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This article examines the role of uric acid (UA) in cognitive changes and neurodegeneration, focusing on its functions as an antioxidant and prooxidant. Research suggests that changes in serum UA levels may be associated with the development or delay of cognitive impairment, especially in the context of neurodegenerative diseases such as Alzheimer's disease. It was revealed that there is a relationship between the level of UA and the dynamics of cognitive functions, indicating the potential neuroprotective properties of UA. Particular attention is paid to the balance between the antioxidant and prooxidant properties of UA, which may play a key role in protecting neurons from damage. However, research results are not clear-cut, highlighting the need for further research to more fully understand the role of UA in cognitive processes. Determining the optimal serum UA level may be an important step in developing strategies for the prevention and treatment of cognitive impairment associated with neurodegeneration. Overall, these studies advance the understanding of the mechanisms underlying the interaction between uric acid metabolism and brain health.

Objective. To study the effect of arthroplasty and anterior interbody fusion in the cervical spine on degenerative changes in the adjacent intervertebral joints. Material and Methods. A retrospective cohort study included 46 patients (22 with cervical total disc arthroplasy – CTDA, and 24 with anterior cervical discectomy and fusion – ACDF) with symptoms of cervical spondylogenic compression myelopathy and/or radiculopathy. The degree of degeneration of facet joints adjacent to the operated segments was evaluated 12 months after surgical treatment. Degenerative changes in the cervical spine were assessed using CT according to the Okamoto classification. Vidar Dicom Viewer 3.2 software was used to view images and evaluate intervertebral joints. Statistical processing was performed using IBM SPSS Statistics 23. Data were presented as median and 25th and 75th percentiles – Me [Q1; Q3]. Results. The mean age of patients in both groups was 47 [39; 52] years (Mann – Whitney U-test, p = 0.047). In the ACDF group it was 48 [42; 55] years and in the CTDA group – 42 [36; 52] years. Comparison of degenerative changes in the ACDF group before and after treatment (Wilcoxon analysis) showed a statistically significant difference in the cranial (p = 0.023), and caudal (p = 0.001) joints, with the progression of degeneration degree. In the CTDA group, no difference between pre- and post-treatment degeneration degree (Wilcoxon analysis) was found in either cranial joints (p = 0.157) or caudal joints (p = 0.161). Conclusion. Surgeries to stabilize spinal segments in degenerative diseases undeniably affect the development of the adjacent level syndrome. However, the use of endoprosthetic technology makes it possible to aggravate the degree of degenerative changes in the intervertebral joints of adjacent segments to a lesser extent.

Background. Calcium pyrophosphate crystal deposition disease (CPPD) may be associated with developing of diastolic dysfunction (DD). Aim. To determine the variability of echocardiographic parameters in patients with CPPD receiving anti-inflammatory therapy. Materials and methods. Twenty six patients with CPPD and osteoarthritis (OA) from 18 to 65 years old were included in the case-control study. All patients underwent echocardiography, laboratory parameters at baseline and after 6 months. Patients with CPPD received methotrexate 15 mg per week or hydroxychloroquine 200 mg once a day, or colchicine 1 mg per day. Diastolic function according to echocardiography was assessed. Results. Diastolic dysfunction was detected in 19 patients: in 11 (42%) patients with CPPD and 8 (31%) patients with OA (p=0.39). The baseline serum CRP level was higher in the CPPD group (p=0.03), no differences were found for other indicators. Twenty-two patients with CPPD and 19 patients with OA completed the study. In patients with OA, there were no significant changes in indicators reflecting the diastolic function of ventricles. Conclusion. CPPD therapy with colchicine, hydroxychloroquine and methotrexate has a positive effect on indicators of diastolic ventricular function.

Endogenous hypercortisolism is a severe endocrine disease characterized by prolonged exposure to excessive amounts of glucocorticoid hormones, accompanied by a wide range of symptoms and complications, including immunosuppression. Timely surgical treatment in most cases allows to save the patient’s life, significantly improve its quality. However, restoration of the normal concentration of glucocorticoid hormones can become a trigger factor in the development or exacerbation of autoimmune and auto-inflammatory diseases. We present a clinical case of atypical gout in a patient with hypercortisolism and a progressive increase in symptoms of the disease after successful surgical treatment for Cushing’s disease and achieving stable remission. The issues of diagnosis and treatment of this group of autoinflammatory diseases are highlighted, the leading clinical and radiological symptoms are considered, the differential diagnosis of microcrystalline (metabolic) arthritis is presented. Despite the widespread, the diagnosis and treatment of this group of diseases still cause difficulties for specialists. A competent choice of drug therapy allows to fully control diseases considered in the article, including when they are combined, and thereby improve the quality of life of the patient.

BACKGROUND: Patients with gout often take glucocorticoids (GCs) and are at high risk of developing type 2 diabetes mellitus (DM2).AIM: Evaluation of the effect of long-term use of low doses of GCs on the risk of developing DM in patients with gout based on the results of a retrospective observationMATERIALS AND METHODS: 317 out of 444 patients with gout and no DM2 who participated in a prospective study of risk factors for DM2 were included. The sample did not include patients who used GCs during the observation period to relieve an acute attack of arthritis, regardless of the method of their use (n=88) and who did not complete the study (n=39). The remaining patients were retrospectively divided into 2 groups: those who continuously took prednisolone at a dose of 5-10 mg/day for ≥180 days and did not use GCs during the observation period. Scheduled visits were carried out at least once every 2 years. During the 1st visit, patients were prescribed or corrected both urate-lowering and prophylactic antiinflammatory therapy, including low doses of GCs. The primary end point was the development of DM2, carbohydrate metabolism indicators (HbA1c levels, serum glucose levels) were compared at baseline and at the end of the study.RESULTS: Of 317 patients with gout, 76 patients (24%) were continuously taking prednisolone at a dose of 5-10 mg/day for ≥180 days, 241 patients (76%) did not receive GCs during the entire follow-up period. The average dose of prednisolone in patients of the main group was 7.9±1.2 mg/day, the duration of treatment was 206.3±20.4 days.DM2 developed during the observation period in 20% of the main group and in 22% of the comparison group (p=0.73). Patients who took GC were older than those who did not take GC (p=0.01), they were more likely to have CHF (p=0.04). There were no significant differences between the groups for the rest of the compared parameters. In patients treated with low doses of GC — a significant increase in the average level of HbA1c (p=0.002); an increase in the number of patients with glucose levels ≥6.1 mmol/l (p=0.004) by the end of the study relative to the baseline. The initial level of HbA1c in patients who developed DM2 was expectedly higher, among them smokers were more often detected (p=0.01), they had a higher level of serum UA (p=0.001). The prevalence of other risk factors for DM in those who developed and did not develop DM2 did not differ significantly.CONCLUSION: Long-term use of low doses of GC in patients with gout does not significantly increase the risk of developing DM2, but may have a negative effect on carbohydrate metabolism.

