In conclusion, the mortality of ARDS caused by miliary TB remains high. Accurate diagnosis and early therapeutic management of therapy including anti-tuberculosis agents and mechanical ventilation are crucial to optimizing outcome. DM, ALT, AST, D-dimer, hemoglobin, and albumin are independent predictors of ARDS development in patients with miliary TB. Symptomatic Venous Thromboembolism Is a Disease Related to Infection and Immune Dysfunction The characteristics of human genomics and cellular immune function between clinically symptomatic venous thromboembolism (VTE) and controls were systematically compared to explore the immunologic pathogenesis of VTE. Microarray assay showed the mRNA expressions of genes related to non-specific cellarer immune and cytokines were significantly down-regulated. Abnormal expressions of CD3+, CD4+, CD8+, NK marker CD16+56+, CD19 and aberrant CD4+/CD8+ ratio were detected in 54 among 56 patients. In PE patients, microarray assay revealed the imbalance in the expressions of genes related to the immune system. The expressions of genes related to non-specific immune cells and cytokines were markedly up-regulated and those associated with cellular immune were dramatically down-regulated. In VTE patients, cytological examination indicated the functions of NK cells were significantly compromised, and the antigen recognition and killing function of T cells markedly decreased. The consistence between genomic and cytological examination suggests the symptomatic VTE is closely associated with the infection and immune dysfunction. Venous thromboembolism (VTE) including acute pulmonary embolism (APE), chronic thromboembolic pulmonary hypertension (CTEPH) and deep venous thrombosis (DVT) is a global disease. The high morbidity, high misdiagnosis rate and high mortality render PE as a worldwide health problem (1) . In 1965, Egeberg et al first described a parentage with inherited antithrombin deficiency, a member of which repeatedly developed DVT. The antithrombin deficiency is an autosomal dominant genetic disease and they first proposed the concept of thrombophilia (2) . However, evidence on the genetic pathogenesis of VTE is rarely identified in a majority of VTE patients (3) . According to the pathogenesis, VTE is classified into genetic VTE and acquired VTE which is frequently found in clinical practice. The symptomatic VTE is an entity of hereditary VTE and acquired VTE.