Metabolic syndrome and gout - approaches to antihypertensive therapy

Metabolic syndrome and gout - approaches to antihypertensive therapy

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Regular issues of "RMZh" No. 27 dated December 25, 2005 p. 1880

Category: General articles

Authors: Shostak N.A. 1, Anichkov D.A. 1 Federal State Budgetary Educational Institution of Russian National Research Medical University named after. N.I. Pirogov Ministry of Health of Russia, Moscow, Russia

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Shostak N.A., Anichkov D.A. Metabolic syndrome and gout - approaches to antihypertensive therapy. RMJ. 2005;27:1880.

Introduction Metabolic syndrome (MS) is a set of cardiovascular risk factors, united by a common pathogenetic mechanism, resistance of peripheral tissues to insulin [1]. The main components of MS are arterial hypertension, abdominal obesity, decreased high-density lipoprotein cholesterol (HDL-C), hypertriglyceridemia and fasting hyperglycemia [2]. At the same time, disturbances in uric acid metabolism, changes in the hemostatic system, endothelial dysfunction, increased levels of C-reactive protein and insufficient reduction in blood pressure at night often accompany MS [3]. These anomalies have pathogenetic, clinical and, in some cases, prognostic significance. Thus, insufficient reduction of blood pressure at night is associated with target organ damage and an increased risk of cardiovascular events in patients with arterial hypertension [4]. Therefore, normalization of the circadian rhythm of blood pressure in patients with MS can be considered as an additional goal of antihypertensive therapy [5].

