Modulation of serum uric acid levels by inosine in patients with multiple sclerosis does not affect blood pressure

The role of uric acid (UA) in human physiology is subject to controversy. Either it is an important radical scavenger, a mostly neutral, waste metabolic product that may cause gout and kidney stones if elevated, or it is involved in the causation of hypertension, vascular and renal diseases. Recently we conducted a clinical trial to determine whether raising the serum UA levels through the oral administration of inosine is well tolerated and may benefit patients with multiple sclerosis. An important aspect of the safety profile is whether raising the serum UA levels elevates blood pressure. During the 1-year trial, blood pressure and serum UA levels were monitored in 16 patients. Both parameters were recorded throughout the trial that included 69 visits by patients at baseline and during the placebo phase as well as 138 visits while receiving inosine treatment. We have observed that although the serum UA levels increased significantly during the inosine treatment phase of the trial, from 4.2+/-0.8 to 7.1+/-1.7 mg per 100 ml, blood pressure remained unchanged, averaging 123+/-15/78+/-9. Our findings indicate that raising the serum UA levels to upper normal physiological levels for a period of up to 1-year does not influence blood pressure significantly.