Gout Attacks Research Articles

The Clinical Significance of Serum Interleukin-36α Levels in Patients with Gout

ABSTRACT Background Gout is a chronic inflammatory diseases caused by monosodium urate crystal deposition. However, the role of interleukin (IL)-36 in gout has not dbeen elucidated. Methods We enrolled 75 subjects, including 20 healthy controls (HC), 30 patients with acute gout attack and 25 patients in remission. Baseline data were obtained through clinical interrogation and laboratory data were obtained through tests of blood samples. Serum levels of IL-36α were detected using enzyme-linked immunosorbent assay. Spearman correlation analysis was used to investigate the correlation of IL-36α with other parameters. The diagnostic value of IL-36α was demonstrated using a receiver operating characteristic curve. Results The serum IL-36α level of gout patients in acute attack and remission stage was significantly higher than that of HC. Serum IL-36α was positively correlated with alanine transaminase (ALT) and aspartate transaminase (AST). Serum amyloid A (SAA) levels positively correlated with C-reactive protein levels and erythrocyte sedimentation rates. Glutamyl transpeptidase levels positively correlated with AST and ALT levels. Conclusion In conclusion, serum IL-36α levels were elevated in patients with gout and correlated with the clinical markers of inflammation. Our findings suggest that IL-36α may be a novel inflammatory indicator for gout.

Is lactic acid a misunderstood trigger of gout attack for a century?

A gout attack could be viewed as a nucleation event. Many reports have shown that the typical molecular structure of crystallization inhibitors usually contains carboxyl and hydroxyl groups, which could interact with solute molecules through hydrogen bonding, thereby suppressing the nucleation and growth of crystals. Since 1923, l-lactic acid (LA), a molecule with structural features of inhibitors, has been speculated to be a trigger for acute gout because metabolized LA temporarily reduces uric acid excretion and leads to a slow increase in serum uric acid concentration. However, many cases of gout presumably triggered by elevated lactate in a very short period of 4 h are often inexplicable. Here, we present the unexpected result that LA has a significant “opposite effect” on the nucleation and growth of gouty pathological crystals, which is that as the concentration of the additive LA increases, the nucleation and growth of the crystals is suppressed and then facilitated. This approach may help our clarifying the long-standing “misunderstandings” and further understanding the association between metabolized LA and increased risk of gout attacks. Finally, a novel mechanism called "tailed-made occupancy (TMO)" was used to explain the nucleation and crystallization effects of LA on sodium urate monohydrate (MSUM).

Cardiovascular safety of using non-steroidal anti-inflammatory drugs for gout: a Danish nationwide case-crossover study.

Gout attacks are treated with uric-lowering and anti-inflammatory drugs. In patients with gout, non-steroidal anti-inflammatory drugs (NSAIDs) could be both cardiovascular beneficial, due to their anti-inflammatory actions, and cardiovascular hazardous, due to their prothrombotic, hypertensive, and proarrhythmic side effects. We, therefore, examined the risk of cardiovascular events associated with NSAID use in patients with gout. We conducted a nationwide, population-based case-crossover study of all Danes ≥ 18years of age with first-time gout during 1997-2020, who experienced a cardiovascular event (myocardial infarction, ischemic stroke, congestive heart failure, atrial fibrillation/flutter, or cardiovascular death) (n = 59,150). The exposure was use of NSAIDs, overall and according to type (ibuprofen, naproxen, or diclofenac). We used the dates 300, 240, 180, and 120 before the outcome date as reference dates. We used the Mantel-Haenszel method to calculate odds ratios (ORs) with 95% confidence intervals (CIs) of the association between NSAID use and cardiovascular events. NSAID use was overall associated with 12% decreased odds of a cardiovascular event (OR = 0.88, 95% CI: 0.85-0.91). This decreased odds ratio was observed for the use of ibuprofen (OR = 0.92, 95% CI: 0.88-0.97) and naproxen (OR = 0.85, 95% CI: 0.74-0.97), but not for the use of diclofenac (OR = 0.97, 95% CI: 0.90-1.05).Overall, use of NSAIDs was associated with decreased odds of all the individual components of the composite outcome. NSAIDs were not associated with an increased cardiovascular event rate when used in gout patients.Ibuprofen and naproxen appeared to have better cardiovascular risk profiles than diclofenac.

