PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33456597-9 2020 Addition of synbiotic to allopurinol leads to a blood uric acid lowering (18.7% vs. 13.3%, p <0.01), CRP reduction (75% vs. 26.3%, p <0.01) as well as decrease of cytokines level: IL-1beta, IL-6, IL-8, IL-10 and TNFalpha (all p <0.001). Allopurinol 25-36 C-reactive protein Homo sapiens 101-104 28093243-17 2017 The protective mechanism of allopurinol might be achieved by suppressing the secretion and release of inflammatory mediators such as TNF-alpha, hs-CRP, OX-LDL and MDA while increasing levels of NO. Allopurinol 28-39 C-reactive protein Homo sapiens 147-150 24625997-4 2014 Serum uric acid (UA) and C-reactive protein levels decreased after allopurinol therapy (P = 0.00 and P = 0.04, respectively), but no change was observed in the control group during the study period. Allopurinol 67-78 C-reactive protein Homo sapiens 25-43 26571421-6 2015 RESULTS: Allopurinol-treated subjects showed a reduction in serum uric acid in association with improvement in fasting blood glucose, fasting insulin, and HOMA-IR index, as well as a reduction in serum high-sensitivity C-reactive protein. Allopurinol 9-20 C-reactive protein Homo sapiens 219-237 24498865-9 2014 After the treatment with allopurinol, colchicine and predonisolone, his symptoms were improved, and serum CRP and UA levels were normalized. Allopurinol 25-36 C-reactive protein Homo sapiens 106-109 20538833-7 2010 RESULTS: Serum uric acid and C-reactive protein levels were significantly decreased in subjects treated with allopurinol. Allopurinol 109-120 C-reactive protein Homo sapiens 29-47 20538833-9 2010 Allopurinol treatment slowed down renal disease progression independently of age, gender, diabetes, C-reactive protein, albuminuria, and renin-angiotensin system blockers use. Allopurinol 0-11 C-reactive protein Homo sapiens 100-118 20538833-13 2010 CONCLUSIONS: Allopurinol decreases C-reactive protein and slows down the progression of renal disease in patients with chronic kidney disease. Allopurinol 13-24 C-reactive protein Homo sapiens 35-53 18330493-1 2008 OBJECTIVE: In this study, we tested in patients with metabolic syndrome whether allopurinol through decreasing oxidative stress improves endothelial function, and ameliorates inflammatory state represented by markers of myeloperoxidase, C-reactive protein (CRP) and fibrinogen. Allopurinol 80-91 C-reactive protein Homo sapiens 257-260 35199285-10 2022 Allopurinol plus standard treatment reduced LDH, ferritin, CRP, procalcitonin, and ET-1 serum level significantly (P < 0.05) compared with Covid-19 patients on standard treatment. Allopurinol 0-11 C-reactive protein Homo sapiens 59-62 17701281-8 2007 In the allopurinol group, serum uric acid levels, GFR, systolic and diastolic blood pressure, and C-reactive protein (CRP) levels significantly improved (P < 0.05). Allopurinol 7-18 C-reactive protein Homo sapiens 98-116 17701281-8 2007 In the allopurinol group, serum uric acid levels, GFR, systolic and diastolic blood pressure, and C-reactive protein (CRP) levels significantly improved (P < 0.05). Allopurinol 7-18 C-reactive protein Homo sapiens 118-121 16514905-13 2005 The relationship between SUA and CRP levels remained statistically significant after adjustment for age, sex, comorbid index, obesity, residual renal function, diuretic and allopurinol treatment, in the multivariate logistic and linear regression models (OR: 1.296, p = 0.0003; and beta: 0.204, p = 0.0002). Allopurinol 173-184 C-reactive protein Homo sapiens 33-36 35120026-8 2022 Patients receiving allopurinol had significant reductions in office systolic and diastolic BP, central systolic BP, pulse pressure, IMT (0.773 +- 0.121 vs. 0.752 +- 0.13 mm, P = 0.044) and hs-CRP (3.36 +- 2.73 vs. 2.74 +- 1.91 mg/L, P = 0.028) compared to controls. Allopurinol 19-30 C-reactive protein Homo sapiens 192-195