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Chest Imaging and Pathology for Clinicians |

A 29-Year-Old Man With Nonproductive Cough, Exertional Dyspnea, and Chest Discomfort29-Year-Old Man With Nonproductive Cough FREE TO VIEW

Darragh Halpenny, MD; James Suh, MD; Suzette Garofano, MD; Jeffrey Alpert, MD
Author and Funding Information

From the Department of Thoracic Radiology (Drs Halpenny and Alpert), the Department of Pathology (Dr Suh), and the Department of Pulmonology (Dr Garofano), New York University Langone Medical Center, New York, NY.

CORRESPONDENCE TO: Darragh Halpenny, MD, Department of Thoracic Radiology, New York University Langone Medical Center, 660 1st Ave, New York, NY 10016; e-mail: darraghhalpenny@hotmail.com


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(3):e80-e85. doi:10.1378/chest.14-2936
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A 29-year-old man presented with a 5-month history of worsening dry cough, exertional dyspnea, chest tightness, and palpitations. He had been treated by his primary care physician with trials of guaifenesin/codeine, azithromycin, albuterol, and omeprazole without improvement. He denied wheezing, fever, sweats, anorexia, joint pain, swelling, or rash. He had no past medical history. He denied a history of tobacco smoking or IV drug use. He kept no pets, worked as a manager in an office environment, and had no history of occupational inhalational exposure. He reported using aerosolized insect spray to eradicate bed bugs in his house shortly before the cough began but did not report any acute symptoms when using the spray.

Figures in this Article

Vital signs were as follows: BP, 120/90 mm Hg; respiratory rate, 16 breaths/min; pulse, 81 beats/min; and arterial oxygen saturation on room air, 94%. Physical examination was remarkable for bilateral rales. Following 1.5 min of stair climbing, oxygen saturation reduced to 91%.

Laboratory investigations demonstrated positive perinuclear antineutrophil cytoplasmic antibodies but were otherwise normal, including a negative HIV test and allergy testing. Pulmonary function test (PFT) results were as follows: total lung capacity, 74%; FVC, 4.28 L (68%); FEV1, 3.32 L (64%); FEV1/FVC, 78%, with no change after bronchodilator trial; and diffusing capacity of the lung for carbon monoxide (Dlco), 73%.

A chest radiograph revealed faint linear opacities in both lower lobes (Fig 1). CT scan of the chest (Figs 2A-D) revealed patchy areas of mainly subpleural ground-glass opacity and mild reticulation throughout all lobes, with a basal predominance. There was mild associated bronchiectasis. No honeycombing, pleural effusion, or lymphadenopathy was identified.

Figure Jump LinkFigure 1 –  Posteroanterior chest radiograph demonstrating faint linear opacities in both lower zones.Grahic Jump Location
Figure Jump LinkFigure 2 –  A-D, High-resolution CT scan images of the chest obtained at varying levels at the time of presentation, demonstrating basally predominant areas of predominantly subpleural ground-glass attenuation with mild subpleural reticulation.Grahic Jump Location

A wedge biopsy demonstrated areas with abundant CD1a-negative macrophages filling distal airways and alveolar spaces, some of which contained fine cytoplasmic pigment. There were foci of reactive type 2 pneumocyte hyperplasia as well as mild interstitial chronic inflammation consisting of lymphocytes and scattered eosinophils and patchy mild interstitial fibrosis without fibroblastic foci or honeycombing that was confirmed by a trichrome stain (Figs 3A, 3B). No tumor, granuloma, organizing pneumonia, hyaline membrane, or viral inclusion was seen. No foreign material or birefringent particles were identified by polarization microscopy. No mycobacteria or fungi were seen on acid-fast bacillus, Gomori methenamine-silver, and periodic acid-Schiff (± diastase) stains. A Von Kossa stain was noncontributory.