Metabolic syndrome (MS) is a set of cardiovascular risk factors, united by a common pathogenetic mechanism, resistance of peripheral tissues to insulin [1]. The main components of MS are arterial hypertension, abdominal obesity, decreased high-density lipoprotein cholesterol (HDL-C), hypertriglyceridemia and fasting hyperglycemia [2]. At the same time, disturbances in uric acid metabolism, changes in the hemostatic system, endothelial dysfunction, increased levels of C-reactive protein and insufficient reduction in blood pressure at night often accompany MS [3]. These anomalies have pathogenetic, clinical and, in some cases, prognostic significance. Thus, insufficient reduction of blood pressure at night is associated with target organ damage and an increased risk of cardiovascular events in patients with arterial hypertension [4]. Therefore, normalization of the circadian rhythm of blood pressure in patients with MS can be considered as an additional goal of antihypertensive therapy [5]. Patients with MS belong to the category of high risk of cardiovascular complications [6]. The European Society of Cardiology/European Society of Hypertension guidelines and the 7th report of the US Joint National Committee (JNC-7) recommend all effective and well-tolerated antihypertensive drugs for patients with diabetes mellitus and metabolic syndrome, with an emphasis in JNC-7 on diuretics and b- blockers. However, the effect of various antihypertensive drugs on lipid, carbohydrate and purine metabolism is different. From this point of view, the most justified is the use of modern long-acting ACE inhibitors (in particular, lisinopril). The drug is metabolically neutral [7,8], and according to some data, even increases tissue sensitivity to insulin [9]. It is relevant to study the effect of lisinopril on the level of uric acid in patients with MS. The rationale is based on the results of several modern studies. Hyperuricemia is a risk factor for cardiovascular morbidity [10]. High levels of uric acid increase the risk of the onset and progression of arterial hypertension [11,12]. Uric acid levels are a strong predictor of cardiovascular mortality in middle-aged men, even after controlling for factors often associated with metabolic syndrome and/or gout [13]. Both asymptomatic hyperuricemia and gout are closely associated with insulin resistance and metabolic syndrome. According to PH Dessein et al. (2000), hyperinsulinemia is observed in 95% of people with gout, metabolic syndrome – in 76% [14]. Hyperuricemia is closely related to hypertriglyceridemia [15]. In addition, hyperuricemia can serve as a surrogate marker of insulin resistance syndrome [16]. The possible relationship between hyperuricemia and vascular complications of arterial hypertension is presented in Figure 1. Thus, the purpose of this study was to evaluate the effects of lisinopril (Sinopril) and the comparator drug atenolol on the 24-hour blood pressure profile and the effect of Sinopril on uric acid levels in patients with MS. Atenolol was chosen due to its widespread clinical use and known hemodynamic and metabolic effects. Atenolol is often used as a comparator in clinical trials of antihypertensive drugs [17,18]. Material and methods An open, non-randomized comparative study was conducted in an outpatient setting. Inclusion criteria were: male or female gender; age from 30 to 60 years; a combination of arterial hypertension stages I and II according to the 2003 WHO classification [19] and two other signs of metabolic syndrome according to ATP III criteria [2]; informed consent. Patients were excluded if at least one of the following criteria was present: secondary arterial hypertension, a history of cardiovascular events, arrhythmias, decompensated diabetes mellitus requiring insulin treatment, extreme obesity (BMI>40 kg/m2), for women - pregnancy or lactation. At the screening stage, 41 patients met the inclusion criteria. However, 3 patients refused to participate in the study and 2 patients did not complete the washout period due to a pronounced increase in blood pressure. Thus, the study group consisted of 36 patients with MS. After a one-week introductory (“wash-out”) period, patients were randomly prescribed lisinopril (Sinopril®, JSC Pharm, Russia, together with Eczacıbaşı Pharmaceutical, Turkey) 10 mg or atenolol 50 mg once in the morning. The duration of therapy was 12 weeks. After 4 weeks Blood pressure and heart rate were monitored; if therapy was insufficiently effective, the dose of the drug (lisinopril or atenolol) was doubled while maintaining a single dose regimen. At baseline and after 12 weeks of therapy, a routine clinical examination was performed, including measurement of office blood pressure and heart rate values; anthropometric measurements (height, body weight, waist circumference). Daily blood pressure monitoring was carried out using Meditech ABPM-04 and Schiller BR-102 devices with assessment of average systolic, diastolic blood pressure and heart rate, as well as the degree of nocturnal decrease in blood pressure and heart rate. Patients were advised to maintain a normal activity schedule and keep a diary indicating the events that occurred and the time of night's sleep. Measurements were carried out at intervals of 15 minutes. afternoon and 30 min. at night. Baseline laboratory examination in the Sinopril and atenolol groups included assessment of the serum lipid profile: total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol (enzymatic method); fasting serum glucose (oxidase method). In the lisinopril group, all of the above parameters were also assessed after 12 weeks of therapy. Levels of uric acid, potassium and creatinine were assessed at baseline and after 12 weeks of therapy in the Sinopril group only. The main criteria for the effectiveness of therapy were: changes in average daily, average daily and average night blood pressure and heart rate, the degree of nocturnal decrease in blood pressure and heart rate, changes in uric acid levels. Additionally, the proportion of patients who responded to therapy (responders rate) was taken into account, with the response criterion being a decrease in office blood pressure to the target level of 140/90 mmHg. or more than 10% of the initial level. The safety of therapy was assessed by the presence of side effects (no side effects; side effects that do not require discontinuation of the drug; side effects requiring discontinuation) and the absence of unfavorable changes in laboratory parameters (creatinine, potassium). Statistical processing Statistical analysis was performed using the Statistica 6.0 software package (StatSoft Inc., USA). Descriptive statistics methods (mean, standard deviation, median, quartiles, absolute and relative frequencies) were used to present the data. To assess the type of distribution, visual analysis of distribution histograms and the Shapiro–Wilk test were used. Comparison of qualitative data was carried out using Fisher's exact test, quantitative (in the case of normal distribution) - using Student's test for related and unrelated samples. When the distribution of a trait differed from normal, nonparametric methods were used (Wilcoxon and Mann–Whitney tests). The significance level was set to 0.05. Results The initial characteristics of patients in the Sinopril and atenolol groups are presented in Table 1. There were no statistically significant differences between the groups, with the exception of office diastolic blood pressure and pulse rate. The initial indicators of 24-hour blood pressure monitoring were comparable, but there were differences in the average daily and average daily values ​​of systolic blood pressure and heart rate (Table 2). After treatment was prescribed, 1 patient in the Sinopril group was excluded due to an allergic reaction (skin rash). In 2 patients in the atenolol group, the drug was discontinued due to severe bradycardia. Thus, 23 patients in the Sinopril group and 10 patients in the atenolol group completed the study. Sinopril and atenolol equally reduced average daily systolic and diastolic blood pressure (Fig. 2). At the same time, Sinopril reduced systolic blood pressure to a greater extent during the night period, while atenolol decreased systolic blood pressure during the daytime period (Fig. 3). During therapy with atenolol, an expected decrease in heart rate was observed (day: –13.6±1.8 beats/min; daytime period: –15.5±2.0 beats/min., night period: –7.6± 1.1 beats/min., for all indicators p The effect of the studied drugs on the daily rhythm of blood pressure and heart rate is presented in Table 3. In the Sinopril group there were no significant changes in the degree of nocturnal decrease in blood pressure; there was a significant (p = 0.048) increase in the degree of nocturnal decrease Heart rate: In the atenolol group, there was a trend toward a decrease in the degree of nocturnal decrease in systolic blood pressure (p = 0.093) and a statistically significant decrease in the degree of nocturnal decrease in heart rate (p = 0.022).Both drugs showed similar effectiveness in relation to office systolic and diastolic blood pressure (-24 ± 4 /–14±2 mmHg in the Sinopril group and –21±6/–12±2 mmHg in the atenolol group; for all indicators – p Data on the effect of Sinopril on uric acid levels, serum lipids , creatinine and potassium are presented in Table 4. The effect on uric acid levels was positive, but did not reach the level of statistical significance. There was an increase in HDL cholesterol (p=0.018), other parameters did not change significantly. Discussion The choice of an antihypertensive drug in a patient with hyperuricemia and/or gout and MS is very difficult. In addition to high antihypertensive effectiveness and a beneficial effect on the characteristics of the circadian rhythm of blood pressure and heart rate, the drug should not increase the level of uric acid. The main drugs recommended by modern guidelines somehow affect the level of uric acid in the blood serum. Thus, therapy with diuretics is accompanied by an increase in uric acid; during treatment with b-blockers, there is a tendency to increase; at the same time, ACE inhibitors (for example, lisinopril) can reduce uric acid levels [20]. Therefore, the drug of choice in this group of patients may be lisinopril. According to our study, lisinopril (Sinopril), like the comparator drug atenolol, effectively reduces average daily blood pressure in patients with MS. At the same time, the response rate to therapy (according to office blood pressure measurements) in the Sinopril group was 79%, in the atenolol group - only 50%. It is interesting to note that Sinopril reduced nocturnal BP to a greater extent, and therefore favorable changes in the circadian BP rhythm were observed, while atenolol worsened the characteristics of the circadian BP rhythm. The data obtained are consistent with the results of other researchers who studied the effect of lisinopril and atenolol on the circadian rhythm of blood pressure [8,21]. Noteworthy is the positive dynamics of the degree of nocturnal decrease in heart rate in the Sinopril group and negative dynamics in the atenolol group. According to the literature, insufficient reduction of heart rate at night worsens the prognosis in patients with arterial hypertension [22]. Therefore, our results may have clinical implications. Sinopril therapy led to a decrease in uric acid levels, which, however, did not reach the level of statistical significance. The drug increased HDL cholesterol levels, but other indicators remained virtually unchanged. Literary data on the effect of ACE inhibitors on uric acid levels are contradictory. Thus, in a study by DeRosa et al. [23] reported an increase in serum uric acid concentration in patients with arterial hypertension during 3 years of enalapril therapy. On the other hand, there is evidence that lisinopril neutralizes the increased level of uric acid caused by hydrochlorothiazide [24]. The positive effect of lisinopril on serum uric acid levels is due to an increase in uricosuria [20]. Thus, Sinopril has a significant antihypertensive effect (response rate 79%), characterized by normalization of the daily blood pressure profile, an increase in the degree of nocturnal decrease in heart rate and blood pressure, and has a beneficial effect on the lipid profile (increased HDL) and uric acid metabolism. Conclusions 1. Sinopril demonstrates an effect comparable to atenolol on 24-hour blood pressure monitoring. 2. The characteristics of the circadian rhythm of blood pressure do not change under the influence of Sinopril therapy; atenolol adversely affects the circadian rhythm of systolic blood pressure. 3. Sinopril, in contrast to atenolol, increases the degree of nocturnal decrease in heart rate. 4. During Sinopril therapy, there is a tendency for uric acid levels to decrease and HDL cholesterol levels to increase. References 1. Reaven GM. Metabolic syndrome. Pathophysiology and implications for management of cardiovascular disease. Circulation 2002;106:286–8 2. Grundy SM, Brewer Jr HB, Cleeman JI, et al. Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation 2004;109:433–8 3. McFarlane SI, Banerji M, Sowers JR. Insulin resistance and cardiovascular disease. J Clin Endocrinol Metab 2001;86:713–8 4. Ohkubo T, Imai Y, Tsuji I. Prognostic significance of the nocturnal decline in blood pressure in individuals with and without high 24-h blood pressure: the Ohasama study. J Hypertens 2002;20:2183–2189. 5. Palatini P, Parati G. Modulation of 24–h blood pressure profiles: a new target for treatment? J Hypertens. 2005;23:1799–1801. 6. Lakka HM, Laaksonen DE, Lakka TA, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle–aged men. JAMA 2002; 288:2709–16 7. Thurig C, Bohlen L, Schneider M, et al. Lisinopril is neutral to insulin sensitivity and serum lipoproteins in essential hypertensive patients. Eur J Clin Pharmacol 1995;49:21–6 8. Reisin E, Weir MR, Falkner B, et al. Lisinopril versus hydrochlorothiazide in obese hypertensive patients: a multicenter placebo–controlled trial. Treatment in Obese Patients With Hypertension (TROPHY) Study Group. Hypertension 1997;30(1pt 1):140–5 9. Fogari R, Zoppi A, Corradi L, et al. Comparative effects of lisinopril and losartan on insulin sensitivity in the treatment of non diabetic hypertensive patients. Br J Clin Pharmacol 1998;46:467–71 10. Wang JG, Staessen JA, Fagard RH, Birkenhager WH, Gong L, Liu L. Prognostic significance of serum creatinine and uric acid in older Chinese patients with isolated systolic hypertension. Hypertension 2001;37(4):1069–74. 11. Nagahama K, Inoue T, Iseki K, et al. Hyperuricemia as a predictor of hypertension in a screened cohort in Okinawa, Japan. Hypertens Res 2004;27:835–41 12. Sundstrom J, Sullivan L, D'Agostino RB, et al. Relations of serum uric acid to longitudinal blood pressure tracking and hypertension incidence. Hypertension 2005;45:28–33. 13. Niskanen LK, Laaksonen DE, Nyyssonen K, et al. Uric acid level as a risk factor for cardiovascular and all-cause mortality in middle-aged men: a prospective cohort study. Arch Intern Med 2004;164:1546–51. 14. Dessein PH, Shipton EA, Stanwix AE, et al. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis 2000;59:539–43 15. Clausen JO, Borch–Johnsen K, Ibsen H, Pedersen O. Analysis of the relationship between fasting serum uric acid and the insulin sensitivity index in a population–based sample of 380 young healthy Caucasians. Eur J Endocrinol 1998;138:63–9 16. Fam AG. Gout, diet, and the insulin resistance syndrome. J Rheumatol 2002;29:1350–5. 17. UK Prospective Diabetes Study Group. Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. BMJ 1998;317:713–20. 18. Dahlof B, Devereux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the losartan intervention for endpoint reduction in hypertension study (LIFE): a randomized trial against atenolol. Lancet 2002;359:995–1003. 19. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. J Hypertens. 2003;21(11):1983–92. 20. Reyes AJ. Cardiovascular drugs and serum uric acid. Cardiovasc Drugs Ther. 2003;17(5–6):397–414 21. Munakata M, Imai Y, Hashimoto J, et al. The influence of antihypertensive agents on circadian rhythms of blood pressure and heart rate in patients with essential hypertension. Tohoku J Exp Med. 1992;166(2):217–27 22. Verdecchia P, Schillaci G, Borgioni C, et al. Adverse prognostic value of a blunted circadian rhythm of heart rate in essential hypertension. J Hypertens 1998;16:1335–43. 23. De Rosa ML, Cardace P, Rossi M, Baiano A, de Cristofaro A. Comparative effects of chronic ACE inhibition and AT1 receptor blocked losartan on cardiac hypertrophy and renal function in hypertensive patients. J Hum Hypertens. 2002;16(2):133–40. 24. Leonetti G. Comparison of metabolic and hemodynamic effects of hydrochlorothiazide in monotherapy and in association with lisinopril. An Italian multicenter study. Minerva Cardioangiol. 1995;43(9):389–98