Upregulation of CD39 During Gout Attacks Promotes Spontaneous Remission of Acute Gouty Inflammation.

Gout is a self-limiting form of inflammatory arthropathy caused by the formation of urate crystals due to hyperuricemia. The resolution of gout involves the transition of proinflammatory M1-type macrophages to anti-inflammatory M2-type macrophages, as well as neutrophil-mediated extracellular trap (NET) formation. However, the underlying mechanisms of these changes are not clear. Studies have confirmed that high expression of CD39 on macrophages and neutrophils can trigger the polarization of macrophages from a proinflammatory state to an anti-inflammatory state. Recent studies have shown that the pathogenesis of gout involves extracellular ATP (eATP), and the synergistic effect of MSU and extracellular ATP can cause gout. CD39 is a kind of ATP hydrolysis enzyme that can degrade eATP, suggesting that CD39 may inhibit the aggravation of inflammation in gout and participate in the remission mechanism of gout. To confirm this hypothesis, using data mining and flow cytometry, we first found that CD39 expression was significantly upregulated on CD14 + monocytes and neutrophils in gout patients during the acute phase. Inhibition of CD39 by lentivirus or a CD39 inhibitor in acute gout models aggravated gouty arthritis and delayed gout remission. Apyrase, a functional analog of CD39, can significantly reduce the inflammatory response and promote gout remission in acute gout model mice. Our findings confirm that the upregulation of CD39 during gout flare-ups promotes spontaneous remission of acute gouty inflammation.

Colchicine's Role in Cardiovascular Disease Management.

Colchicine-an anti-inflammatory alkaloid-has assumed an important role in the management of cardiovascular inflammation ≈3500 years after its first medicinal use in ancient Egypt. Primarily used in high doses for the treatment of acute gout flares during the 20th century, research in the early 21st century demonstrated that low-dose colchicine effectively treats acute gout attacks, lowers the risk of recurrent pericarditis, and can add to secondary prevention of major adverse cardiovascular events. As the first Food and Drug Administration-approved targeted anti-inflammatory cardiovascular therapy, colchicine currently has a unique role in the management of atherosclerotic cardiovascular disease. The safe use of colchicine requires careful monitoring for drug-drug interactions, changes in kidney and liver function, and counseling regarding gastrointestinal upset. Future research should elucidate the mechanisms of anti-inflammatory effects of colchicine relevant to atherosclerosis, the potential role of colchicine in primary prevention, in other cardiometabolic conditions, colchicine's safety in cardiovascular patients, and opportunities for individualizing colchicine therapy using clinical and molecular diagnostics.

Gout: physical activity in therapy and prevention of the disease

Gout is a systemic chronic inflammatory disease associated with purine metabolism disorders. Risk factors for gout are a combination of genetic and environmental factors. Taking into account such features of the pathogenesis of gout as hyperuricemia and the deposition of monosodium urate crystals in tissues and joints, the development of the inflammatory, researchers studied the effect of physical activity on its main links. The intensity of the load and the type of physical exercise were taken into account due to their possible effect on metabolic processes. There is currently no reliable evidence on the importance of physical activity in reducing serum uric acid levels. Research has shown that physical activity has a positive effect on inflammation between gout attacks. The use of physical exercise can indirectly affect uric acid levels by reducing body weight in comorbid pathologies. EULAR emphasizes physical activity to prevent cardiovascular risks, which is also important for gout. Conclusions. Physical activity as one of the components of lifestyle is important for gout due to its effect on the inflammatory process and the prevention of relapses, a general strengthening effect on the body, an effect on hyperuricemia due to the positive effect associated with comorbid pathology, and a decrease in cardiovascular risk and associated him premature death. Physical activity of low and moderate intensity is effective for gout. Preference is given to aerobic exercise, taking into account the nature of metabolism and the possible impact on the occurrence of gout attacks. Further study and development of the characteristics of physical activity in gout are necessary to improve the prevention and treatment of the disease, and the development of individual recommendations for patients (for the management of gout).

