Search Results (84)

Background and Objectives: The nomenclature of calcium pyrophosphate deposition (CPPD) disease remains confusing, with different labels used interchangeably to describe the disease. Although ‘CPPD disease’ is the term that has been recommended by EULAR since 2011, ‘pseudogout’ remains the most frequently used label in the medical literature. This study aimed to investigate how the labels ‘CPPD disease’ versus ‘pseudogout’ affect the public’s perceptions of the illness. Methods: In this randomized controlled single-blind study, 200 members of the public watched a 2 min video describing a form of arthritis labeled as either ‘CPPD disease’ or ‘pseudogout’. Participants then completed a questionnaire assessing their perceptions of the illness using the Brief Illness Perception Questionnaire (BIPQ), with additional questions about their perceived seriousness of the illness and embarrassment associated with it, and beliefs about causes and management strategies. The primary outcome was the level of embarrassment associated with the illness. Results: Overall, embarrassment scores were low with no significant difference between the ‘CPPD disease’ and ‘pseudogout’ groups. Participants in both groups viewed the illness as being serious. There were no differences between the groups in their responses to the BIPQ, nor in their beliefs on the likely causes and management strategies. Even after a video intervention, participants’ understanding of the illness remained low. Conclusions: The labels ‘CPPD disease’ and ‘pseudogout’ do not differentially influence perceptions about the illness among members of the public. This could be due to the lack of knowledge about CPPD disease, highlighting the need to increase public awareness of this important condition. Full article

Humans and other great apes are unique among animals in lacking functional uricase, an enzyme that breaks down urate and allows its excretion. Modern-day humans have elevated serum urate, which is associated with various chronic health issues, including gout, metabolic syndrome, and hypertension. This prompts the question: what is the evolutionary benefit of the loss of uricase function, given that it may confer an increased risk of these chronic diseases? In this review, we explore numerous possible advantages, including some less commonly discussed, such as urate’s function as an antioxidant, its roles in ancestral survival, and its metabolic role in the context of our evolutionary history and the environmental pressures that have shaped human biology. We go on to examine the tradeoffs of urate’s evolutionary advantages, and how these features may be a double-edged sword for our health in our modern environment characterized by a caloric abundance of key nutrients, such as fructose, which are intimately linked with urate production and/or metabolism. Moving forward, we suggest that future work should explore the role of our evolutionary history in the rising prevalence of gout and other modern-day metabolic diseases. We further recommend that drugs and therapeutic strategies for diseases such as gout be informed by an understanding of the rich evolutionary context from which these maladies emerged and the unifying role of serum urate across these disease states. Full article

Gout is one of the most common inflammatory arthritides worldwide, and its burden is rising in Southeast Asia alongside rapid demographic and socioeconomic transitions. This region, characterized by diverse healthcare systems, cultural practices, and levels of economic development, presents a unique context in which the epidemiology and management of gout are evolving. Despite the availability of effective urate-lowering therapy (ULT) and well-established treat-to-target (T2T) strategies, real-world outcomes remain suboptimal. Barriers to optimal gout care operate at multiple levels. Physician-related factors include clinical inertia and limited awareness of evidence-based recommendations. Patient-related factors include limited understanding of gout and its treatment, compounded by socioeconomic disadvantages. System-level challenges include inequitable access to healthcare services, limited health insurance coverage, and resource-strained health systems. The current evidence base in Southeast Asia remains limited and heterogeneous, raising uncertainty regarding the applicability of global data to local populations. Nevertheless, emerging studies suggest that multidisciplinary, context-oriented approaches can improve gout outcomes. The objective of this review is to explore the evolving epidemiological landscape and barriers to gout management in Southeast Asia. Full article