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Difficulties in managing patients with gout

For citation. Bashkova I.B., Madyanov I.V. Difficulties in managing patients with gout // RMZh. 2015. No. 25. pp. 1508–1514.

Gout is a systemic tophi disease characterized by the deposition of monosodium urate crystals in various tissues and the resulting inflammation in individuals with hyperuricemia (HU) caused by environmental and/or genetic factors [1]. In the last two decades, there has been a steady increase in the incidence of gout, probably associated both with the characterological characteristics of patients (increased living standards, changes in diet, excessive alcoholism) [2] and with the spread of metabolic diseases in the population (obesity, metabolic syndrome, diabetes mellitus (DM), arterial hypertension (AH)), often accompanying gout [3–5]. Despite advances in diagnosis, understanding of pathogenesis and development of effective drugs for the treatment of gout, managing this category of patients can present certain difficulties for internists. The diagnosis of gout is made in the first year of the disease only in 1/4 of cases, but on average 7–8 years pass before the correct diagnosis is made [1]. The reason for late diagnosis may be the natural course of the disease - the alternation of rare, and short-term attacks of monoarthritis, with longer “bright intervals” of the disease due to the inherent self-limiting nature of gouty arthritis. Another explanation for the late diagnosis of gout can be the fact that the “first contact” doctor for this disease is often a surgeon or traumatologist, who, seeing a patient with acute, extremely painful arthritis, sends him for an X-ray examination of the affected joint, with the help of which diagnosis can be made. the debut of gout is often not possible, since large cysts in the subchondral zone of the bone (the so-called “puncture” symptom or X-ray negative intraosseous tophi) appear much later - on average 7–8 years from the moment of the first attack of gout [6, 7]. In the absence of bone-destructive changes on radiographs of the distal foot, the condition is regarded as a “soft tissue contusion,” which is usually accompanied by recommendations for taking nonsteroidal anti-inflammatory drugs (NSAIDs), which, due to their effectiveness in this situation, convince the doctor and patient of the validity of the incorrect diagnosis. In some cases, it is possible to predict the scenario for the further development of the disease: the patient will try to stop each subsequent attack of monoarthritis on his own, taking the NSAID that he “liked the first time,” until either an adverse reaction to the drug appears, or the NSAIDs cease to have the expected effect. Among the typical mistakes that doctors make when treating patients with acute gouty arthritis are: prescribing physiotherapeutic procedures, analgesics, ointments/gels applied locally in the area of ​​the affected joint, prescribing allopurinol at the time of an attack, delay in prescribing effective analgesic and anti-inflammatory therapy [8 ]. Untimely and ineffective treatment of gout contributes not only to the aggravation of comorbid pathology, which is typical for this category of patients, in particular coronary heart disease (CHD) [9], but also to the development of fatal complications. We present our own observation when a combination of gout, GU, disorders of carbohydrate and lipid metabolism, hypertension, as well as the patient’s inattention to his health caused the death of a young man.

