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Diagnosing sarcoidosis

imagePurpose of review: The usual diagnostic criteria for sarcoidosis include the documentation of a compatible clinicoradiologic scenario, biopsy proof of granulomas, and exclusion of alternate causes for the findings. Establishing the presence of multisystem disease, and longitudinal assessment for the emergence of potential sarcoidosis mimics both strengthen the diagnosis. These principles have constituted a ‘diagnostic modus operandi’ for several decades, but the emergence of several new technologies has begun to transform their application.

Recent findings: The widespread availability of high-resolution chest computed tomography, endobronchial ultrasound-guided transbronchial needle aspiration, rapid on-site cytopathology and to a lesser degree, fluorodeoxyglucose positron emission tomography have facilitated more convenient diagnosis. They also have identified possibilities for biopsy-less diagnosis in appropriate clinical contexts, similar to idiopathic pulmonary fibrosis, and allowed for more comprehensive assessment of the extent and activity of disease. Nonetheless, these new technologies cannot replace the central role of the clinician, whose judgment and circumspection are keys to accurate diagnosis.

Summary: The diagnosis of sarcoidosis and the assessment of its extent should be tailored to the clinical situation. The application of new technologies may permit some evolution of the diagnostic approach in many patients.

Progress in the management of acute pulmonary embolism

imagePurpose of review: Pulmonary embolism is a major contributor to global disease burden worldwide. The 2014 guidelines of the European Society of Cardiology, endorsed by the European Respiratory Society, emphasize the need for initial and advanced risk stratification as well as risk-adapted treatment to ensure the highest quality of care.

This review summarizes the progress in pulmonary embolism diagnosis, risk assessment, and treatment. Recent findings: Major advances of the past 12 months include age-related biomarker cutoff levels for optimising pulmonary embolism diagnosis and risk stratification; detection of (isolated) subsegmental pulmonary embolism by computed tomographic pulmonary angiography, raising the question of appropriate treatment in these cases; benefits versus risks of systemic thrombolytic therapy in normotensive patients at intermediate-high risk of an adverse early outcome; catheter-directed reperfusion with low-dose thrombolytics for patients at high bleeding risk; lack of efficacy of retrievable vena cava filters in the prevention of pulmonary embolism recurrence; and specific antidotes for nonvitamin K-dependent oral anticoagulants.

Summary: Recent advances in the diagnosis, risk stratification, and treatment of acute pulmonary embolism now permit, for the first time, the implementation of an integrated risk-adapted approach to the disease such as recommended by the recent European guidelines.

Circulating MACC1 as a novel diagnostic and prognostic biomarker for nonsmall cell lung cancer.

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PURPOSE: Metastasis-associated in colon cancer-1 (MACC1) is a newly identified gene that plays an important role in cancer progression and metastasis. MACC1 has important functions in the differentiation, invasion, and metastasis of nonsmall cell lung cancer (NSCLC). However, the value of circulating MACC1 as a potential diagnostic and prognostic biomarker for NSCLC remains unknown.

METHODS: Plasma MACC1 mRNA levels were examined in 272 patients with NSCLC, 61 with benign lung disease, and 80 healthy volunteers using reverse transcription quantitative real-time polymerase chain reaction.

RESULTS: MACC1 was more highly expressed in NSCLC patients than in patients with benign disease (P < 0.001) or in healthy volunteers (P < 0.001). High MACC1 expression was significantly associated with NSCLC stage (P = 0.013) and lymph node metastasis (P = 0.016). The area under the receiver operating characteristic curve was 0.766, and the optimal cutoff value was 0.105, providing a sensitivity of 71.4 % and a specificity of 89.1 %. The diagnostic capability of circulating MACC1 mRNA was higher than that of carcinoembryonic antigen (P = 0.025) or cytokeratin-19 (P = 0.010). Furthermore, high MACC1 expression was associated with poor overall survival (OS) and disease-free survival (DFS) and predicted poor survival in NSCLC patients. Consequently, MACC1 mRNA was an independent prognostic factor of OS and DFS.

CONCLUSION: We concluded that circulating MACC1 mRNA represents a potential noninvasive, diagnostic and prognostic marker for NSCLC.

Osteopontin is a novel prognostic biomarker in early-stage non-small cell lung cancer after surgical resection.

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PURPOSES: Osteopontin (OPN), an extracellular matrix-secreted phosphorylated glycoprotein, has been reported overexpressed in many solid tumors. As an important part of lung cancer, the high recurrence of non-small cell lung cancer (NSCLC) also attracted great attention of scientists.

METHODS: In this study, we investigated the expression of OPN and the relationship with prognosis of NSCLC patients. We measured the expression of OPN among 163 NSCLC samples by immunohistochemical method and compared the expression of these 28 matched cDNA between tumor and peritumoral tissue by real-time polymerase chain reaction.

RESULTS: We demonstrated that the percentages of positive OPN expression is 66.8 % and OPN expression in tumor site was much higher than the tissue adjacent to carcinoma (p = 0.0046). By further analysis, we found that OPN expression was significantly correlated with poor prognosis of NSCLC. Moreover, for early-stage patients, OS and DFS rates of OPN (-) group were significantly higher than OPN (+) group. For advanced-stage patients, OPN expression was only associated with OS rates.

CONCLUSIONS: These results suggest that OPN is commonly expressed in NSCLC and may guide the evaluation of prognosis with NSCLC, especially for early-stage patients.

Exposure to cigarette smoke downregulates β2-adrenergic receptor expression and upregulates inflammation in alveolar macrophages.

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Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary disease (COPD). β2-Adrenergic receptor (β2-AR) is abundantly expressed on inflammatory cells, which is associated with inflammation regulation. To observe alterations in inflammation, pathological changes in lung tissues, and detect changes in β2-AR expression, rats were exposed for 4 months to cigarette smoke.

Pathological changes were observed in lung tissue sections. The levels of inflammatory mediators tumor necrosis factor (TNF)-α, interleukin (IL)-1β in bronchoalveolar lavage fluid (BALF), and lung tissues were measured using enzyme-linked immunosorbent assay (ELISA). Nuclear factor (NF)-κB activity was detected by electrophoretic mobility shift assay (EMSA). Exposure to this regimen of cigarette smoke induced peribronchial and perivascular lymphocytic aggregates and parenchymal accumulation of macrophages in rats. EMSA demonstrated that smoke exposure enhanced NF-κB activation in rats' alveolar macrophages (AMs). Compared with the control group, smoke exposure induced a notable increase in TNF-α and IL-1β in BALF, lung tissues, and a decrease of β2-AR expression of AMs.

The expression of β2-AR from AMs was inversely correlated with TNF-α and IL-1β levels of BALF. These data demonstrated that chronic smoke-triggered lung inflammation was accompanied by down-regulation of β2-AR in rat lungs' AMs.

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