Background In contemporary Western settings, higher occupational class is associated with lower risk for cardiovascular disease ( CVD ) incidence, including coronary heart disease ( CHD ) and stroke. However, in non‐Western settings (including Japan), the occupational class gradient for cardiovascular disease risk has not been characterized. Methods and Results Using a nationwide, multicenter hospital inpatient data set (1984–2016) in Japan, we conducted a matched hospital case‐control study with ≈1.1 million study subjects. Based on a standard national classification, we coded patients according to their longest‐held occupational class (blue‐collar, service, professional, manager) within each industrial sector (blue‐collar, service, white‐collar). Using blue‐collar workers in blue‐collar industries as the referent group, odds ratios and 95% CI s were estimated by conditional logistic regression with multiple imputation, matched for sex, age, admission date, and admitting hospital. Smoking and drinking were additionally controlled. Higher occupational class (professionals and managers) was associated with excess risk for CHD . Even after controlling for smoking and drinking, the excess odds across all industries remained significantly associated with CHD , being most pronounced among managers employed in service industries (odds ratio, 1.19; 95% CI , 1.08–1.31). On the other hand, the excess CHD risk in higher occupational class was offset by their lower risk for stroke (eg, odds ratio for professionals in blue‐collar industries, 0.77; 95% CI , 0.70–0.85). Conclusions The occupational “gradient” in cardiovascular disease (with lower risk observed in higher status occupations) may not be a universal phenomenon. In contemporary Japanese society, managers and professionals may experience higher risk for CHD .

Prostaglandin E synthase (PGES) is a recently identified terminal enzyme that acts downstream of cyclooxygenase and catalyzes the conversion of prostaglandin (PG) H2 to PGE2. At least three isozymes have been cloned so far, which are called membrane-associated PGES (mPGES)-1, mPGES-2, and cytosolic PGES. Among them, mPGES-1 is induced by various inflammatory stimuli in some cells and tissues. Induction of mPGES-1 in the component of articular tissues of patients with rheumatoid arthritis and osteoarthritis has been demonstrated in vitro. Recent studies using adjuvant induced arthritis model have shown the increase of mPGES-1 expression resulted in the increase of PGE2 production at the sites of inflammation. In addition, reports of mPGES-1-deficient mice clearly suggest the role of mPGES-1 in the process of chronic inflammation such as collagen-induced arthritis and collagen antibody induced arthritis in vivo. Thus, recent in vitro and in vivo findings suggest that mPGES-1 may be a novel therapeutic target for arthritis. This paper introduces recent advances in research about the role of PGES in the pathophysiology of arthritis.

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