Figure Jump LinkFigure 3 –  A, High-power image shows macrophages with fine cytoplasmic pigment within alveoli and focal mild interstitial chronic inflammation consisting of lymphocytes and a few eosinophils (hematoxylin and eosin [H&E], original magnification × 400). B, Low-power image shows diffusely abnormal lung parenchyma with abundant macrophages filling distal airways and alveolar spaces as well as scattered lymphoid aggregates (H&E, original magnification × 20).Grahic Jump Location
What is the diagnosis?
Diagnosis: Desquamative interstitial pneumonia
Clinical Discussion

Desquamative interstitial pneumonia (DIP) is strongly associated with cigarette smoking, with up to 91% of patients giving a smoking history.1,2 Multiple other potential precipitants have been described (Table 1), including inorganic particle exposure, collagen vascular disease, infection (eg, cytomegalovirus and hepatitis C), and certain medication use (eg, sirolimus and nitrofurantoin).1,3-16 DIP is rare in children, is often associated with surfactant deficiency, and typically has a worse prognosis than in adults.9,10 Very rare cases of DIP have been associated with congenital conditions such as Gaucher disease15 and Hermansky-Pudlak syndrome.16 The average age of diagnosis is between 40 and 60 years, and it is twice as common in male patients. Overall survival varies from between 70% to 94%.1,17

Table Graphic Jump Location
TABLE 1 ]  Summary of the Causes of Non-Smoking-Related Desquamative Interstitial Pneumonia, Most of Which Are Rare1,3-16

The most common presenting symptoms are the insidious development of exertional dyspnea and nonproductive cough. Chest pain, hemoptysis, weight loss, and fatigue may also be present.1 Occasionally the onset of symptoms can be rapid, with a fulminant clinical course.18 On examination, bibasilar crackles and cyanosis are common. Clubbing is less frequent but has been reported in up to 50% of patients.2

Dlco is reduced in up to 87% of patients and is the most commonly abnormal PFT.2,4,19 Systemic arterial oxygen saturation measurements typically reduce following exercise. Mild restrictive defects are also frequently found on PFTs.20 It should be noted that performance of a 6-min walk test or other assessment of oxygenation with exertion may unmask a subtle abnormality in pulmonary function, particularly in patients with supranormal baseline values. The results of serologic investigations are generally nonspecific and frequently normal.1

Long-term oral corticosteroid treatment is central to the treatment of patients with DIP. In the absence of steroid treatment, two-thirds of patients will continue to deteriorate clinically.21 The potential role for the use of immunosuppressive agents or other medical therapies has yet to be defined. Clinical improvement in steroid-refractory DIP has been demonstrated following the use of cyclophosphamide and macrolide antibiotics.22,23 Smoking cessation is central to the management of this patient cohort. A variety of clinical courses have been described in patients with occupational exposure-associated DIP. For example, Lougheed et al24 report five patients with occupational DIP, two of whom returned to work and suffered relapse of symptoms, two of whom did not return to work and improved without steroid therapy, and one who did not return to work but who had a slow and incomplete response to steroid therapy.

The patient in this case is a male nonsmoker, slightly outside the typical age distribution for cases of DIP. However, he had exposure to insect spray prior to the onset of symptoms, and in the absence of other potential etiologic agents or a history of cigarette smoking we believe this is the probable causative agent (to our knowledge, no prior reports of DIP resulting from exposure to aerosolized insecticide exist, although Liebow et al4 report DIP resulting from aerosolized hairspray). The presenting symptoms of dry cough, increasing exertional dyspnea, chest tightness, and weight loss are all nonspecific and are associated with many respiratory and cardiac diseases. The PFT abnormalities in this case are similarly nonspecific. It is the combination of clinical findings with characteristic pathologic and radiologic findings that allows a diagnosis of DIP to be made.

Radiologic Discussion

The imaging features of DIP are nonspecific.25 The most common abnormality on chest radiograph is the presence of irregular basal-predominant opacity.26 On CT scan, patchy basally/peripherally predominant ground-glass opacities (corresponding to areas of intra-alveolar macrophage accumulation on histology27) are the dominant finding. Ground-glass attenuation will typically improve following treatment with steroids.27

Irregular linear opacities suggestive of fibrosis can be identified in up to 63% of patients.28 The degree of reported architectural distortion and bronchiectasis varies considerably in the literature but tends to be mild, described in between 13% to 100% of patients.28,29 Small cystic spaces are also frequently described and can be seen in up to 75% of cases.28 The cysts differ from areas of honeycombing seen in usual interstitial pneumonia (UIP) both morphologically and in their potential for resolution following treatment.28 Frank honeycombing can be seen in cases of DIP but is rare. Centrilobular nodular opacities have been described but are also rare.29 The dominant imaging findings in this case are peripherally and basally predominant ground-glass opacities. There were foci of mild bronchial dilation but no evidence of cyst formation.