The frequency and risk factors for the development of diastolic function in patients with calcium pyrophosphate crystal deposition disease (CPPD) and osteoarthritis (OA) have not been studied.The aim – to determine the frequency and to identify risk factors (RF) for the development of diastolic dysfunction (DD) of the left (LV) and right (RV) ventricles in patients with calcium pyrophosphate crystal deposition disease and osteoarthritis.Material and methods. 26 patients (18–65 years) each were included with CPРD and with knee OA, matched in age and gender, without cardiovascular disease (CVD), type 2 diabetes mellitus, rheumatic diseases. Traditional risk factors of CVD were assessed, echocardiography was performed.Results. The frequency of DD in patients with CPРD and OA was quite high and almost did not differ in both groups: it was detected in 19 patients, of which 11 (42%) with CPРD and 8 (31%) with OA (p=0.39). Type 1 LV DD was detected in 10 (39%) patients with CPРD and in 8 (31%) with OA (p=0.11); type 1 RV DD – in 8 (31%) patients with CPРD and in 7 (27%) patients with OA (p=0.17); type 1 LV DD and RV DD – in 7 (27%) patients with both CPРD and with OA. DD types 2 and 3 were not detected in both groups. There were no differences in both groups in CV risk factors, except for the level of C-reactive protein (CRP) – it was higher in CPРD (p=0.03). In the CPРD group, mean values of LV E/E′ (p=0.02), LV DT (p=0.03), LV MI (p=0.04) were significantly higher than in patients with OA. On the contrary, in patients with OA, the following indicators: EDV (p=0.004), TVC (p=0.02) were higher.There were direct correlations between diastolic function indices and the following factors in CPРD: LVL, PWLV and PTH level (r=0.7; p

Gout is a disease characterized by deposition of sodium monourate crystals in tissues which is the reason of inflammation among persons with hyperuricemia (HU). The prevalence of HU, which can be considered the first stage of gout formation, varies in different countries. Despite this, only a small number of persons with HU have been shown to develop symptoms of gout. Recent data suggest that HU is an independent risk factor for cartilage and bone damage. UA, both in the form of crystals and in a dissolved form, activates damage and potentiates cell death by releasing reactive oxygen species, activating the necroptosis pathway, neutrophil traps, synthesis of pro-inflammatory cytokines, and other pathogenetic mechanisms that cause the negative effects of HU and gout on articular cartilage and subchondral bone. The association of HU and osteoarthritis (OA) is well known and based on the common pathogenesis, but the direction of this relationship is still a debatable issue. The accumulated data suggest the need for a deeper study of the relationship of gout and asymptomatic HU with pathological processes leading to the development and progression of OA and disorders of bone metabolism.

The article presents current data on the effect of drugs for the treatment of gout on the composition and function of the intestinal microbiota. The potential possibilities of pre- and probiotics use for the prevention and complex therapy of gout are discussed, therapeutic effect may be associated with their impact on the uric acid synthesis and intestinal excretion, as well as with anti-inflammatory properties. The need for further research in this area is emphasized.

The gut microbiota plays a key role in metabolism and immune regulation, and imbalance in microbial composition can contribute to various diseases. We present up-to-date data on the role of the gut microbiota in the occurrence of chronic hyperuricemia (HU) and gout, which is associated with the influence of the microbiota on the synthesis of purine-metabolizing enzymes and pro-inflammatory cytokines. It has been shown that the gut microbiota plays an important role in the pathophysiology of gout and can serve as a new target for therapy. Currently, the microbial index of gout is considered as a potential method for early diagnosis of the disease, possibly already at the preclinical stage. The gut microbiota can be a starting point in the study of the pathogenesis of HU and gout. This makes it necessary to assess the pathogenetic relationship between individual specific microorganisms, the microbiota as a whole, and the development of uric acid (UA) metabolism disorders that contribute to the onset of HU and its transformation into gout. It is assumed that this approach will provide a more complete understanding of the gut microbiota participation in the synthesis of UA and its extrarenal excretion, as well as of bacteria and bacterial enzymes that can be used as a probiotic coadjuvant for the treatment and prevention of gout.

Colchicine is an alkaloid isolated from plants of the Colchicum genus. Colchicine has been used for thousands of years and remains one of the few drugs whose use remains relevant today. The therapeutic use of colchicine is widely known for gout, familial Mediterranean fever, Behcet’s disease, cardiovascular diseases (pericarditis, coronary heart disease, pericarditis, after coronary artery bypass grafting, etc.) and other diseases and is due to anti-inflammatory effects, which are based, including , inhibition of NLRP3 inflammasome and interleukin (IL)-1β production. The mechanisms of anti-inflammatory action of colchicine are diverse. It is primarily an inhibitor of mitosis and microtubule assembly. Colchicine destroys the structure of microtubules and reduces the elasticity and relaxation of neutrophils, thereby preventing the extravasation of neutrophils from blood vessels to the site of inflammation. Systemic inflammation is also a hallmark of coronavirus disease (COVID-19), which develops immunological disorders accompanied by the production of a large number of pro-inflammatory cytokines, including interleukin-1. Coronavirus disease 2019 (COVID-19), which has become the most urgent medical problem in the world in the last 2 years, given the mechanisms of inflammation similar to rheumatic diseases, is also considered a disease with the potential effectiveness of colchicine treatment. SARS-CoV-2 vaccines also have a trigger factor for the development of an exacerbation of arthritis. On average, colchicine use was associated with a 47% reduction in post-vaccination arthritis. This article provides an update on the mechanisms of action and current experience with colchicine in COVID-19, including in patients with microcrystalline arthritis.

It is assumed that the risk of developing type 2 diabetes mellitus (T2DM) in patients with gout is influenced by both generally accepted risk factors and factors related to gout.Objective. To evaluate the impact of various risk factors for T2DM in patients with gout.Material and methods. 444 patients (49 women, 395 men) ≥18 years old with gout and without DM were included. Duration of observation was 5.66 [2.69; 7.64] g. To identify factors associated with the risk of developing T2DM, multivariate logistic regression was used, which included: sex; T2DM in relatives; insufficient physical activity; unbalanced diet; age ≥45 years; ≥4 attacks per year; presence of tophi; BMI≥30 kg/m2 ; allopurinol, febuxostat, glucocorticoids, diuretics, metformin, colchicine; GFR˂ 60 ml/min/1.73 m2 ; serum uric acid level (sUA) ≥420 μmol/l and ≥480 μmol/l.Results. T2DM developed in 108 (24.3%) patients. According to the multivariate model, the presence of ≥4 attacks of arthritis per year increased the risk of T2DM (OR=5.23; 95% CI: 2.98–9.19; p=0.0001); presence of tophi (OR=2.61; 95% CI: 1.50–4.54; p=0.001); sUA≥480 μmol/l (OR=2.26; 95% CI: 1.02–5.00; p=0.144), diuretics (OR=2.35; 95% CI: 1.19–4.64; p=0.014). Febuxostat (OR=0.31; 95% CI: 0.11–0.84; p=0.022) and metformin (OR=0.49; 95% CI: 0.21–1.16; p=0.107) reduced the risk of developing T2DM.Conclusion. Risk of T2DM in patients with gout is associated with high incidence of arthritis attacks, MK≥480 μmol/l, hypertension, diuretic use, and febuxostat and metformin reduces risk.

