Objectives <p>Massive hemoptysis caused by cavitary lesions containing aspergillomas has a poor prognosis. However, the histological changes in the pulmonary vasculature of such lesions are unclear. The goal of the present study was to clarify the histological and immunohistochemical changes in pulmonary vessels in specimens from patients with massive hemoptysis caused by aspergillomas.</p> Methods <p>In this prospective observational case series, specimens from three patients for whom bronchial artery embolization (BAE) failed and who ultimately underwent lung resection were analyzed. Lung sections from paraffin-embedded blocks were subjected to hematoxylin and eosin (HE) staining and were immunostained for CD31 and alpha-smooth muscle actin. Gordon–Sweets and&#xa0;Victoria blue staining were performed to identify reticulin and elastic fibers, respectively.</p> Results <p>Increased microvessel density as well as unbalanced hypertrophic bronchial arteries (BAs) and pulmonary arteries were detected in all patients. Destroyed and compressed vessels caused by intimal fibrosis and collagen deposition were observed in the lesions. Potential anastomoses between the microvessels and BAs and plexiform-like lesions with multiple sinusoidal channels were identified in all three patients.</p> Conclusions <p>Microvascular proliferation and vascular remodeling are ubiquitous in cavitary lesions containing aspergillomas. Potential intrapulmonary bronchopulmonary anastomoses and plexiform-like lesions may constitute the anatomic basis of angiographic fistulas, which may ultimately contribute to massive hemoptysis in cavitary lesions containing aspergillomas.</p>

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Neoangiogenesis, potential intrapulmonary bronchopulmonary anastomoses and plexiform-like lesions may contribute to massive hemoptysis in lung cavitary lesions containing aspergillomas

  • Geping Li,
  • Lu Wang,
  • Qiuhong Yang,
  • Yu Mao,
  • Jing Han,
  • Wei Luo

摘要

Objectives

Massive hemoptysis caused by cavitary lesions containing aspergillomas has a poor prognosis. However, the histological changes in the pulmonary vasculature of such lesions are unclear. The goal of the present study was to clarify the histological and immunohistochemical changes in pulmonary vessels in specimens from patients with massive hemoptysis caused by aspergillomas.

Methods

In this prospective observational case series, specimens from three patients for whom bronchial artery embolization (BAE) failed and who ultimately underwent lung resection were analyzed. Lung sections from paraffin-embedded blocks were subjected to hematoxylin and eosin (HE) staining and were immunostained for CD31 and alpha-smooth muscle actin. Gordon–Sweets and Victoria blue staining were performed to identify reticulin and elastic fibers, respectively.

Results

Increased microvessel density as well as unbalanced hypertrophic bronchial arteries (BAs) and pulmonary arteries were detected in all patients. Destroyed and compressed vessels caused by intimal fibrosis and collagen deposition were observed in the lesions. Potential anastomoses between the microvessels and BAs and plexiform-like lesions with multiple sinusoidal channels were identified in all three patients.

Conclusions

Microvascular proliferation and vascular remodeling are ubiquitous in cavitary lesions containing aspergillomas. Potential intrapulmonary bronchopulmonary anastomoses and plexiform-like lesions may constitute the anatomic basis of angiographic fistulas, which may ultimately contribute to massive hemoptysis in cavitary lesions containing aspergillomas.