In general, the radiologic differential diagnosis includes respiratory bronchiolitis interstitial lung disease (RB-ILD), hypersensitivity pneumonitis (HP), nonspecific interstitial pneumonia (NSIP), and atypical infections such as Pneumocystis jiroveci pneumonia (PJP). There is some overlap in the imaging features of DIP and RB-ILD. RB-ILD, however, in addition to ground-glass opacities, is classically associated with centrilobular nodules and bronchial wall thickening. Both of these latter features were absent in this case. In combination with the lack of smoking history, this makes RB-ILD very unlikely.

In patients with NSIP, high-resolution CT scan findings are most frequent in the lower lobes but often lack a clear apicobasal gradient. As with DIP, the dominant finding is that of ground-glass attenuation, in addition to associated reticular opacities and micronodules.30 Although there was no definite reticulation in the images in this case, NSIP is a diagnostic consideration.

Ground-glass opacity, which is usually bilateral and symmetric, but which can be patchy or in a bronchovascular distribution, is also a typical feature of HP. HP is also frequently associated with centrilobular nodular opacities. In addition, air trapping may be seen as a consequence of bronchiolar inflammation. The images in this case lack evidence of air trapping and centrilobular nodularity; however, given the close temporal link to insecticide exposure, HP remains on the radiologic differential diagnosis.31

Centrally distributed ground-glass attenuation is also the most frequent finding on high-resolution CT scan in cases of PJP.32 This case lacks the typical CT scan distribution of PJP which, in combination with the absence of typical clinical features predisposing to PJP, makes it an unlikely diagnosis.

To our knowledge, there is no radiologic method to distinguish the pattern of DIP in smokers compared with nonsmokers. In a patient without a smoking history, chest CT scans or radiographs should be examined for ancillary imaging signs that may suggest a systemic disorder, for example, the presence of esophageal dilation to suggest systemic sclerosis or the presence of arthritis to suggest rheumatoid arthritis (although interstitial lung disease associated with these entities is more likely to be NSIP or UIP).13

Pathologic Discussion

DIP is characterized by marked diffuse intra-alveolar macrophage accumulation, which corresponds to areas of ground-glass attenuation on CT scan.25,30,33 The pathologic differential diagnosis of DIP includes NSIP, UIP, and HP, as well as smoking-related interstitial processes such as RB-ILD, Langerhans cell histiocytosis (LCH), and airspace enlargement with fibrosis (AEF)/smoking-related interstitial fibrosis (SRIF).33-35 The presence of interstitial chronic inflammation and fibrosis may lead to confusion with NSIP, UIP, or HP, but extensive intra-alveolar macrophage accumulation should not be seen in any of these interstitial lung diseases.25,33 Furthermore, the absence of fibroblastic foci and honeycombing and the lack of bronchiolocentricity and granulomas distinguish DIP from UIP and HP, respectively.17

DIP, RB-ILD, LCH, and AEF/SRIF are usually smoking related, so “smoker’s macrophages” that have lightly pigmented cytoplasm staining for iron can be identified in BAL specimens.1,25,33 In contrast to RB-ILD, the distribution of alveolar macrophages in DIP is diffuse rather than patchy and centrilobular (as seen on CT scan).17,30,34 Peribronchiolar stellate-shaped nodules with traction emphysema and CD1a-positive Langerhans cells are characteristic of LCH but are absent in DIP. There is much morphologic overlap between DIP and AEF/SRIF, which may represent incidental findings in the nonneoplastic parenchyma of lung cancer resection specimens.35

Some investigators have reported that macrophages in nonsmokers tend to have homogenously eosinophilic or slightly vacuolated cytoplasm in comparison with the presence of fine pigmented granules typically seen in cigarette smokers and the coarse pigmented granules typically seen in those with a history of heavy marijuana use17; however, the reliability of using these methods to histologically differentiate between non-smoking-related and smoking-related causes has not been established.17 In a series of 20 patients, Craig et al6 found no differences in histologic features of DIP comparing smokers and never smokers. We did not see coarse granules in our case, which, in combination with the absence of a history of cigarette smoking, suggested inhalational toxicity from pesticide exposure as the etiological agent.

