What Causes Gout?
Gout: A Metabolic Disorder and Its Causes
Gout is a metabolic disorder characterized by excessively high levels of uric acid in the blood, exceeding the solubility limit of the blood, leading to its precipitation from the bloodstream. This uric acid accumulates in joints, forming crystals that trigger periodic bouts of severe pain and inflammation. Clinically, factors such as excessive alcohol consumption, high-purine diets, obesity, and smoking can all contribute to the development of gout.
Excessive alcohol intake facilitates uric acid production while inhibiting its excretion, thereby elevating the risk of gout. Additionally, certain alcoholic beverages, like beer, contain increased levels of purines, which are also contributors to high uric acid levels. Consumption of high-purine foods, including animal organs, seafood, and meat, can increase uric acid production and thus, the risk of gout.
Smoking or passive smoking also heightens the risk of hyperuricemia and gout. Therefore, middle-aged men with unrestrained diets, particularly those who frequently indulge in social gatherings, are more prone to developing gout. Obesity is another significant factor in the onset of gout, particularly in children, where the prevalence is higher among obese individuals. This is often attributed to unhealthy dietary patterns, including the consumption of excessive amounts of carbonated beverages and fructose-laden drinks.
The primary medications used to treat gout are analgesics and uric acid-lowering drugs. Analgesics include non-steroidal anti-inflammatory drugs (NSAIDs), while uric acid-lowering drugs primarily encompass benzbromarone, allopurinol, and febuxostat. Among these, febuxostat (such as Feili Febuxostat) offers superior uric acid-lowering efficacy with fewer adverse effects. It is excreted through multiple pathways, requiring smaller doses and not entirely reliant on renal excretion, making it suitable for gout patients with mild to moderate renal insufficiency.
The latest gout treatment guidelines recommend an initial dose of 20mg/d. If blood uric acid levels remain unsatisfactory after 2-4 weeks, the dose may be increased by 20mg/d, up to a maximum of 80mg/d. The specific dosage and frequency should be determined based on individual patient conditions and in accordance with medical advice.