Gout is a systemic metabolic inflammatory disease driven by hyperuricemia and monosodium urate crystal deposition, and is frequently accompanied by chronic kidney disease and uric acid nephrolithiasis. Current evidence indicates that acidic urine, hypocitraturia, and insufficient ammonium excretion are common in gout patients, and may be associated with insulin resistance, impaired renal ammoniagenesis, and abnormalities in tubular acid-base regulation. Persistent urinary acidification may contribute to the development and progression of uric acid stone formation and gout-related renal injury by reducing uric acid solubility, promoting crystal formation and intratubular deposition, and decreasing renal uric acid clearance. Urinary alkalization therapy can increase urine pH, thereby enhancing uric acid solubility and excretion, and has shown potential in some studies to improve serum urate levels, proteinuria, renal function parameters, and gout flare frequency, especially when using citrate-based alkali. However, the currently available evidence is mainly derived from observational studies and small prospective investigations, and recommendations across international guidelines remain inconsistent. High-quality evidence is still lacking regarding the optimal target population, urine pH range, choice of alkalizing agents, monitoring strategies, and long-term efficacy. Well-designed prospective studies are therefore needed to clarify the clinical role of urinary alkalization in renal protection among patients with gout. Full article

Background and Objectives: Despite evidence demonstrating the advantages of rheumatology-led point-of-care (POC) polarised light microscopy (PLM), it remains underutilised in many hospital settings. We aimed to identify barriers to its use and assess typical caseloads of crystal arthropathy, diagnostic methods and frequency of rheumatology-led POC PLM in practice in Ireland. We also assessed reliance on laboratory-led crystal analysis and the turnaround time for results to be reported. Solutions to improve implementation of rheumatologist-led POC PLM were also explored. Material and Methods: We surveyed 29 rheumatologists registered to the Irish Society of Rheumatology via SurveyMonkey, between May and October 2024. Textual responses were categorised into key themes, and word clouds were generated using Tagcrowd to visualise thematic content. Results: Fifty-five percent of respondents faced challenges using POC PLM for crystal analysis. Common barriers included lack of access to a microscope, lack of a polarising light function and lack of training in performing and interpreting of PLM. Fifty-two percent of rheumatologists highlighted the critical need for accessible and functional microscopes. Ninety-two percent of respondents relied on in-house laboratory crystal analysis. Thirty-two percent received inaccurate or incomplete results from laboratory reports and 28% of respondents reported delays in sample analysis from the laboratory. Laboratory turnaround was 1–2 days for 43% of rheumatologists and 3–5 days for 33%. Sixty-nine percent had not received training on PLM and 48% emphasised the need for improved education on POC PLM, including improved integration into the national rheumatology training. Conclusions: Rheumatology-led POC PLM remains underutilised despite its clinical advantage primarily due to equipment and training deficits. Addressing these barriers through improved infrastructure, education and equipment is essential to ensure effective and timely care for patients with crystal arthropathy. Full article

Calcific tendinitis (CT) is a condition that most commonly affects the rotator cuff tendons of the shoulder joint. Fundamental crystal morphology and composition underlying different radiological stages of CT remained insufficiently characterized. We collected human tendon samples from 33 patients with CT and 12 control patients. CT patients exhibited an increased incidence of comorbidities, especially high blood pressure and disorders of fat metabolism. Based on the Gärtner classification, calcific deposits were classified as type I in two patients, type II in 14 patients, and type III in 17 patients. Tendon calcification of the controls was significantly lower compared to the CT group. No differences in the amount of histological calcification between the Gärtner groups were observed. A correlation between the radiological size of calcification and the amount of calcification detected in histology was found. SEM-EDS and Raman identified basic calcium phosphate to be the predominant crystal type in tendons from CT patients, with only two calcium pyrophosphate detections. CT is mainly associated with BCP deposition. Calcified depot size was associated with pain intensity, while diabetes mellitus was observed more frequently in CT patients than in controls. BCP may be a focus of future mechanistic studies on CT. Full article