Medial Ankle Impingement Syndrome due to Talar Osteochondroma and Gout Attack: A Case Report

Medial Ankle Impingement Syndrome due to Talar Osteochondroma and Gout Attack: A Case Report

History of Treatments Used to Treat Gout and Hyperuricemia

ABSTRACT: Treatment of arthritis has been gaining momentum most recently with new advancement in technology and various modes of treatment available. But; with changing life-style and unhealthy dietary habits; cases of hyperuricemia and gout are increasing at an alarming rate. Gout attacks joints and the Heat, inflammation, discomfort, inflammation, and intense discomfort are a few symptoms. Inhibitors of Xanthine Oxidase used in treatment for hyperuricemia and arthritis which reduce the serum urate level. Study on further applications of medications to combat hyperuricemia and gout is currently under way which has a scope for further development. synthesis of inhibitors of Xanthine Oxidase has been showing for preventing tophaceous deposits from accumulating. Many different methods have been used to combat hyperuricemia throughout the history and many different modes of treatment are currently employed which provide relief from hyperuricemia and gout due to the advancement in technology. The advancement in modern science has ensured that the treatment of hyperuricemia and gout has developed rapidly to effectively treat the disease which has been increasing at an alarming rate in the last two decades. Emphasis has also been given to find out new breakthroughs in the discovery of alternatives for traditional drugs that are used to treat hyperuricemia and gout which will provide relief to patients.

Comparative Study to Assess the Safety and Effectiveness of Allopurinol & Febuxostat in Patients Diagnosed with Gout

Introduction: Gout is placed under the umbrella term ‘arthritis’ - a wide variety of joint illness and joint pain. Some types of arthritis cause inflammation in the joints, while others do not. It is the most prevalent form of inflammatory arthritis which arises due to the elevated levels of Serum Uric acid (SUA), leading to the deposition of Mono Sodium Urate (MSU) crystals in and around joints. burden of gout has risen in recent decades with a prevalence rate of <1% to 6.8% and the patients with gout may have significant medical comorbidity load asociated with pain, disability and activity limitation which inturn affects the patients’ Health-related quality of life (HRQOL). Several drugs are used to treat acute attacks of gout which includes Colchicine, Non steroidal anti inflammatory drugs (NSAIDs), and Corticosteroids. Long term management of gout focuses on lowering SUA level to normal (<0.36mmol/L). There are two major classes of drugs used to reduce SUA levels, Urate-lowering therapy (ULT), specifically Uricosuric drugs and Xanthine oxidase inhibitors (XOIs). Hence, it is necessary to compare the safety and effectiveness of Allopurinol and Febuxostat used in the management of gout and there is a growing need to research the impact of gout on patients’ HRQOL inorder to improve productivity and QOL of patients. Objectives: The goal of the study was to compare the safety and effectiveness of Allopurinol and Febuxostat in patients diagnosed with Gout. The study also aimed to assess the effect of these on renal profile and the study further assessed the Health-related quality of life of the patients. Methodology: This was an observational study conducted in the selected Orthopedic clinics in T. Dasarahalli, Bengaluru District for a period of 6 months by enrolling 50 subjects, based on various inclusion and exclusion criteria. The subject’s demographic details, laboratory data and responses were collected with the help of a self-designed questionnaire. ...........

Single-cell transcriptomics reveals variations in monocytes and Tregs between gout flare and remission.

Gout commonly manifests as a painful, self-limiting inflammatory arthritis. Nevertheless, the understanding of the inflammatory and immune responses underlying gout flares and remission remains ambiguous. Here, based on single-cell RNA-Seq and an independent validation cohort, we identified the potential mechanism of gout flare, which likely involves the upregulation of HLA-DQA1+ nonclassical monocytes and is related to antigen processing and presentation. Furthermore, Tregs also play an essential role in the suppressive capacity during gout remission. Cell communication analysis suggested the existence of altered crosstalk between monocytes and other T cell types, such as Tregs. Moreover, we observed the systemic upregulation of inflammatory and cytokine genes, primarily in classical monocytes, during gout flares. All monocyte subtypes showed increased arachidonic acid metabolic activity along with upregulation of prostaglandin-endoperoxide synthase 2 (PTGS2). We also detected a decrease in blood arachidonic acid and an increase in leukotriene B4 levels during gout flares. In summary, our study illustrates the distinctive immune cell responses and systemic inflammation patterns that characterize the transition from gout flares to remission, and it suggests that blood monocyte subtypes and Tregs are potential intervention targets for preventing recurrent gout attacks and progression.

