Ma N, Pan Q, Qi Y, Shao F. Thrombosis in Severe Influenza A Pneumonia: Distribution and Risk Factors in Hangzhou, China. Infect Drug Resist. 2026;19:590329
Background: Severe viral pneumonia, including that caused by influenza A, can trigger a systemic inflammatory response that can lead to coagulation abnormalities, which substantially increases the risk of life-threatening thrombotic complications.
Objective: This study aimed to examine the distribution of thrombosis and its risk factors among patients with severe influenza A pneumonia to inform early clinical identification and intervention.
Methods: A retrospective analysis was performed on 175 patients with severe influenza A pneumonia who were admitted to the Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine between January 2024 and March 2025. Patients were categorised into a thrombosis group (n = 82) and a control group (n = 93). Clinical data were analysed using univariate and multivariate logistic regression to identify independent risk factors.
Results: The thrombosis group showed significantly higher D-dimer (3.06 [0.95, 12.42] vs 0.90 [0.54, 1.53] μg/mL, p < 0.001) and prolonged prothrombin time (PT) (14.90 [13.56, 18.58] vs 13.70 [13.20, 14.50] s, p < 0.001) than the controls. Multivariate analysis identified elevated D-dimer (odds ratio [OR] = 1.016, p = 0.021) and decreased haemoglobin (OR = 1.026, p = 0.013) as independent risk factors, whereas prolonged PT was independently associated with a lower risk of thrombosis (OR = 0.751, p = 0.010). Venous thrombosis predominated (78.0%), with isolated muscular vein thrombosis (IMVT) being the most common subtype (36.6%).
Conclusion: This study clarified that venous thrombosis, predominantly IMVT and pulmonary embolism, is the primary thrombotic complication in severe influenza A pneumonia. We identified a unique biomarker profile for risk stratification; elevated D-dimer and decreased haemoglobin are independent risk factors, whereas prolonged PT was independently associated with a lower risk of thrombosis. This combination provides a practical tool for early clinical identification of patients at high risk, guiding tailored thromboprophylaxis.
Objective: This study aimed to examine the distribution of thrombosis and its risk factors among patients with severe influenza A pneumonia to inform early clinical identification and intervention.
Methods: A retrospective analysis was performed on 175 patients with severe influenza A pneumonia who were admitted to the Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine between January 2024 and March 2025. Patients were categorised into a thrombosis group (n = 82) and a control group (n = 93). Clinical data were analysed using univariate and multivariate logistic regression to identify independent risk factors.
Results: The thrombosis group showed significantly higher D-dimer (3.06 [0.95, 12.42] vs 0.90 [0.54, 1.53] μg/mL, p < 0.001) and prolonged prothrombin time (PT) (14.90 [13.56, 18.58] vs 13.70 [13.20, 14.50] s, p < 0.001) than the controls. Multivariate analysis identified elevated D-dimer (odds ratio [OR] = 1.016, p = 0.021) and decreased haemoglobin (OR = 1.026, p = 0.013) as independent risk factors, whereas prolonged PT was independently associated with a lower risk of thrombosis (OR = 0.751, p = 0.010). Venous thrombosis predominated (78.0%), with isolated muscular vein thrombosis (IMVT) being the most common subtype (36.6%).
Conclusion: This study clarified that venous thrombosis, predominantly IMVT and pulmonary embolism, is the primary thrombotic complication in severe influenza A pneumonia. We identified a unique biomarker profile for risk stratification; elevated D-dimer and decreased haemoglobin are independent risk factors, whereas prolonged PT was independently associated with a lower risk of thrombosis. This combination provides a practical tool for early clinical identification of patients at high risk, guiding tailored thromboprophylaxis.
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