The results of gout therapy in many patients remain unsatisfactory, despite the availability of drugs and recommendations for its treatment. In addition to poor adherence to treatment by patients, medical errors and other reasons influence this situation. The article considers several clinical cases demonstrating the possibilities of a rational choice of urate-lowering therapy.

The development of type 2 diabetes mellitus (DM) (DM2) in patients with gout can be influenced by both conventional and directly linked to gout risk factors (RFs).Objective: to identify RFs for the development of DM2 in patients with gout, including those directly associated with gout, based on long-term prospective follow-up data.Patients and methods. The study included 444 patients with gout older than 18 years (49 women, 395 men) who did not have DM. The followup period ranged from 2 to 8 years. The studied RFs for DM2 were: gender, age, family history of DM2, obesity, alcohol consumption >20 units per week, insufficient physical activity, unbalanced nutrition, history of hyperglycemia, coronary heart disease (CHD), arterial hypertension (AH), chronic heart failure, antihypertensive drugs, diuretics, glucocorticoids (GCs), urate-lowering therapy, serum levels of cholesterol, triglycerides, CRP, uric acid (UA), glucose, creatinine, glomerular filtration rate 4 attacks of gout per year, ≥5 affected joints during the disease.Results and discussion. DM2 developed in 108 (24.3%) patients. These patients were older, had a family history of DM, more often received antihypertensive therapy, diuretics, and glucocorticoids (49.1; 73.1; 27.8 and 47.2%, respectively) than patients who did not develop DM2 (25.6; 50.5; 14.8 and 36.4%, respectively; p4 attacks per year). UA levels >480 and 600 μmol/l were also significantly more frequent (p=0.0002) in patients with DM2 (71.3 and 34.3%, respectively).According to logistic regression data, factors that increase the risk of developing DM2 were: family history of DM, a history of hyperglycemia, CHD, AH, intake of GCs, antihypertensive drugs, the presence of tophi, >4 exacerbations of gout per year. Febuxostat use and UA

BACKGROUND: Gout is associated with a high incidence of type 2 diabetes mellitus (T2DM).AIM: To calculate the risk of T2DM on the FINDRISС scale, to assess the sensitivity and specificity of the scale in patients with gout based on the results of prospective follow-up.MATERIALS AND METHODS: A prospective single-center study included 444 patients with gout over 18 years of age (49 women, 395 men) without diabetes. The duration of follow-up ranged from 2 to 8 years. Initially, the risk of developing diabetes mellitus 2 was calculated according to the Russian version of the FINDRISС scale. The risk of developing T2DM was assessed as «low» with a total score (CC) 25 kg / m2 — 85.6% of patients, taking antihypertensive drugs — 81.3% of patients, age over 45 years in 70.5% of patients. The sensitivity and specificity of the FINDRISС scale were 52.8% and 66.3%, respectively. According to these data, the quality of the model was assessed as moderate. 9% vs 31.1% (p = 0.014)), serum MK level ≤300 μmol / L. Developed type 2 diabetes 33.3% of patients with moderate / high / very high risk 18.1% of patients with low or slightly increased risk (p = 0.0002).CONCLUSION: The FINDRISС scale can have sufficient sensitivity (52.8%) and specificity (66.3%) and can be used to calculate the risk of T2DM in patients with gout.

Achieving the target serum uric acid (UA) level is a priority in the treatment of gout.Objective: to study the relationship of the ABCG2 gene polymorphism (rs2231142) with the efficacy of allopurinol and febuxostat in patients with gout.Patients and methods. The study included 82 patients with gout over 18 years of age with serum UA level >360 μmol/L who did not take uratelowering therapy.All patients were prescribed allopurinol 100 mg daily, followed by its titration until the target UA level was reached (A polymorphism (rs2231142) of the ABCG2 gene. We compared the probability of achieving the target UA level, the mean values of a decrease in the serum UA level, and the mean doses of urate-lowering drugs in patients with different genotypes (CC, CA, AA) of the ABCG2 gene.Results and discussion. The target UA level in 45 (55%) of 82 patients was defined as A polymorphism of the ABCG2 gene, but the presence of CA and AA genotypes is identified with a higher dose of the drug. The C>A (rs2231142) polymorphism of the ABCG2 gene does not affect the ability to achieve the goal of therapy when using febuxostat in patients with allopurinol ineffectiveness.

Anti-inflammatory therapy, such as colchicine (COL), has been suggested to affect the incidence of cardiovascular events in patients with calcium pyrophosphate crystal deposition disease (CPPD).Objective: to study the effect of anti-inflammatory therapy with COL, hydroxychloroquine (HC), and methotrexate (MT) on cardiovascular outcomes in patients with CPPD.Patients and methods. The study included 305 patients with CPPD, the majority (62.30%) were women. The average follow-up period was 3.9±2.7 years. Among factors influencing cardiovascular outcome were considered: gender; age; smoking; alcohol intake >20 conventional doses per week; arterial hypertension; a history of cardiovascular diseases (CVD), in particular ischemic heart disease, acute myocardial infarction, acute cerebrovascular accident, chronic heart failure >III stage according to NYHA, as well as type 2 diabetes mellitus (DM); body mass index >25 kg/m2 and >30 kg/m2; cholesterol level (CHOL) >5.1 mmol/l; glomerular filtration rate (GFR) < 60 ml/min/1.73 m2; serum uric acid level >360 μmol/l; hypercalcemia (serum calcium level >2.62 mmol/L); CRP level >2 mg/l; the presence of hyperparathyroidism (parathyroid hormone level >65 pg/ml); CPPD phenotypes (asymptomatic, osteoarthritis with calcium pyrophosphate crystals, chronic arthritis, acute arthritis); intake of COL, HC, MT, glucocorticoids and non-steroidal anti-inflammatory drugs (NSAIDs).Results and discussion. 264 patients were under dynamic observation. Any of the studied cardiovascular events were registered in 79 (29.9%) patients. During the observation period, 46 (17.4%) patients died, in 76.1% of cases the cause of death was CVD. Death from other causes was diagnosed in 11 (23.9%) patients. Non-fatal cardiovascular events were reported in 44 (16.7%) cases. The risk of cardiovascular events was higher in patients over 65 years of age (odds ratio, OR 5.97; 95% confidence interval, CI 3.33–10.71), with serum cholesterol levels ≥5.1 mmol/L (OR 1,95; 95% CI 1.04–3.65), GFR

The main direction of drug therapy for gout and other diseases associated with hyperuricemia is the long-term use of drugs aimed at correcting the level of uric acid. However, in addition to the urate-lowering effect, these drugs may have other beneficial pleiotropic effects. The article will discuss the additional effects of xanthine oxidase inhibitors, as well as drugs used to treat gout-related diseases that have urate-lowering effects.

