Hypouricemia or hypouricaemia is a level of uric acid in blood serum that is below normal. In humans, the normal range of this blood component has a lower threshold set variously in the range of 2 mg/dL to 4 mg/dL, while the upper threshold is 530 μmol/L (6 mg/dL) for women and 619 μmol/L (7 mg/dL) for men. Hypouricemia usually is benign and sometimes is a sign of a medical condition. Presentation
Complications
Although normally benign, idiopathic renal hypouricemia may increase the risk of exercise-induced acute kidney failure. There is also evidence that hypouricemia can worsen conditions such as rheumatoid arthritis, especially when combined with low Vitamin C uptake, due to free radical damage. Causes
Hypouricemia is not a medical condition itself (i.e., it is benign), but it is a useful medical sign. Usually hypouricemia is due to drugs and toxic agents, sometimes it is due to diet or genetics, and rarely it is due to an underlying medical condition. When one of these causal medical conditions is present, hypouricemia is a common sign. Medication
The majority of drugs that contribute to hypouricemia are uricosurics (drugs that increase the excretion of uric acid from the blood into the urine). Others include drugs that reduce the production of uric acid:  xanthine oxidase inhibitors, urate oxidase (rasburicase), and sevelamer. Diet
Hypouricemia is common in vegetarians due to the low purine content of most vegetarian diets. Vegetarian diet has been found to result in mean serum uric acid values as low as 239 μ mol/L (2.7 mg/dL).
These genetic factors influence the rate at which alcohol and its initial metabolic product, acetaldehyde, are metabolized. They are found at different frequencies in people from different parts of the world. The alcohol dehydrogenase allele ADH1B*2 causes a more rapid metabolism of alcohol to acetaldehyde, and reduces risk for alcoholism; it is most common in individuals from East Asia and the Middle East. The alcohol dehydrogenase allele ADH1B*3 also causes a more rapid metabolism of alcohol. The allele ADH1B*3 is only found in some individuals of African descent and certain Native American tribes. African Americans and Native Americans with this allele have a reduced risk of developing alcoholism. Native Americans, however, have a significantly higher rate of alcoholism than average; risk factors such as cultural environmental effects (e.g. trauma) have been proposed to explain the higher rates. The aldehyde dehydrogenase allele ALDH2*2 greatly reduces the rate at which acetaldehyde, the initial product of alcohol metabolism, is removed by conversion to acetate; it greatly reduces the risk for alcoholism.A genome-wide association study (GWAS) of more than 100,000 human individuals identified variants of the gene KLB, which encodes the transmembrane protein β-Klotho, as highly associated with alcohol consumption. The protein β-Klotho is an essential element in cell surface receptors for hormones involved in modulation of appetites for simple sugars and alcohol. Several large GWAS have found differences in the genetics of alcohol consumption and alcohol dependence, although the two are to some degree related.