Chung WJ, et al. J Korean Med Sci. 2015 Oct;30(10):1429-1438. https://doi.org/10.3346/jkms.2015.30.10.1429

Objective Plasma C reactive protein (CRP) is a marker of inflammation, and increased plasma CRP is reported in many diseases, including cardiovascular disease, diabetes, metabolic syndrome, arthritis and malignancies. The aim of the study was to evaluate the association between plasma CRP levels and cardiovascular disease, metabolic syndrome, malignancies and other comorbidities. Design A retrospective, cross-sectional survey study. Setting Large population survey in Korea. Methods A total of 5887 (weighted n=40 251 868) participants aged 19 years or older from the 2016 Korea National Health and Nutrition Examination Survey were included for analysis. Weighted prevalence and OR of comorbidities were analysed according to the continuous variable of log plasma high-sensitivity CRP levels. Results The mean age was 46.7±0.37 years and the median plasma CRP was 0.58 mg/L (IQR 0.36–1.09). The mean plasma CRP levels were higher in participants with cardiovascular diseases and cardiovascular risk factors, osteoarthritis, rheumatoid arthritis, pulmonary tuberculosis, and several cancers, including gastric, colon, breast and cervix, than in the general population. In the multivariable analysis, plasma CRP concentration was associated with increased prevalence of hypertriglyceridaemia (OR 1.157, 95% CI 1.040 to 1.287, p=0.007), diabetes (OR 1.204, 95% CI 1.058 to 1.371, p=0.005) and metabolic syndrome (OR 1.228, 95% CI 1.112 to 1.357, p<0.001) after adjustment for socioeconomic and lifestyle characteristics. There was no significant association between plasma CRP level and cancers. Conclusion Plasma CRP was associated with an increased risk of dyslipidaemia, diabetes and metabolic syndrome in the general population.

Ankylosing spondylitis (AS) is a male-predominant disease, and radiographic evidence of damage is also more severe in males. Estrogen modulates immune-related processes such as T cell differentiation and cytokine production. This study aimed to evaluate the effect of estrogen on the disease activity of spondyloarthritis (SpA). The effects of estrogen on the development of arthritis were evaluated by performing ovariectomy and 17β-estradiol (E2) pellet implantation in zymosan-treated SKG mice. Clinical arthritis scores were measured, and ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) small-animal positron emission tomography/computed tomography performed to quantify joint inflammation. The expression of inflammatory cytokines in joint tissue was measured. E2-treated mice showed remarkable suppression of arthritis clinically and little infiltration of inflammatory cells in the Achilles tendon and intervertebral disc. ¹⁸F-FDG uptake was significantly lower in E2-treated mice than in sham-operated (sham) and ovariectomized mice. Expression of TNF, interferon-γ, and IL-17A was significantly reduced in E2-treated mice, whereas expression of sclerostin and Dickkopf-1 was increased in E2-treated mice compared with sham and ovariectomized mice. Estrogen suppressed arthritis development in SKG mice, a model of SpA. Results of this study suggest that estrogen has an anti-inflammatory effect on the spondyloarthritis manifestations of the SKG arthritis model.

Jeon CH. J Korean Med Sci. 2016 Nov;31(11):1846-1850. https://doi.org/10.3346/jkms.2016.31.11.1846