• Title/Summary/Keyword: Acute fibrinous and organizing pneumonia

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A Case of Acute Fibrinous and Organizing Pneumonia (급성 섬유소성 기질화 폐렴 1예)

  • Cho, Joo Yeon;Lee, Hyun Kyung;Lee, Sung Soon;Lee, Hye Kyung;Lee, Young Min;Lee, Hyuk Pyo;Kim, Joo In;Choi, Soo Jeon;Yum, Ho-Kee
    • Tuberculosis and Respiratory Diseases
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    • v.61 no.5
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    • pp.479-483
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    • 2006
  • Acute fibrinous and organizing pneumonia (AFOP) is a histological pattern consisting of prominent intra-alveolar fibrin and organizing pneumonia, with out hyaline membranes or prominent eosinophilia. The clinical manifestations of AFOP resemble those of acute lung injury such as acute interstitial pneumonia (AIP). However, the classic histological patterns of AFOP differ from diffuse alveolar damage (DAD), bronchiolitis obliterans with organizing pneumonia (BOOP) or acute eosinophilic pneumonia (AEP). The characteristic intra-alveolar fibrin ball and lack of classic hyaline membrane are the predominant histological features of AFOP. Although some reports suggest that its clinical course is less catastrophic than DAD, the clinical entity that distinguishes AFOP from DAD has not been established. We present a case of pathologically demonstrated AFOP in a 79-year-old man. The radiological findings of our case were similar to those of DAD, presented with diffuse bilateral lung infiltrations. However, despite the rapid development of respiratory failure, the patient had a better response and outcome to steroid therapy than what would be expected for DAD.

Pathological interpretation of connective tissue disease-associated lung diseases

  • Kwon, Kun Young
    • Journal of Yeungnam Medical Science
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    • v.36 no.1
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    • pp.8-15
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    • 2019
  • Connective tissue diseases (CTDs) can affect all compartments of the lungs, including airways, alveoli, interstitium, vessels, and pleura. CTD-associated lung diseases (CTD-LDs) may present as diffuse lung disease or as focal lesions, and there is significant heterogeneity between the individual CTDs in their clinical and pathological manifestations. CTD-LDs may presage the clinical diagnosis a primary CTD, or it may develop in the context of an established CTD diagnosis. CTD-LDs reveal acute, chronic or mixed pattern of lung and pleural manifestations. Histopathological findings of diverse morphological changes can be present in CTD-LDs airway lesions (chronic bronchitis/bronchiolitis, follicular bronchiolitis, etc.), interstitial lung diseases (nonspecific interstitial pneumonia/fibrosis, usual interstitial pneumonia, lymphocytic interstitial pneumonia, diffuse alveolar damage, and organizing pneumonia), pleural changes (acute fibrinous or chronic fibrous pleuritis), and vascular changes (vasculitis, capillaritis, pulmonary hemorrhage, etc.). CTD patients can be exposed to various infectious diseases when taking immunosuppressive drugs. Histopathological patterns of CTD-LDs are generally nonspecific, and other diseases that can cause similar lesions in the lungs must be considered before the diagnosis of CTD-LDs. A multidisciplinary team involving pathologists, clinicians, and radiologists can adequately make a proper diagnosis of CTD-LDs.

Severe Acute Fibrinous and Organizing Pneumonia with Acute Respiratory Distress Syndrome

  • Kang, Hyo-Jae;Choi, Sun-Mi;Jeong, Yun-Jeong;Park, Jong-Sun;Lee, Sei-Won;Yoon, Ho-Il;Lee, Jae-Ho;Lee, Choon-Tack;Cho, Young-Jae
    • Tuberculosis and Respiratory Diseases
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    • v.71 no.5
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    • pp.368-372
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    • 2011
  • Acute fibrinous and organizing pneumonia is a newly recognized pattern of acute lung injury. A 49-year-old female presented with a cough and worsening dyspnea on exertion. She had no history of smoking and no specific past medical history except exposure of home humidifier containing sterilizer. A chest computed tomography scan showed patchy consolidation with fibrosis in the right lower lobe and ill-defined centrilobular ground glass opacity in both lungs. The pathological findings were patchy areas of lung parenchyma with fibrin deposits in the alveolar ducts and alveoli, and fibrin balls with hemosiderin deposition in the alveolar spaces. The histological pattern of our case is differentiated from diffuse alveolar damage by the absence of hyaline membranes, and from eosinophilic pneumonia by the lack of eosinophils. In our case, the patient was treated with corticosteroid pulse therapy. However, the clinical course became aggravated and she died within two weeks.