| Objective To observe the effect of allopurinol, fenofibrate and combination therapy on hyperuricemia and hypertriglyceridemia, and evaluate the impact of durgs on serum uric acid(UA), blood lipids, liver and kidney function, high sensitive C reactive protein (hsCRP) and momocyte chemoattractant protein-1(MCP-1) in patients. To analyse the role of lowering uric acid by different drugs and the inflammatory factors with hyperuricemia and hypertriglyceridemia.Methods Select 40 patients with hyperuricemia,40 patients with hyperuricemia and hypertriglyceridemia, and 30 patients without hyperuricemia. Patients with hyperuriemia were randomly divided into allopurinol group(n=20) and control group(n=20). The allopurinol group was given allopurinol 0.1g 3 times/day and sodium bicarbonate 0.5g 3 times/day, control group was given sodium bicarbonate 0.5g3 times/ day. Patients with hyperuriemia and hypertriglyceridemia were randomly divided into fenofibrate group(n=20) and combination therapy group(n=20). The fenofibrate group was given fenofibrate 0.2g 1 time/day and sodium bicarbonate 0.5g 3 times/day, combination therapy group was given allopurinol 0.1g 3 times/day, fenofibrate 0.2g 1 time/day and sodium bicarbonate 0.5g 3 times/day. Blood goucose, blood lipids, liver and kidney function, hsCRP, UA, MCP-1 were observed before and after 8 weeks treatment, and the side effects of the drug were also observed.Results (1) All patients accomplished observation, and no serious side effects happened. In hyperuricemia group, UA, hsCRP, MCP-1 were significantly higher than non-hyperuricemia group. After 8 weeks treatment, UA in allopurinol group(471.03±77.16vs316.68±102.92), fenofibrate group(460.29±73.29vs340.09±74.47), combination therapy group(489.72±70.89vs303.91±72.57) decreased significantly after treatment(P<0.01), but not for control group(P=0.291). Comparison between groups showed that degree of UA drop in combination therapy group and allpurinol group was greater than fenofibrate group(P<0.05).(2) HsCRP decreased in 4 goups of hyperuricemia patients after treatment (P<0.05). The degree of hsCRP drop in combination therapy group(4.19±1.94vs0.93±0.39), fenofibrate group(4.76±2.43vs0.99±0.56) was greater than control group (3.95±1.97vs1.04±0.47), allpurinol group (4.13±2.02vs1.17±0.85), (P<0.05).(3) MCP-1 in allopurinol group(336.24±39.49vs175.85±45.15), fenofibrate group (342.85±48.26vs200.37±42.48), combination therapy group (359.74±50.26vsl28.27±47.31) decreased significantly after treatment P<0.01), but not for control group(P=0.139). The degree of MCP-1 drop in combination therapy group was greater than allpurinol group and fenofibrate group(P<0.01).(4) Triglyceride(TG) in fenofibrate group(3.66±1.14vs1.43±1.04), combination therapy group (3.80±1.03vsl.35±0.89)decreased after treatment (P<0.05), and high density lipoprotein(HDL) were higher than that before treatment (P<0.05).(5) Correlation regression analysis showed that the decrease of UA, TG (r=0.457, r=0.321,P<0.05) were associated with the MCP-1 derease. Drugs and decrease of UA, TG were independent impact factors of the MCP-1.Conclusion Patients with hyperuricemia had higher MCP-1 and hsCRP than patients without hyperuricemia which suggests that hyperuricemia was a chronic inflammatory state. Allopurinol, fenofibrate and combination therapy can reduce the level of UA, hsCRP and MCP-1. With the decline in UA, amelioration in blood lipids the inflammation state can be improved in patients with hyperuricemia and hypertriglyceridemia. Allopurinol and fenofibrate are safe and effective in the treatment of hyperuricemia and hypertriglyceridemia. The decline in MCP-1 was associated with the change of serum UA and triglyceride. |
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