Basic calcium phosphate (BCP) and calcium pyrophosphate dihydrate (CPPD) crystals drive the degenerative and inflammatory pathways that lead to crystal arthropathy. Although recent classification criteria and imaging recommendations have improved standardisation for CPPD disease, it remains underdiagnosed in practice. In contrast, BCP disease lacks validated classification criteria and standardised diagnostic descriptors, limiting translational research and clinical recognition. Accurate diagnoses are limited by varied reference standards, operator-dependent techniques, and the absence of validated bedside tools. As the population ages and the burden of crystal disease rises, there will be increased demand for reliable diagnostic tools in clinical practice. This review summarises current and emerging diagnostic tools for identifying BCP and CPPD, with emphasis on bridging the diagnostic gap from research to routine care. Polarised light microscopy remains a highly specific test for the diagnosis of CPPD but is limited by inter-observer variability and access to polarising light microscopes. Imaging tools such as ultrasound, conventional radiography, computed tomography (CT) and dual-energy CT can identify CPPD, although performance varies by anatomical site, disease stage and technical parameters. Ultrasound is a useful bedside tool for identifying BCP disease, whereas CT and DECT also have diagnostic utility but lack validation for routine use. Emerging technologies such as computational polarised light microscopy and Raman spectroscopy are promising techniques, but require further research to evidence their use in clinical practice. Development of clear diagnostic reference standards, classification criteria for BCP disease, and evidence-based multimodal diagnostic pathways are essential to bridge the gap between research and routine clinical diagnosis. Full article

The crystal arthropathies gout and calcium pyrophosphate deposition (CPPD) disease represent a significant subset of rheumatic and musculoskeletal diseases, yet their overlap with common entities such as osteoarthritis (OA), rheumatoid arthritis (RA), and psoriatic arthritis (PsA) remains underrecognized. We conducted a structured narrative review of studies published through August 2025, exploring the epidemiology, clinical presentation, imaging characteristics, and treatment implications of these overlapping conditions. We particularly examine how crystal deposition may mimic or complicate the clinical course of OA, RA, and PsA, especially in older adults with multimorbidity. Recognizing these overlaps is critical to avoid misdiagnosis, inappropriate escalation of immunomodulatory therapy, and missed opportunities for targeted crystal-directed treatment. Full article

Prior research suggests a connection between osteoarthritis and gout at sites commonly affected by gouty attacks. Whether this connection exists at sites with known monosodium urate crystal deposition but less commonly affected by gouty attacks, such as the lumbosacral spine, has not been previously investigated. We assessed whether lumbosacral osteoarthritis is more prevalent and more severe in subjects with gout compared with controls, and whether lumbosacral osteoarthritis is associated with higher levels of spinal monosodium urate deposition. Fifty gout subjects and 25 controls underwent dual-energy computed tomography imaging of the lumbosacral spine. We assessed lumbosacral osteoarthritis using a modification of a validated computed tomography scoring system, incorporating grade of intervertebral disc narrowing and facet joint osteoarthritis, and presence of spondylolysis and spondylolisthesis. We quantified spinal monosodium urate deposition using the default post-processing algorithm, plus a maximally specific algorithm to exclude potential artefacts. Forty-six gout subjects and 25 controls, average age 62 years, were included in the final analysis. Both gout and control subjects exhibited high rates of facet joint osteoarthritis and degenerative disc disease, with no difference in prevalence or severity between groups. Gout subjects did not have differing prevalence of spondylolysis and spondylolisthesis vs. controls. Subjects with lumbosacral osteoarthritis did not have higher levels of spinal monosodium urate deposition. Overall, lumbosacral osteoarthritis was not more prevalent or more severe in gout patients compared with controls, and spinal monosodium urate crystal deposition did not differ between patients with and without lumbosacral osteoarthritis. Full article

Hyperuricemia influences several aspects of the immune system. It enhances cytokine production by monocytes and activates neutrophils and natural killer cells. Within the adaptive immune system, hyperuricemia enhances antigen presentation, skews T helper cell differentiation toward the Th17 lineage and may also activate B cells. Beyond its established role in the pathogenesis of gout, hyperuricemia may therefore contribute to other rheumatic diseases. In this review, we summarize current evidence on the role of hyperuricemia in osteoarthritis, psoriatic arthritis, axial spondylarthritis, rheumatoid arthritis, systemic sclerosis, primary Sjögren’s disease and systemic lupus erythematosus. Available data do not support a causal role for hyperuricemia in the disease onset of osteoarthritis or rheumatoid arthritis. In contrast, hyperuricemia is associated with the development of psoriatic arthritis and may be linked to a more severe disease course. Small, predominantly cross-sectional studies further suggest a potentially adverse role of hyperuricemia in systemic sclerosis, Sjögren’s disease, and systemic lupus erythematosus. Across several rheumatic diseases, hyperuricemia is associated with cardiovascular disease, renal dysfunction and interstitial lung disease. However, both mechanistic and causal evidence remain limited, underscoring the need for more studies. Full article

