Hyperurikemie se vyskytuje u 60 % pacientů s chronickým onemocněním ledvin (CKD) a dna asi u 25 % těchto pacientů. I přes častý společný výskyt není vliv kyseliny močové na progresi onemocnění ledvin jednoznačně objasněn. O indika- cích k léčbě asymptomatické urikemie u pacientů s CKD se vedou spory. Převaha důkazů naznačuje, že asymptomatická hyperurikemie je pravděpodobně škodlivá, ale může se týkat zejména určitých podskupin pacientů, a to pacientů se systémovými depozity urátu, urátovou krystalurií nebo urolitiázou a pacientů s vysokou intracelulární hladinou kyseliny močové. Současné důkazy nepodporují nasazení inhibitorů xantinoxidázy ke zmírnění progrese CKD u pacientů s asymp- tomatickou hyperurikemií.
Hyperuricaemia occurs in 60% of patients with chronic kidney disease (CKD) and gout in about 25% of these patients. Despite the frequent co-occurrence, the influence of uric acid on the progression of kidney disease is not clearly understood. There is controversy over the indications for treatment of asymptomatic uricemia in patients with CKD. The preponderance of evidence suggests that asymptomatic hyperuricaemia is likely to be harmful, but may be particularly relevant to certain subgroups of patients, namely those with systemic crystal deposits, urate crystalluria or urolithiasis, and those with high intracellular uric acid levels. Current evidence does not support the deployment of xanthine oxidase inhibitors to ameliorate the progression of CKD in patients with asymptomatic hyperuricaemia.
- MeSH
- Acute Kidney Injury etiology therapy MeSH
- Renal Insufficiency, Chronic * diagnosis etiology drug therapy MeSH
- Hyperuricemia diagnosis drug therapy complications MeSH
- Clinical Studies as Topic MeSH
- Uric Acid blood MeSH
- Humans MeSH
- Kidney Diseases etiology MeSH
- Xanthine Oxidase antagonists & inhibitors MeSH
- Check Tag
- Humans MeSH
Kyselina močová (UA) se převážně tvoří v játrech, střevech a cévním endotelu jako konečný produkt metabolismu purinů získaných exogenně z potravy a endogenně z poškozených nebo mrtvých buněk. Ledviny hrají hlavní roli ve vylučování UA, eliminují asi 70 % denní produkce. Zbytek (přibližně 30 %) je vylučován střevem. Pokud tvorba UA překračuje její vylučování, vzniká hyperurikemie. Hyperurikemie je silně spojena s rozvojem a závažností metabolického syndromu. Nadměrná exprese urátového transportéru 1 (URAT1) a glukózového transportéru 9 (GLUT9) a narušení glykolýzy kvůli inzulinové rezistenci mohou souviset s rozvojem hyperurikemie u metabolického syndromu. Dříve se hyperurikemie po- važovala pouze za hlavní příčinu dny a dnavé artritidy. Také se předpokládalo, že hyperurikemie u pacientů s renálními onemocněními je důsledkem nedostatečného vylučování UA kvůli ledvinnému selhání, a proto nebyla cílem intenzivní léčby. Základní vědecké poznatky nyní naznačují, že hyperurikemie hraje patogenní roli při vzniku chronického onemocnění ledvin a kardiovaskulárních onemocnění, protože způsobuje endoteliální dysfunkci, proliferaci cévních hladkých svalových buněk a aktivaci renin-angiotenzinového systému. Další nashromážděné údaje naznačují, že léčba snižující hladinu UA zpomaluje progresi těchto onemocnění. Snížení hladiny UA je účinnou metodou pro zlepšení stavu, ale ne všechny látky snižující hladinu UA fungují stejně. V klinické praxi je třeba tyto látky používat s opatrností.