Patient S., 42 years old,

was hospitalized in the rheumatology department of the Republican Clinical Hospital (Cheboksary) on April 29, 2014 with complaints of constant intense pain in the left knee, ankle, metatarsophalangeal joints of the first toes of both feet, a number of proximal interphalangeal joints of the hands, worsening at night. From the medical history: the first attack of acute arthritis of the metatarsophalangeal joint of the 1st toe of the right foot developed 10 years ago, subsequently the arthritis recurred, the articular process gradually became polyarthritic in nature, and there was a natural reduction in the intervals between attacks to 2–3 months. The patient did not consult a doctor; he occasionally took nimesulide on his own. In 2009, he suffered an acute anteroseptal-apical myocardial infarction with a Q wave; in the same year, hyperglycemia (fasting blood sugar level 13.6 mmol/l) and GU (serum uric acid level 572 μmol/l) were first detected. Prescribed antiplatelet (acetylsalicylic acid 100 mg/day, clopidogrel 75 mg/day), oral hypoglycemic (metformin 1000 mg/day), lipid-lowering (atorvastatin 20 mg/day), uricodepressor (allopurinol 100 mg/day) drugs, β-blockers ( The patient did not take bisoprolol 5 mg/day after discharge from the hospital. Since 2010, there has been a rapid growth of tophi localized on the ears, in the area of ​​the joints of the hands and feet, and an exacerbation of gouty arthritis with an increase of up to 5–6 rubles/year. In April 2014, after an alcoholic excess (alcohol abuse for 7 days), a severe exacerbation of chronic gouty arthritis developed: pain, swelling, local hyperemia and hyperthermia of the left knee joint, ankle, metatarsophalangeal joints of the first toes, a number of metacarpophalangeal and proximal interphalangeal joints of both hands. Intramuscular administration of diclofenac 75 mg 2 times / day and oral administration of nimesulide 400 mg / day - without effect. In the left heel area there is a wound measuring 1.5x1.0 cm (ulcerated tophi) with a white curdled discharge. The patient independently consulted a surgeon; on an outpatient basis, an increase in blood sugar level to 27.8 mmol/l and uric acid level to 686 μmol/l was detected, and therefore the patient was sent to a rheumatology hospital on April 29, 2014. Upon admission, the patient’s condition severe, forced position due to pain in the left knee joint, deformation of the knee (more than the left), ankle joints, multiple non-ulcerated tophi localized on the auricles, in the area of ​​​​the joints of the hands (Fig. 1) and feet (Fig. 2), ulcerated tophi in the left calcaneal area. There is no peripheral edema. Body mass index – 25.6 kg/m2. On percussion there is a clear pulmonary sound throughout all pulmonary fields. In the lungs there is vesicular breathing, there are no wheezes at the time of examination. The boundaries of relative dullness of the heart: right - along the right edge of the sternum, upper - in the third intercostal space, left - 1.0 cm outward from the midclavicular line. Blood pressure (BP) – 160/100 mmHg. Art. Heart sounds are rhythmic, systolic murmur on the left edge of the sternum. The abdomen is soft, sensitive to palpation in the right hypochondrium. Liver - along the edge of the costal arch. The effleurage symptom is negative on both sides.

In the general blood test: red blood cells – 4.93×1012/l, hemoglobin – 149 g/l, platelets – 61×109/l, leukocytes – 4.2×109/l, leukoformula shift to the left (young neutrophils – 2%, band neutrophils – 35%), absolute lymphopenia (0.38×109/l), ESR according to the Panchenkov method – 36 mm/h. General urine analysis: proteinuria (0.36 g/l), microscopy of urinary sediment revealed: leukocyturia (10–12 per field of view), microhematuria (6–8 red blood cells per field of view), cylinduria (hyaline and granular), urates a lot. In the biochemical blood test: total bilirubin - 21 µmol/l, ALT - 89 U/l (with the upper limit of normal up to 40 U/l), AST - 135 U/l (with the upper limit of normal up to 40 U/l), urea – 14.4 mmol/l, creatinine – 215 µmol/l, total protein – 62 g/l, total cholesterol – 3.64 mmol/l, glucose – 15.0 mmol/l, uric acid – 761 µmol/l, high-sensitivity C-reactive protein (CRP) – 426 mg/l (with the upper limit of normal up to 5 mg/l). On a radiograph of the joints of the feet in a direct projection (dated April 28, 2014): large cysts in the subchondral zone of the metatarsal and proximal phalanges of the 1st toe and small erosions on the articular surfaces, significant compaction of the periarticular soft tissues in the area of ​​the metatarsophalangeal joint of the 1st toe right foot (Fig. 3).

A diagnosis was made of “Primary chronic tophi gout, predominantly of a severe metabolic type. Chronic gouty polyarthritis, activity level 3, radiological stage II. Functional joint insufficiency of the 3rd degree. GU (761 µmol/l). Multiple large non-ulcerated tophi localized on the ears, in the area of ​​​​the joints of the hands and feet, ulcerated tophi in the left heel area. Chronic gouty nephropathy, azotemic stage, CKD stage 3B. Type 2 diabetes, diabetic nephropathy, diabetic macroangiopathy, target level of glycosylated hemoglobin less than 7%. Risk category for developing diabetic foot syndrome 2. IHD: post-infarction cardiosclerosis (acute myocardial infarction with Q wave from 2009). Stage III hypertension. Degree of hypertension 2. Risk 4 (very high). Chronic heart failure (CHF) stage IIA (FC3).” Taking into account the decrease in excretory function of the kidneys due to the patient's renal failure (glomerular filtration rate according to EPI - 35 ml/min), type 2 diabetes, the use of NSAIDs and glucocorticoids (GC) to relieve exacerbation of chronic gouty polyarthritis was contraindicated. For analgesic purposes, intramuscular injections of tramadol 200 mg/day were prescribed, and therapy with short-acting insulin (10 U every 4 hours) was started. On April 30, 2014, at 8:30 p.m., the patient felt severe general weakness, increased thirst, dry mouth, and cold sweat. Blood pressure – 85/40 mm Hg. Art. An urgent blood test for sugar was performed - a slight hyperglycemia (9.3 mmol/l) was detected, the patient was administered a 5% glucose solution, prednisolone 90 mg, after which the patient's condition improved somewhat, but after 1 hour there was again a sharp increase in general weakness, profuse sweating When trying to get up, the patient fell, lost consciousness, cyanosis of the face and shoulder girdle appeared, blood pressure was 40/15 mm Hg. Art. The electrocardiogram recorded signs of overload of the right parts of the heart (deviation of the electrical axis of the heart to the right, P-pulmonale, deep S wave in lead I, negative T wave in lead III, right bundle branch block). To exclude acute myocardial infarction, the serum level of troponin I was examined, which was 0.148 μg/L (normally less than 0.5 μg/L). At the same time, the concentration of D-dimer in the blood serum turned out to be increased several times and amounted to 2021 μg/l (with the norm being up to 500 μg/l). Resuscitation measures were started, but they were unsuccessful - with increasing symptoms of acute cardiopulmonary failure, biological death was declared after 80 minutes. The cause of death was pulmonary embolism.