"Dialogue Between Franklin and the Gout" Reexamined.

Benjamin Franklin, one of the founding fathers of the United States, was not just a politician and a political philosopher but an inventor with a scientific temperament. He was overweight and likely suffered from the consequences of metabolic syndrome including gout. He woke up with a gout attack on October 22, 1780 and wrote the "Dialogue Between Franklin and the Gout." His observations on the risk factors for gout are re-examined in the modern context 243 years later.

Maresin1 ameliorates MSU crystal-induced inflammation by upregulating Prdx5 expression

BackgroundMaresin1 (MaR1) is a potent lipid mediator that exhibits significant anti-inflammatory activity in the context of several inflammatory diseases. A previous study reported that MaR1 could suppress MSU crystal-induced peritonitis in mice. To date, the molecular mechanism by which MaR1 inhibits MSU crystal-induced inflammation remains poorly understood.MethodsMousebone marrow-derived macrophages (BMDMs) were pretreated with MaR1 and then stimulated with FAs (palmitic, C16:0 and stearic, C18:0) plus MSU crystals (FAs + MSUc). In vivo, the effects of MaR1 treatment or Prdx5 deficiency on MSUc induced peritonitis and arthritis mouse models were evaluated.ResultsThe current study indicated that MaR1 effectively suppressed MSUc induced inflammation in vitro and in vivo. MaR1 reversed the decrease in Prdx5 mRNA and protein levels induced by FAs + MSUc. Further assays demonstrated that MaR1 acceleratedPrdx5 expression by regulating the Keap1-Nrf2 signaling axis. Activation of AMPK by Prdx5 improved homeostasis of the TXNIP and TRX proteins and alleviated mitochondrial fragmentation. In addition, Prdx5 overexpression inhibited the expression of CPT1A, a key enzyme for fatty acid oxidation (FAO). Prdx5 protected against defects in FA + MSUc induced FAO and the urea cycle.ConclusionMaR1 treatment effectively attenuated MSUc induced inflammation by upregulating Prdx5 expression. Our study provides a new strategy by which Prdx5 may help prevent acute gout attacks.

On the venous origin of primary gout: The barotoxicity hypothesis

Gout is the oldest and the most prevalent inflammatory joint disease worldwide exhibiting a steady increase in both incidence and prevalence. Despite millennia of rigorous clinical research, specific pivotal questions still need to be fully elucidated. Presently, the exact initial defect that induces its most prevalent type—primary hyperuricemia and primary gout—remains idiopathic. Additionally, the remarkable predilection for foot involvement (podagra), its exceptionally intense pain, and the precise mechanism triggering acute gout attack all lack clear pathological processes. This manuscript aims to demystify the aforementioned dilemmas by presenting the barotoxicity hypothesis which introduces the barotoxic effect of intra-abdominal pressure on the renal and pedal venous circulations as the potential origin of primary hyperuricemia and the subsequent podagra formation in addition to presenting evidence in support of this hypothesis. If validated, the barotoxicity hypothesis could radically transform our modern understanding of this ancient ailment, reframing gout from being a metabolic arthropathy to a mechanical phlebopathy. Moreover, future therapeutic interventions could pivot towards alleviating intra-abdominal pressure and subsequent peripheral venous stasis, offering innovative preventative and therapeutic approaches.

