The Uricolysis Of Gut In Patients With Coronary Heart Disease And Chronic Renal Insufficiency

Objective：To evaluate the uricolysis of gut in patients with coronaryheart disease (CHD) by using the model of feces, to discuss the underlyingmechanisms of the disturbance of serum uric acid (SUA) in patients withCHD.Methods：Totally 70 consenting subjects were recruited in this study,among them, 40 were normal; 30 were diagnosed CHD (15 with elevatedSUA and 15 with normal level of SUA). Clinical data including the genderand age, the routine examination of blood, urine and stool as well as theindicators reflecting the functions of kidney and liver were recorded. All thesubjects were informed to reserve feces themselves the day before samplingand according to weight, the feces were evenly mixed with phosphate buffersolution (PBS) by the ratio of 1:2 once obtained then centrifuged at 3000rpmfor 10 minutes to deposit the residues like the undigested food. Thesuspensions were then equally divided into different reaction systems and beadded with the standard uric acid solution or lithium carbonate solution.Some reaction systems were subjected to 100℃for 30 minutes then all reaction systems were placed in 37℃for 2 hours. During this step, theuricolysis would take place and the intestinal flora was then deposited duringthe centrifuge at 15000rpm for 15 minutes later. The suspension wascollected again and the enzyme colorimetric method was immediately usedfor the detection of the uric acid in the heating group and the non heatinggroup. The amount of the uric acid metabolized by the flora in 1g feces andthe uric acid contained in the feces per se were the main statisticalparameters in our study. All the data were analyzed by SPSS 13.0. P＜0.05was considered to be statistically different.Results：The metabolized uric acid by the flora in 1g feces of CHDwith normal level of SUA was absolutely higher than that of the normal(P<0.05)；and that of those with elevated SUA was comparable to thatof the normal. There was no statistical significance between thesubgroups of CHD. The endogenous uric acid in feces of CHD withelevated SUA was absolutely higher than that of the CHD with normallevel of SUA and the normal (P<0.05). The TG of the CHD wassignificantly higher and the HDLC was distinctly lower than that of thenormal with the P<0.01 and P<0.001 respectively. The TC, LDL-C,VLDL of patients with CHD had no statistic difference when comparedwith that of the normal. The serum total bilirubin of CHD was significantly lower than that of the normal (P<0.05).Conclusions：The uricolysis of gut in patients with CHD isabsolutely higher than that of the normal, the gut may partly contributeto the abnormal metabolism of SUA which is commonly seen in CHD.Patients with CHD have lower antioxidant capacity. Objective：To evaluate the uricolysis of gut in patients with chronicrenal insufficiency (RI) and the possible influence of antibiotics on it byusing the model of feces, to discuss the underlying mechanisms of the uricacid disturbance from the perspective of gut.Methods：Totally 40 consenting subjects were recruited in this study,among them, 26 were normal; 7 were established chronic RI and incombined antibiotics therapy; the others were chronic RI too but withoutantibiotics intervention. Clinical data including the gender and age, theroutine examination of blood, urine and stool as well as the indicatorsreflecting the functions of kidney and liver were recorded. All the subjectswere informed to reserve feces themselves the day before sampling andaccording to weight, the feces were evenly mixed with phosphate buffersolution (PBS) by the ratio of 1:2 once obtained then centrifuged at 3000rpmfor 10 minutes to deposit the residues like the undigested food. Thesuspensions were then equally divided into different reaction systems and beadded with the standard uric acid solution or lithium carbonate solution.Some reaction systems were subjected to 100℃for 30 minutes then all reaction systems were placed in 37℃for 2 hours. During this step, theuricolysis would take place and the intestinal flora was then deposited duringthe centrifuge at 15000rpm for 15 minutes later. The suspension wascollected again and the enzyme colorimetric method was immediately usedfor the detection of the uric acid in the heating group and the non heatinggroup. The amount of the uric acid metabolized by the flora in 1g feces andthe uric acid contained in the feces per se were the main statisticalparameters in our study. All the data were analyzed by SPSS 13.0. P＜0.05was considered to be statistically different.Results：The metabolized uric acid by the flora in 1g feces of group 3was obviously higher than that of group 2（P<0.001）and group 1（P<0.05）；The endogenous uric acid in feces of group 3 was evidentlylower than that of the group 3（P<0.001）and was comparable to that of thegroup 1；For subjects with chronic RI and were receiving two kinds ofantibiotics simultaneously, the endogenous uric acid in feces was positivelycorrelated with the serum uric acid (r=0.801, P<0.05). The RBC (P<0.01),HGB (P<0.05) were lower and the serum urea (P<0.001) as well as thecreatine (P<0.05) in subjects with chronic RI were higher than that of thenormals respectively.Conclusions：The gut is a potential tract in elimination of uric acid and the intestinal flora which expressing the uricase is the main spot where theuricolysis take place. Under the condition of chronic RI, the gut canimplement compensating mechanisms aimed to eliminate the excessive uricacid, but effective bacteriostasis, for example, the combined use ofantibiotics can suppress the uricolysis of the intestinal flora and lead to anevident increase of the uric acid in feces.