Gout is often accompanied by comorbid diseases [10–12], which can affect its course and prognosis. Hypertension and coronary artery disease are complicated by the development of chronic heart failure (CHF), which, undoubtedly, requires the doctor to prescribe diuretic drugs. In this situation, it is important to remember that all diuretics increase uric acid levels. In a population-based study of 4249 UK residents over the age of 30 years, a clinically verified diagnosis of gout was established in 164 patients, while in 25 (15%) patients, gout was induced by taking diuretics, 16 (64%) of them still continued take diuretics [13]. GU that occurs during treatment with diuretics may be due to an increase in reverse reabsorption and a decrease in urate secretion in the renal tubules, which, against the background of decreased renal circulation, leads to an increase in the production of angiotensin, which further inhibits the secretion of uric acid [14]. In addition, furosemide leads to an increase in lactic acid levels, which in turn inhibits urate excretion [15]. There is an immutable rule - diuretics prescribed for health reasons (CHF) to patients with gout must be compensated by taking allopurinol with dose titration under the supervision of a rheumatologist [7]. It is necessary to take into account the increasing incidence of abuse of diuretics by young women for cosmetic reasons (to improve their figure, etc.) [14, 16]. We present our own observation - a case of autoiatrogenicity - the development of secondary gout in a young woman, induced by long-term use of furosemide.

Patient A., 34 years old

, was admitted to the rheumatology department of the Republican Clinical Hospital (Cheboksary) on October 5, 2014 with complaints of constant intense pain, swelling and redness in the area of ​​the metatarsophalangeal joint of the 1st toe of the left foot, which persisted for a week. From the medical history: in 2000 (at the age of 20 years), the patient, for cosmetic purposes, in a short period of time, adhering to a strict diet with limited animal protein, reduced her body weight by 20 kg. Subsequently, in order to maintain the “ideal” body weight, she independently began to take furosemide, ½ tablet 1 time/2–4 weeks. Without taking a diuretic, the patient began to subjectively feel shortness of breath, heaviness in the heart area, linking these phenomena with fluid retention, she increased the dose of the drug to 10-12 tablets per dose. In 2005 (5 years of constant use of furosemide), she first noted the appearance of pain, swelling and local hyperemia in the area of ​​the right ankle joint, which stopped spontaneously after 3 days, but despite this, she continued to take furosemide at the same dose. In 2010, pain and swelling in the area of ​​the right ankle joint arose again and subsequently recurred every 2–3 months, and arthritis of the metatarsophalangeal joint of the 1st toe of the left foot was added. To relieve joint pain, the patient increasingly began to resort to intramuscular injections of ketorolac. Due to the lack of effect from the use of NSAIDs, in 2014 she turned to a rheumatologist at the RCH. When examining the patient, rheumatoid arthritis, urogenital form of reactive arthritis, spondyloarthritis, and systemic lupus erythematosus were excluded. In the biochemical blood test, attention was drawn to an increase in serum levels of urea (25.5 mmol/l), creatinine (128 μmol/l), total cholesterol (9.4 mmol/l), and uric acid (495 μmol/l). To clarify the diagnosis, the patient was hospitalized in the rheumatology department. From physical examination: body mass index – 18.2 kg/m2; for organs and systems – without features; pain on palpation and deformation of the metatarsophalangeal joint of the 1st toe of the left foot with local hyperemia and hyperthermia (Fig. 4). An additional laboratory study revealed an increase in ESR to 54 mm/h, hypoisosthenuria, nocturia, hyper-alpha-2-globulinemia (14%), Fredrickson type IIb hyperlipoproteinemia, GU (654 µmol/l), a decrease in daily uric acid excretion to 0.8 mmol/day (with a norm of 1.5–4.5 mmol/day). According to esophagogastroduodenoscopy, mucus and clear bile were detected in the gastric cavity; the gastric mucosa was diffusely hyperemic and edematous. An X-ray of the foot joints in a direct projection (dated October 12, 2014) showed a slight narrowing of the joint spaces of the metatarsophalangeal joints of the 1st toes, and single cyst-like lucencies in the head of the 1st metatarsal bone on the left (Fig. 5).

A diagnosis was made of “Secondary gout induced by long-term use of furosemide, renal (hypoexcretory) type. Chronic gouty arthritis of the right ankle joint, metatarsophalangeal joint of the 1st toe of the left foot, activity of the 3rd degree, X-ray stage I. GU (654 µmol/l). Chronic interstitial nephritis, latent course. CKD stage 2. Hyperlipoproteinemia type IIb. Chemical gastropathy caused by bile reflux.” Furosemide was immediately stopped, and the drinking regimen was expanded to 1.5–2 l/day (previously I drank no more than 300–500 ml). The uric acid level dropped to 631 µmol/L within 14 days. To relieve arthritis, the patient was prescribed amtolmetin guacil (AMG) at a dose of 1200 mg/day in 2 divided doses. The drug was well tolerated. After complete relief of inflammatory phenomena in the joint (after 7 days) against the background of continued use of AMH in the hospital, therapy with allopurinol was initiated at an initial dose of 100 mg/day with recommendations for titrating the dose of the latter until normouricemia is achieved (the target level of uric acid in the blood serum is less than 360 µmol/ k) on an outpatient basis.