Endothelial dysfunction associated with chronic microcrystalline inflammation plays a role in the progression of atherosclerosis in calcium pyrophosphate crystal deposition diseases (CPPD).The aim of the study was to assess the dynamics of the development of atherosclerosis based on changes in the thickness of the intima-media complex (ICIM) of the carotid arteries (CA) in patients with CPPD receiving long-term anti-inflammatory therapy (colchicine, methotrexate, hydroxychloroquine).Materials and methods. 26 patients with CPPD and 26 patients with osteoarthritis aged over 18 years old were included. Exclusion criteria: age >65 years; presence of cardiovascular diseases. The blood lipid spectrum, hs-CRP level, anthropometric parameters were determined for all, and Doppler ultrasound ultrasonography of the carotid arteries (CA) was performed. Patients were followed up for not 0.9 mm were detected in 11 of 22 (50%) patients with CPPD and in OA in 8 of 19 (42%) (p=0.39). In dynamics, patients with CPPD revealed a decrease in the number of patients with ICIM>0.9 mm from 42 to 18%. At the same time, in 8 patients with CPPD, ICIM>0.9 mm was combined with a CRP level >0.2 mg/l. Out of 22 patients with CPPD, 14 (64%) patients showed a decrease in the mean values of ICIM, in 2 (9%) patients - an increase, in 5 patients the mean values of ICIM did not change. After 6 months of therapy, out of 11 patients with CPPD with ICIM >0.9 mm, after 6 months of therapy, in 7 cases there was a decrease in the indicator less than the specified value, in 5 of them a decrease in serum CRP level

Calcium pyrophosphate deposition disease (CPPD) is characterized by polymorphism of clinical manifestations: from asymptomatic course to severe chronic arthropathy with destruction of bone structures. It is believed that calcium pyrophosphate crystals are more often found in the knee and so-called root joints (hip and shoulder), as well as in the triangular fibro-cartilaginous complex. However, CPPD can also affect the axial skeleton. A pathological process localized in the spine is more common in older people and is rare at a young age. The article presents a case of chondrocalcinosis of the cervical spine in a 62-year-old female patient who did not have risk factors.

To this date there have been no studies of subclinical atherosclerosis in the patients with calcium pyrophosphate crystal deposition disease (CPPD); in osteoarthritis (OA) such works are rare.Objective: to assess the prevalence of subclinical atherosclerosis of carotid arteries (CA) in patients with CPPD and OA.Patients and methods. The case-control study included 26 patients with CPPD and OA. The diagnosis of CPPD was based on the criteria of D.J. McCarty, diagnosis of OA was based on national clinical practice guidelines. We recorded data on smoking, blood pressure level. Assessed blood lipid spectrum, serum levels of glucose, creatinine, uric acid, CRP. Obesity was diagnosed in accordance with the WHO recommendations. All patients underwent CA Doppler ultrasonography (DUS). An increase in intima-media thickness (IMT) >0.9 mm was considered a manifestation of subclinical atherosclerosis. The SCORE index was calculated for all patients.Results and discussion. The median serum CRP level was comparable in CPPD and OA. The CRP level >5 mg/L was detected in 8 patients with CPPD and in 3 patients with OA (p=0.09). Initial signs of atherosclerosis were present in 11 (42%) patients with CPPD and in 8 (31%) patients with OA (p=0.39). In CPPD, an increase in IMT was associated with a CRP level of ≥5 mg/L in 19% of cases, and in OA – in 12.5% (p=0.08). An increase in IMT >1.3 mm was not found in patients of both groups.Conclusion. In patients with CPPD and OA, subclinical atherosclerosis is often present according to the CA ultrasound. Early detection of uncomplicated subclinical atherosclerosis in CPPD and OA is necessary for timely initiation of treatment aimed to prevent the progression of atherosclerosis and the development of cardiovascular diseases.

Gout is the most common inflammatory arthritis in adults and has continued to increase in prevalence over the past decades. Gout is characterized by hyperuricemia with the obligatory crystallization of urates and an associated inflammatory reaction, as well as metabolic effects caused, among other things, by these processes. In particular, the diagnosis of gout is identified with a high risk of carbohydrate metabolism disorders, which is 2 times higher than the population risk: according to various sources, from 21 to 26% of patients with gout have type 2 diabetes mellitus (DM 2). However, the role of uric acid and urate-lowering drugs in its development in patients with gout remains controversial. The possibility of influencing the risk of developing diabetes mellitus type 2 of chronic inflammation, the activity of interleukin-1β and other pro-inflammatory cytokines, hyperuricemia, xanthioxidase and other factors associated with gout is discussed. It is possible that the level of uric acid is associated with diabetes and other metabolic diseases, causing pathophysiological changes not only through inflammation, but also oxidative stress, damage to the vascular endothelium. It is also suggested that gout and DM 2 may share genetic markers. The interrelation of violations of purine and carbohydrate metabolism prompts the search for drugs that have a simultaneous positive effect on purine and carbohydrate metabolism. However, it is not clear what the level of uric acid should be considered as a risk factor, there are conflicting data on the possibility of reducing the risk of developing diabetes with various anti-gout therapies.

Calcium pyrophosphate crystal deposition disease (CPPD) is a disease caused by the deposition of calcium pyrophosphate crystals, mainly in the articular cartilage, and often manifests as severe acute or chronic arthritis. Therapy given in such cases with non-steroidal anti-inflammatory drugs, colchicine, methotrexate and glucocorticoids is often effective. In these cases, the possibility of prescribing biological drugs, primarily interleukin 1 (IL-1) inhibitors, is being considered. The article analyzes the experience of using Anakinra, an IL-1 receptor antagonist, registered in the Russian Federation in 2021, in 5 patients with persistent arthritis in CPPD. The article also presents an analysis of data from key studies on the use of the drug in patients with CPPD.

