Bracco, Milan, Italy) were administered intravenously before treatment
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For instance, the promoter regions of inflammation-related genes (e.g., IL-6 and TNF-) in patients with gouty arthritis exhibit hypomethylation, potentially promoting inflammation directly and independently of hyperuricemia ( CXCL8 and PTGS2 ) within macrophages, thereby prolonging inflammatory responses ( 2.1.4 Impaired intestinal and renal excretion Approximately 90% of patients with gout exhibit impaired uric acid excretion, primarily due to reduced renal urate clearance ( 2.1.5 Synergism with metabolic syndrome Gout is closely associated with metabolic syndrome components, including obesity, insulin resistance, and hypertension ( 2.1.6 Transition from asymptomatic hyperuricemia to gout Only 10%20% of individuals with hyperuricemia develop gout, implicating critical roles for other regulatory factors (e.g., local tissue microenvironment and crystal-promoting factors) (Zhang, 2023)
Drop one dose level every 4 weeks (for example, from 10mg to 7.5mg to 5mg to 2.5mg)
However, this relationship needs further investigation [79]
