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The skeletal system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
NSAIDs are a mainstay for treating the inflammation associated with gout. Drugs called uricosuric agents (e.g., probenecid) may be used to enhance the elimination of gout by the kidneys. Agents such as allopurinol and febuxostat may be used to inhibit xanthine oxidase, a key enzyme involved in the production of uric acid.
Crystal deposition disorders
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Paul Creamer, Dimitris Kassimos
Other ULT agents are ‘uricosuric’, increasing excretion of urate at the kidney. In general they are less effective than allopurinol and are contraindicated in urolithiasis. Examples include probenecid and sulphinpyrazone, which act by inhibiting URAT1. Benzbromarone is an effective uricosuric but is not widely available.
Gout and Pseudogout
Published in Louis Solomon, David Warwick, Selvadurai Nayagam, Apley and Solomon's Concise System of Orthopaedics and Trauma, 2014
Louis Solomon, David Warwick, Selvadurai Nayagam
Uricosuric drugs (probenecid or sulfinpyrazone) can be used if renal function is normal. However, allopurinol, a xanthine oxidase inhibitor, is usually preferred, and for patients with renal complications or chronic tophaceous gout allopurinol is definitely the drug of choice.
Advances in pharmacotherapies for hyperuricemia
Published in Expert Opinion on Pharmacotherapy, 2023
Federica Piani, Davide Agnoletti, Claudio Borghi
As seen in the previous paragraphs, hyperuricemia may occur from ‘overproduction’ or ‘underexcretion.’ The ‘underexcretion’ type is the most common form of hyperuricemia and is mainly caused by a reduced renal secretion of uric acid. Uric acid is readily filtered, and up to 90% is reabsorbed in the proximal tubular cells by the apical transporters URAT1 and OAT4, and the basolateral GLUT9. Furthermore, uric acid can also be secreted in variable amounts into the proximal tubular lumen by the apical transporters ABCG2, NPT1 and NPT4, GLUT9, and the basolateral OAT1 and OAT3 [13]. The uricosuric agents act on the proximal tubule of the kidney inhibiting uric acid reabsorption and/or increasing uric acid secretion. Uricosuric drugs are second-line agents indicated in refractory hyperuricemia in combination with XO inhibitors, or in patients who cannot tolerate XO inhibitors [59].
Extending the ambit of SGLT2 inhibitors beyond diabetes: a review of clinical and preclinical studies on non-diabetic kidney disease
Published in Expert Review of Clinical Pharmacology, 2021
Saurabh Nayak, Vinay Rathore, Joyita Bharati, Kamal Kant Sahu
Four decades ago, a nonselective SGLT inhibitor, phloridzin, was reported to exert a uricosuric effect [119]. Earlier findings suggested the importance of tubular glucose (osmotic diuresis) for uric acid-lowering action. However, a recent preclinical study confirmed the role of GLUT9 and URAT1 transporter in the mediation of the uricosuric potential of SGLT2i [120,121]. Glucosuria also mediates the uricosuric effect through the alteration of uric acid reabsorption. Numerous clinical data confirm the lowering of serum uric acid levels with the administration of SGLT2i within days [122]. Fractional excretion of uric acid is affected by euglycemia and CKD (eGFR< 60 ml/min) stage. The uricosuric effect of SGLT2i among non-diabetics has not been tested in any study involving humans. In non-diabetic mice, URAT1 inhibition is required for the acute uricosuric effect of canagliflozin [120]. In a post hoc analysis, canagliflozin reduced gout flare among T2DM [123]. To date, several clinical studies have provided evidence that uric acid-lowering therapy may help to prevent and delay the decline of renal function in patients with CKD [124]. Also, uric acid-lowering therapy is indicated for cardiovascular protection in CKD patients. The uricosuric effect would be complementary to the overall renoprotection offered by SGLT2i.
Effect of Curcumin on Serum Urate in Asymptomatic Hyperuricemia: A Randomized Placebo-Controlled Trial
Published in Journal of Dietary Supplements, 2021
Pannipa Bupparenoo, Rattapol Pakchotanon, Pongthorn Narongroeknawin, Paijit Asavatanabodee, Sumapa Chaiamnuay
Three types of drugs are currently used in practice to lower the SU level. These include uricostatic (allopurinol and febuxostat), uricosuric (probenecid, benzbromarone, sulfinpyrazone, and lesinurad), and uricolytic drugs (rasburicase and plegoticase). According to recommendation of the Thai Rheumatism Association, the first-line drug is allopurinol (Thai Rheumatism Association 2012), which inhibits xanthine oxidase, resulting in decreasing urate production. However, allopurinol-related severe cutaneous drug reaction was reported at 0.1% to 0.4%, leading to a high mortality rate of 30%. There were reports of allopurinol-induced recurrent meningoencephalitis, acute febrile neutrophilic dermatosis, and severe cholestatic liver failure (Baker and Schumacher 2010; Strilchuk et al. 2019). On the other hand, febuxostat has a high cost and is inaccessible in some circumstances. This drug also has a similar incidence of skin rashes to allopurinol and may cause elevation of liver enzymes (Strilchuk et al. 2019). In addition, uricosuric agents have limitations to use in patients with chronic kidney disease or preexisting uric acid stone. Finally, uricolytic drugs are not available in Thailand. Therefore, there is undoubtedly a treatment gap in the management of gout. A safe and lower-cost drug that can reduce SU is needed to fill this gap.