To explore the clinical application value of procalcitonin in acute attack of gout.

A retrospective design was used in this study, and a total of 440 subjects were  included. According to the clinical diagnosis, they were divided into acute gout infection  group ( n = 33 ), acute gout non-infection group ( n = 111 ), and gout remission noninfection group ( n = 50 ). Rheumatoid arthritis ( n = 61 ), ankylosing spondylitis ( n =  51 ), osteoarthritis group ( n = 69 ), and normal group ( n = 65 ) were used as control  groups. Non-parametric analysis Kruskal-Wallis was used to compare the six groups of  inflammatory indicators between groups, and further pairwise comparison ; independent  sample t test or Mann-Whitney U test was used to compare the differences in baseline  data and blood indicators between the infected group and the non-infected group.  Multivariate logistic regression model was used to evaluate the independent correlation  between inflammatory indicators and gout co-infection. For the abnormal increase of  procalcitonin ( PCT ) in the non-infected group, Pearson / Spearman correlation analysis  and multiple linear regression were used to evaluate the influencing factors. Finally, the  receiver operating characteristic ( ROC ) curve was used to evaluate the diagnostic value  of PCT and combined indicators for acute gout attack and the diagnostic efficacy of each  indicator for gout complicated with infection, and the area under the curve ( AUC ) was  calculated. P < 0.05 was considered statistically significant

1. There were significant differences in white blood cell count ( WBC ), C-reactive  protein ( CRP ), erythrocyte sedimentation rate ( ESR ) and procalcitonin ( PCT ) between  the acute gout non-infection group, gout remission group, normal group, rheumatoid  3 arthritis group, ankylosing spondylitis group and osteoarthritis group ( all p < 0.001 ).  The results of pairwise comparison showed that the inflammatory indexes of gout acute  non-infection group were higher than those of the other 5 groups ( all p < 0.05 ). 2. Compared with the non-infected group, in the general data, the tophi ulceration  rate in the infected group was higher than that in the non-infected group ( 16 ( 48.5 % )  vs 7 ( 6.0 % ), P < 0.05 ). Age, smoking history, drinking history, dyslipidemia, fatty liver,  liver dysfunction, renal insufficiency, coronary heart disease, cerebral infarction, kidney  stones, hypertension, and diabetes were not statistically significant in the two groups.  Among the blood indexes, uric acid ( 492.67 ± 141.86 umol / L vs 429.62 ± 140.37 umol  / L ) and procalcitonin ( 1.20 ng / ml ( 0.829,4.010 ) vs 0.65 ng / ml ( 0.237,1.007 ) ) were  higher in the infected group than in the non-infected group. There was no significant  difference in white blood cell count, CRP, D-dimer, SIRI, NLP, LMR, D-dimer, serum  ferritin, creatinine, hemoglobin and platelet count between the two groups. Logistic  regression analysis showed that tophi rupture 10.309 ( 3.195,33.333 ) and procalcitonin  ( 1.331 ( 1.041,1.702 ), P < 0.05 ) were independent risk factors for infection. 3. In patients with acute gout, the procalcitonin in the tophi group was significantly  higher than that in the non-tophi group, the procalcitonin in the tophi ulceration group  was significantly higher than that in the non-ulceration group, and the procalcitonin in the  renal insufficiency group was significantly higher than that in the non-renal insufficiency  group ( P < 0.001 ). 4. In the non-infected group, Spearman correlation analysis showed that  procalcitonin was correlated with creatinine, IL-6, white blood cell count, SIRI,  hemoglobin, D-dimer, CRP, erythrocyte sedimentation rate ( r = 0.407, r = 0.5, r = 0.54,  r = 0.453, r = -0.289, r = 0.496, r = 0.657, r = 0.387 ) ( P < 0.05 ). Further multivariate  linear regression analysis showed that IL-6 was a significant predictor of PCT levels in  the non-infected group ( P < 0.05 ). 5. ROC curve analysis showed that the AUC of PCT in the diagnosis of acute gout  attack was 0.854 ( 95 % CI : 0.798-0.910, P < 0.001 ). The AUC of IL-6 combined with  PCT was 0.901 ( 95 % CI : 0.853-0.949, P < 0.001 ). The AUC of TNF-α combined with  PCT was 0.916 ( 95 % CI : 0.875-0.958, P < 0.001 ). The AUC of combined diagnosis  4was higher than that of single PCT index. 6. ROC curve analysis showed that the diagnostic efficacy of PCT ( AUC = 0.659,95 %  CI = 0.534-0.784 ), WBC ( AUC = 0.471,95 % CI = 0.317-0.624 ), CRP ( AUC = 0.578,95 %  CI = 0.435-0.720 ), ESR ( AUC = 0.521,95 % CI = 0.384-0.657 ) and SIRI ( AUC =  0.430,95 % CI = 0.277-0.583 ) were at a low level. The results confirmed that PCT and  traditional inflammatory markers were not sensitive enough to identify whether gouty  arthritis was complicated with infection, and the diagnostic value was limited.

1. In the context of no bacterial infection, the level of PCT in patients with acute  gout was significantly higher than that in patients with gout remission, rheumatoid  arthritis, ankylosing arthritis, osteoarthritis and healthy people. 2. Gout stone rupture and abnormal increase of PCT level are independent risk  factors for bacterial infection in acute gout attack. 3. The clinical value of PCT combined with IL-6 or TNF-α in the acute attack of  gout is better than that of single index. 4. In acute gout attacks, PCT is not an effective indicator of infection, but a  quantitative indicator of inflammatory load.