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Introduction: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting multiple systems and classified under connective tissue disorders. Ocular involvement occurs in up to 30% of SLE cases, with the cornea being particularly susceptible to thinning due to immune-complex deposits and its predominantly type I collagen composition. This corneal thinning is clinically significant in glaucoma, where patients with reduced central corneal thickness (CCT) may have up to a threefold increased risk of developing glaucoma, as well as in refractive surgery. However, existing studies on CCT in SLE are limited and marked by substantial heterogeneity in methodology, technology, criteria, and participant numbers, resulting in conflicting findings. Based in our hypothesis that SLE-related corneal lysis may result in decreased CCT, this study aims to determine and compare the mean CCT values between SLE patients and healthy controls to obtain a more precise understanding of the potential relationship., Methods and Analysis: A cross-sectional observational study will be conducted, enrolling SLE patients and age-and sex-matched healthy controls recruited from ophthalmology consultations. Exclusion criteria will be applied to rule out other corneal thinning risk factors. A pilot study estimated a minimum sample size of 34 participants per group. CCT measurements will be obtained using Zeiss HD Cirrus 5,000 optical coherence tomography (OCT) on a randomly selected eye, following concordance analysis using the Kappa index. Statistical analysis will include descriptive, bivariate, and multivariate methods. The study protocol was approved by the ethics committee., Discussion: The cornea's vulnerability to thinning and lysis in SLE, which impacts CCT, is crucial for the accurate assessment of glaucoma, the leading cause of irreversible blindness worldwide and the second leading cause in Europe. Given that patients with reduced CCT are at a significantly higher risk of developing glaucoma, further research is necessary to understand the association between SLE and CCT. Our study aims to enhance methodological rigor compared to prior research by determining an appropriate sample size and exclusively enrolling SLE patients to increase participant homogeneity. If a significant difference in CCT between groups and an association between CCT and SLE are found, a prospective study will be considered., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Saldaña-Garrido, Cantó-Cerdán, Gil-Guillén, Alfaro-Beltrá and Sivera.)

Objective: The study objective was to examine the disease, demographic, and imaging features associated with different inflammatory phenotypes of calcium pyrophosphate deposition (CPPD) disease, ie, recurrent acute calcium pyrophosphate (CPP) crystal arthritis, chronic CPP crystal inflammatory arthritis, and crowned dens syndrome (CDS)., Methods: Data from an international cohort (assembled from 25 sites in 7 countries for the development and validation of the 2023 CPPD classification criteria from the American College of Rheumatology/EULAR) that met the criteria were included. Three cross-sectional studies were conducted to determine the phenotypic characteristics of recurrent acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis, and CDS. Multivariable logistic regression analysis was used to calculate adjusted odds ratio (aOR) and 95% confidence interval (CI) to examine the association between potential risk factors and the inflammatory phenotype., Results: Among the 618 people included (56% female; mean age [standard deviation] 74.0 [11.9] years), 602 (97.4%) had experienced acute CPP crystal arthritis, 332 (53.7%) had recurrent acute arthritis, 158 (25.6%) had persistent inflammatory arthritis, and 45 (7.3%) had had CDS. Recurrent acute CPP crystal arthritis associated with longer disease duration (aOR 2.88 [95% CI 2.00-4.14]). Chronic CPP crystal inflammatory arthritis was associated with acute wrist arthritis (aOR 2.92 [95% CI 1.81-4.73]), metacarpophalangeal joint osteoarthritis (aOR 1.87 [95% CI 1.17-2.97]), and scapho-trapezo-trapezoid (STT) joint osteoarthritis (aOR 1.83 [95% CI 1.15-2.91]), and it was negatively associated with either metabolic or familial risk for CPPD (aOR 0.60 [95% CI 0.37-0.96]). CDS was associated with male sex (aOR 2.35 [95% CI 1.21-4.59]), STT joint osteoarthritis (aOR 2.71 [95% CI 1.22-6.05]), and more joints affected with chondrocalcinosis (aOR 1.46 [95% CI 1.15-1.85])., Conclusion: CPPD disease encompasses acute and chronic inflammatory phenotypes, each with specific clinical and imaging features that need to be considered in the diagnostic workup., (© 2024 The Author(s). Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.)

Crystallization of monosodium urate monohydrate (MSU) leads to painful gouty arthritis. Despite extensive research it is still unknown how this pathological biomineralization occurs, which hampers its prevention. Here we show how inflammatory MSU crystals form after a non-inflammatory amorphous precursor (AMSU) that nucleates heterogeneously on collagen fibrils from damaged articular cartilage of gout patients. This non-classical crystallization route imprints a nanogranular structure to biogenic acicular MSU crystals, which have smaller unit cell volume, lower microstrain, and higher crystallinity than synthetic MSU. These distinctive biosignatures are consistent with the template-promoted crystallization of biotic MSU crystals after AMSU at low supersaturation, and their slow growth over long periods of time (possibly years) in hyperuricemic gout patients. Our results help to better understand gout pathophysiology, underline the role of cartilage damage in promoting MSU crystallization, and suggest that there is a time-window to treat potential gouty patients before a critical amount of MSU has slowly formed as to trigger a gout flare., (© 2024. The Author(s).)