Objectives: Sarcopenia is the progressive loss of muscle mass and strength, and has a risk of adverse outcomes such as disability, poor quality of life and death. As prognosis depends not only on disease aggressiveness, but also on a patient's physical condition, sarcopenia can predict survival in patients with various cancer types. However, its effects on postoperative prognosis in patients with localized non-small cell lung cancers (NSCLC) have never been reported. Methods: We retrospectively investigated 215 male patients with pathological Stage I NSCLC. L3 muscle index is defined as the cross-section area of muscle at the third lumbar vertebra level, normalized for height, and is a clinical measurement of sarcopenia. We then investigated the effect of preoperative sarcopenia on their postoperative prognosis. Results: Our 215 subjects included 30 patients with sarcopenia. Sarcopenia was significantly associated with body mass index, nutritional condition, serum CYFRA 21-1 level and pathological stage, but not with preoperative respiratory function or performance status. Frequency of postoperative complications, length of postoperative hospital stay, thoracic drainage period or causes of death were not correlated with the presence of sarcopenia. The sarcopenia group had a significantly shorter median overall survival (32 months) than the no-sarcopenia group. Conclusion: Sarcopenia might not affect short-term outcomes in patients with early-stage lung cancer. Sarcopenia was a predictor of poor prognosis in male patients with Stage I NSCLC. As sarcopenic patients with NSCLC patients are at risk for significantly worse outcomes, their treatments require careful planning, even for those with Stage I disease.

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BackgroundThe aim was to determine the prognostic value of the neutrophil-lymphocyte ratio (NLR) in patients with completely resected stage 1 non-small cell lung cancer (NSCLC).MethodsThe study enrolled 382 NSCLC patients, and an optimal NLR cutoff value was determined by ROC analysis. Patients were divided by preoperative NLR into low (< 1.5, n = 99), intermediate (1.5 ≤ NLR < 3.5, n = 245), and high (NLR ≥ 3.5, n = 38) value groups. Serum diacron-reactive oxygen metabolites (d-ROMs) were assayed in 33 consecutive patients and used as an indicator of oxidative stress.ResultsThe mean NLR in patients with high d-ROMs (> 300 U.CARR, n = 16) was 1.72 ± 0.67, which was significantly higher than that in patients with low d-ROMs (1.41 ± 0.39, n = 17; P = 0.018). The 3-, 5- and 10-year survival rates in the three NLR groups were 92, 77, and 59% (low); 82, 70, and 50% (intermediate); and 76, 58, and 32% (high) (P = 0.034). The 1-, 3- and 5-year recurrence-free survival rates in the three groups were 98, 90, and 86% (low), 91, 77, and 74% (intermediate); and 92, 77, and 68% (high) (P = 0.033). Multivariate analysis found that although NLR was not predictive of overall survival, high NLR was an independent risk factor of recurrence (hazard ratio: 2.03, 95% confidence interval: 1.17–3.79, P = 0.011) as were as age, pathological stage, tumor differentiation, and lymph-vascular invasion.ConclusionsA low preoperative NLR predicted good prognosis, and was associated with low systemic inflammation status in patients with stage 1 NSCLC. It may be helpful when considering intervals of routine follow-up or choice of adjuvant therapy.

Pirfenidone is a representative medication to treat interstitial pulmonary fibrosis. Researchers reported pirfenidone (>100 µg/ml) significantly suppressed fibroblast growth in vitro. However, clinically, the maximum concentration of pirfenidone in the blood is approximately 10 µg/ml. We hypothesized there might be an additional mechanism of pirfenidone to fibroblasts indirectly. Macrophages are known to control the activation of fibroblasts via the regulation of inflammatory M1 and suppressive M2 polarization. The aim of this study was to investigate the effects of pirfenidone on alveolar macrophage polarization. Rat alveolar macrophages (NR8383) were stimulated in vitro with lipopolysaccharide (LPS) + interferon (IFN)-γ, or interleukin (IL)-4 + IL-13. Expression of M1 and M2 markers and supernatant’s levels of TGF-β1 were assessed after pirfenidone treatment (0–100 µg/ml). Treatment with LPS + INF-γ or IL-4 + IL-13 significantly increased the expression of M1 and M2 markers, respectively. In macrophage polarization assays, pirfenidone significantly reduced the expression of M2 markers at concentrations greater than 10 µg/ml but had no effect on the expression of M1 markers. At these concentrations, pirfenidone significantly reduced TGF-β1 levels in NR8383 culture supernatants. In rat lung fibroblasts treated with NR8383 culture supernatants, pirfenidone significantly suppressed proliferation, and the collagen mRNA and protein levels. In conclusion, our results demonstrated that pirfenidone suppressed polarization to M2 macrophages at clinically relevant concentrations and suppressed the rat lung fibroblasts fibrogenic activity.