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Pulmonary Alveolar Microlithiasis.

Brian M Shaw¹, Steven D Shaw¹, Francis X McCormack^1,2

¹Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio.

Seminars in Respiratory and Critical Care Medicine

|April 13, 2020

Summary

This summary is machine-generated.

Pulmonary alveolar microlithiasis (PAM) is a rare genetic disorder caused by faulty phosphate transport. This leads to calcium-phosphate buildup in the lungs, forming distinctive microliths visible on imaging.

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Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages

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Area of Science:

Pulmonology
Genetics
Radiology

Background:

Pulmonary alveolar microlithiasis (PAM) is a rare autosomal recessive disorder.
It stems from mutations in the SLC34A2 gene, impacting the Npt2b phosphate cotransporter.
This dysfunction leads to inorganic phosphate accumulation in alveolar lining fluid.

Purpose of the Study:

To describe the genetic basis, pathophysiology, and clinical presentation of Pulmonary Alveolar Microlithiasis.
To highlight diagnostic imaging findings and management strategies for PAM.

Main Methods:

Review of existing literature on Pulmonary Alveolar Microlithiasis.
Analysis of diagnostic imaging characteristics (radiographs, CT scans).
Discussion of genetic mutations and their functional consequences.

Main Results:

Mutations in SLC34A2 impair Npt2b function, causing phosphate export failure.
Accumulated phosphate binds calcium, forming hydroxyapatite microliths in alveoli.
Chest imaging reveals characteristic hyperdense infiltrates; diagnosis often non-invasive.
Dyspnea on exertion is a common symptom; incidental findings are frequent.

Conclusions:

PAM is characterized by genetic defects in phosphate transport leading to lung microlithiasis.
Diagnosis is often achievable through characteristic imaging findings.
Disease progression can lead to pulmonary fibrosis, hypertension, and respiratory failure; treatment is supportive, with lung transplantation for end-stage cases.