ReviewEuropean respiratory review : an official journal of the European Respiratory Society2024
Pathogenesis-driven treatment of primary pulmonary alveolar proteinosis.
Review in European respiratory review : an official journal of the European Respiratory Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of recombinant human GM-CSF compared to placebo for autoimmune pulmonary alveolar proteinosis: a systematic review and meta-analysis.BMC pulmonary medicine · 2026Pooled it
- Pulmonary Alveolar Proteinosis-Like Presentation of Murine Typhus in a Previously Healthy Adult.Cureus · 2026Article
- Targeting the PPAR-γ-ABC transporter axis ameliorates secondary pulmonary alveolar proteinosis induced by indium oxide nanoparticles.Particle and fibre toxicology · 2026Article
- Successful Whole-Lung Lavage in Anti-GM-CSF-Negative Pulmonary Alveolar Proteinosis: A Case Report.The American journal of case reports · 2026Article
- Clinical characterization of 39 patients with autoimmune pulmonary alveolar proteinosis.The Journal of international medical research · 2026Article
- Pulmonary alveolar proteinosis andFrontiers in pediatrics · 2026Article
- Beyond the Graft: Recurrence of Interstitial Lung Diseases Post Transplant.Journal of clinical medicine · 2025Review
- Case Report: Innovative anesthetic approaches for whole lung lavage in an infant with pulmonary alveolar proteinosis.Frontiers in pediatrics · 2025Article
- Hyaluronan in the pathogenesis of lung fibrosis associated to autoimmune pulmonary alveolar proteinosis (aPAP).Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary alveolar proteinosis (PAP) is a syndrome that results from the accumulation of lipoproteinaceous material in the alveolar space. According to the underlying pathogenetic mechanisms, three different forms have been identified, namely primary, secondary and congenital. Primary PAP is caused by disruption of granulocyte-macrophage colony-stimulating factor (GM-CSF) signalling due to the presence of neutralising autoantibodies (autoimmune PAP) or GM-CSF receptor genetic defects (hereditary PAP), which results in dysfunctional alveolar macrophages with reduced phagocytic clearance of particles, cholesterol and surfactant. The serum level of GM-CSF autoantibody is the only disease-specific biomarker of autoimmune PAP, although it does not correlate with disease severity. In PAP patients with normal serum GM-CSF autoantibody levels, elevated serum GM-CSF levels is highly suspicious for hereditary PAP. Several biomarkers have been correlated with disease severity, although they are not specific for PAP. These include lactate dehydrogenase, cytokeratin 19 fragment 21.1, carcinoembryonic antigen, neuron-specific enolase, surfactant proteins, Krebs von Lungen 6, chitinase-3-like protein 1 and monocyte chemotactic proteins. Finally, increased awareness of the disease mechanisms has led to the development of pathogenesis-based treatments, such as GM-CSF augmentation and cholesterol-targeting therapies.
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Registered trials
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