While a vegetarian diet is typically seen as beneficial with respect to conditions such as gout, care should be taken to avoid associated health conditions.Transient hypouricemia sometimes is produced by total parenteral nutrition. Paradoxically, total parenteral nutrition may produce hypouricemia followed shortly by acute gout, a condition normally associated with hyperuricemia. The reasons for this are unclear. Genetics
Genetic mutations known to cause hypouricemia are of two kinds:  mutations causing xanthine oxidase deficiency, which reduces the production of uric acid;  and mutations causing abnormal kidney function that increases the excretion of uric acid. Collectively known as familial renal hypouricemia, these latter mutations are of two types, involving defects of presecretory and postsecretory reabsorption.A genetic mutation in Dalmatian dogs causes hypouricemia due to a kidney defect that interferes with reabsorption of uric acid. A similar mutation has been reported in a human brother and sister.In humans, loss-of-function mutations in the gene URAT1 are associated with presecretory reabsorption defects. Medical conditions
Medical conditions that can cause hypouricemia include:

Fanconi syndrome
Hyperthyroidism
Multiple sclerosis
Myeloma
Nephritis
Wilsons disease
Purine nucleoside phosphorylase (PNP) deficiency

Diagnosis
Uric acid clearance should also be performed, increase in clearance points to proximal tubular defects in the kidney, normal or reduced clearance points to a defect in xanthine oxidase. Treatment
Idiopathic hypouricemia usually requires no treatment. In some cases, hypouricemia is a medical sign of an underlying condition that does require treatment. For example, if hypouricemia reflects high excretion of uric acid into the urine (hyperuricosuria) with its risk of uric acid nephrolithiasis, the hyperuricosuria may require treatment.
There was no rebound effect following withdrawal of treatment, but a gradual return to pre-treatment bowel movement frequency should be expected. Minimal distribution of the drug occurs beyond the immediate gastrointestinal tissues. Lubiprostone is rapidly metabolized by reduction/oxidation, mediated by carbonyl reductase. There is no metabolic involvement of the hepatic cytochrome P450 system. The measurable metabolite, M3, exists in very low levels in plasma and makes up less than 10% of the total administered dose. Data indicate that metabolism occurs locally in the stomach and jejunum. References
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