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Background: Hemocoagulase batroxobin is used to prevent hemostasis or bleeding in surgical and trauma patients; however, the role of batroxobin in patients with hemoptysis is not well understood. We evaluated the risk factors and prognosis of acquired hypofibrinogenemia in hemoptysis patients treated systemically with batroxobin.Methods: We retrospectively reviewed the medical charts of hospitalized patients who were administered batroxobin for hemoptysis. Acquired hypofibrinogenemia was defined as a plasma fibrinogen level >150 mg/dL at baseline, decreasing to <150 mg/dL after batroxobin administration.Results: Overall, 183 patients were enrolled, of whom 75 had acquired hypofibrinogenemia after the administration of batroxobin. There was no statistical difference in the median age of the patients in the non-hypofibrinogenemia and hypofibrinogenemia groups (72.0 vs. 74.0 years, respectively). The patients in the hypofibrinogenemia group showed a higher rate of intensive care unit (ICU) admission (11.1% vs.22.7%; P=0.041) and tended to have more massive hemoptysis than those in the non-hyperfibrinogenemia group (23.1% vs. 36.0%; P=0.068). The patients in the hypofibrinogenemia group further showed a higher requirement for transfusion (10.2% vs. 38.7%; P<0.000) than those in the non-hyperfibrinogenemia group.Low levels of baseline plasma fibrinogen and a prolonged and higher total dose of batroxobin were associated with the development of acquired hypofibrinogenemia. Acquired hypofibrinogenemia was associated with increased 30-day mortality [hazard ratio (HR), 4.164; 95% confidence interval (CI), 1.318-13.157]. Conclusions:The plasma fibrinogen levels in patients who were administered batroxobin for hemoptysis should be monitored, and batroxobin should be discontinued if hypofibrinogenemia occurs.

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This study aimed to investigate the feasibility of Krebs von den Lungen-6 (KL-6) as potential biomarker for treatment-related ILD (TR-ILD) in lung cancer. We recruited patients with lung cancer in whom serum KL-6 was measured for differentiating between pneumonia and ILD (category 1), diagnosing and assessing the severity of suspicious TR-ILD (category 2), or evaluating baseline levels before cancer treatment (category 3). Among 1297 patients who underwent KL-6 testing, 422 had lung cancer, and TR-ILD was detected in 194 patients. In lung cancer patients, median KL-6 level was higher in patients with drug-induced ILD than in those without ILD or those with radiation pneumonitis, and it was correlated with the severity of TR-ILD. Elevated serum KL-6 (cutoff: 449.9 U/mL) was an independent risk factor of severe TR-ILD, and elevated serum KL-6 with normal serum procalcitonin was associated with severe TR-ILD rather than non-ILD respiratory disease or non-severe TR-ILD. Patients with high serum KL-6 levels had worse overall survival compared with those with low serum KL-6 levels, regardless of patients’ categories. Therefore, serum KL-6 may be surrogate marker for predicting the occurrence and assessing the severity of TR-ILD at the time of suspicious ILD events and before lung cancer treatment.