The most severe form of the condition begins in infancy. The first symptom is a bladder or kidney stone. If treated promptly with proper medications and diet, gout and kidney impairments can be detoured. In cases were the diagnosis is delayed these conditions will occur along with hearing loss, weak low muscle tone, ataxia, and developmental delay. This condition is a result of a mutation in the PRPS1 gene (phosphoribosyl pyrophosphate synthetase 1). This mutation causes a poorly regulated and overactive PRS, generating an excessive amount of purines and resulting in a great amount of uric acid, a waste product of purine breakdown, allowing it to accumulate in the body (Becker, 2001). This condition is treated with allopurinol or febuxostat. Febuxostat is a non- purine xanthine oxidase inhibitor, designed to minimize the production of uric acid. It is an alternative for patients with poor tolerance to allopurinol (Bisht &Bist, 2011).
Another most recent identified cause of gout in young children (and very alarming) is high blood pressure accompanied by being overweight or obese. Children normally complaint of joint pain and swelling. This condition falls into the metabolic syndrome that includes a group of disorders increasing the risk of heart diseases, stroke, and diabetes (Tang, Kubota, Nagai, Mamemoto, & Tokuda, 2010).
In all three above mentioned conditions related to gout, it is recommended to have medications combined with proper fluid intake, and a low -fat dairy, low-purine, low fructose diet. If possible also urate -retaining medications should be avoided such as low-dose aspirin and thiazide diuretics (de Brouwer, et al.,