Cardiovascular safety of non-steroidal anti-inflammatory drug use for gout: A Danish nationwide case-crossover study

Abstract Background Gout is associated with increased cardiovascular risk through inflammation and shared risk factors. Gout attacks are treated with a uric-lowering drug, such as allopurinol, and an anti-inflammatory drug, such as a non-steroidal anti-inflammatory drug (NSAID). Thus, NSAIDs could be both cardiovascular beneficial, due to their anti-inflammatory actions, and cardiovascular hazardous, due to their prothrombotic, hypertensive, and proarrhythmic actions. Yet, no study has examined the cardiovascular safety of NSAIDs for the treatment of gout. Purpose To examine the risk of major adverse cardiovascular events (MACEs) associated with NSAID use in gout patients. Methods We conducted a nationwide, population-based case-crossover study of all Danes ≥18 years of age with first-time gout during 1997–2020, who experienced a MACE (myocardial infarction, ischemic stroke, congestive heart failure, atrial fibrillation or flutter, or all-cause death) (n=103,522). The patients were identified either via a hospital diagnosis for gout (12%) or via a filling of an allopurinol prescription (88%). The exposures were use of NSAIDs overall and according to subtype (ibuprofen, naproxen, or diclofenac). An individual was considered exposed from the time of a filled prescription until the end of a use period, estimated from average use of two tablets per day. In the case-crossover design, we used four reference dates at 120, 180, 240, and 300 days before the outcome. An individual was considered exposed if the use period covered a reference date or the outcome date. We used the Mantel-Haenszel method to calculate odds ratios (ORs) with 95% confidence intervals (CIs) of the association between NSAID use and MACE. Results NSAID use was overall associated with a 15% decreased risk of MACE (OR=0.85, 95% CI: 0.83–0.87). The ORs of the association between NSAID use and the individual cardiovascular events were 0.91 (95% CI: 0.84–0.99) for myocardial infarction, 0.88 (95% CI: 0.81–0.95) for ischemic stroke, 0.89 (95% CI: 0.83–0.94) for congestive heart failure, 0.80 (95% CI: 0.75–0.85) for atrial fibrillation or flutter, and 0.77 (95% CI: 0.75–0.80) for all-cause death. The decreased risk of MACE was observed for use of ibuprofen (OR=0.91, 95% CI: 0.88–0.95) and naproxen (OR=0.78, CI: 0.70–0.86), but not for use of diclofenac (OR=1.03, 95% CI: 0.97–1.09). Conclusions In patients with first-time gout, use of ibuprofen and naproxen was associated with a slightly decreased cardiovascular risk, whereas diclofenac was not.

New Inflammatory Marker Associated with Disease Activity in Gouty Arthritis: The Systemic Inflammatory Response Index.

The systemic immune-inflammatory index (SII) and systemic inflammatory response index (SIRI), as novel non-specific inflammatory markers, have recently drawn attention. At present, no studies have been conducted to investigate the value of SII and SIRI in gouty arthritis (GA), so we explored their possible association with GA disease activity. The study enrolled 474 patients with acute gouty arthritis (AG), 399 patients with intercritical gouty arthritis (IG) and 194 healthy controls (HC). The differences in Monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), SII, and SIRI levels among different groups were assessed. The changes in the above indicators before and after treatment in the AG and IG groups were evaluated. Multivariate logistic regression analysis was assessed influencing factors for the acute gout attack. ROC curves were plotted to evaluate their diagnostic value for AG. Compared with the IG group, the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), PLR, and incidence of hyperlipidemia in the AG group were significantly higher, and the duration of disease was significantly shorter (P < 0.05). The MLR, NLR, SII and SIRI in the AG group were significantly higher than those in the IG and HC groups (P < 0.05). Compared with baseline, decreased MLR, NLR, PLR, SII and SIRI were observed in the AG group after treatment (P < 0.05), while there was no significant difference in the IG group before and after treatment (P > 0.05). SIRI was positively correlated with ESR and CRP (P < 0.05). Multivariate logistic regression analysis result showed that duration of disease, hyperlipidemia, ESR, CRP, and SIRI were influencing factors of acute gout attack (P < 0.05). The AUC of ESR, CRP and SIRI on the diagnosis in AG were 0.664, 0.755, and 0.674, respectively. SIRI may be used as a new inflammatory marker of disease activity with gouty arthritis.