Objective: to investigate the efficacy and safety of low-dose colchicine in patients with gout receiving urate-lowering therapy (ULT).Patients and methods. A single-center prospective study included 113 patients with gout. The main group consisted of 92 patients who were prescribed colchicine 0.5 mg/day combined with ULT (allopurinol or febuxostat), control group – 21 patients with contraindications to colchicine therapy who received only ULT. Patient data were entered into individual registration cards at the first visit, as well as on the 90th and 180th day after the start of drug intake. The presence of arthritis attacks was recorded by doctor or patient using a validated questionnaire. We compared the mean frequency of arthritis attacks in the groups, their duration and maximum pain intensity according to the visual analogue scale (VAS). Laboratory tests included: complete blood count test, general urinary test, uric acid (UA), blood glucose, alanine aminotransferase, aspartate aminotransferase, creatinine, serum creatine phosphokinase.Results and discussion. Patients who did not receive prophylactic anti-inflammatory therapy had significantly longer duration of the disease and higher number of affected joints. For 6 months of follow-up, there were no arthritis attacks in 54% of patients who were prescribed colchicine, and only in 19% of patients who did not use prophylactic anti-inflammatory therapy (p=0.004). The duration of arthritis attacks and the intensity of pain according to the VAS were also statistically significantly lower in the colchicine group (p

Colchicine is a drug that has been known for several millennia, since the days of Ancient Egypt, but has been successfully used to treat gout to this day. The action of colchicine is based on microtubule damage, mitosis suppression, as well as the ability to inhibit the activation of NLRP3 inflammasoma by monosodium urate crystals and block the release of interleu-kina (IL)-1p - key cytokine in the development of gout inflammation. However, the mechanism of action of colchicine is still not fully understood.Colchicine should be considered as the optimal drug not only for relieving an acute attack of arthritis in gout, but also as the best method for preventing attacks of gouty arthritis when choosing urate-lowering therapy. Recent studies have confirmed the good efficacy and safety profile of the drug when used correctly in patients with gout. Currently, it is recommended to use low doses of the drug (1-1.5 mg per day to relieve an acute attack of arthritis and 0.5-1.0 mg to prevent attacks when initiating uratelowering therapy). At the same time, according to the results of recent studies on the effectiveness, low doses are not inferior to high doses, but when low doses are used, the frequency of undesirable effects is much less. Unlike non-steroidal anti-inflammatory drugs and glucocorticoids, the drug does not have a negative effect on the cardiovascular system and can be used in patients with diabetes mellitus. This allows the drug to be used for a long time, which is especially important, since it is recommended to prevent arthritis attacks for at least 6 months from the start of taking urate-lowering drugs. This avoids the exacerbation of arthritis in most patients and significantly reduces their frequency. In addition, in the light of the accumulating data on the effect of the drug on the cardiovascular system of the drug, in conjunction with the high safety profile, other points of application should be considered where both anti-inflammatory and cardioprotective properties of colchicine can be used.

The article presents a case of periodic fever (PF) in a 35-year-old patient, who did not have hereditary and proven genetic factors of the disease, which was characterized by an atypical course with variable in duration and frequency severe abdominal pain and febrile fever attacks, increased acute phase reactants and ineffectiveness of colchicine intake. Differential diagnosis with a wide range of febrile conditions was performed. Daily subcutaneous therapy of interleukin 1 inhibitor (iIL1) at a dose of 100 mg was used as a diagnostic marker to confirm the diagnosis of PF. As a result of the therapy, a rapid (within a few hours after injection) relief of the current attack of the disease, normalization of serum CRP levels, and further complete control over the disease (no relapses) were achieved. Our observation shows that a positive response to iIL1 therapy can serve as a diagnostic marker of PF.

Gout can have a significant impact on the quality of life (QoL) of patients.Objective: to assess the dynamics of QoL indicators and the possibility of achieving the target level of uric acid (UA) in patients with gout on febuxostat therapy, with ineffectiveness and / or contraindications to the allopurinol administration.Patients and methods. The prospective, single-center study included 80 patients with gout. The follow-up period was at least 6 months of allopurinol or febuxostat (Azurix®) therapy in doses required to achieve the target UA level. When urate-lowering therapy was initiated, allopurinol 100 mg per day was prescribed, followed by dose titration (up to maximum of 900 mg per day) until the target UA level was reached (

The community of many national and international recommendations dedicated to the treatment of a specific disease, including gout, is fully justified, since it allows taking into account, for example, regional, ethnic characteristics of the manifestations of the disease, which can be important when choosing a therapy. However, this is often associated with dissonance regarding the solution of key issues facing the practitioner. The publication in 2020 of the updated American College of Rheumatology (ACR) guidelines for the management of gout revealed controversy with some of the previous version’s postulates, as well as with other similar work, for example, with the guidelines published in the same year and the French Association of Rheumatology. Among the controversial provisions of the new version of the ACR recommendations are the unified target level of uric acid for all patients, indications for drug therapy, the choice of a drug in patients with reduced renal function, prevention of arthritis attacks when starting uratelowering therapy. This article discusses these and other controversial issues in gout therapy based on an analysis of the latest ACR guidelines.

Non-steroidal anti-inflammatory drugs (NSAIDs), colchicine and glucocorticoids (GC) are used to prevent arthritis attacks in gout, but data on their comparative effectiveness is lacking.Objective: to compare the efficacy and safety of various anti-inflammatory drugs at the start of treatment in patients with gout.Patients and methods. Of the 108 patients with gout, observed in the V.A. Nasonova Research Institute of Rheumatology, 97 (94%), mostly men, entered a single-center prospective study. The observation period was at least 24 weeks, patients received combined urate-lowering and prophylactic anti-inflammatory therapy unintermittingly. The control group included 12 patients in whom anti-inflammatory drugs were contraindicated. At the start of urate-lowering therapy, allopurinol 100 mg per day was prescribed, followed by dose titration until the target uric acid (UA) level of < 360 μmol/L level was reached, in patients with severe tophus gout it was < 300 μmol/L. The maximum dose of allopurinol was 900 mg per day; in patients with reduced glomerular filtration rate (

Updated ACR recommendations for the treatment of gout concerning lifestyle are discussed. Factors related to a lifestyle, above all food habits, for many years were of leading importance in the treatment of patients with gout, even after application of effective drugs. The authors of the updated ACR recommendations for the first time offered to reconsider the role of environmental factors in the genesis of gout and objectively assess the possibility of its non-drug treatment. On the one hand, regardless of the activity of the disease, the need for restrictions of the alcohol, purine-rich products and fructose-containing beverages, as well as the decrease of body weight in obese patients and vitamin C usage unviability are confirmed. On the other hand, these recommendations are conditional. Their new version of ACR recommendations is significantly different from both its previous version and other international and national recommendations, including recommendations on the diagnosis and treatment of gout used in the Russian Federation.

Clinical guidelines have long been one of the working tools of the modern doctor, helping him quickly navigate the most effective proven methods of treatment and prevention of various diseases, and also to adapt these methods to the specific tasks of their patients and to achieve maximum personalization of treatment. Clinical practice guidelines are drawn up by professional non-profit associations and are approved by the Scientific Council of the Ministry of Health of the Russian Federation, while often one recommendation is prepared by two or even three associations. The peculiarity of the recommendations offered to your attention is that not only endocrinologists, but also therapists, cardiologists, gynecologists, gastroenterologists, and experts of many other specialties are involved in the prevention and treatment of obesity. The Multidisciplinary Working Group presents this a project in a multidisciplinary journal to bring together the efforts of several professional associations that associated with the need to pay attention not only to obesity itself but also to comorbid conditions. We are looking forward to constructive criticism and a comprehensive discussion of the problem on the pages of our journal.

