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Management of idiopathic pulmonary fibrosis
Published in Muhunthan Thillai, David R Moller, Keith C Meyer, Clinical Handbook of Interstitial Lung Disease, 2017
Damian AD Bruce-Hickman, Helen Garthwaite, Melissa Heightman, Bibek Gooptu
Things become even less clear where clinico-radiologic evaluation supports diagnosis of a different non-auto-immune ILD that shows evidence of progressive fibrosis. This can be observed in relatively young patients with CT appearances suggestive of cryptogenic organizing pneumonia or hypersensitivity pneumonitis in the absence of a clearly identified inhalational trigger. Fibroblastic foci are not entirely specific for IPF, and even surgical biopsy may miss characteristic features of a disease process. Therefore, what histologic criteria should constitute ‘sufficiently characteristic’ UIP histology to switch the consensus diagnosis of a MDT to a diagnosis of IPF? In cases where the radiology is suggestive of chronic HP or COP, how robustly reproducible are such judgments of UIP histology between histopathologists? To what extent does the confidence of identifying a dominant UIP process in these circumstances depend upon the experience of the histopathologist? Do such patients have ‘IPF-like’ responses to treatment, deriving benefit from anti-fibrotic treatment and harm from immune suppressive treatment? If so, it might make sense to recommend a lower threshold for biopsy, even in non-IPF ILDs where radiology seemed conclusive.
Pathology of drug-induced respiratory disease
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
William D Travis, Douglas B Flieder
This pattern consists of patchy areas of consolidation consisting of intraluminal plugs of loose connective tissue within distal airways including alveoli, alveolar ducts and bronchioles (Fig. 5.2). The architecture of the lung is preserved, interstitial chronic inflammation is usually mild, and dense scarring fibrosis is absent. This pattern can be seen in a wide variety of settings including infection, collagen vascular disease, eosinophilic pneumonia, vasculitis, as a secondary reaction adjacent to other mass lesions, and as an idiopathic condition known as cryptogenic organizing pneumonia.19,22 The latter condition is also known as idiopathic bronchiolitis obliterans organizing pneumonia (BOOP). The term ‘COP’ would not be used in the setting of a known drug reaction; in this situation the term BOOP could be used clinically with mention of the specific drug association (e.g. ‘BOOP due to amiodarone toxicity’). Various drugs are known to cause this reaction, including amiodarone, bleomycin, interferons, nitrofurantoin, radiation and statins.1,11,12,20 With bleomycin, the organizing pneumonia can present radiologically with discrete nodules.
Pulmonary Hemorrhage
Published in Philip T. Cagle, Timothy C. Allen, Mary Beth Beasley, Diagnostic Pulmonary Pathology, 2008
Andras Khoor, Henry D. Tazelaar
Diffuse alveolar hemorrhage is defined by the presence of blood in alveolar spaces, which is similar regardless of etiology, but this may be accompanied by other features (see below), some of which are helpful in limiting the diagnostic possibilities (35). Hemorrhage is manifest by the presence of red blood cells, fibrin, and hemosiderin-laden macrophages in the airspaces (Fig. 6). The alveolar walls may show evidence of acute lung injury in the form of hyaline membranes and reactive type II cells. Foci of organization may be prominent (Fig. 7). The degree of organization can be so prominent as to suggest the diagnosis of cryptogenic organizing pneumonia. Recognition of the presence of abundant hemosiderin-laden macrophages in the plugs of granulation tissue may suggest the diagnosis of organizing hemorrhage (Fig. 8).