Errors made in the management of patients with chronic gouty arthritis are also quite common. Among them: 1) prescription of allopurinol during the acute period of the disease; 2) in some cases, the dose of allopurinol is not titrated to the most effective one, allowing to achieve the target value of uric acid level; 3) discontinuation of allopurinol when normouricemia is achieved; 4) unreasonable prescription of glucocorticoids (GC) to relieve exacerbation of chronic gouty arthritis, which in turn can lead to aggravation of metabolic disorders associated with gout (hypertension, type 2 diabetes, dyslipidemia), the development of secondary adrenal insufficiency when treatment is discontinued, and the rapid growth of intradermal tophi with long-term use, a decrease in the effectiveness of GCs after 1 year of therapy (the strength of their action of GCs becomes comparable to NSAIDs) [8, 17, 18]; 5) resection of subcutaneous tophi without achieving normouricemia, which creates a threat of infection of long-term non-healing skin defects [19]. Similar therapeutic errors made by primary care physicians in the management of patients with gouty arthritis are pointed out by M.V. Sklyanov and A.N. Kalyagin. When they conducted an anonymous survey of 50 local therapists in Irkutsk, it turned out that 56% of doctors admit the possibility of prescribing allopurinol in the acute period of the disease, every fourth (26%) indicated the necessary withdrawal of allopurinol after achieving normouricemia, 10% of doctors in their clinical practice have never prescribed patients with gout received allopurinol, while 44% of respondents indicated the advisability of using allopurinol in people with asymptomatic HU [20]. We present our own observation when the uncontrolled use of GC in the absence of achieving normouricemia served as the reason for the surgical removal of subcutaneous deposits of uric acid salts, which was inevitably accompanied by an exacerbation of chronic gouty arthritis and led to long-term non-healing of the wound surface.

Patient A., 60 years old,

was admitted to the rheumatology department of the Russian Clinical Hospital (Cheboksary) on October 19, 2015 with complaints of constant intense pain, swelling and redness in the area of ​​the right ankle joint, a number of metatarsophalangeal joints of the right foot, a wound that did not heal within 1 year in the area of ​​the 2nd toe of the right foot after amputation performed on September 8, 2014. From the medical history: at the age of 45 years, acute arthritis of the metatarsophalangeal joint of the 1st toe of the right foot developed for the first time, which resolved on its own after 7 days. The first visit to a general practitioner was several years after a series of recurrent arthritis of the same metatarsophalangeal joint. The examination revealed GU (serum uric acid level at that time was 456 µmol/l). A diagnosis of gout, chronic gouty arthritis was made; after the gouty attack was relieved by NSAIDs (diclofenac 150 mg/day for 10 days), therapy with allopurinol at a dose of 100 mg/day was started. The dose of the latter drug has not been revised for 12 years. Against this background, the patient notes the addition of arthritis of the joint of the same name in the left foot, ankle, elbow, wrist joints, and metacarpophalangeal joint of the 2nd finger of the right hand. Exacerbation of the disease - more than 5 rubles / year; in the area of ​​​​the joints of the hands and feet, subcutaneous formations (tophi) have appeared in the area of ​​​​the joints of the hands and feet over the last 7-8 years, with an increase in their size and number. Attacks of arthritis, on the recommendation of a general practitioner, were treated with intramuscular injections of ketorolac, less commonly, diclofenac or taking nimesulide. I constantly used ointments/gels on the area of ​​the affected joints at the time of joint attacks, and took dietary supplements widely advertised in the media in order to reduce the level of uric acid in the blood. Retrospective review of outpatient medical records revealed persistent HU with a minimum uric acid value of 571 μmol/L. In September 2014, he consulted a surgeon due to the appearance of intense pain, swelling, redness in the area of ​​the 2nd toe of the right foot with swelling and hyperemia spreading to the back of the foot, as well as an increase in body temperature. Blood tests revealed neutrophilic leukocytosis without a shift to the left (11.0×109/l), increased ESR (46 mm/h) and CRP level (85.8 mg/l). An X-ray of the joints of the right foot in a direct projection (dated 09/08/2014): multiple cysts of the epiphyses of the metatarsal bones and phalanges of the fingers and erosions on the articular surfaces, compaction of the periarticular soft tissues in the area of ​​the metatarsophalangeal joints of the right foot (Fig. 6). The condition was regarded as “acute purulent arthritis”, as a result of which on 08.0.2014 amputation of the 2nd toe of the right foot was performed (Fig. 7), followed by the prescription of antibacterial therapy. At the time of surgery, a large amount of cheesy white discharge was obtained in the absence of purulent exudate. The wound healed by secondary intention; to this day, a skin defect remains at the base of the 2nd toe of the right foot with periodic discharge of tophi masses from the wound. In the last 2 years, the patient noted frequent relapses of arthritis of the right wrist, knee and ankle joints; the use of NSAIDs (diclofenac, ketorolac, nimesulide, meloxicam) became ineffective, as a result of which intramuscular injections of prolonged betamethasone were used to relieve chronic gouty arthritis in the following months. Rapid growth of tophi was observed (Fig. 8). In March 2015, due to an increase in body temperature to 39°C, the appearance of pain in the lumbar region, and an increase in general weakness, he was hospitalized in the nephrology department of City Clinical Hospital No. 1 (Togliatti). Laboratory testing revealed leukocytosis (13.0×109/l) with a shift of the leukoformula to the left (band neutrophils - 8%), an increase in ESR to 55 mm/h; in urine analysis - proteinuria (1.19 g/l), leukocyturia and bacteriuria during microscopy of urinary sediment. There was a decrease in the glomerular filtration rate according to EPI to 61 ml/min against the background of hypercreatininemia (125 µmol/l) and renal concentration function (diurnal fluctuations in the relative density of urine from 1004 to 1009, nocturia - nighttime versus daytime diuresis - 1.49 l versus 0. 8 l). An ultrasound examination of the kidneys revealed a decrease in the thickness of the parenchyma with an increase in its echodensity with multiple foci of fibrosis up to 4–5 mm, tuberosity of the kidney contour, and an expansion of the renal collecting system, which indicated that the patient had chronic pyelonephritis, which was probably secondary. A diagnosis of “Chronic gouty nephropathy with kidney damage similar to chronic interstitial nephritis” was made. Secondary chronic pyelonephritis, exacerbation. CKD stage 2." Against the background of antibacterial (ceftriaxone 2 g/day) and antihypertensive (amlodipine 10 mg/day and losartan 100 mg/day) therapy, improvements in general blood and urine tests, normalization of blood pressure, and a decrease in serum creatinine levels to 102 μmol/l were observed. (GFR according to EPI - 79 ml/min). Upon discharge, the patient was recommended to consult a rheumatologist to select a dose of allopurinol, but the patient continued to take the drug at a dose of 100 mg/day, followed by a series of exacerbations of chronic gouty arthritis, for the relief of which GCs were repeatedly used. From the life history it is known that the patient suffers from gastric ulcer with rare recurrence of ulcers. Denies alcohol abuse. During a physical examination at the time of hospitalization in the rheumatology department: body mass index – 23.2 kg/m2; for organs and systems – without features; pain on palpation and deformation of the right wrist and ankle joints with local hyperemia and hyperthermia, swelling of the dorsum of the right foot, mainly at the base of the fingers, multiple tophi localized on the hands and feet. An additional laboratory study revealed an increase in ESR (according to the Panchenkov method) to 21 mm/h and CRP to 18.9 mg/l, hypoisosthenuria, GU (551 µmol/l) with a decrease in daily excretion of uric acid to 1.0 mmol/day (at a norm of 1.5–4.5 mmol/day). On the radiograph of the joints of the hands in a direct projection: cyst-like clearings in the epiphyses of the bones, small erosions on the articular surfaces, narrowing of the joint spaces of a number of metacarpophalangeal and interphalangeal joints, significant compaction of the periarticular soft tissues in the projection of the metatarsophalangeal joints of the 3 fingers of both hands (Fig. 9 ).

