A fifty year old female with extensive gout!
Numerous large tophi with associated joint deformity in the hand of this young patient. Gout is a form of inflammatory arthritis characterized by recurrent attacks of a red, tender, hot, and swollen joint, where crystals in the form of monosodium urate form inside and around joints (called tophi). The most known hallmark of the disease is hyperuricemia, but by itself it does not indicate gout. Hyperuricemia means an increased production of uric acid due either a defect or hyperactivity in an enzyme, HGPRT (Hypoxanthine Guanine Phosphoribosyl Transferase) and increased cell turnover (or cell breakdown) in patients that use chemotherapy for cancer, have chronic hemolysis, or have hematologic malignancies. Another, even more common reason for gout is decreased excretion of uric acid by the kidneys due to renal disease, NSAID or diuretics usage. Inflammation typically develops when uric acid collect in the synovial fluid as the extracellular fluid becomes saturated with the acid which is then phagocytized by polymorphonuclear cells. This process develops inflammation. Pain typically comes on rapidly in less than 12 hours. The joint at the base of the big toe is affected in about half of cases. It may also result in kidney stones, or urate nephropathy. Severe gout is characterised by frequent polyarticular flares, numerous tophi, joint damage, and musculoskeletal disability. This is a preventable condition and in many cases, represents a disease that has been insufficiently managed for years. Standard management recommendations may be insufficient for patients with severe gout; these patients frequently require intensive individualised pharmacological management with combinations of urate-lowering therapy and anti-inflammatory agents.