Persistent anti-tumor response in cancer patients experiencing pneumonitis related to immune checkpoint blockade
Published in Acta Clinica Belgica, 2021
Laila Belcaid, Soizic Garaud, Joseph Kerger, Sideris Spyridon, Sandrine Aspeslagh
Diagnosing ICI-induced pneumonitis requires ruling out infection, tumor progression and radiation-induced pneumonitis. One study has examined the CT findings of PD-1 inhibitor-related pneumonitis and revealed a pattern of findings for 20 patients, including ground-glass opacities (100%) reticular opacities (95%), traction consolidation (60%), bronchiectasis (10%), and centrilobular nodularity (10%). According to ATS/ERS classification, a cryptogenic organizing pneumonia pattern was found in 65% patients suffering from melanoma, lung cancer or lymphoma [11]. Cases have been reported of patients treated by pembrolizumab monotherapy presenting with a misleading metastasis-like multiple pulmonary nodules by CT-scan [12]. Therefore, it has been proposed to perform a biopsy to obtain a histological diagnosis, especially in cases of dissociated responses, i.e. a response to the immunotherapy extra-pulmonary. Hence the absence of a specific biomarker for immune-related pneumonitis the integration of anamnesis, clinical presentation and imaging data is essential for correct diagnosis [5].
Daptomycin associated eosinophilic pneumonia: case report and differential diagnoses
Published in Journal of Community Hospital Internal Medicine Perspectives, 2018
Sijan Basnet, Niranjan Tachamo, Rashmi Dhital, Biswaraj Tharu
Conditions that can have a similar presentation of dyspnea and bilateral ground glass pulmonary infiltrates include pneumonia, hypersensitivity pneumonitis, alveolar proteinosis and cryptogenic organizing pneumonia. The patient did not have constitutional symptoms, sputum production with negative pneumococcal and Legionella urinary antigens making pneumonia unlikely. Pneumocystis jirovecii pneumonia without constitutional symptoms, history of exposure to HIV or high-risk behavior can be ruled out. Alveolar proteinosis is a rare diagnosis which is uncommon with no history of smoking. Lastly, cryptogenic organizing pneumonia is characteristically associated with a change in location of consolidation which was absent in our patient on serial imaging.
Describing and expanding the clinical phenotype of anti-MDA5-associated rapidly progressive interstitial lung disease: case series of nine Canadian patients and literature review
Published in Scandinavian Journal of Rheumatology, 2018
S Hoa, Y Troyanov, MJ Fritzler, IN Targoff, S Chartrand, AM Mansour, E Rich, H Boudabbouz, J Bourré-Tessier, M Albert, JR Goulet, M Landry, JL Senécal
Patient 9, a 61-year-old white woman, was diagnosed 2 years (in 2013) before her most recent hospitalization with ‘cryptogenic’ organizing pneumonia, and treated with high-dose corticosteroids and antibiotics for acute exacerbations attributed to infection. Lung disease was steroid-dependent, with difficulty tapering prednisone below 10 mg daily. Six weeks before hospitalization, she developed new-onset polyarthritis of the hands, wrists, and elbows, with morning stiffness and strongly positive RF and anti-CCP serology; along with a new rash consisting of mechanic’s hands, Gottron’s papules and sign, periungueal erythema, lateral finger papules, oral ulcers, alopecia, and shawl and V-signs. Two weeks before hospitalization, she experienced significant worsening of dyspnoea, now occurring at rest, and a 9 kg weight loss. She was clinically amyopathic, with normal CK, and had mild hyperferritinaemia (370 µg/L; normal 10–150 µg/L) and liver transaminitis (aspartate aminotransferase 58 U/L, alanine aminotransferase 45 U/L; normal 0–40 U/L). At this point, a diagnosis of anti-MDA5-associated RPILD was suspected, and she was treated with intravenous methylprednisolone pulses (500 mg weekly), prednisone (5–7.5 mg/day), MMF (3 g/day), and tacrolimus (2–3 mg/day), resulting in significant improvements in lung, joint, and skin disease over the following 4 months. Methylprednisolone pulses were discontinued thereafter without disease recurrence, and disease has remained quiescent with over 8 months of follow-up on MMF, tacrolimus, and low-dose prednisone (2–3 mg/day). Anti-MDA5 and anti-Ro52/TRIM21 autoantibodies were subsequently confirmed to be positive.