Antioxidant, Antiinflammatory, and Anti Uric Acid Bioactivity Correlation of some Family Acanthaceae Plants (A Review)

Uric acid is a naturally occurring antioxidant that is produced in the body as a byproduct of the enzymatic breakdown of xanthine. Inflammation of the blood vessel cells in the human body can be brought on by abnormally high amounts of uric acid in the serum. An acute inflammatory response often manifests with symptoms similar to those of gout attacks. XO is a major contributor to the production of superoxide free radicals, which are a factor in chronic inflammatory diseases. Existing drugs have been used to treat gout and inflammatory diseases, but have negative effects in humans. Medicinal plants are a source of active chemicals, which are particularly significant in the process of developing new medications due to the variety and distinctive chemical structures of these active compounds. Justicia gendarussa, Andrographis paniculata (Burn.f.) Nees, Ruellia tuberosa L, and Clinacanthus nutans Lindau are examples of plant species in the Acanthaceae family. The results of existing publications show that the bioactive compounds contained in these plants have a relationship between antioxidant activity, anti-uric acid and anti-inflammatory properties.

Diurnal Variations in Serum Uric Acid, Xanthine, and Xanthine Oxidoreductase Activity in Male Patients with Coronary Artery Disease.

Hyperuricemia is influenced by diet and can cause gout. Whether it is a potential risk factor for cardiovascular disease (CVD) remains controversial, and the mechanism is unclear. Similar to CVDs, gout attacks occur more frequently in the morning and at night. A possible reason for this is the diurnal variation in uric acid (UA), However, scientific data regarding this variation in patients with CVD are not available. Thus, we aimed to investigate diurnal variations in serum levels of UA and plasma levels of xanthine, hypoxanthine, and xanthine oxidoreductase (XOR) activity, which were measured at 18:00, 6:00, and 12:00 in male patients with coronary artery disease. Thirty eligible patients participated in the study. UA and xanthine levels significantly increased from 18:00 to 6:00 but significantly decreased from 6:00 to 12:00. By contrast, XOR activity significantly increased both from 18:00 to 6:00 and 6:00 to 12:00. Furthermore, the rates of increase in UA and xanthine levels from night to morning were significantly and positively correlated. In conclusion, UA and xanthine showed similar diurnal variations, whereas XOR activity showed different diurnal variations. The morning UA surge could be due to UA production. The mechanism involved XOR activity, but other factors were also considered.

Prednisolone Versus Colchicine for Acute Gout in Primary Care (COPAGO): protocol for a two-arm multicentre, pragmatic, prospective, randomized, double-blind, controlled clinical trial of prednisolone and colchicine for non-inferiority with a parallel group design

BackgroundGout is the most common form of rheumatic disease in which monosodium urate crystals are deposited in the joints followed by acute inflammatory reactions. There are various approved drugs that can be prescribed for pain relief during an acute gout attack. However, to date, no direct comparison of efficacy of colchicine and prednisolone for the treatment of acute gout attacks has been investigated. Furthermore, the majority of previous research studies were not only conducted in tertiary centres but also excluded patients with common comorbidities due to contraindications to naproxen.MethodsThis pragmatic, prospective, double-blind, double-dummy, parallel-group, randomized, non-inferiority trial investigates whether prednisolone (intervention) is non-inferior to treatment with colchicine (active control) in patients with acute gout. Adult patients presenting with acute gout to their general practitioners in 60 practices across 3 university sites (Greifswald, Göttingen, and Würzburg) are eligible to participate in the study. Participants in the intervention group receive 30 mg prednisolone for 5 days. Those in the control group receive low-dose colchicine (day 1: 1.5 mg; days 2–5: 1 mg). The primary outcome is the absolute level of the most severe pain on day 3 (in the last 24 h) measured with an 11-item numerical rating scale. Day 0 is the day patients take their study medication for the first time. They are then asked to fill out a study diary the same time each day for pain quantification. Pain scores are used for comparison between the two medications. Secondary outcomes are average response to treatment, swelling, tenderness and physical function of the joint, patients’ global assessment of treatment success, use of additional pain medication and non-pharmacological pain therapies. For safety reasons, potential side effects and course of systolic blood pressure are assessed.DiscussionThis trial will provide evidence on the effectiveness of pain reduction and side effects of colchicine and prednisolone in acute gout in primary care.Trial registrationClinicalTrials.gov Identifier: NCT05698680 first posted on January 26, 2023 (retrospectively registered). URL of trial registry record: https://clinicaltrials.gov/study/NCT05698680