The patient was started on treatment with prednisone 60 mg/d. His dyspnea gradually improved during his 3 months of steroid therapy to date. His steroid dose was tapered to 15 mg/d, and he restarted mild exercise. A follow-up CT scan performed 5 weeks following the commencement of steroids demonstrated marked improvement in aeration in both lungs, with near resolution of the previously demonstrated ground-glass opacities (Figs 4A-D). PFTs repeated 3 months after the commencement of steroid therapy also demonstrated improvement: total lung capacity, 88% (previously 74%); FVC, 5.27 L (82%) (previously 4.28 L, 68%); FEV1, 4.06 L (76%) (previously 3.32, 64%); FEV1/FVC, 77% (previously 78%); Dlco 89% (previously 73%). His response to steroid therapy was typical of the clinical and radiologic course in the majority of patients with DIP.

Figure Jump LinkFigure 4 –  A-D, High-resolution CT scan images of the chest obtained at varying levels following 2 mo of steroid therapy, demonstrating considerable improvement in the previously identified areas of subpleural ground-glass attenuation.Grahic Jump Location

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Godbert B, Wissler MP, Vignaud JM. Desquamative interstitial pneumonia: an analytic review with an emphasis on aetiology. Eur Respir Rev. 2013;22(128):117-123. [CrossRef] [PubMed]
 
Ryu JH, Colby TV, Hartman TE, Vassallo R. Smoking-related interstitial lung diseases: a concise review. Eur Respir J. 2001;17(1):122-132. [CrossRef] [PubMed]
 
Kroll RR, Flood DA, Srigley J. Desquamative interstitial pneumonitis in a non-smoker: a rare diagnosis. Can Respir J. 2014;21(2):86-88. [PubMed]
 
Liebow AA, Steer A, Billingsley JG. Desquamative interstitial pneumonia. Am J Med. 1965;39:369-404. [CrossRef] [PubMed]
 
Abraham JL, Hertzberg MA. Inorganic particulates associated with desquamative interstitial pneumonia. Chest. 1981;80(1_suppl):67-70. [CrossRef] [PubMed]
 
Craig PJ, Wells AU, Doffman S, et al. Desquamative interstitial pneumonia, respiratory bronchiolitis and their relationship to smoking. Histopathology. 2004;45(3):275-282. [CrossRef] [PubMed]
 
Moon J, du Bois RM, Colby TV, Hansell DM, Nicholson AG. Clinical significance of respiratory bronchiolitis on open lung biopsy and its relationship to smoking related interstitial lung disease. Thorax. 1999;54(11):1009-1014. [CrossRef] [PubMed]
 
Esmaeilbeigi F, Juvet S, Hwang D, Mittoo S. Desquamative interstitial pneumonitis in a patient with systemic lupus erythematosus. Can Respir J. 2012;19(1):50-52. [PubMed]
 
Langston C, Dishop MK. Diffuse lung disease in infancy: a proposed classification applied to 259 diagnostic biopsies. Pediatr Dev Pathol. 2009;12(6):421-437. [CrossRef] [PubMed]
 
Deutsch GH, Young LR, Deterding RR, et al; Pathology Cooperative Group; ChILD Research Co-operative. Diffuse lung disease in young children: application of a novel classification scheme. Am J Respir Crit Care Med. 2007;176(11):1120-1128. [CrossRef] [PubMed]
 
Swartz JS, Chatterjee S, Parambil JG. Desquamative interstitial pneumonia as the initial manifestation of systemic sclerosis. J Clin Rheumatol. 2010;16(6):284-286. [CrossRef] [PubMed]
 
de Lauretis A, Veeraraghavan S, Renzoni E. Review series: aspects of interstitial lung disease: connective tissue disease-associated interstitial lung disease: how does it differ from IPF? How should the clinical approach differ? Chron Respir Dis. 2011;8(1):53-82. [PubMed]
 
Lamblin C, Bergoin C, Saelens T, Wallaert B. Interstitial lung diseases in collagen vascular diseases. Eur Respir J Suppl. 2001;32:69s-80s. [PubMed]
 
Tillie-Leblond I, Colin G, Lelong J, Cadranel J. Pulmonary involvement in polymyositis and dermatomyositis [in French]. Rev Mal Respir. 2006;23(6):671-680. [CrossRef] [PubMed]
 
Copley SJ, Coren M, Nicholson AG, Rubens MB, Bush A, Hansell DM. Diagnostic accuracy of thin-section CT and chest radiography of pediatric interstitial lung disease. AJR Am J Roentgenol. 2000;174(2):549-554. [CrossRef] [PubMed]
 
van der Vis JJ, ten Klooster L, van Oosterhout MFM, Grutters JC, van Moorsel CHM. The occurrence of Hermansky Pudlak syndrome in patients with idiopathic pulmonary fibrosis–a cohort study. J Genet Syndr Gene Ther. 2013;4:141.
 