Uric acid (UA) is predominantly formed in the liver, intestine and vascular endothelium as an end product of the metabolism of purines derived from food and endogenously from damaged or dead cells. The kidneys play a major role in the excretion of UA, eliminating about 70 % of the daily production. The remainder (approximately 30 %) is excreted by the intestine. If the production of UA exceeds the capacity of its excretion, hyperuricaemia results. Overexpression of urate transporter 1 (URAT1), glucose transporter 9 (GLUT9) and impaired glycolysis due to insulin resistance may be related to the development of hyperuricaemia in metabolic syndrome. Hyperuricemia is associated with the development and severity of metabolic syndrome. Previously, hyperuricaemia was thought to be the main cause of gout and gouty arthritis only. It was also assumed that hyperuricemia in patients with renal disease was a consequence of inadequate UA excretion due to renal failure and therefore was not a target for intensive treatment. Basic scientific evidence now suggests that hyperuricemia plays a pathogenic role in the development of chronic kidney disease and cardiovascular disease by causing endothelial dysfunction, vascular smooth muscle cell proliferation, and activation of the renin- angiotensin system. Lowering UA levels is an effective method for improving the condition, but not all UA lowering agents work the same. In clinical practice, these agents should be used with caution. Further accumulating data suggest that UA-lowering therapy slows the progression of these diseases.
- MeSH
- Allopurinol administration & dosage therapeutic use MeSH
- Gout Suppressants antagonists & inhibitors pharmacology therapeutic use MeSH
- Febuxostat administration & dosage therapeutic use MeSH
- Hyperuricemia drug therapy complications MeSH
- Cardiovascular Diseases prevention & control MeSH
- Uric Acid blood MeSH
- Humans MeSH
- Metabolic Syndrome * diagnosis etiology therapy MeSH
- Check Tag
- Humans MeSH
Dna (arthritis urica) je chronické metabolické multifaktorové ochorenie, ktoré vzniká v dôsledku hyperurikémie. Ide o poruchu v metabolizme purínov. Patrí medzi liečiteľné reumatické ochorenia. Vzniká na hereditárnom podklade alebo pod vplyvom vonkajších faktorov. Medzi patologické prejavy dny patrí akútna dnová artritída, chronická dnová artritída, tvorba tofov, poškodenie obličiek a urolitiáza. Akútnemu dnovému záchvatu predchádza obdobie asymptomatickej hyperurikémie. Najdôležitejším laboratórnym nálezom je hyperurikémia. V liečbe dny sa využívajú nefarmakologické opatrenia a farmakoterapia. K nefarmakologickým opatreniam patrí nízkopurínová diéta a úprava životosprávy. Z farmakoterapie sa na liečbu dny používajú liečivá s protizápalovým účinkom (nesteroidné antiflogistiká (NSA), kolchicín, monoklonálne protilátky, glukokortikoidy) a liečivá znižujúce hyperurikémiu (urikostatiká, urikozuriká, urikázy). Urikozuriká sa momentálne v Slovenskej republike nepoužívajú, rovnako nie sú v súčasnosti dostupné ani v Českej republike, pegylovaná urikáza nie je aktuálne registrovaná v Európskej únii. Liekmi prvej voľby na zníženie zápalu a bolesti pri dne sú kolchicín a NSA, na zníženie hyperurikémie alopurinol. Liekom druhej voľby na zníženie hyperurikémie je febuxostat. Nové liečebné možnosti – monoklonálne protilátky a urikázy – sú liekmi druhej voľby. Lieky druhej voľby sú určené pre pacientov, ktorí netolerujú klasickú farmakoterapiu alebo trpia na ťažkú polyartikulárnu dnu.
Gout (arthritis urica) is chronic metabolic multifactor disease as a result of the hyperuricaemia. The disease is purine metabolism disorder. It belongs to treatable rheumatic diseases. Its origin is based on genetic or external factors. Gout's pathological manifestations are acute and chronic gouty arthritis, tophi formation, kidney impairment and urolithiasis. The asymptomatic hyperuricaemia period comes before acute gouty attack. Hyperuricaemia is the most crucial laboratory finding. In treatment management of gout there are used nonpharmacological measures and pharmacotherapy. To nonpharmacological measures there belong low purine diet and lifestyle modifications. Pharmacotherapy of gout is as follows: anti-inflammatory drugs (non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, monoclonal antibodies, glucocorticoids) and hyperuricaemia decreasing drugs (uricostatics, uricosuric agents, uricases). Uricosuric agents are not being presently used in the Slovak Republic just as in the Czech Republic, pegloticase is not being registered in the European Union at the moment. Colchicine and NSAIDs are first choice medicine for inflammation and pain reduction and allopurinol for hyperuricaemia reduction. Febuxostat is second choice medicine for hyperuricaemia reduction. Monoclonal antibodies and uricases as a new treatment management are second choice medicine. Second choice medicine is recommended for the patients with traditional pharmacotherapy intolerance or suffering from severe polyarticular gout.
