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hURAT1 Transgenic Mouse Model for Evaluating Targeted Urate-Lowering Agents.
Int J Rheum Dis
January 2025
Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China.
Background: Urate transporter 1 (URAT1) is a well-known therapeutic target for reducing urate levels in the treatment of hyperuricemia and gout. However, current pharmacological studies have failed to evaluate the efficacy of URAT1 inhibitors in non-primate animal models. We established a human URAT1 (hURAT1) transgenic knock-in (KI) mouse model to assess uricosuric agents' effectiveness and characterize URAT1-caused pathogenesis.
View Article and Find Full Text PDFAn update on the pharmacotherapy of gout.
Expert Opin Pharmacother
January 2025
Department of Rheumatology, Royal Free London NHS Foundation Trust, London, UK.
Introduction: Gout is a common form of acute inflammatory arthritis caused by the deposition of monosodium urate crystals within synovium of joints. This leads to severe pain, reducing quality of life for patients with this condition.
Areas Covered: This review summarizes the treatment of both acute flares of gout and urate-lowering therapy based on guidance from various major international societies.
Hyperuricemia causes not only gout but also organ damage, such as through cerebrovascular, cardiovascular, and lifestyle-related diseases. The relationship between the serum urate(SUA)level and organ damage has recently been redefined as dysuricemia, as follows: 1)SUA level is positively associated with the occurrence of gout and intra-arterial gout(gout pattern); 2)occurrence of neurodegenerative diseases is negatively correlated with SUA level(ND pattern); and 3)the relationship between SUA level and chronic kidney disease(CKD)and cardiovascular disease(CVD)forms a J-shaped curve(CKD/CVD pattern). CVDs accompanied by dysuricemia include gout, ND, and CKD/CVD patterns; therefore, optimal SUA levels must be maintained to reduce organ damage.
View Article and Find Full Text PDFAnalysis of the Efficacy and Safety of Benzbromarone Combined with Sodium Bicarbonate Tablets in the Treatment of Hyperuricemia.
Br J Hosp Med (Lond)
November 2024
Department of Endocrinology, Zhongda Hospital Southeast University, Nanjing, Jiangsu, China.
Hyperuricemia is a metabolic disorder characterized by elevated levels of uric acid in the blood. If left untreated, hyperuricemia can progress to gout, which manifests as acute arthritic attacks, and may also lead to uric acid nephrolithiasis and other renal conditions. This widespread condition poses significant risks to human health and quality of life.
View Article and Find Full Text PDFProbenecid Inhibits Extracellular Signal-Regulated Kinase and c-Jun N-Terminal Kinase Mitogen-Activated Protein Kinase Pathways in Regulating Respiratory Syncytial Virus Response.
Int J Mol Sci
November 2024
Department of Infectious Diseases, University of Georgia, Athens, GA 30602, USA.
Unlabelled: We examined the effect of probenecid in regulating the ERK and JNK downstream MAPK pathways affecting respiratory syncytial virus replication.
Background: We have previously shown that probenecid inhibits RSV, influenza virus, and SARS-CoV-2 replication in vitro in preclinical animal models and in humans. In a Phase two randomized, placebo-controlled, single-blind, dose range-finding study using probenecid to treat non-hospitalized patients with symptomatic, mild-to-moderate COVID-19, we previously showed that a 1000 mg twice daily treatment for 5 days reduced the median time to viral clearance from 11 to 7 days, and a 500 mg twice daily treatment for 5 days reduced the time to viral clearance from 11 to 9 days more than the placebo.
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