Eleven old male patients with hyperuricemia were collected ( hyperuricemia group,65-90 years old ).10 healthy middle-aged males ( middle-aged group,30-40 years old) and 10 healthy old males ( older group 60-70 years old ) with normal blood uric acid level were used as controls.All of the subjects were given low purine content diet ( 250 mg/d ) for 3 days followed by high purine content diet ( 800 mg/d ) consecutively for another three days.The samples of fasting blood and 24 h urine were collected for assay.The results showed that there were no significant changes of serum uric acid ( UA ) concentration in three groups after low purine content diet.But the levels of serum UA in three groups all increased significantly after high purine content diet,and the change was higher in hyperuricemia group than middle-aged group [ ( 507.7 ± 108.1 vs 378.9 ± 80.1 ) μmol/L,P＜0.05 ].24 h urine uric acid excretion in three groups was all significantly decreased after low purine content diet and increased after high purine content diet.After high purine content diet,24 h urine uric acid was lower in hyperuricemia group than middle-aged group [ ( 2.99 ± 1.21 vs 3.62 ± 1.02 ) mmol/24 h,P＜0.05 ].Blood urea nitrogen levels in all subjects decreased after low purine content diet and increased after high purine content diet ( P＜0.05 or P＜0.01 ).Creatinine clearance rate in hyperuricemia group was decreased after high purine content diet compared with baseline [ (75.3 ± 20.3 vs 80.7 ±20.0) ml/min ],and there were no significant changes in other groups after low and high purine content diet.24 h urine protein in hyperuricemia group was higher than middle-aged group ( P＜0.05 ),and increased after high purine content diet with significant difference ( P＜0.05 ).These results suggest that high purine content diet and decreased by renal uric acid clearance mainly contribute to hyperuricemia in old people.

This paper assembled immunotherapy methods for neuromyelitis optica spectrum disorder (NMOSD) in recent years, including the treatment of acute stage, the prevention of relapse and the potential immunotherapy. The treatment of acute stage is mainly to inhibit inflammatory response and reduce aquaporin 4 (AQP4) antibody(Ab) titer, and this is done mainly by using high-dose hormone shock therapy and plasmapheresis. Remission treatment is to inhibit the proliferation of T cells and B cells and also remove B cells from the body, for the purpose of reducing the number of relapses. Azathioprine, rituximab and mycophenolate mofetil are mainly given during remission stage. The treatment of NMOSD will become more targeted/specific in the future. The mechanism of action of the new drug is mainly through blocking the binding of pathogenic AQP4-Ab and its antigen (Ag), reducing the generation of pathogenic AQP4-Ab, and blocking the downstream reaction after pathogenic Ab-Ag binding. The new drugs mainly include aquaporumab, tocilizumab, DNA vaccine, anti-CD19 monoclonal Ab (MEDI-551), eculizumab and bevacizumab.