Chylothorax is a rare condition that results from thoracic duct damage with chyle leakage from the lymphatic system into the pleural space, usually on the right side. It has multiple aetiologies and is usually discovered after it manifests itself as a pleural effusion. Diagnosis involves cholesterol and triglyceride measurement in the pleural fluid. Complications include malnutrition, immunosuppression and respiratory distress. Treatment may be either conservative or aggressive depending on the clinical scenario. In this review, we discuss the aetiology, diagnosis and treatment of chylothorax. English language publications in MEDLINE and references from relevant articles from January 1, 1980 to February 28, 2008 were reviewed. Keywords searched were chylothorax, aetiology, diagnosis and treatment.

Key Points Neutrophil lifespan is extended in patients with gain-of-function HIF2A mutations. HIF-2α regulates in vivo neutrophil longevity and thus tissue inflammation and repair.

The death ligand TRAIL plays a role in physiologic resolution of inflammation and exogenous TRAIL has potential therapeutic benefits in neutrophil-dominant inflammation.

In most diseases related to pleural effusion, the fluid analysis yields important diagnostic information, and in certain cases, fluid analysis alone is enough for diagnosis. The many important characteristics of pleural fluid are described, as are other complementary investigations that can assist with the diagnosis of common and rare pleural effusions. For a systematic review of pleural effusion, a literature search for articles on the practical investigation and diagnosis of pleural effusion was done. Articles included guidelines, expert opinion, experimental and nonexperimental studies, literature reviews, and systematic reviews published from May 2003 through June 2009. The search yielded 1 guideline, 2 meta-analyses, 9 literature reviews, 1 randomized control trial, and 9 clinical studies. On the basis of class IIa or class I evidence from these articles, a step by step approach is recommended for investigating a pleural effusion, beginning with assessment of the medical history, clinical examination, radiology, pleural fluid evaluation, and finally, if no diagnosis is forthcoming, a pleural biopsy under image guidance or thoracoscopy.

BackgroundThe death receptor ligand tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) shows considerable clinical promise as a therapeutic agent. TRAIL induces leukocyte apoptosis, reducing acute inflammatory responses in the lung. It is not known whether TRAIL modifies chronic lung injury or whether TRAIL has a role in human idiopathic pulmonary fibrosis (IPF). We therefore explored the capacity of TRAIL to modify chronic inflammatory lung injury and studied TRAIL expression in patients with IPF.MethodsTRAIL−/− and wild-type mice were instilled with bleomycin and inflammation assessed at various time points by bronchoalveolar lavage and histology. Collagen deposition was measured by tissue hydroxyproline content. TRAIL expression in human IPF lung samples was assessed by immunohistochemistry and peripheral blood TRAIL measured by ELISA.ResultsTRAIL−/− mice had an exaggerated delayed inflammatory response to bleomycin, with increased neutrophil numbers (mean 3.19±0.8 wild type vs 11.5±5.4×104 TRAIL−/−, p<0.0001), reduced neutrophil apoptosis (5.42±1.6% wild type vs 2.47±0.5% TRAIL−/−, p=0.0003) and increased collagen (3.45±0.2 wild type vs 5.8±1.3 mg TRAIL−/−, p=0.005). Immunohistochemical analysis showed induction of TRAIL in bleomycin-treated wild-type mice. Patients with IPF demonstrated lower levels of TRAIL expression than in control lung biopsies and their serum levels of TRAIL were significantly lower compared with matched controls (38.1±9.6 controls vs 32.3±7.2 pg/ml patients with IPF, p=0.002).ConclusionThese data suggest TRAIL may exert beneficial, anti-inflammatory actions in chronic pulmonary inflammation in murine models and that these mechanisms may be compromised in human IPF.