Therapeutic Strategies for the Treatment of Chronic Hyperuricemia: An Evidence-Based Update

Cicero, Arrigo F G; Fogacci, Federica; Kuwabara, Masanari; Borghi, Claudio

doi:10.3390/medicina57010058

Cited by 70 publications

(65 citation statements)

References 112 publications

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“…There are two main classes of hypouricemic agents: UA production inhibitors and UA excretion promoters [101,102]. So far, there have been only a few studies that have analyzed the effects of UA-lowering drugs in patients with hypertension [44][45][46][48][49][50][51][52][53][54][55][56][57][58][59]103] (Table 2).…”

Section: Ua Lowering-therapies Effects On Blood Pressurementioning

confidence: 99%

“…A recent systematic review of clinical practice guidelines and consensus statements on the treatment of hyperuricemia and gout recommended long-term treatment of patients with gout or with comorbities and SUA > 6.0 mg/dL (or 360 µmol/L) [102]. Even if treatment of asymptomatic patients without comorbities is still not recommended, large population studies such as the multicenter Uric Acid Right for Heart Health (UR-RAH) Study showed that the optimal SUA cut-off for reducing CV mortality was under 5.6 mg/dL [111][112][113].…”

Section: How To Choose the Right Hypouricemic Agentmentioning

confidence: 99%

“…The recommended first-line treatment was allopurinol, unless the patient had the genetic variant HLA-B*5801, which is commonly found in Han Chinese, South East Asians, and African Americans [102].…”

Section: How To Choose the Right Hypouricemic Agentmentioning

confidence: 99%

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Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

Piani

Cicero

Borghi

2021

JCM

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The relationship between serum uric acid (SUA) and hypertension has been a subject of increasing interest since the 1870 discovery by Frederick Akbar Mahomed. Several epidemiological studies have shown a strong association between high SUA levels and the presence or the development of hypertension. Genetic analyses have found that xanthine oxidoreductase (XOR) genetic polymorphisms are associated with hypertension. However, genetic studies on urate transporters and Mendelian randomization studies failed to demonstrate a causal relationship between SUA and hypertension. Results from clinical trials on the role of urate-lowering therapy in the management of patients with hypertension are not uniform. Our study sought to analyze the prognostic and therapeutic role of SUA in the hypertensive disease, from uric acid (UA) biology to clinical trials on urate-lowering therapies.

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Section: Ua Lowering-therapies Effects On Blood Pressurementioning

confidence: 99%

Section: How To Choose the Right Hypouricemic Agentmentioning

confidence: 99%

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Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

Piani

Cicero

Borghi

2021

JCM

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“…Uricosuric drugs lower serum uric acid levels by blocking urate reabsorption transporters expressed by the renal tubular epithelial cells, including urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) [16,17]. However, commonly used uricosuric agents such as probenecid, benzbromarone, and febuxostat have also been known to interact with urate secretion transporters ABCG2, OAT1, and OAT3 [18,19]. The ability of benzbromarone and febuxostat, among other urate-lowering drugs, to inhibit urate secretion activity of ABCG2 has been demonstrated [20].…”

Section: Discussionmentioning

confidence: 99%

“…Considering the role of ABCG2 in both renal and intestinal urate excretion, this could have a somewhat canceling effect on the hypouricemic activity of these drugs [16,20,21]. Furthermore, potent inhibitors of OAT seem to reduce the renal clearance of organic acids e.g., salicylates and methotrexate, resulting in drug-drug interactions [18,22,23]. Given the above, and the finding that URAT1 is the primary protein involved in the reabsorption of urate [23], the attention of new uricosuric agents is focused on selective inhibition of URAT1 to maximize efficacy and minimize unfavorable effects.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and Safety of Dotinurad in Hyperuricemic Patients With or Without Gout: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Iqbal¹,