Gout is the most common form of inflammatory arthritis in men, driven by hyperuricemia and the deposition of monosodium urate (MSU) crystals. The innate immune response to these crystals leads to acute inflammatory episodes, called flares, characterized by intense joint pain, swelling, and temporary disability. Although gout flares are self-limiting, they impose a considerable burden on patients’ quality of life and contribute to increased healthcare utilization. A detailed understanding of the inflammatory processes triggered by MSU crystals is critical for developing targeted therapies to prevent and manage flares effectively. This review provides an overview of experimental models used to study the inflammatory phase of gout, with a focus on both in vivo and in vitro models of MSU crystal-induced inflammation. We concentrate on models that reproduce the acute inflammatory response following MSU crystal deposition, including the air pouch, intraarticular injection, and peritonitis rodent models, alongside the larval zebrafish model. In addition, we discuss in vitro approaches using primary immune cells and cell lines. We discuss the strengths, limitations, and translational relevance of these models and highlight some examples of how they have contributed to our understanding of the etiology of gout. Of note, models of hyperuricemia are not included here as these have been extensively reviewed elsewhere. Full article

‘Irregular gout’ is an obsolete term that was used in the past to describe both trivial and serious health issues seemingly related to gouty arthritis. This article looks back at what physicians such as George Cheyne, William Oliver, William Cullen and William Heberden thought about ‘irregular gout’. It examines to what degree the concept is still relevant, knowing what we now know about uric acid and the local and systemic inflammatory effects of urate crystal formation. In parallel, the article traces the trajectory from Cullen’s ‘asthenic gout’ to nineteenth century ‘uric acid poisoning’ and thence to possible hidden consequences of asymptomatic hyperuricaemia. ‘Irregular gout’ in its various guises has greatly influenced both orthodox and unorthodox treatments over the years. Although the term is no longer used, the concept is by no means dead. Full article

The 1st Joint Ectopic Calcification Meeting (JECM) was held in Nancy, France on 24–26 September 2025. In response to the growing need for unified scientific dialogue on soft tissue ectopic calcification, the Joint Ectopic Calcification Meeting (JECM) brought together the communities of INTEC, ISSEC, BBC, iSCCa, and the PXE Budapest meeting. This initiative emerged from concerns over fragmentation in the field, with multiple smaller meetings diluting collaborative potential. By consolidating efforts, JECM aims to foster interdisciplinary exchange, highlight cutting-edge research, and build a flagship event for the ectopic calcification community. With over 100 participants, the inaugural meeting in Nancy marks a promising step toward a more integrated and dynamic future for the field. The abstracts of this year’s meeting oral and poster presentations are collected in this conference paper, with permission from the corresponding authors. Full article

Allopurinol, the most used urate-lowering drug for the treatment of gout, is associated with rare but life-threatening severe cutaneous adverse reactions (SCARs) such as Stevens–Johnson Syndrome (SJS), Toxic Epidermal Necrolysis (TEN), and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome, but not Acute Generalised Exanthematous Pustulosis (AGEP). They are characterised by severe skin and systemic involvement and are associated with substantial morbidity and a high risk of mortality. This narrative review summarises evidence on the clinical presentation, epidemiology, risk factors, and preventive strategies for allopurinol-induced SCARs. Key risk factors include the presence of the HLA-B*58:01 allele, renal impairment, older age, female sex, heart disease, higher starting doses of allopurinol, and certain ethnicities, e.g., South Asian, Han Chinese, and African populations likely due to the higher prevalence of the HLA-B*58:01 allele. Risk mitigation strategies include genetic testing for HLA-B*58:01 in high-risk ethnic groups and avoiding allopurinol in those that are positive for the HLA-B*58:01 allele, starting allopurinol at a low-dose (e.g., 50–100 mg/day) and up-titrating it gradually at 4-week intervals, and avoiding high-dose allopurinol in those with risk factors (e.g., chronic kidney disease stage ≥3). In addition, risk stratification using prediction tools may enable a safer use of allopurinol. Full article