Tazelaar HD, Wright JL, Churg A. Desquamative interstitial pneumonia. Histopathology. 2011;58(4):509-516. [CrossRef] [PubMed]
 
Gould TH, Buist MD, Meredith D, Thomas PD. Fulminant desquamative interstitial pneumonitis. Anaesth Intensive Care. 1998;26(6):677-679. [PubMed]
 
Ryu JH, Myers JL, Capizzi SA, Douglas WW, Vassallo R, Decker PA. Desquamative interstitial pneumonia and respiratory bronchiolitis-associated interstitial lung disease. Chest. 2005;127(1):178-184. [CrossRef] [PubMed]
 
Wells AU, Nicholson AG, Hansell DM. Challenges in pulmonary fibrosis. 4: smoking-induced diffuse interstitial lung diseases. Thorax. 2007;62(10):904-910. [CrossRef] [PubMed]
 
Carrington CB, Gaensler EA, Coutu RE, FitzGerald MX, Gupta RG. Natural history and treated course of usual and desquamative interstitial pneumonia. N Engl J Med. 1978;298(15):801-809. [CrossRef] [PubMed]
 
Flusser G, Gurman G, Zirkin H, Prinslo I, Heimer D. Desquamative interstitial pneumonitis causing acute respiratory failure, responsive only to immunosuppressants. Respiration. 1991;58(5-6):324-326. [CrossRef] [PubMed]
 
Knyazhitskiy A, Masson RG, Corkey R, Joiner J. Beneficial response to macrolide antibiotic in a patient with desquamative interstitial pneumonia refractory to corticosteroid therapy. Chest. 2008;134(1):185-187. [CrossRef] [PubMed]
 
Lougheed MD, Roos JO, Waddell WR, Munt PW. Desquamative interstitial pneumonitis and diffuse alveolar damage in textile workers. Potential role of mycotoxins. Chest. 1995;108(5):1196-1200. [CrossRef] [PubMed]
 
American Thoracic Society/European Respiratory Society international multidisciplinary consensus classification of the idiopathic interstitial pneumonias. This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Executive Committee, June 2001. Am J Respir Crit Care Med. 2002;165(2):277-304. [CrossRef] [PubMed]
 
Feigin DS, Friedman PJ. Chest radiography in desquamative interstitial pneumonitis: a review of 37 patients. AJR Am J Roentgenol. 1980;134(1):91-99. [CrossRef] [PubMed]
 
Lynch DA, Travis WD, Müller NL, et al. Idiopathic interstitial pneumonias: CT features. Radiology. 2005;236(1):10-21. [CrossRef] [PubMed]
 
Akira M, Yamamoto S, Hara H, Sakatani M, Ueda E. Serial computed tomographic evaluation in desquamative interstitial pneumonia. Thorax. 1997;52(4):333-337. [CrossRef] [PubMed]
 
Heyneman LE, Ward S, Lynch DA, Remy-Jardin M, Johkoh T, Müller NL. Respiratory bronchiolitis, respiratory bronchiolitis-associated interstitial lung disease, and desquamative interstitial pneumonia: different entities or part of the spectrum of the same disease process? AJR Am J Roentgenol. 1999;173(6):1617-1622. [CrossRef] [PubMed]
 
Mueller-Mang C, Grosse C, Schmid K, Stiebellehner L, Bankier AA. What every radiologist should know about idiopathic interstitial pneumonias. Radiographics. 2007;27(3):595-615. [CrossRef] [PubMed]
 
Hirschmann JV, Pipavath SN, Godwin JD. Hypersensitivity pneumonitis: a historical, clinical, and radiologic review. Radiographics. 2009;29(7):1921-1938. [CrossRef] [PubMed]
 
