Proposed Pathogenesis of Diffuse Alveolar Hemorrhage in Idiopathic Pulmonary Hemosiderosis.
Eosinophilic cationic protein
Histamine
Idiopathic pulmonary hemosiderosis
Pathogenesis
Pulmonary hemorrhage
Journal
Lung
ISSN: 1432-1750
Titre abrégé: Lung
Pays: United States
ID NLM: 7701875
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
received:
05
01
2022
accepted:
27
02
2022
pubmed:
11
3
2022
medline:
28
4
2022
entrez:
10
3
2022
Statut:
ppublish
Résumé
Idiopathic pulmonary hemosiderosis (IPH) is a rare disease that causes diffuse alveolar hemorrhage (DAH). The latest data suggests an immunologic origin of IPH, and a new name, immune mediated pulmonary hemosiderosis (ImPH), has been proposed. However, the exact immunologic mechanism has remained elusive for nearly eight decades despite extensive research, including detailed histopathologic analysis. Although several hypotheses have been proposed to describe the pathobiology of IPH, none of them explain the clinical and histopathologic findings conclusively. In this manuscript, we have presented a new hypothesis for the pathogenesis of DAH in IPH. We hypothesize that DAH in IPH is not immunocomplex mediated but due to histamine, eosinophilic cationic protein (ECP), and possibly vascular endothelial growth factor (VEGF). These bioactive proteins induce endothelial and alveolar epithelial damage, leading to the peri-capillary and intraalveolar escape of RBCs. The deformability of the RBC likely also plays a role. The supranormal secretion of histamine, ECP and VEGF occurs in genetically predisposed individuals with an aberrant immunologic response. The histamine is released from the basophils and possibly the mast cells in response to cytokines secreted by activated lymphocytes. The lymphocyte activation occurs after exposure to a known (gluten) or unknown antigen. The same lymphocyte-derived cytokines also induce eosinophilic degranulation of ECP and VEGF in the pulmonary circulation. We believe that our hypothesis unifies the observed clinical variabilities and histopathologic findings in IPH, and we hope that would promote future research in the field of IPH.
Identifiants
pubmed: 35267072
doi: 10.1007/s00408-022-00523-4
pii: 10.1007/s00408-022-00523-4
doi:
Substances chimiques
Cytokines
0
Vascular Endothelial Growth Factor A
0
Histamine
820484N8I3
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
205-215Informations de copyright
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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