or corticosteroids, and urate levels are managed with allopurinol. Allopurinol, which weakly inhibits xanthine oxidase, is an analog of hypoxanthine that is hydroxylated by xanthine oxidoreductase at the 2-position to give oxipurinol. Tumor lysis syndrome Tumor lysis syndrome, an emergency condition that may result from blood cancers, produces high uric acid levels in blood when tumor cells release their contents into the blood, either spontaneously or following chemotherapy. Tumor lysis syndrome may lead to acute kidney injury when uric acid crystals are deposited in the kidneys. Treatment includes hyperhydration to dilute and excrete uric acid via urine, rasburicase to reduce levels of poorly soluble uric acid in blood, or allopurinol to inhibit purine catabolism from adding to uric acid levels. Lesch–Nyhan syndrome Lesch–Nyhan syndrome, a rare inherited disorder, is also associated with high serum uric acid levels. Spasticity, involuntary movement, and cognitive retardation as well as manifestations of gout are seen in this syndrome. Cardiovascular disease Hyperuricemia is associated with an increase in risk factors for cardiovascular disease. It is also possible that high levels of uric acid may have a causal role in the development of atherosclerotic cardiovascular disease, but this is controversial and the data are conflicting. Type 2 diabetes Hyperuricemia may be a consequence of insulin resistance in diabetes rather than its precursor. One study showed high serum uric acid was associated with higher risk of type 2 diabetes, independent of obesity, dyslipidemia, and hypertension. Hyperuricemia is associated with components of metabolic syndrome, including in children. Uric acid stone formation Kidney stones can form through deposits of sodium urate microcrystals. Saturation levels of uric acid in blood may result in one form of kidney stones when the urate crystallizes in the kidney. These uric acid stones are radiolucent, so do not appear on an abdominal plain X-ray. Uric acid crystals can also promote the formation of calcium oxalate stones, acting as "seed crystals". Metabolic Myopathies Metabolic myopathies, such as glycogenoses, impair the ability of the muscle cell to create ATP (energy). When ATP reservoirs are low, ATP is produced via the Purine Nucleotide Cycle. In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in plasma after exercise and decrease over hours with rest. Excess IMP (inosine monophosphate) is converted into uric acid. IMP → Inosine → Hypoxanthine → Xanthine → Uric Acid Excessive Alcohol Consumption Hyperuricemia can be caused by excessive alcohol