Abstract

BackgroundMalaria-associated acute respiratory distress syndrome (MA-ARDS) is an understudied complication of malaria and is characterized by pulmonary inflammation and disruption of the alveolar-capillary membrane. Its pathogenesis remains poorly understood. Since endothelial activation plays an important role in other malarial complications, the expression of two endothelial activation markers, von Willebrand factor (VWF) and angiopoietin-2 (ANG-2), was investigated in the lungs of patients with MA-ARDS.MethodsPost-mortem lung sections of Plasmodium falciparum-infected patients without alveolar oedema (NA), P. falciparum-infected patients with alveolar oedema (MA-ARDS), and uninfected people who died accidentally with no pathological changes to the lungs (CON) were immunohistochemically stained for VWF and ANG-2, and were evaluated with semi-quantitative analysis.ResultsAlveolar oedematous VWF and ANG-2 and intravascular VWF staining were significantly increased in patients with MA-ARDS versus infected and uninfected control groups. The levels of VWF in the alveolar septa and endothelial lining of large blood vessels of patients with MA-ARDS was significantly decreased compared to controls. ANG-2 expression was increased in the alveolar septa of malaria patients without alveolar oedema versus control patients, while ANG-2+ leukocytes were increased in the alveoli in both infected patient groups.ConclusionsThis study documents a high level of VWF and ANG-2, two endothelial activation markers in the oedematous alveoli of post-mortem lung sections of Thai patients with MA-ARDS. Decreased detection of VWF in the endothelial lining of blood vessels, in parallel with an increased presence of intravascular VWF staining suggests marked endothelial activation and Weibel–Palade body release in the lungs of patients with MA-ARDS.

Highlights

  • Malaria-associated acute respiratory distress syndrome (MA-ARDS) is an understudied complication of malaria and is characterized by pulmonary inflammation and disruption of the alveolar-capillary membrane

  • There was no significant difference in age, days of hospitalization, parasitaemia, haemoglobin levels and circulating white blood cells between the no alveolar oedema (NA) and MA-ARDS group

  • von Willebrand factor (VWF) and ANG-2 stained alveolar oedema and intravascular VWF staining were significantly increased in patients with MA-ARDS versus infected and uninfected control groups

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Summary

Introduction

Malaria-associated acute respiratory distress syndrome (MA-ARDS) is an understudied complication of malaria and is characterized by pulmonary inflammation and disruption of the alveolar-capillary membrane. Since endothelial activation plays an important role in other malarial complica‐ tions, the expression of two endothelial activation markers, von Willebrand factor (VWF) and angiopoietin-2 (ANG-2), was investigated in the lungs of patients with MA-ARDS. Despite the availability of efficient antimalarial treatment, transmission and severe disease. MA-ARDS has a poor prognosis and leads to a lethality rate of up to 80%, despite anti-malarial treatment. MA-ARDS has been described to emerge at hospital admission and during anti-malarial treatment [2]. MA-ARDS is characterized by disruption of the alveolar-capillary membrane, which results into alveolar oedema and leads to a decreased gas exchange and hypoxaemia.

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