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Serum CRP in patients with gout and effects of benzbromarone
C Okuda1, H Koyama, Z Tsutsumi
1Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan.
Insights
Hyperuricemia may not increase C-reactive protein (CRP) levels. However, benzbromarone treatment significantly reduced CRP and increased adiponectin in gout patients, suggesting a beneficial cardiovascular effect.
Area of Science:
- Cardiovascular Science
- Rheumatology
- Biochemistry
Background:
- C-reactive protein (CRP) is a marker for cardiovascular disease risk.
- Elevated serum uric acid (hyperuricemia) is linked to cardiovascular mortality.
- The relationship between hyperuricemia and CRP requires further investigation.
Purpose of the Study:
- To compare serum CRP levels in healthy individuals and gout patients.
- To evaluate the effect of benzbromarone on serum CRP in gout patients.
- To assess benzbromarone's impact on CRP gene expression in vitro.
Main Methods:
- Compared serum CRP in 40 healthy males and 43 male gout patients.
- Administered benzbromarone to 42 male gout patients for 1 year, measuring CRP and adiponectin.
- Investigated benzbromarone's effect on IL-1beta-induced CRP expression in HuH7 cells.
Main Results:
- No significant difference in log serum CRP between gout patients and healthy subjects.
- Benzbromarone treatment decreased log serum CRP by 11% (p < 0.01) and increased log serum adiponectin by 2% (p < 0.01).
- In vitro studies showed benzbromarone down-regulated IL-1beta-stimulated CRP gene expression.
Conclusions:
- Hyperuricemia does not appear to elevate serum CRP levels.
- Benzbromarone demonstrates a potential beneficial effect on CRP levels and expression.
- Benzbromarone may favorably impact cardiovascular markers in gout patients.
Objective:
C-reactive protein (CRP) is associated with increased risk for myocardial infarction, atherosclerosis, and peripheral artery diseases, while increased serum uric acid level is suggested to be independently associated with an increased risk of cardiovascular mortality. Accordingly, to investigate whether hyperuricemia is associated with serum CRP, we compared serum CRP levels between healthy subjects and patients with gout. In addition, we also examined whether benzbromarone has effects on serum CRP levels in patients with gout and the expression of CRP messenger RNA of CRP in the hepatoma cell line HuH7.
Methods:
In the first experiment, 40 healthy males and 43 male patients with gout were enrolled, then blood samples were drawn from each after an overnight fast. In the second experiment, 42 male patients with gout were given uric acid-lowering therapy with benzbromarone. Blood samples were drawn after an overnight fast before and 1 year after beginning benzbromarone treatment. In the third experiment, the effects of benzbromarone on IL1beta-induced CRP expression were determined in HuH7 cells.
Results:
Log serum CRP levels were not significantly different between the patients with gout and healthy subjects, while log serum CRP levels were decreased by 11% after benzbromarone treatment, as compared to the values before treatment (p < 0.01). In addition, log serum adiponectin levels were elevated by 2% after treatment (p < 0.01). Furthermore, our in vitro findings demonstrated that benzbromarone down-regulated IL1beta-stimulated CRP gene expression.
Conclusions:
These results suggest that hyperuricemia may not contribute to an increase in serum CRP level, while benzbromarone may have a favorable effect on CRP.
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