Iqbal²,

Farid³

et al. 2021

Cureus

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IntroductionA systematic review and meta-analysis of the available randomized controlled trials (RCTs) were conducted to investigate the efficacy and safety of dotinurad in hyperuricemic patients with or without gout. Dotinurad is a novel selective urate reabsorption inhibitor (SURI) that increases uric acid excretion by selectively inhibiting urate transporter 1 (URAT1). To the best of our knowledge, this is the first meta-analysis conducted to gauge the efficacy and safety of dotinurad. MethodsElectronic databases (PubMed, the Cochrane Library, and ClinicalTrials.gov) were searched from inception till March 2, 2021, according to the Preferred Reporting Items for Systematic Review and Meta-Analysis statement. Randomized controlled trials comparing the efficacy and safety of dotinurad with placebo-or active (febuxostat or benzbromarone) control were included. The eligible studies were analyzed with RevMan 5.3 Software (The Nordic Cochrane Centre, Cochrane Collaboration, Copenhagen). ResultsFour eligible studies, consisting of 684 hyperuricemic patients were included. The number of patients who achieved serum uric acid (sUA) levels ≤ 6.0 mg/dl favoured dotinurad 1 mg group as compared to placebo group (risk ratio {RR} = 39.27, 95% onfidence interval {CI}, 5.59 to 275.65; p = 0.0002), dotinurad 2 mg group compared with placebo group (RR = 45.36, 95% CI, 6.48 to 317.38; p= 0.0001), and dotinurad 4 mg group compared with placebo group (RR = 54.16, 95% CI, 7.76 to 377.77; p < 0.0001). Conversely, there was no significant difference in the number of patients who achieved the target sUA levels between dotinurad 2 mg and active control (RR = 1.00, 95% CI, 0.92 to 1.08; p = 0.91). Moreover, the percentage change in sUA levels from baseline to final visit favoured dotinurad 1 mg vs. placebo ((RR = 36.51, 95% CI, 33.00 to 40.02; p < 0.00001), dotinurad 2 mg vs. placebo (RR = 46.70, 95% CI, 42.53 to 50.87; p < 0.00001), and dotinurad 4 mg vs. placebo (RR = 63.84, 95% CI, 60.51 to 67.16; p < 0.00001), while no significant difference was seen in dotinurad 2 mg vs. active control (RR = -0.08, 95% CI, -4.27 to 4.11; p= 0.97). Compared with active or placebo control, dotinurad 2 mg showed no significant difference in the number of events of gouty arthritis (RR= 1.31, 95% CI, 0.47 to 3.71; p = 0.60), the number patients with adverse events (RR = 1.09, 95% CI, 0.91 to 1.30; p = 0.36), and the number of patients who experienced adverse drug reactions (RR = 1.00, 95% CI, 0.68 to 1.47; p = 0.99). ConclusionDotinurad shows significant improvement in serum uric acid levels in hyperuricemic individuals with or without gout. Its urate-lowering effect is comparable to the commonly available anti-hyperuricemic agents. Moreover, it is effective at doses 1 mg, 2 mg, and 4 mg and well-tolerated at a dose of 2 mg.

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Si Miao San relieves hyperuricemia by regulating intestinal flora

Qian,

Shen

2023

Biomedical Chromatography

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This study seeks to investigate the therapeutic effects of Si Miao San (SMS) on hyperuricemia and its underlying mechanisms, particularly focusing on the role of intestinal flora. The key components of SMS were identified using high‐performance liquid chromatography (HPLC). To establish a rat model of hyperuricemia, an intraperitoneal injection of potassium oxonate was performed, followed by oral administration of various concentrations of SMS. The study evaluated the status of hyperuricemia, renal pathology, xanthine oxidase (XO) activity, and intestinal flora. Utilizing HPLC, we identified five active components of SMS. Following SMS intervention, there was a significant reduction in serum levels of uric acid (UA), blood urea nitrogen, and creatinine, accompanied by an increase in urine UA levels in rats with hyperuricemia. Distinct pathological injuries were evident in the renal tissues of hyperuricemic rats, and these were partially alleviated following SMS intervention. Moreover, SMS exhibited a dose‐dependent reduction in XO activity both in the serum and hepatic tissues. Notably, SMS contributed to an enhancement in the diversity of intestinal flora in hyperuricemic rats. The intervention of SMS resulted in a reduction in the abundance of certain bacterial species, including Parabacteroides johnsonii, Corynebacterium urealyticum, and Burkholderiales bacterium. This suggests that SMS may exert anti‐hyperuricemia effects, potentially by modulating the composition of intestinal flora.

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Therapeutic Strategies for the Treatment of Chronic Hyperuricemia: An Evidence-Based Update

Cited by 70 publications

References 112 publications

Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

Efficacy and Safety of Dotinurad in Hyperuricemic Patients With or Without Gout: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Si Miao San relieves hyperuricemia by regulating intestinal flora

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