Asymptomatic and Symptomatic Hyperuricemia: an Innovative Treatment Strategy

Asymptomatic hyperuricemia is associated with many somatic diseases, the onset and progression of chronic kidney disease (CKD), with an increase in cardiovascular and general mortality. Symptomatic hyperuricemia – gout and various variants of kidney damage, despite the availability of modern rheumatological, urological and nephrological guidelines, does not lose its relevance, as it is characterized by a severe course, significantly worsens the quality of life, increases cardiovascular risk and leads to disability. Hyperuricemia is a persistent increase in the concentration of uric acid (UA) in blood serum (above 360 μmol/l). The appointment of urate-lowering therapy (ULT) for gout is based on the Guidelines of the American College of Rheumatology (ACR, 2020), the European League Against Rheumatism (EULAR, 2016), the National Institute for Health and Care Excellence (NICE, 2022), in the case of urolithiasis – the Guidelines of the European Association of Urology (EAU, 2023) and the American Urological Association (AUA, 2019). Asymptomatic hyperuricemia, from the point of view of the evidence base, requires only the use of lifestyle modification measures. The Austrian Society of Rheumatology and Rehabilitation for patients with gout and hyperuricemia in 2022 proposed dietary and lifestyle recommendations, including sour cherries (Montmorency), which can lower UA levels. Combination of concentrated Montmorency tart cherry powder (1:50) and dry willow extract is an innovative strategy for the treatment of asymptomatic and symptomatic hyperuricemia, a natural hypouricemic agent with an anti-inflammatory effect, which is prescribed as a complementary therapy for gout and hyperuricemia in: cardiovascular diseases, diabetes and metabolic syndrome, CKD, urolithiasis. The appointment of сombination of concentrated Montmorency tart cherry powder (1:50) and dry willow extract will contribute to the achievement of the target value of the UA level in the blood serum of patients with asymptomatic and symptomatic hyperuricemia, the initiation of reno- and cardioprotection, the reduction of the risk of gout attacks, and the achievement of a stable and long interrelapse period.

Epidemiology and risk factors associated with gout control among adult Asians: a real-world retrospective cohort study.

Gout is associated with significant morbidity and mortality, yet suboptimal gout control remains a problem globally. Identifying the risk factors associated with poor gout control among patients in primary care allows targeted interventions to improve their clinical management. This study aimed to determine the prevalence of poor gout control and its associated demographic and clinical factors among urbanized community-dwelling Asian patients. This retrospective study was based on data extracted from the electronic medical records of 8 public primary care clinics in Singapore. Patients with a diagnostic code of gout who had 2 or more visits between 1st January 2018 and 31st December 2019 were included in the analysis. Data extracted included: demographics, anthropological measurements, comorbidities, serum uric acid levels and medication prescription. A patient is defined to have poor gout control if they suffer two or more acute gout attacks within a year. Chi-Squared test was used for categorical parameters. For continuous variables, univariate logistic regression analysis was first performed. Significant factors (p ≤ 0.1) were then included in the logistics regression model to account for confounders. A total of 7,970 patients and 24,624 visits were included in the analysis. The prevalence of poorly controlled gout was 28.2% (n = 2,244/7,970); only 46.3% of them (n = 1,039/2,244) were prescribed allopurinol and 13.4% (n = 301/2,244) were taking doses ≥300 mg. Using logistic regression, factors associated with poor gout control were: male gender [adjusted OR (AOR) =1.66, p < 0.001], Malay ethnicity (AOR = 1.27, p = 0.007), congestive heart failure (AOR = 1.64, p = 0.037). Patients prescribed allopurinol (AOR = 1.52, p < 0.001), NSAIDs (AOR = 2.76, p < 0.001) and corticosteroids (AOR = 2.83, p < 0.001) were more likely to have poorly-controlled gout. Nearly 30% of patients had poor gout. Interventions should focus on male and Malay patients and those with congestive cardiac failure.