IntroductionThe association of idiopathic inflammatory myositis (IIM) and malignancies has been reported, but rarely in Asian countries. Our aim was to investigate the risk of cancer among IIM patients without a prior history of malignancies, in Taiwan.MethodsWe conducted a nationwide cohort study of 1,012 patients with dermatomyositis (DM) and 643 patients with polymyositis (PM), but without prior history of malignancies, utilizing the National Health Insurance Database from 1997 to 2007. Standardized incidence ratios (SIRs) of cancers were analyzed.ResultsA total of 95 cancers (9.4%) in DM and 33 cancers (4.4%) in PM were identified. Overall cancer risk was significantly elevated in DM patients (SIR = 5.11, 95% confidence interval [CI] = 5.01 to 5.22) and PM patients (SIR = 2.15, 95% CI = 2.08 to 2.22). Most cancers were detected in the first year of observation. The risk of cancer decreased with observation time, yet remained elevated compared with the general population in both study groups after 5 years of follow-up. DM was associated with sustained elevated risk of cancers in every age group, whereas the risk of cancer in PM was highest in younger patients and decreased with age. DM patients were at the greatest risk of cancers of the nasopharynx, lungs and hematopoietic malignancies.ConclusionsPatients with IIM are at increased risk for cancer and should receive age-appropriate and gender-appropriate malignancy evaluations, with additional assessment for nasopharyngeal, lung and hematologic malignancy following diagnosis, and with continued vigilance for development of cancers in follow-up.

To evaluate the role of leptin, a 16-kDa adipocyte-derived hormone, in the development of metabolic dysregulation of psoriasis.

The two independent predictive factors for malignancy (P < 0.05) in patients with DM/PM were an older age at onset (> 45 years) and male gender. The primary idiopathic DM group was shown to have higher risk of developing internal malignancies, especially NPC. However, this was not identified as an independent predictive factor for concomitant neoplastic diseases in multivariate analysis. In addition, patients who had the complication of interstitial lung disease had a significantly lower frequency of malignancies (P < 0.001).

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Proliferation of hepatic stellate cells (HSCs) plays a key role in the pathogenesis of liver fibrosis. Induction of HSC apoptosis by natural products is considered an effective strategy for treating liver fibrosis. Herein, the apoptotic effects of 7,20-epoxy-ent-kaurane (oridonin), a diterpenoid isolated from Rabdosia rubescens, and its underlying mechanisms were investigated in rat HSC cell line, HSC-T6. We found that oridonin inhibited cell viability of HSC-T6 in a concentration-dependent manner. Oridonin induced a reduction in mitochondrial membrane potential and increases in caspase 3 activation, subG1 phase, and DNA fragmentation. These apoptotic effects of oridonin were completely reversed by thiol antioxidants, N-acetylcysteine (NAC) and glutathione monoethyl ester. Moreover, oridonin increased production of reactive oxygen species (ROS), which was also inhibited by NAC. Significantly, oridonin reduced intracellular glutathione (GSH) level in a concentrationand time-dependent fashion. Additionally, oridonin induced phosphorylations of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 OPEN ACCESSMolecules 2014, 19 3328 mitogen-activated protein kinase (MAPK). NAC prevented the activation of MAPKs in oridonin-induced cells. However, selective inhibitors of MAPKs failed to alter oridonin-induced cell death. In summary, these results demonstrate that induction of apoptosis in HSC-T6 by oridonin is associated with a decrease in cellular GSH level and increase in ROS production.