Background. Cardiovascular diseases (CVD) is the leading cause of death for gout. Arterial hypertension is a proven CVD risk factor (CVD-RF).Objective. To assess the factors influencing on development of an arterial hypertension in patients with a gout. Subjects and methods. 286 male patients fulfilling Wallace proposed criteria for gout were included in the study: age 51.2 [42.8; 59.4] years, disease duration - 6.2 [3.8; 12.1] years, number of joints involved during disease course - 7 [4; 12], subcutaneous tophi - in 35% of patients, intraosseous tophi - in 44%, nephrolithiasis - in 69%, abdominal obesity - in 71%. All patients underwent standard clinical examination, C-reactive protein (CRP), total cholesterol, triglycerides, low and high density lipoproteins, serum uric acid, serum creatinine, smoking, family history of arterial hypertension, body mass index (BMI), diabetes mellitus was performed by standard procedure. We estimated the adjusted odds ratio (OR) and 95% confidence interval (95% CI).Results. There were two groups of patients with arterial hypertension diagnosed on clinical data: group 1 (with arterial hypertension) - 244 (85%) patients, group 2 (without arterial hypertension) - 42 (15%) patients. The group 1 patients were older (52.3 [44.5; 61.1] vs 41.9 [38.3; 50.1] years old), had longer duration of gout (6.7 [3.9; 13.7] vs 4.5 [3; 7.9]), a higher number of joints involved during disease course (8 [4; 12] vs 5 [3; 9]). The frequency of family history of arterial hypertension (68.3 vs 48.8%), abdominal obesity (55.3 vs 33.3%), nephrolithiasis (71 vs 54.7%), intraosseous tophi (48 vs 21%) was higher in group 1 as compared with group 2, р

Hyperuricemia is an increase of uric acid (UA) concentration in blood serum >420 pmol/L in men or >360 pmol/L in women and is considered to be a common biochemical abnormality. This condition shows that the extracellular fluid is oversaturated with urates, which concentration exceeds the limit of their solubility. This fact predisposes to the formation of crystals of sodium salt of UA and results in gout, urolithiasis, and other diseases. The frequent combination and relationship between purine and carbohydrate metabolism were noted in previous studies. In this regard, the choice of drugs for correcting these disorders should consider the possibility of a combined positive effect on the UA and serum glucose levels. The hypoglycemic drugs with pleiotropic effects on several metabolic syndrome components are considered to be of particular interest. Currently, one of the most frequently prescribed groups of drugs in the treatment of diabetes mellitus type 2 are dipeptidyl peptidase-4 inhibitors, which affect the level of incretins (gliptins). These drugs can be potentially attractive in patients with purine metabolism disorders since the available data indicate that these drugs affect UA level.

Low compliance in patients with gout is one of the reasons for inadequate disease control.Objective: to study treatment adherence in compliance with the national guidelines for the management of gout patients, which provide for the continuous use of urate-lowering drugs, a gradual increase in their dose until the target serum uric acid (UA) level is reached, prophylactic antiinflammatory therapy, and regular patient monitoring.Patients and methods. This was a prospective single-center study. By now, 60 of the 80 enrolled gout patients had completed the study. The follow-up period was at least 24 weeks, during which allopurinol or febuxostat was used at the final dose. During initiation of urate-lowering therapy, allopurinol 100 mg/day was prescribed, followed by dose titration to reach the target UA level (

Cardiovascular risk (CVR) in patients with calcium pyrophosphate crystal deposition disease (CPPD) has not been studied, and the optimal method for assessing it has not been established yet.Objective: Evaluation of CVR and comparison of results using Adult Treatment Panel III (ATP III) and Reynolds Risk Score (RRS) scales in patients with CPPD, gout, rheumatoid arthritis (RA) and in the control group.Materials and methods: Cross-sectional, single-center study performed by case-control method. There are 42 patients with CPPD in main group, 42 patients with gout and RA in the comparison groups are, 42 healthy volunteers in the control group. The survey included measurements of anthropometric measures, blood pressure (BP), serum glucose, creatinine, cholesterol (TC), high density lipoproteins (HDL), low density lipoproteins (LDL), C-reactive protein (CRP). CVR was assessed on ATP III and RRS scales, comparison of its evaluation results was carried out between groups and between scales within groups.Results and discussion: Most of the parameters in the compared groups did not differ. However, HDL CS levels were significantly higher in patients with CPPD and in the control group than in RA and gout (p0.05). The CRP > 5 mg/L in CPPD and in the control group was greater than in RA (p

The curation of patients with gout involves the mandatory prescription of pathogenetic therapy with urate-lowering drugs, among which xanthine oxidase inhibitors, such as allopurinol and febuxostat, are most widely used. According to various national and international guidelines, allopurinol is the first line drug for gout. However, there is a large cohort of patients, in whom the use of febuxostat is not only justified, but is also preferable. First of all, these are patients who are intolerant to allopurinol and at a high risk of severe skin reactions. There is a high risk of mortality and a low probability of achieving the target uric acid level when allopurinol is prescribed for patients with diminished renal function. Taking into account the fact that febuxostat has a pronounced nephroprotective effect, prescribing the drug in these patients will be a more effective way to achieve normouricemia. At the same time, the presence of cardiovascular diseases, although this requires additional caution when choosing therapy, should not be a reason for refusal to take febuxostat, since the results of many studies not only have failed to confirm a higher risk for cardiovascular events during therapy with this drug, but also have shown that it has cardioprotective properties.

The emergence of updated American College of Rheumatology (ACR) guidelines for the management of gout may serve as a prerequisite for revising the draft Russian Federal Clinical Guidelines (FCGs). Despite some differences, it should be noted that both guidelines are similar in key points concerning the principles of drug correction of hyperuricemia, indications for prescription and algorithms for the use of specific medicaments. The proximity of positions can be also traced in the need for the priority use of xanthine oxidase inhibitors (allopurinol and febuxostat) for urate-lowering therapy (ULT), which is aimed at implementing the target principle of gout management – the strict, constant control of serum levels of uric acid (its value should not exceed 6 mg/dl, or 360 μmol/l). The practical results of ULT in accordance with the basic principles outlined in the FCG have been published earlier.

Gout is an auto-inflammatory tophaceous disease characterized by the deposition of crystals of monosodium urate and developing in connection with this inflammation in people with hyperuricemia (HU). Except to genetic factors, risk factors for the development of HU and gout are many modifiable factors, including metabolic syndrome and obesity, and their correction is the most important component of successful disease control. Obesity can change the clinical picture of gout, characterized by an earlier onset, a large number of affected joints. Weight loss helps reduce uric acid (UA) serum levels. Bariatric / metabolic surgery significantly reduces the incidence of comorbid obesity and mortality, and is by far the most effective way to combat obesity. In addition to improving health, an important goal of bariatric surgery is to improve the quality of life. Bariatric surgery can prevent the development of HU in subjects with an initially normal level of serum UA before surgery. The dynamics of the concentration of UA in serum can be a predictor of successful bariatric surgery and help in predicting the severity of postoperative weight loss. The decrease in body weight after bariatric surgery leads to a decrease in UA in the long-term postoperative period, however, there is a high frequency of acute gout attacks in the early postoperative period. Thus, bariatric surgery has a significant effect on HU and gout and can be an effective treatment for this disease.

