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Interstitial lung disease: time to rethink the snapshot diagnosis?

An accurate and early diagnosis of idiopathic pulmonary fibrosis (IPF) is critically required for patients and care providers because it dictates very specific management decisions that include referral to transplant, access to new approved drugs, avoidance of immunosuppression and potential referral to palliative care.1 While the original diagnosis of IPF was highly dependent on patterns observed on histology, in 2002 the American Thoracic Society (ATS)/European Respiratory Society (ERS) guideline altered the approach to diagnosis so as to include a clinical–radiological–pathological multidisciplinary diagnosis.2

A careful history, searching for subtle evidence of connective tissue disease, exposures and other known causes for interstitial lung disease (ILD), was emphasised. A radiographic pattern of usual interstitial pneumonia (UIP) on high-resolution CT (HRCT) was described, characterised by basal-predominant fibrosis with peripheral reticular markings, traction airway change, architectural distortion and honeycombing.

With this new classification system, it was proposed, characteristic HRCT findings...

What defines latent infection with Mycobacterium tuberculosis in patients with autoimmune diseases?

Screening for latent infection with Mycobacterium tuberculosis (LTBI) and treatment of test-positives is the cornerstone in the prevention of TB and should be performed preferably among individuals with risk for progression.

Progression from LTBI to active TB is highest in recent contacts of patients with active TB. Moreover, it is considered particularly high in latently infected patients if they are also immunodeficient. Therefore, screening for evidence of LTBI is recommended for HIV-infected individuals, patients with chronic renal failure, individuals receiving immunosuppressive drug therapy following solid organ or stem cell transplantation, and patients with autoimmune diseases.1 2 Since by definition LTBI lacks the gold standard of bacteriological confirmation, the condition is diagnosed indirectly by detection of an immune response towards mycobacterial antigens with either the tuberculin skin test (TST) or interferon- release assays (IGRA) performed from whole blood. IGRA may have test-intrinsic and operational advantages over...

Effect of immunosuppressive therapy on interferon {gamma} release assay for latent tuberculosis screening in patients with autoimmune diseases: a systematic review and meta-analysis

Objective : Interferon release assay (IGRA) is commonly used to diagnose latent TB infection (LTBI). Immunosuppressive therapy may affect its performance but data are conflicting. We aimed to determine the effect of immunosuppressive therapy on the performance of IGRA in patients with autoimmune diseases.

Methods : We searched PubMed, MEDLINE, EMBASE and the Cochrane Library up to December 2014. We included studies that reported the IGRA results in patients with autoimmune disease with or without immunosuppressive therapy. The pooled effect of immunosuppressive therapy on IGRA was estimated using a Peto fixed-effects model.

Results : We included 17 studies with 3197 participants in the meta-analysis. Among the subjects, 71.5% were taking immunosuppressive therapy and 56.7% had received Bacillus Calmette–Guérin vaccination. Compared with patients not on immunosuppressants, patients receiving immunosuppressive therapy were less likely to have a positive IGRA result (OR 0.66, 95% CI 0.53 to 0.83, I2=23%), especially patients receiving anti-tumour necrosis factor (anti-TNF) treatment (OR 0.50, 95% CI 0.29 to 0.88). The use of immunosuppressive therapy was also associated with a lower rate of positive tuberculin skin test result (OR 0.51, 95% CI 0.42 to 0.61).

Conclusions : Our meta-analysis showed that IGRA results are negatively affected by immunosuppressive therapy. IGRA alone may not be sufficiently sensitive to diagnose LTBI in patients on immunosuppressive therapy. Patients should preferably be screened for LTBI before initiation of immunosuppressive therapy, especially before anti-TNF therapy.

Surgery for Stage IIIA Non-Small-cell Lung Cancer: Lack of Predictive and Prognostic Factors Identifying Any Subgroup of Patients Benefiting From It.

Although a trimodality regimen for patients with stage IIIA/pN2 non-small-cell lung cancer (NSCLC) has been variably used owing to limited evidence for its benefits, it remains unknown whether any patient subgroup actually receives benefit from such an approach. To explore this question, the published data were reviewed from 1990 to 2015 to identify the possible predictors and prognosticators in this setting. Overall survival was the endpoint of our study.

Of 27 identified studies, none had studied the predictors of improved outcomes with trimodality treatment. Of the potential patient- and tumor-related prognosticators, age, gender, and histologic type were the most frequently formally explored. However, none of the 3 was found to influence overall survival. The most prominent finding of the present review was the substantial lack of data supporting a trimodality treatment approach in any patient subgroup.

As demonstrated in completed prospective randomized studies, the use of surgery for stage IIIA NSCLC should be limited to well-defined clinical trials.

Middle East respiratory syndrome coronavirus infection: virus-host cell interactions and implications on pathogenesis.

Middle-East Respiratory Syndrome coronavirus (MERS-CoV) was identified to cause severe respiratory infection in humans since 2012. The continuing MERS epidemic with a case-fatality of more than 30 % poses a major threat to public health worldwide.

Currently, the pathogenesis of human MERS-CoV infection remains poorly understood. We reviewed experimental findings from human primary cells and ex vivo human lung tissues, as well as those from animal studies, so as to understand the pathogenesis and high case-fatality of MERS. Human respiratory epithelial cells are highly susceptible to MERS-CoV and can support productive viral replication. However, the induction of antiviral cytokines and proinflammatory cytokines/chemokines are substantially dampened in the infected epithelial cells, due to the antagonistic mechanisms evolved by the virus. MERS-CoV can readily infect and robustly replicate in human macrophages and dendritic cells, triggering the aberrant production of proinflammatory cytokines/chemokines. MERS-CoV can also effectively infect human primary T cells and induce massive apoptosis in these cells. Although data from clinical, in vitro and ex vivo studies suggested the potential for virus dissemination, extrapulmonary involvement in MERS patients has not been ascertained due to the lack of autopsy study. In MERS-CoV permissive animal models, although viral RNA can be detected from multiple organs of the affected animals, the brain of human DPP4-transgenic mouse was the only extrapulmonary organ from which the infectious virus can be recovered.

More research findings on the pathogenesis of MERS and the tissue tropisms of MERS-CoV may help to improve the treatment and infection control of MERS.

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