Chest
Desquamative Interstitial Pneumonitis Associated with Monomyelocytic Leukemia
Section snippets
Methods
Open lung biopsies from both patients and autopsy lung tissue from case 2 were fixed in 10 percent buffered formaldehyde, processed routinely, and embedded in paraffin. Sections were stained with hematoxylin and eosin, periodic acid-Schiff, reticulin, trichrome, Prussian blue, gram, methenamine silver, and acid-fast stains. The lung biopsy from case 1 and post mortem tissue from case 2 were also studied by the chloroacetate esterase (CAE) technique13 and by immunoperoxidase for intracellular
Case 1
A previously healthy, 51-year-old woman who smoked, presented in February, 1978 with a three-week history of low grade fever, right pleuritic chest pain, and increasing dyspnea. The chest radiograph had the “classic” appearance for DIP: bilateral, hazy, ground glass infiltrates in the medial aspects of the lung bases.15 This illness was unresponsive to oral penicillin. After a white blood cell count was interpreted as acute leukemia, the patient was referred to the Peter Bent Brigham Hospital.
Discussion
Both the underlying etiology and pathogenesis of DIP are unknown. Although the masses of intra-alveolar mononuclear cells were originally thought to be desquamated granular pneumocytes,1 subsequent ultrastructural studies have proven them to be alveolar macrophages.2,6,12 Farr et al12 suggested PAMs in DIP migrate into the air spaces in response to abnormal secretions produced by granular pneumocytes, which in turn may be reacting to an underlying immunologic, toxic, hormonal, or infectious
Acknowledgments
The writers wish to thank Dr. Geraldine Pinkus for the special histochemical and immunoperoxidase stains performed on these specimens.
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2012, Diffuse Lung Disease: A Practical Approach, Second Edition
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Supported in part by National Research Service Award No. 4 T32 HL07066-5.