The data accumulated to date suggests that it is extremely rare for a gout patient to have only his or her main disease and no accompanying pathology. One of the frequent situations is a combination with another microcrystal arthritis, a disease of calcium pyrophosphate crystals deposition. In addition, diseases of the kidneys (including chronic renal failure), cardiovascular system, gastrointestinal tract, as well as metabolic disorders directly associated with gout or indirectly related to taking medications necessary to control the disease, not only affect the quality and longevity of life of the patient, but also create difficulties for its curation. The prescription of drug therapy, both symptomatic and pathogenetic, in such cases involves an assessment of all the associated risks, and the choice of drugs, in addition to efficiency, should be based on their safety profile in relation to comorbid pathology. This article analyzes the main principles and approaches to the treatment of gout and the disease of calcium pyrophosphate crystals deposition in the presence of concomitant diseases (arterial hypertension, chronic kidney disease, chronic heart failure, obesity, dyslipidemia, etc.) on the example of a 50-year-old patient. The possibilities of combined symptomatic therapy including colchicine, non-steroidal anti-inflammatory drugs and glucocorticoids are shown. The necessity and tactics of choice of preventive prophylactic therapy for arthritis attacks and use of phebuxostat in the presence of contraindications for prescription or ineffectiveness of allopurinol are also discussed.

Currently, only two drugs for reducing uric acid (UA), allopurinol and febuxostat, are registered in the Russian Federation, but their use does not allow to achieve the target level of UA in all cases. According to the results of numerous randomized trials, hyperuricemia and gout are associated with the corresponding components of the metabolic syndrome, including diabetes mellitus. The influence of factors is due to the need to search for new drugs that have a complex effect on several components of metabolic syndrome at once. Potentially attractive in this regard is a new group of drugs for the treatment of type 2 diabetes mellitus inhibitors of the sodium-glucose cotransporter of type 2, which, in addition to the main hypoglycemic actions, showed positive effects on the cardiovascular system, kidneys, as well as lowering UA.

The 2018 national guidelines for the management of gout provide a consistent scheme for urate-lowering drugs; however, the possibility of achieving uric acid (UA) targets in its use has not been studied.Objective: to evaluate the effectiveness and safety of the urate-lowering therapy algorithm presented in the national guidelines for the management of gout.Patients and methods. This investigation was a prospective single-center study. It has been currently included 54 patients (91% males) with gout. The follow-up period is not less than 12 weeks of continuous use of allopurinol or febuxostat (Azurix) at the final dose.After the initiation of urate-lowering therapy, allopurinol 100 mg/day was prescribed, followed by dose titration to achieve the UA target that was defined as

Interview with a leading expert in the treatment of gout, head of the laboratory of microcrystalline arthritis of the Federal State Budget Scientific Institution “Scientific Research Institute of Rheumatology named after V.A. Nasonova“ candidate of medical sciences Maxim Sergeevich Eliseev.

Abstract The determination of the effective electron neutrino mass via kinematic analysis of beta and electron capture spectra is considered to be model-independent since it relies on energy and momentum conservation. At the same time the precise description of the expected spectrum goes beyond the simple phase space term. In particular for electron capture processes, many-body electron-electron interactions lead to additional structures besides the main resonances in calorimetrically measured spectra. A precise description of the $$^{163}$$ 163 Ho spectrum is fundamental for understanding the impact of low intensity structures at the endpoint region where a finite neutrino mass affects the shape most strongly. We present a low-background and high-energy resolution measurement of the $$^{163}$$ 163 Ho spectrum obtained in the framework of the ECHo experiment. We study the line shape of the main resonances and multiplets with intensities spanning three orders of magnitude. We discuss the need to introduce an asymmetric line shape contribution due to Auger–Meitner decay of states above the auto-ionisation threshold. With this we determine an enhancement of count rate at the endpoint region of about a factor of 2, which in turn leads to an equal reduction in the required exposure of the experiment to achieve a given sensitivity on the effective electron neutrino mass.

Calcium pyrophosphate deposition disease (CPPD) is more common at an old age. The age-related features of the disease have not been studied.Objective: to study age-related features of CPPD.Subjects and methods. A total of 113 patients (54 men and 59 women) who had received inpatient or outpatient treatment at the V.A. Nasonova Research Institute of Rheumatology were retrospectively analyzed. The inclusion criteria were age older than 18 years, crystal-verified diagnosis of CPPD, and a signed informed consent.The patients were divided into two groups: 1) older than 55 years (n=38) and younger than 55 years (n=75). The investigators compared the frequency of clinical symptoms, including phenotypes in accordance with the EULAR recommendations, the intensity of pain with a visual analogue scale (VAS), the need for symptomatic therapy, detection rates for chondrocalcinosis (CC) in the knee and wrist joints by radiography, anthropometric and laboratory (the serum levels of C-reactive protein (CRP), creatinine, uric acid, parathyroid hormone, magnesium, phosphorus, and total calcium) features, the presence of CPPD-associated factors (a history of joint injuries, family CC cases, hypomagnesemia, hyperparathyroidism (HPT), hemochromatosis, hypomagnesemia, rheumatoid arthritis (RA), gout, chronic kidney disease (CKD) Stage >3, and use of diuretics).Results and discussion. Thirty-eight (33.6%) of the 113 examined patients with CPPD were aged less than 55 years. The most common clinical form of CPPD was chronic arthritis (n=54; 47.8%), the less common forms were osteoarthritis (OA) with calcium pyrophosphate (CPP) crystals (n=35; 31%) and acute arthritis (n=24; 21.2 %); their rates did not differ in the formed groups.In patients older than 55 years, the pain intensity according to VAS was higher than that at a younger age (50 [40; 70] mm and 40 [25; 54] mm, respectively; p5 mg/dL was comparable for both groups. Family CPPD cases were recorded in two patients less than 55 years of age. Knee joint radiography significantly more frequently revealed CC in 65 (57.5%) patients aged older than 55 years than that at a younger age (68 and 36.8%, respectively; p=0.001). Hand radiography detected CC in 21 (18.6%) patients, it was also more common in those aged older than 55 years (25.3 and 5.3%, respectively; p=0.001).The CPPD-associated factors include OA, gout, HPT, RA, and CKD >3 Stage; these diseases detected in this study were seen in 91 (80.5%), 28 (24.8%), 14 (12.4%), 5 (4.4%), and 12 (11%) cases, respectively. There were no significant differences in the detection rates for these diseases in patients younger and older than 55 years of age. Also, one patient had hypomagnesemia and one patient had hemochromatosis; both were younger than 55 years old.Conclusion. The prevalence of CPPD at a young age can be underestimated: 33.6% of the patients with CPPD confirmed by the detection of CPP crystals in synovial fluid were aged less than 55 years. Moreover, the frequency of individual phenotypes and main CPPD-associated factors is identical in different age groups. At the age of older than 55 years, CPPD is characterized by the more frequent detection of radiographic signs of CC, a greater need for NSAIDs and colchicine, and a high level of CRP.