Kanne JP, Yandow DR, Meyer CA. Pneumocystis jirovecipneumonia: high-resolution CT findings in patients with and without HIV infection. AJR Am J Roentgenol. 2012;198(6):W555-W561. [CrossRef] [PubMed]
 
Hidalgo A, Franquet T, Giménez A, Bordes R, Pineda R, Madrid M. Smoking-related interstitial lung diseases: radiologic-pathologic correlation. Eur Radiol. 2006;16(11):2463-2470. [CrossRef] [PubMed]
 
Caminati A, Cavazza A, Sverzellati N, Harari S. An integrated approach in the diagnosis of smoking-related interstitial lung diseases. Eur Respir Rev. 2012;21(125):207-217. [CrossRef] [PubMed]
 
Travis WD, Costabel U, Hansell DM, et al; ATS/ERS Committee on Idiopathic Interstitial Pneumonias. An official American Thoracic Society/European Respiratory Society statement: update of the international multidisciplinary classification of the idiopathic interstitial pneumonias. Am J Respir Crit Care Med. 2013;188(6):733-748. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  Posteroanterior chest radiograph demonstrating faint linear opacities in both lower zones.Grahic Jump Location
Figure Jump LinkFigure 2 –  A-D, High-resolution CT scan images of the chest obtained at varying levels at the time of presentation, demonstrating basally predominant areas of predominantly subpleural ground-glass attenuation with mild subpleural reticulation.Grahic Jump Location
Figure Jump LinkFigure 3 –  A, High-power image shows macrophages with fine cytoplasmic pigment within alveoli and focal mild interstitial chronic inflammation consisting of lymphocytes and a few eosinophils (hematoxylin and eosin [H&E], original magnification × 400). B, Low-power image shows diffusely abnormal lung parenchyma with abundant macrophages filling distal airways and alveolar spaces as well as scattered lymphoid aggregates (H&E, original magnification × 20).Grahic Jump Location
Figure Jump LinkFigure 4 –  A-D, High-resolution CT scan images of the chest obtained at varying levels following 2 mo of steroid therapy, demonstrating considerable improvement in the previously identified areas of subpleural ground-glass attenuation.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  Summary of the Causes of Non-Smoking-Related Desquamative Interstitial Pneumonia, Most of Which Are Rare1,3-16

References

Godbert B, Wissler MP, Vignaud JM. Desquamative interstitial pneumonia: an analytic review with an emphasis on aetiology. Eur Respir Rev. 2013;22(128):117-123. [CrossRef] [PubMed]
 
Ryu JH, Colby TV, Hartman TE, Vassallo R. Smoking-related interstitial lung diseases: a concise review. Eur Respir J. 2001;17(1):122-132. [CrossRef] [PubMed]
 
Kroll RR, Flood DA, Srigley J. Desquamative interstitial pneumonitis in a non-smoker: a rare diagnosis. Can Respir J. 2014;21(2):86-88. [PubMed]
 
Liebow AA, Steer A, Billingsley JG. Desquamative interstitial pneumonia. Am J Med. 1965;39:369-404. [CrossRef] [PubMed]
 
Abraham JL, Hertzberg MA. Inorganic particulates associated with desquamative interstitial pneumonia. Chest. 1981;80(1_suppl):67-70. [CrossRef] [PubMed]
 
Craig PJ, Wells AU, Doffman S, et al. Desquamative interstitial pneumonia, respiratory bronchiolitis and their relationship to smoking. Histopathology. 2004;45(3):275-282. [CrossRef] [PubMed]
 
Moon J, du Bois RM, Colby TV, Hansell DM, Nicholson AG. Clinical significance of respiratory bronchiolitis on open lung biopsy and its relationship to smoking related interstitial lung disease. Thorax. 1999;54(11):1009-1014. [CrossRef] [PubMed]
 
Esmaeilbeigi F, Juvet S, Hwang D, Mittoo S. Desquamative interstitial pneumonitis in a patient with systemic lupus erythematosus. Can Respir J. 2012;19(1):50-52. [PubMed]
 
Langston C, Dishop MK. Diffuse lung disease in infancy: a proposed classification applied to 259 diagnostic biopsies. Pediatr Dev Pathol. 2009;12(6):421-437. [CrossRef] [PubMed]
 