Hyperurikemie, patologické zvýšení hladin kyseliny močové v séru, je nejvýznamnějším ovlivnitelným rizikovým faktorem vývoje dny. Prevalence hyperurikemie v populaci v posledních desetiletích narůstá. Riziko vývoje manifestní dny významně roste s výší urikemie. Pacienti s asymptomatickou hyperurikemií a dnou mají zvýšené riziko rozvoje komorbidit, zejména hypertenze, chronického onemocnění ledvin a metabolického syndromu. Asymptomatická hyperurikemie a dna je spojena se zvýšenou celkovou a kardiovaskulární mortalitou. Základem úspěšné léčby hyperurikemie je poučení pacienta o podstatě onemocnění, o principech a cílech léčby i o jejích možných komplikacích. Léčba asymptomatické hyperurikemie by měla vždy zahrnovat režimová a dietní opatření, léčbu komorbidit, racionalizaci farmakoterapie a u některých pacientů rovněž hypourikemickou léčbu. U pacientů s manifestní dnou by hypourikemická léčba měla být zvažována již od prvních projevů. Léčba musí směřovat k dlouhodobému udržení urikemie nižší než 360 μmol/l. Důležitou součástí hypourikemické léčby by měla být i profylaktická léčba dnavých záchvatů. Účinnost a bezpečnost hypourikemické léčby je nutné monitorovat a na nesplnění cílů léčby reagovat změnou léčebné strategie.
Hyperuricaemia, a pathological increase in serum uric acid levels, is the most significant modifiable risk factor for the development of gout. The prevalence of hyperuricaemia in the population has been increasing during recent decades. The risk of developing gout increases significantly with the increase in uricaemia. Patients with asymptomatic hyperuricaemia and gout have an increased risk of developing comorbidities, especially hypertension, chronic kidney disease, and metabolic syndrome. Asymptomatic hyperuricaemia and gout are associated with increased overall and cardiovascular mortality. The basis of successful treatment of hypeuricaemia is the patient's awareness of the nature of the disease, the principles and objectives of the treatment, and its possible complications. The management of asymptomatic hyperuricaemia should include lifestyle and dietary measures, treatment of comorbidities, rationalization of pharmacotherapy and, in some patients, urate-lowering therapy as well. In patients with gout, hypouricaemic treatment should be considered since the first manifestations. Urate-lowering therapy should be aimed at long-term maintenance of uricaemia below 360 μmol/l. Prophylactic treatment of gout attacks should also be an important part of urate-lowering therapy. The efficacy and safety of hypouricaemic treatment should be monitored and responded to by changing the treatment strategy in the case of failure to meet treatment objectives.
- MeSH
- Allopurinol administration & dosage adverse effects therapeutic use MeSH
- Anti-Inflammatory Agents, Non-Steroidal therapeutic use MeSH
- Gout Suppressants pharmacology therapeutic use MeSH
- Renal Insufficiency, Chronic ethnology physiopathology prevention & control MeSH
- Gout * diagnosis drug therapy physiopathology MeSH
- Arthritis, Gouty drug therapy physiopathology MeSH
- Febuxostat administration & dosage adverse effects therapeutic use MeSH
- Hyperuricemia * diagnosis drug therapy physiopathology MeSH
- Uric Acid blood metabolism adverse effects MeSH
- Humans MeSH
- Primary Health Care MeSH
- Practice Guidelines as Topic MeSH
- Urate Oxidase therapeutic use MeSH
- Uricosuric Agents administration & dosage adverse effects therapeutic use MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
Kyselina močová (KM) je konečným produktem metabolismu purinů u člověka. KM pochází u člověka ze tří zdrojů: z nukleotidů z potravy, z rozpadu tkáňových nukleoproteinů a z vlastní syntézy. KM je ze 75-80 % vylučována ledvinami, zbylá část je z těla vylučována gastrointestinálním traktem a potem. Koncentrace KM v plazmě závisí na příjmu purinů potravou, na intenzitě vlastní tvorby a na jejím vylučování. Klinický význam mají zvýšené hodnoty KM v krvi (hyperurikemie) a zvýšené vylučování KM do moči (hyperurikosurie). Při poruchách metabolismu KM bývá největším a nejčastějším problémem pro člověka hyperurikemie, neboť pokud není léčena a není pod kontrolou, vede ke vzniku dny (Athritis uratica) se všemi dalšími negativními důsledky pro lidský organismus včetně tvorby urátové litiázy. Závažné následky pro člověka má i hyperurikosurie, která nemusí být nutně provázena hyperurikemií. V přehledném článku jsou podrobně uvedeny nemoci, k nimž dochází na podkladě poruch metabolismu KM, v závěru článku jsou uvedeny možnosti terapie a prevence při poruchách metabolismu KM.
