Gout Revisited: A Complete Review of Hyperuricemia and Crystal-Induced Arthritis

Abstract

The most common form of inflammatory arthritis, gout, develops when crystals of monosodium urate (MSU) form in joints and soft tissues, which leads to hyperuricemia. Increased purine consumption, metabolic issues, oxidative stress, and insufficient uric acid excretion all lead to high levels of urate in the blood. Because of these factors, gout is commonly associated with obesity, hypertension, and cardiovascular and chronic kidney diseases. It is now more common all over the world due to an increase in gout-derived diseases coupled with an aging population. Epidemiological studies find the cause of this increase to be an increase in poor lifestyle choices. MSU crystals form and chronic inflammation along with the development of tophi occur. This is due to local proteomics and synovial physicochemical factors. Diagnosis is confirmed through an analysis of the synovial fluid, sometimes with the aid of imaging and sometimes without. Once diagnosed, gout can be managed through adapted diets, weight loss, and medications that lower uric acid levels. Certain foods can lead to the uric acid level spiking and other foods can lower it. It is thought that high levels of purines, fructose, and alcohol increase the levels of urate in the blood. On the other hand, a more balanced diet, more drinking of water, and avoiding dehydration lowers the risk of a gout flare. Nonetheless, even with successful methods, numerous individuals continue to be under-involved due to insufficient compliance, slow recognition, and unawareness. A more inclusive, patient-centric method that incorporates the patient's lifestyle, diet, and continued medication management is critical to alleviating the disease burden and preventing the resulting effects from complications related to gout.