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Published ahead of print on October 3, 2002, doi:10.1164/rccm.200202-135OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 3, February 2003, 438-443

A more recent version of this article appeared on February 1, 2003
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Submitted on February 22, 2002
Accepted on October 2, 2002

Interstitial vascularity in fibrosing alveolitis

Elisabetta A Renzoni1*, David A Walsh2, Michael Salmon3, Athol U Wells1, Piersante Sestini4, Andrew G Nicholson5, Srihari Veeraraghavan1, Anne E Bishop6, Hanna M Romanska6, Panagiotis Pantelidis1, Carol M Black7, and Roland M du Bois1

1 Interstitial lung disease unit, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, United Kingdom, 2 Academic Rheumatology, University of Nottingham, Nottingham, United Kingdom, 3 Department of Thoracic medicine, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, United Kingdom, 4 Division of Respiratory diseases, University of Siena, Siena, Italy, 5 Department of Pathology, Royal Brompton Hospital, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, United Kingdom, 6 Department of Histochemistry, Hammersmith hospital, Imperial college of science Technology and medicine, London, United Kingdom, 7 Division of Academic Rheumatology, Royal Free Hospital, London, United Kingdom

* To whom correspondence should be addressed. E-mail: e.renzoni{at}ic.ac.uk.

The aim of this study was to evaluate interstitial vascularity in cryptogenic fibrosing alveolitis (CFA) and in fibrosing alveolitis associated with systemic sclerosis (FASSc). Open lung biopsies from 8 patients with CFA, 9 patients with FASSc, and normal lung from 12 patients undergoing surgery for lung cancer, were studied. Markers for endothelial cells (CD34) and cell proliferation (proliferating cell nuclear antigen, PCNA) were localised by sequential immunohistochemistry and quantified using computer-assisted analysis. Vascular distribution was evaluated at increasing distances (up to 160µ) from the airspaces. Vessel density was markedly reduced in both FASSc (3.9%) and in CFA (4.5%) compared to controls (20.4%, p<0.0001). The percentage of tissue occupied by vessels decreased with increasing distance from alveoli in control samples, but not in CFA or FASSc samples. Endothelial cell proliferation indices were increased in FASSc but not in CFA, compared to controls (p=0.006). In conclusion, there is net vascular ablation and redistribution of blood vessels in areas of interstitial thickening in both CFA and FASSc, which may contribute to gas exchange impairment.
Key words: pulmonary fibrosis, scleroderma, pathologic neovascularization, endothelial proliferation




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