Uric acid (UA) is the end product of purine metabolism in man. There are three sources of UA in man: food nucleotides, degradation of tissue nucleoproteins, and biosynthesis. UA is eliminated by the kidneys in 75-80%, with the remainder being excreted from the body by the gastrointestinal tract and through perspiration. Plasma UA concentration depends on dietary purine intake, intensity of its intrinsic formation, and its elimination rate. Elevated levels of UA in the blood (hyperuricaemia) and increased urinary UA excretion (hyperuricosuria) are of clinical significance. In the case of disorders of UA metabolism, hyperuricaemia tends to be the major and most common problem for man since, when it is untreated and uncontrolled, it leads to the development of gout (gouty arthritis) with all its negative consequences for the human body, including uric acid lithiasis. Serious consequences for man are also associated with hyperuricosuria which may not necessarily be accompanied by hyperuricaemia. The review article presents in detail diseases that occur in the setting of underlying disorders of UA metabolism; also discussed are the options of treatment and prevention for disorders of UA metabolism.
- MeSH
- Hyperuricemia etiology classification pathology MeSH
- Uric Acid * metabolism adverse effects MeSH
- Humans MeSH
- Kidney Diseases * chemically induced etiology pathology MeSH
- Urolithiasis etiology classification pathology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
Hyperurikemie, patologické zvýšení hladin kyseliny močové v séru, je nejvýznamnějším ovlivnitelným rizikovým faktorem vývoje dny. Prevalence hyperurikemie v populaci v posledních desetiletích narůstá. Riziko vývoje manifestní dny významně roste s výší urikemie. Pacienti s asymptomatickou hyperurikemií a dnou mají zvýšené riziko rozvoje komorbidit, zejména hypertenze, chronického onemocnění ledvin a metabolického syndromu. Asymptomatická hyperurikemie a dna je spojena se zvýšenou celkovou a kardiovaskulární mortalitou. Základem úspěšné léčby hyperurikemie je poučení pacienta o podstatě onemocnění, o principech a cílech léčby i o jejích možných komplikacích. Léčba asymptomatické hyperurikemie by měla vždy zahrnovat režimová a dietní opatření, léčbu komorbidit, racionalizaci farmakoterapie a u některých pacientů rovněž hypourikemickou léčbu. U pacientů s manifestní dnou by hypourikemická léčba měla být zvažována již od prvních projevů. Léčba musí směřovat k dlouhodobému udržení urikemie nižší než 360 µmol/l. Důležitou součástí hypourikemické léčby by měla být i profylaktická léčba dnavých záchvatů. Účinnost a bezpečnost hypourikemické léčby je nutné monitorovat a na nesplnění cílů léčby reagovat změnou léčebné strategie.
Hyperuricaemia, a pathological increase in serum uric acid levels, is the most significant modifiable risk factor for the development of gout. The prevalence of hyperuricaemia in the population has been increasing during recent decades. The risk of developing gout increases significantly with the increase in uricaemia. Patients with asymptomatic hyperuricaemia and gout have an increased risk of developing comorbidities, especially hypertension, chronic kidney disease, and metabolic syndrome. Asymptomatic hyperuricaemia and gout are associated with increased overall and cardiovascular mortality. The basis of successful treatment of hypeuricaemia is the patient's awareness of the nature of the disease, the principles and objectives of the treatment, and its possible complications. The management of asymptomatic hyperuricaemia should include lifestyle and dietary measures, treatment of comorbidities, rationalization of pharmacotherapy and, in some patients, urate-lowering therapy as well. In patients with gout, hypouricaemic treatment should be considered since the first manifestations. Urate-lowering therapy should be aimed at long-term maintenance of uricaemia below 360 μmol/l. Prophylactic treatment of gout attacks should also be an important part of urate-lowering therapy. The efficacy and safety of hypouricaemic treatment should be monitored and responded to by changing the treatment strategy in the case of failure to meet treatment objectives.
