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Less Common Lung and Bronchial Tumours; Bronchiolo-Alveolar Ca., Carcinoids, Hamartomas, Reticuloses, Protein Disorders, Lung Deposits and Leukaemia.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
The first description of this tumour was by Melassey (1876), with a multiple nodular form found at autopsy. Musser (1903), also on autopsy material, described a diffuse or pneumonic form. The first in vivo diagnosis was probably by Skorpil (1941), the patient having hilar metastases at autopsy. Post-mortem examinations often suggested a multicentric origin, but in some cases it was more localised, and was often associated with lung scarring from previous disease. Lipoid pneumonia (see also p. 6.14) was suggested as a precursor by Felson and Ralaisomay (1983) and Maesen et al. (1985). Others, e.g. Woodring and Stelling (1983a) incriminated tobacco smoking. It may follow desquamative interstitial pneumonia (DIP - p. 19.119) or scleroderma (see ps. 19.85 - 87).
Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Usual interstitial pneumonitis may also be seen in Sjögren syndrome and should be considered if honeycomb destruction of the lung parenchyma is the main abnormality. Desquamative interstitial pneumonia is more common in men and strongly associated with smoking. It is not associated with Sjögren syndrome. Acute interstitial pneumonitis is an acute form of the interstitial pneumonias; however it is of unknown aetiology and not associated with Sjögren syndrome.
Lymphoproliferative Disorders of The Lung
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Lymphoid interstitial pneumonia (LIP) is an uncommon nonmalignant lymphoproliferative disorder histologically defined as diffuse interstitial infiltration of lung parenchyma with mature lymphocytes, plasma cells, and reticuloendothelial cells.80 It is less common than desquamative interstitial pneumonia (see Chapter 41).
Clinical significance of microscopic polyangiitis with interstitial lung disease and bronchiectasis: probability of preexisting comorbidities
Published in Annals of Medicine, 2023
Yun Zhang, Qunli Ding, Chengna Lv, Yanan Ying, Zekai Cen, Haijun Zhou, Tingting Wu
In our present study, the frequency of smoking was obviously higher in MPA-ILD patients than in MPA-BE patients, although there was no statistically significant difference between the two groups. Cigarette smoking is considered a principal pathogenetic factor for the development of certain diffuse interstitial and bronchiolar lung diseases, such as respiratory bronchiolitis-interstitial lung disease (RB-ILD), desquamative interstitial pneumonia (DIP) and adult pulmonary Langerhans cell histiocytosis (PLCH) [31]. In addition, previous studies have shown that cigarette smoking has an independent detrimental effect on the risk of IPF and works synergistically [31,32]. In our opinion, multiple factors, such as the environment, smoking, infection and genetic susceptibility, lead to the occurrence and development of ILD, with a small number of ILD patients being ANCA positive and diagnosed with AAV-ILD. In addition, a recent study showed that patients with AAV were more likely to be current or former smokers and that this association was largely driven by MPO-ANCA-positive AAV [33]. This finding indicated that cigarette smoking may also induce ANCA production, especially MPO-ANCA.
Bronchoalveolar lavage: role in the evaluation of pulmonary interstitial disease
Published in Expert Review of Respiratory Medicine, 2020
Stanca-Patricia Hogea, Emanuela Tudorache, Camelia Pescaru, Monica Marc, Cristian Oancea
Desquamative interstitial pneumonia is a rare type of smoking-related ILD which is characterized by accumulation of alveolar macrophages in alveolar lumens and septa [49]. BAL fluid typically shows an increased total cell count (about 50 × 106 cells) with predominance of alveolar macrophages with golden or black pigmented inclusions. The absence of these cells excludes DIP and indicates other types of ILD [47,50]. Also, these patients may have an increased number of eosinophils and/or neutrophils in BAL fluid [7,47,51]. Kawabata Y. et al showed in their study a mild to moderate increase in total cell numbers (mean of 5.0 × 105 cells ⁄ml), moderate to marked eosinophilia (mean 18%) and moderate neutrophilia (mean 11%) in patients with DIP. Six cases out of seventeen showed >25% eosinophils [52].
Pathogenesis and treatment of idiopathic and rheumatoid arthritis-related interstitial pneumonia. The possible lesson from COVID-19 pneumonia
Published in Expert Review of Clinical Immunology, 2020
A Manfredi, F Luppi, G Cassone, C Vacchi, C Salvarani, M Sebastiani
Ishikawa evaluated 263 patients with interstitial pneumonia of different etiologies and diagnosed both as IPF, and other idiopathic interstitial pneumonias (namely desquamative interstitial pneumonia, respiratory bronchiolitis interstitial lung disease, acute interstitial lung disease, nonspecific interstitial pneumonia, etc.), CTD-ILD, or chronic pulmonary fibrosis with emphysema. Patients with elevated D-dimer levels (more than 0.4 mcg/mL) had an increased risk of developing AE in ILD within three months from each measurement. Since the median time to AE was between the first and second month from D-dimer measurement the Authors raised a question about the efficacy of prophylactic anticoagulation for subjects with high D-dimer levels [78]. Previous studies on animal and human with pulmonary fibrosis supported anticoagulation as a therapeutic approach in IPF [96,97]. The mortality rate from AE in subjects with IPF receiving anticoagulation (i.e., warfarin for maintenance and switching to low-molecular-weight heparin after developing AE) was low at 18% compared with 71% in patients who did not receive anticoagulation [79,81].