 cells contribute to sustained inflammation through IL-17 production. On the other hand, , whereas Tregs serve to counteract this effect and maintain immune tolerance. An imbalance between these cell types has been associated with exacerbated inflammation in gout (54). Notably, microbial-derived metabolites such as acetate short-chain fatty acids (SCFAs) modulate the immune system. Of these SCFAs, acetate have been shown to promote the differentiation of naïve T cells into Th17 cells. This effect involves suppression of histone deacetylases and modulation of the mTOR-S6K pathway (Figure 1). Al together,, thereby potentially amplifying inflammatory responses (56) (Figure 1).In addition, short-chain fatty acid (SCFA)-sensing receptors such as GPR43 (FFAR2) and GPR41 (FFAR3), presentexpressed on neutrophils and macrophages, have emerged as important modulators of the inflammatory response (76). The recognition of microbiota-derived SCFA, particularly, by GPR43 may trigger acute inflammatory arthritis by promoting IL-1β maturation and release through NLRP3 inflammasome activation in macrophage lineage cells (87).Recent research has highlightedEmerging evidence demonstrated how the gut microbiota may influence both urate metabolism but and the immunometabolic pathways involved in gout (98,910). E xtensive evidence suggests that certain bacteria have developed adaptive mechanisms for purine biosynthesis and salvage, potentially altering systemic urate levels. Additionally, microbial metabolites from the gut microbiota may reach the liver via the portal vein, promoting the synthesis of purinogenic amino acids and urate (11). Notably, fecal microbiota transplants from hyperuricemic (HUA) rats towards germ-free recipients have been shown to increase serum urate levels (12).While most early studies focused on the role of the microbiota in urate metabolism, there is now growing evidence that it also plays a crucial role in modulating the inflammatory response in gout. In a paradigm-shifting study, Vieira et al. (103) demonstrated that germ-free mice had an impaired inflammatory response to MSU crystals, which and that it was reversed by introducing acetate. This was the first study to highlight the essential role of the gut microbiota in regulating immune responses in gout. Furthermore, it pointed to acetate and it receptor GPR43 as key factors in the development and severity of gout attacks (130).Studies in in several populations have demonstrated the presence of gut dysbiosis in gout patients, supported by reduced Building on this, Martínez-Nava GA and colleagues investigated the gut microbiota composition and functionality in patients with gout. Their first study identified microbial dysbiosisα diversity measures, such as Chao1 and Abundance-base coverage estimator (ACE) indices (14,15). This dysbiosis is characterized by reduced beneficial taxa (e.g. Faecalibacterium, Ruminococcus) and increased pro-inflammatory genera in gout patients (e.g. Prevotella and Bacteroides) (910). Moreover, Iin a follow-up metatranscriptomic analysis, Martínez-Nava and colleagues they identifiedfound that at least three orthologues genes (K00161, K00162 and K01621) involved in pathways related to acetate production pathways that were differentially expressed in the gut microbiota of gout patients compared in comparison to normouricemic and asymptomatic hyperuricemic individuals (116).Together, these findings suggest that the gut microbiota not only shapes host immunity but also participates in key metabolic and inflammatory processes relevant to gout pathophysiology. This highlights its potential as a therapeutic target in the management of gout.The influence of the gut microbiota on systemic immunity has become a focal point in the understanding of chronic inflammatory diseases. While Maciel-Fiuza et al.(1) address conditions such as rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus, the omission of gout overlooks a critical intersection of metabolic and inflammatory pathology. Like rheumatoid arthritis, gout is...

Objective: Conventional radiography (CR) and ultrasound (US) are used interchangeably for identification of calcium pyrophosphate deposition (CPPD). The aim of this study was to assess whether combining US and CR offers greater accuracy over either modality alone for the identification of CPPD.Methods: Consecutive patients scheduled for knee replacement surgery for osteoarthritis were enrolled. Before surgery, patients underwent CR and US of the knee. Menisci and hyaline cartilage were collected and analyzed using polarized light microscopy to confirm the presence of CPPD (gold standard). CR and US were assessed for absence/presence of CPPD by expert radiologists and sonographers. Diagnostic performance statistics were calculated. Poisson models with robust variance estimators were used to determine the likelihood of identifying CPPD.Results: Fifty-one patients (63% female, mean age 71.4 [SD 8] years) were enrolled. US demonstrated higher overall accuracy than CR for CPPD identification (0.78 vs 0.73). Sequential use of both modalities provided an advantage when only 1 knee site was positive in 1 of the 2 techniques; however, when 2 or 3 sites were positive, no additional advantage was observed. When US was negative, subsequent CR did not improve CPPD detection, but in cases of a negative CR, a positive US increased the likelihood of CPPD by 4.21 times, whereas a negative US substantially reduced the probability of CPPD, increasing the likelihood of its absence by 76%.Conclusion: US was more accurate than CR for identification of CPPD. Performing both exams can be an added value for CPPD identification only in a few specific cases.

Osteoarthritis (OA) is a prevalent condition with significant clinical and epidemiological consequences, requiring a multidisciplinary approach. One potential solution is the establishment of specialized, comprehensive healthcare centers to address OA effectively. A previous initiative focused on the development of Centers of Excellence (CoEs) for rheumatoid arthritis (RA), and endorsed by the Pan American League of Associations for Rheumatology (PANLAR), aimed to establish CoEs for select rheumatic conditions, providing a framework for their accreditation.