Deutsch GH, Young LR, Deterding RR, et al; Pathology Cooperative Group; ChILD Research Co-operative. Diffuse lung disease in young children: application of a novel classification scheme. Am J Respir Crit Care Med. 2007;176(11):1120-1128. [CrossRef] [PubMed]
 
Swartz JS, Chatterjee S, Parambil JG. Desquamative interstitial pneumonia as the initial manifestation of systemic sclerosis. J Clin Rheumatol. 2010;16(6):284-286. [CrossRef] [PubMed]
 
de Lauretis A, Veeraraghavan S, Renzoni E. Review series: aspects of interstitial lung disease: connective tissue disease-associated interstitial lung disease: how does it differ from IPF? How should the clinical approach differ? Chron Respir Dis. 2011;8(1):53-82. [PubMed]
 
Lamblin C, Bergoin C, Saelens T, Wallaert B. Interstitial lung diseases in collagen vascular diseases. Eur Respir J Suppl. 2001;32:69s-80s. [PubMed]
 
Tillie-Leblond I, Colin G, Lelong J, Cadranel J. Pulmonary involvement in polymyositis and dermatomyositis [in French]. Rev Mal Respir. 2006;23(6):671-680. [CrossRef] [PubMed]
 
Copley SJ, Coren M, Nicholson AG, Rubens MB, Bush A, Hansell DM. Diagnostic accuracy of thin-section CT and chest radiography of pediatric interstitial lung disease. AJR Am J Roentgenol. 2000;174(2):549-554. [CrossRef] [PubMed]
 
van der Vis JJ, ten Klooster L, van Oosterhout MFM, Grutters JC, van Moorsel CHM. The occurrence of Hermansky Pudlak syndrome in patients with idiopathic pulmonary fibrosis–a cohort study. J Genet Syndr Gene Ther. 2013;4:141.
 
Tazelaar HD, Wright JL, Churg A. Desquamative interstitial pneumonia. Histopathology. 2011;58(4):509-516. [CrossRef] [PubMed]
 
Gould TH, Buist MD, Meredith D, Thomas PD. Fulminant desquamative interstitial pneumonitis. Anaesth Intensive Care. 1998;26(6):677-679. [PubMed]
 
Ryu JH, Myers JL, Capizzi SA, Douglas WW, Vassallo R, Decker PA. Desquamative interstitial pneumonia and respiratory bronchiolitis-associated interstitial lung disease. Chest. 2005;127(1):178-184. [CrossRef] [PubMed]
 
Wells AU, Nicholson AG, Hansell DM. Challenges in pulmonary fibrosis. 4: smoking-induced diffuse interstitial lung diseases. Thorax. 2007;62(10):904-910. [CrossRef] [PubMed]
 
Carrington CB, Gaensler EA, Coutu RE, FitzGerald MX, Gupta RG. Natural history and treated course of usual and desquamative interstitial pneumonia. N Engl J Med. 1978;298(15):801-809. [CrossRef] [PubMed]
 
Flusser G, Gurman G, Zirkin H, Prinslo I, Heimer D. Desquamative interstitial pneumonitis causing acute respiratory failure, responsive only to immunosuppressants. Respiration. 1991;58(5-6):324-326. [CrossRef] [PubMed]
 
Knyazhitskiy A, Masson RG, Corkey R, Joiner J. Beneficial response to macrolide antibiotic in a patient with desquamative interstitial pneumonia refractory to corticosteroid therapy. Chest. 2008;134(1):185-187. [CrossRef] [PubMed]
 
Lougheed MD, Roos JO, Waddell WR, Munt PW. Desquamative interstitial pneumonitis and diffuse alveolar damage in textile workers. Potential role of mycotoxins. Chest. 1995;108(5):1196-1200. [CrossRef] [PubMed]
 
American Thoracic Society/European Respiratory Society international multidisciplinary consensus classification of the idiopathic interstitial pneumonias. This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Executive Committee, June 2001. Am J Respir Crit Care Med. 2002;165(2):277-304. [CrossRef] [PubMed]
 
Feigin DS, Friedman PJ. Chest radiography in desquamative interstitial pneumonitis: a review of 37 patients. AJR Am J Roentgenol. 1980;134(1):91-99. [CrossRef] [PubMed]
 
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