A diagnosis was made of “Primary chronic tophi gout, predominantly of a severe metabolic type. Chronic gouty polyarthritis, activity level 2, radiological stage II. Functional joint insufficiency of the 2nd degree. GU (551 µmol/l). Multiple large non-ulcerated tophi localized in the joints of the hands and feet. Chronic gouty nephropathy of the type of chronic interstitial nephritis, azotemic stage, stage 2 CKD. Condition after disarticulation of the 2nd toe of the right foot. Stage II hypertension. The achieved degree of hypertension is 1. Risk 3 (high).” To relieve arthritis, the patient was prescribed AMG 600 mg twice a day (with recommendations to take the drug strictly on an empty stomach). Against the background of continued AMH intake, the dose of allopurinol was increased to 200 mg/day after 1 week. The serum uric acid level was re-determined to be 370 µmol/L, which required further titration of the allopurinol dose until normouricemia was achieved (target uric acid level less than 360 µmol/L) while continuing preventive anti-inflammatory therapy for AMH.

At the time of exacerbation of chronic gouty arthritis, the doctor is faced with the task of stopping the arthritis as quickly, effectively and safely as possible. In this case, NSAIDs become the first-line drugs. According to M.S. Eliseev and V.G. Barskova, it can be either a non-selective or a selective inhibitor of cyclooxygenase-2, provided that its anti-inflammatory and analgesic effect is realized as quickly as possible with a minimum incidence of adverse reactions [18]. In recent years, a fundamentally new non-selective NSAID has appeared in the arsenal of domestic doctors - amtolmetin guacil (Naisylat®, Dr. Reddy's Lab), which, along with a pronounced analgesic and anti-inflammatory effect, has a gastroprotective effect. The latter became possible thanks to the modification of the tolmetin molecule by introducing the amino acid vanillin, which made it possible to achieve the protective effect of AMH in relation to the mucous membrane of the gastrointestinal tract (GIT) while maintaining the class-specific positive effects of NSAIDs. The gastroprotective properties of the drug are associated with stimulation of capsaicin receptors (the so-called vanilloid receptors, the name of which comes from the presence of a vanillin group in the AMH molecule) located in the walls of the gastrointestinal tract. Excitation of capsaicin receptors leads to the release of a peptide encoded by the calcitonin gene, which in turn leads to a local increase in the production of nitric oxide (NO) in the gastric mucosa, and not in other organs and tissues [21, 22]. As is known, NO is one of the important components of the endogenous system for protecting the mucous membrane of the upper gastrointestinal tract from damage; it maintains the integrity of the structure by increasing mucus formation and bicarbonate secretion, increasing blood flow and repair of epithelial cells, reducing neutrophil chemotaxis and lipid peroxidation. The effectiveness and safety of AMH have been demonstrated in a number of clinical studies. Thus, A. Tavella and G. Ursini showed greater effectiveness of 4-week therapy with AMH compared to diclofenac in patients with musculoskeletal pain in reducing the severity of pain at rest, during movement, as well as dysfunction [23]. A meta-analysis of 18 clinical studies by R. Marcolongo et al. to evaluate the safety of AMH in patients with osteoarthritis and rheumatoid arthritis compared with other non-selective NSAIDs, such as diclofenac, tolmetin, indomethacin, naproxen, piroxicam and ibuprofen, showed that the incidence of side effects and cases of premature discontinuation of therapy was lower in the AMH group . The odds ratio (OR) for adverse reactions of AMH compared with those of other NSAIDs assessed together was 0.2 (95% CI 0.1–0.3). During endoscopic assessment, the frequency and severity of damage to the mucous membrane of the upper gastrointestinal tract in the group of patients taking AMH were significantly lower than in the control groups - the OR for moderate and severe erosive and ulcerative changes was 0.1 (95% CI 0.1–04 ) [24]. Another study on the safety and effectiveness of AMH in patients with rheumatoid arthritis was conducted by a group of Croatian scientists. The 24-week randomized, placebo-controlled trial included 180 patients with rheumatoid arthritis, of which 85 patients received AMH 1200 mg/day and 95 received celecoxib 200 mg/day. Both NSAIDs demonstrated the same clinical efficacy (according to ACR-20) when assessed at 4, 12 and 24 weeks. therapy. When analyzing endoscopic data, there was no statistically significant difference in the groups using AMH or celecoxib; any gastrointestinal changes according to esophagogastroduodenoscopy were noted in 24.8% and 22.3% of patients, respectively. While the clinical manifestations of the symptom of dyspepsia (pain and discomfort in the epigastric region) after 4 weeks. therapies were less common when taking AMH [25]. The recommended dose of AMG is 600 mg 2 times / day (maximum daily dose - 1800 mg), the maintenance dose is 600 mg 1 time / day; to maintain the gastroprotective effect of the drug, AMG should be taken on an empty stomach. Studies have shown that AMH was well tolerated by patients even with long-term use (for 6 months). Among the registered rheumatological indications for the use of AMG are not only rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, damage to periarticular soft tissues (bursitis, tendovaginitis), but also articular syndrome with exacerbation of gout. And although there are currently no studies on the use of AMH in patients with gout, our positive experience of using a new effective non-selective NSAID with its own gastroprotective effect in relieving exacerbations of chronic gouty arthritis gives us the right to hope for the successful use of the drug in the fight against acute and chronic pain.