Calcium pyrophosphate crystal deposition disease (CPCDD) is among the most common inflammatory rheumatic diseases; however, studies of cardiovascular risks in CPCDD have not been conducted.Objective: to stratify a cardiovascular risk in patients with CPCDD according to the systematic coronary risk evaluation (SCORE) algorithm that allows determination of an individual 10-year risk of cardiovascular death.Subjects and methods. The one-stage, single-center study of a cardiovascular risk enrolled 118 patients (43 men and 75 women) with CPCDD. Laboratory studies included determination of fasting serum glucose, total cholesterol, uric acid, magnesium, phosphorus, and total calcium. The level of C-reactive protein (CRP) was measured by a highly sensitive method; CRP >5 mg/L was taken as a high level; parathyroid hormone was determined by chemiluminescence immunoassay. The SCORE table was used to assess the total cardiovascular risk in all the patients.Results and discussion. The patients' mean age was 60.7±12.4 years. According to the SCORE scale, very high and high risks of cardiovascular death were found in 59 (50%) and 6 (5%) patients, respectively; only in 10% of cases this risk was associated exclusively with age (> 65 years); 60 (50.8%) of the 118 patients did not have previous cardiovascular events or atherosclerosis risk factors. Coronary heart disease was detected in 28.8% of the 118 patients; hypertension was identified in 64%; diabetes mellitus (DM) was found in almost 15%. The mean SCORE values did not significantly differ in men and women. The level of CRP was higher in men than that in women (8.6±4.6 and 7.3±3.5 mg/dL, respectively; p = 0.04). Glomerular filtration rate (GFR) 100 ml/min: 61% (60/98) and 25% (5/20) of patients, respectively (p = 0.003). Hyperparathyroidism (HPT) was detected in 12 (10%) patients, and 7 of them were at a very high risk by the SCORE scale; however, hypercalcemia was diagnosed in only three cases. The results of the SCORE stratification of the whole group showed that 64 (54.2%) of the 118 patients with CPCDD were at a very high or high risk, the latter was very high in exactly half of the cases (n = 59.Conclusion. One-half of patients with CPCDD have a very high cardiovascular risk. In addition to the high detection rate of traditional cardiovascular risk factors (hypertension, smoking, hypercholesterolemia, and DM), the presence of chronic microcrystalline inflammation, concomitant metabolic disorders and diseases (hyperuricemia, HPT, decreased renal function) should be taken into account when determining the cardiovascular risk in patients with CPCDD.

Asymptomatic hyperuricemia (AHU) is a condition, in which the serum concentration of uric acid (UA) is increased (>420 μmol/l in men or >360 μmol/l in women) and there are no signs of the formation of urate crystals. The worldwide prevalence rate of AHU has been on the increase in recent decades: it has been detected in approximately every five inhabitants of the Earth. In 10% of adults, hyperuricemia (HU) occurs at least once in a lifetime. In the process of evolution, HU has been useful; it has contributed to the intellectual development of man, owing to the activation of neurostimulating adenosine receptors, and to his survival under cold and hunger conditions. However, the negative role of UA in the genesis of different metabolic disorders, cardiovascular diseases (CVD), and kidney diseases has been discussed in recent decades. The association of elevated UA levels with almost all CVD risk factors makes it difficult to answer the question of whether UA plays a causative role in the development of heart disease, kidney disease, or carbohydrate metabolism disorders, or it is only a marker for their increased risk.Whether HU that is uncomplicated by joint damage, urolithiasis, or urate nephropathy should be treated is another question that is currently being actively discussed. Although the routine prophylactic urate-lowering therapy is not indicated in the vast majority of cases of AHU, there is growing evidence that this correction is necessary in some groups of patients. The use of xanthine oxidase (XO) inhibitors in a number of trials was accompanied by a reduction in the risk of CVD and by an improvement in renal function. Epidemiological studies have also established that there is a significant positive correlation of the serum concentration of UA with obesity, dyslipidemia, insulin resistance, and cerebrovascular and peripheral vascular diseases. Further investigations are needed to study the impact of lowering UA levels and that of therapy with XO inhibitors on the progression of different diseases.

The frequency of vascular calcification in patients with osteoarthritis (OA) and calcium pyrophosphate crystal deposition disease (CPPD) has not yet been studied, and the role of calcium crystals (basic and pyrophosphates) in the development of calcification is also unknown.Objective. Determine the presence and degree of calcification of the coronary vessels in patients with calcium pyrophosphate crystal deposition disease and osteoarthritis of the knee joints with no clinical signs of cardiovascular diseases.Materials and methods. One-stage, single-center study, performed by the “case – control” method. The main group – 20 patients with CPPD, the comparison group – 20 patients with OA of the knee joints. Inclusion criteria: age from 18 to 65 years; absence of clinical signs of cardiovascular disease at the time of examination and indications of a history of cardiovascular accidents. Exclusion criteria: unsigned informed consent; pregnancy; breastfeeding; other rheumatic disease; cancer; high and very high cardiovascular risk on the SCORE scale. The survey included an assessment of anthropometric data, blood pressure (BP), lipid profile, serum levels of glucose, creatinine, uric acid, C-reactive protein, vitamin D, osteoprotegerin, parathyroid hormone, and the levels of magnesium, phosphorus, and total calcium were studied. All patients underwent multispiral computed tomography with determination of calcium count and the number of affected arteries. To calculate the coronary score, the A.S. Agatston et al.Results and discussion. Most of the parameters in the compared groups did not differ. When assessing the calcification of the coronary arteries according to the A.S. Agatston et al. 9 (45%) patients with CPPD and 8 (40%) patients with OA had a coronary calcium score >1. Quantitative indicators of calcium score can correspond to coronary artery stenosis ≥20% in 8 (40%) patients with CPPD and in 5 (25%) patients with OA according to J.A. Rumberger et al. The serum level of osteoprotegerin was significantly higher in patients with a calcium score ≥27 according to J.A. Rumberger et al. (p=0.04). Calcification was detected in 9 (56%) of 16 patients with serum vitamin D levels 30 ng/ml.Conclusions. In patients with an initially low cardiovascular risk, the probability of a combination of chondrocalcinosis and cardiovascular calcification is 45%, in OA it is 40%. The risk factors for coronary calcification in patients with CPPD and OA should be studied further.