- MeSH
- Allopurinol administration & dosage adverse effects therapeutic use MeSH
- Anti-Inflammatory Agents, Non-Steroidal therapeutic use MeSH
- Gout Suppressants pharmacology therapeutic use MeSH
- Renal Insufficiency, Chronic ethnology physiopathology prevention & control MeSH
- Gout * diagnosis drug therapy physiopathology MeSH
- Arthritis, Gouty drug therapy physiopathology MeSH
- Febuxostat administration & dosage adverse effects therapeutic use MeSH
- Hyperuricemia * diagnosis drug therapy physiopathology MeSH
- Uric Acid blood metabolism adverse effects MeSH
- Humans MeSH
- Primary Health Care MeSH
- Practice Guidelines as Topic MeSH
- Urate Oxidase therapeutic use MeSH
- Uricosuric Agents administration & dosage adverse effects therapeutic use MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
Although gout is the most common inflammatory arthritis, it is still frequently misdiagnosed. New data on imaging and clinical diagnosis have become available since the first EULAR recommendations for the diagnosis of gout in 2006. This prompted a systematic review and update of the 2006 recommendations. A systematic review of the literature concerning all aspects of gout diagnosis was performed. Recommendations were formulated using a Delphi consensus approach. Eight key recommendations were generated. A search for crystals in synovial fluid or tophus aspirates is recommended in every person with suspected gout, because demonstration of monosodium urate (MSU) crystals allows a definite diagnosis of gout. There was consensus that a number of suggestive clinical features support a clinical diagnosis of gout. These are monoarticular involvement of a foot or ankle joint (especially the first metatarsophalangeal joint); previous episodes of similar acute arthritis; rapid onset of severe pain and swelling; erythema; male gender and associated cardiovascular diseases and hyperuricaemia. When crystal identification is not possible, it is recommended that any atypical presentation should be investigated by imaging, in particular with ultrasound to seek features suggestive of MSU crystal deposition (double contour sign and tophi). There was consensus that a diagnosis of gout should not be based on the presence of hyperuricaemia alone. There was also a strong recommendation that all people with gout should be systematically assessed for presence of associated comorbidities and risk factors for cardiovascular disease, as well as for risk factors for chronic hyperuricaemia. Eight updated, evidence-based, expert consensus recommendations for the diagnosis of gout are proposed.
- MeSH
- Gout diagnosis diagnostic imaging epidemiology pathology MeSH
- Hyperuricemia diagnosis epidemiology MeSH
- Uric Acid MeSH
- Humans MeSH
- Tomography, X-Ray Computed MeSH
- Radiography MeSH
- Risk Factors MeSH
- Synovial Fluid MeSH
- Ultrasonography MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Consensus Development Conference MeSH
- Practice Guideline MeSH
OBJECTIVES: Genome-wide meta-analyses of clinically defined gout were performed to identify subtype-specific susceptibility loci. Evaluation using selection pressure analysis with these loci was also conducted to investigate genetic risks characteristic of the Japanese population over the last 2000-3000 years. METHODS: Two genome-wide association studies (GWASs) of 3053 clinically defined gout cases and 4554 controls from Japanese males were performed using the Japonica Array and Illumina Array platforms. About 7.2 million single-nucleotide polymorphisms were meta-analysed after imputation. Patients were then divided into four clinical subtypes (the renal underexcretion type, renal overload type, combined type and normal type), and meta-analyses were conducted in the same manner. Selection pressure analyses using singleton density score were also performed on each subtype. RESULTS: In addition to the eight loci we reported previously, two novel loci, PIBF1 and ACSM2B, were identified at a genome-wide significance level (p<5.0×10-8) from a GWAS meta-analysis of all gout patients, and other two novel intergenic loci, CD2-PTGFRN and SLC28A3-NTRK2, from normal type gout patients. Subtype-dependent patterns of Manhattan plots were observed with subtype GWASs of gout patients, indicating that these subtype-specific loci suggest differences in pathophysiology along patients' gout subtypes. Selection pressure analysis revealed significant enrichment of selection pressure on ABCG2 in addition to ALDH2 loci for all subtypes except for normal type gout. CONCLUSIONS: Our findings on subtype GWAS meta-analyses and selection pressure analysis of gout will assist elucidation of the subtype-dependent molecular targets and evolutionary involvement among genotype, phenotype and subtype-specific tailor-made medicine/prevention of gout and hyperuricaemia.