Medical Internet conferences

Long-term uncontrolled use of thiazide-like and loop diuretics leads to a decrease in renal blood flow and glomerular filtration rate, hyperuricemia. We present a clinical observation demonstrating the development of gout during diuretic therapy. Patient P., 36 years old, was admitted to the nephrology department of the Regional Clinical Hospital (RCH) in Saratov with complaints of weakness and shortness of breath on exertion. In 2005, she suffered from infective endocarditis with damage to the mitral valve, partial separation of the chordae of the posterior leaflet of the mitral valve. For 5 years, I took furosemide almost every day, 1-2 tablets per day, and triampur compositum for circulatory failure. In April 2010, at the age of 35 years, acute arthritis of the 1st metatarsophalangeal joint on the right developed, followed by arthritis of the interphalangeal joints of the hands. In August 2010, tophi appeared in the area of ​​the distal interphalangeal joints of the hands. In September 2010, during an examination before the planned surgical treatment of a heart defect, an increase in the blood creatinine level to 475.9 µmol/l was first detected, and therefore the patient was hospitalized in the nephrology department of the Regional Clinical Hospital. During the examination, anemia (hemoglobin 92 g/l), hyperazotemia (blood creatinine 316.3 µmol/l, urea 20.6 mmol/l), a decrease in serum iron levels to 8.3 µmol/l, hyperuricemia (uric acid - 1033.6 mmol/l), hyposthenuria (urine specific gravity 1003), glomerular filtration rate 24 ml/min. Ultrasound of the kidneys shows signs of bilateral nephrosclerosis. An X-ray of the feet shows signs of gouty arthritis; in the heads of the 1st metatarsal bones and in the head of the main phalanx of the 1st toe on the right there is an oval-shaped defect of bone tissue with sclerotic contours. An X-ray of the hands shows diffuse osteoporosis, cyst-like restructuring of the bone structure, narrowing of the joint spaces, and isolated lesions. The patient was entered into the register of people awaiting renal replacement therapy; conservative therapy for chronic renal failure was recommended, allopurinol at a dose of 50 mg/day under the control of blood uric acid and creatinine levels. This clinical case illustrates the development of gout associated with the use of diuretics, manifested by damage to the joints of the upper and lower extremities, rapid development of tophi, kidney damage with severe impairment of their functions.

Gout pills sir

Despite the successive economic crises, deteriorating environmental conditions and decreasing quality of products, life expectancy in most countries of the world is growing. We begin to live longer, and eat tastier and more varied than just half a century ago. It is these trends that are associated with the increase in the prevalence of gout.

Over the past 30 years, people have become twice as likely to suffer from the disease, the cause of which was determined even before our era by the famous physician Galen, who said that incontinence was to blame. Followers of Gargantua and Pantagruel, connoisseurs of tasty but not very healthy food, doom themselves to the risk of developing chronic arthritis, which is characterized by periodically recurring extremely painful attacks of inflammation, most often in the joint at the base of the thumb.

Like on broken glass

The immediate cause of the inflammatory process in gout is the accumulation of sharp uric acid salts and urates in the joint, like glass fragments. They physically damage the joint membrane, which is accompanied by excruciating pain, swelling and redness in the affected area.

The trigger, i.e. the trigger, for the development of an attack is often a hearty lunch or a hearty dinner. It is with foods, in particular meat, fish, coffee, tea, alcohol (especially beer), that purines enter the body, as a result of the decomposition of which uric acid is formed.

Gout almost always comes at night, suddenly. Overtaking a lover of delicious food in bed, it often does not allow him to leave the bedroom for several days - the pain is so severe. After the attack ends, usually after 5–7 days, the uric acid level returns to normal, and gout goes away on its own for a period of time.

Fortunately, in our time, there is no need to wait a week, languishing in excruciating pain in the tight fetters of gout, because there are drugs that can quickly improve your well-being.

And again NSAIDs

Gout is arthritis. And any inflammatory disease of the joints is treated primarily with the help of non-steroidal anti-inflammatory drugs. They do not affect the level of uric acid, but they allow you to quickly and effectively relieve pain and reduce the severity of inflammation.

The group of NSAIDs is extensive. And although all its representatives have both anti-inflammatory and analgesic properties, in case of an acute attack of gout, preference is given to those drugs that exhibit a powerful and rapid analgesic effect: naproxen, ketoprofen, ibuprofen, diclofenac and indomethacin. To achieve optimal results, the maximum dosage of drugs is prescribed for 10–14 days, depending on the response to therapy.

It should be remembered that while taking NSAIDs, gastrointestinal side effects may develop, and therefore for people suffering from peptic ulcers, gastritis and other gastrointestinal diseases, drugs from this group may be contraindicated.

Uricosuric drugs

Uricosuric drugs block the reabsorption of uric acid in the renal tubules, resulting in a decrease in its level in the blood. But while the urate content in the joints decreases, on the contrary, there is more of it in the urine (they are simply filtered from the blood into the urine). And this is already associated with the risk of stones and the development of kidney stones.

Uricosuric drugs include colchicine and probenecid. They are included in international recommendations for the treatment of an acute attack of gout. In order to prevent the formation of stones, colchicine and probenecid are prescribed in short courses and in low doses. However, Russians will not have to worry about the tolerability of uricosuric drugs, since today they are not registered in our country.

Uric acid synthesis blockers

Their name in pharmacology for most consumers sounds very “heavy” - xanthine oxidase inhibitors. However, most gout sufferers know this name by heart and take the appropriate medications.

Xanthine oxidase inhibitors include the well-known anti-gout drug allopurinol, which combines fairly pronounced activity with availability, as well as the much less economical febuxostat. Both the first and second block the enzyme involved in the synthesis of uric acid, which leads to a decrease in the level of urate in the blood.

Xanthine oxidase inhibitors are prescribed for both treatment and prevention of gout attacks (in long courses). However, starting to take drugs in this group can provoke an exacerbation of the disease, so they are not recommended to be prescribed during an acute inflammatory process.

Hit with hormones!

But drugs of adrenal hormones, glucocorticosteroids, unlike xanthioxidase inhibitors, are capable of stopping an acute attack of gout in a short time and very effectively. However, they are not prescribed to everyone and not always - the list of side effects when taking drugs from this group systemically is too long. Among the most common are edema, excretion of potassium, calcium, increased blood pressure, increased blood glucose levels, increased blood clotting, and menstrual irregularities.

To avoid the development of adverse reactions, corticosteroid hormones are prescribed only to those who cannot tolerate NSAIDs and colchicine, and only in short courses. Most often, prednisolone, triamcinolone, and corticotropin are used for this purpose in the form of tablets or injections.

Marina Pozdeeva

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