- MeSH
- ATP Binding Cassette Transporter, Subfamily G, Member 2 genetics MeSH
- Genome-Wide Association Study * MeSH
- Gout epidemiology genetics MeSH
- Phenotype MeSH
- Genetic Predisposition to Disease ethnology MeSH
- Genetic Loci MeSH
- Genotype MeSH
- Risk Assessment MeSH
- Incidence MeSH
- Humans MeSH
- Aldehyde Dehydrogenase, Mitochondrial genetics MeSH
- Neoplasm Proteins genetics MeSH
- Prognosis MeSH
- Reference Values MeSH
- Case-Control Studies MeSH
- Severity of Illness Index MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
- Meta-Analysis MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Japan MeSH
OBJECTIVE: The first ever genome-wide association study (GWAS) of clinically defined gout cases and asymptomatic hyperuricaemia (AHUA) controls was performed to identify novel gout loci that aggravate AHUA into gout. METHODS: We carried out a GWAS of 945 clinically defined gout cases and 1003 AHUA controls followed by 2 replication studies. In total, 2860 gout cases and 3149 AHUA controls (all Japanese men) were analysed. We also compared the ORs for each locus in the present GWAS (gout vs AHUA) with those in the previous GWAS (gout vs normouricaemia). RESULTS: This new approach enabled us to identify two novel gout loci (rs7927466 of CNTN5 and rs9952962 of MIR302F) and one suggestive locus (rs12980365 of ZNF724) at the genome-wide significance level (p<5.0×10-8). The present study also identified the loci of ABCG2, ALDH2 and SLC2A9. One of them, rs671 of ALDH2, was identified as a gout locus by GWAS for the first time. Comparing ORs for each locus in the present versus the previous GWAS revealed three 'gout vs AHUA GWAS'-specific loci (CNTN5, MIR302F and ZNF724) to be clearly associated with mechanisms of gout development which distinctly differ from the known gout risk loci that basically elevate serum uric acid level. CONCLUSIONS: This meta-analysis is the first to reveal the loci associated with crystal-induced inflammation, the last step in gout development that aggravates AHUA into gout. Our findings should help to elucidate the molecular mechanisms of gout development and assist the prevention of gout attacks in high-risk AHUA individuals.
- MeSH
- ATP Binding Cassette Transporter, Subfamily G, Member 2 genetics MeSH
- Asymptomatic Diseases MeSH
- Genome-Wide Association Study MeSH
- Gout blood genetics MeSH
- Adult MeSH
- Genetic Loci genetics MeSH
- Genotyping Techniques MeSH
- Hyperuricemia genetics MeSH
- Contactins genetics MeSH
- Uric Acid blood MeSH
- Middle Aged MeSH
- Humans MeSH
- MicroRNAs genetics MeSH
- Aldehyde Dehydrogenase, Mitochondrial genetics MeSH
- Neoplasm Proteins genetics MeSH
- Glucose Transport Proteins, Facilitative genetics MeSH
- Risk Factors MeSH
- Zinc Fingers genetics MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
- Meta-Analysis MeSH
- Research Support, Non-U.S. Gov't MeSH
V posledných desaťročiach sa dokázal vzťah zvýšenej hladiny kyseliny močovej ku viacerým klinickým stavom v internej medicíne. Dnes už je k dispozícii dostatok dôkazov o tom, že zvýšená hladina kyseliny močovej je užitočným biomarkerom aj z hľadiska preventívneho. Z tohto dôvodu je potrebná cielená liečba a celkový manažment rizikového pacienta s hyperurikémiou či dnou.
During last decades potential relationship of increased acid uric to many clinical states in internal medicine was described. However nowadays there are eviden-ces, that hyperuricaemia represents an useful biomarker, also from the preven-tive point of view. Therefore targeted therapy and complex management of risk patient with hyperuricaemia and gout is of importance.
- MeSH
- Gout Suppressants therapeutic use MeSH
- Diet Therapy methods MeSH
- Hyperuricemia * diet therapy drug therapy prevention & control MeSH
- Uric Acid blood MeSH
- Humans MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
