Explore chapters and articles related to this topic
Interstitial lung diseases
Published in Louis-Philippe Boulet, Applied Respiratory Pathophysiology, 2017
Dion Geneviève, Cormier Yvon, Boulet Louis-Philippe
Respiratory bronchiolitis-interstitial lung disease (RB-ILD) and desquamative interstitial pneumonia (DIP) are two rare idiopathic interstitial pneumonias, associated in more than 90% of cases with smoking [120]. These two interstitial pathologies are characterized by an accumulation of pigmented macrophages. In RB-ILD, this accumulation is greater in the lumen of the respiratory bronchioles while it predominates in the alveolar spaces in DIP [5]. Centrilobular emphysema is often associated [121]. In regard to its strong association with smoking, the first treatment is smoking cessation.
Smoking and interstitial lung disease
Published in Muhunthan Thillai, David R Moller, Keith C Meyer, Clinical Handbook of Interstitial Lung Disease, 2017
Joshua J Solomon, Kevin K Brown
In 1987, Myers et al. described a series of active smokers with clinicoradiographic evidence of interstitial lung disease (ILD) who were found to have RB as the sole pathologic pattern on surgical lung biopsy (SLB) (17). They speculated that this RB-associated ILD might be on a clinical spectrum with desquamative interstitial pneumonitis (DIP), a more diffuse and symptomatic smoking-related lung disease. Eighteen additional cases were subsequently reported by Yousem and the term ‘respiratory bronchiolitis-interstitial lung disease’ (RB-ILD) was proposed to distinguish the clinical disease from the histologic finding seen in asymptomatic smokers (18).
Test Paper 4
Published in Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike, Get Through, 2017
Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike
In acute hypersensitive pneumonitis, symptoms may begin after patients return to an environment from which they have been absent for a while (e.g., resuming work following weekends or holidays). Chest radiographs obtained in many patients with hypersensitivity pneumonitis are normal. HRCT typically shows patchy ground-glass opacities and centrilobular nodules. Respiratory bronchiolitis–interstitial lung disease is a smoking-related lung disease that has similar imaging features.
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.
Smoking-associated interstitial lung disease: update and review
Published in Expert Review of Respiratory Medicine, 2020
Yaser T Dawod, Noah E Cook, William B Graham, Farah Madhani-Lovely, Choua Thao
Smoking-associated interstitial lung diseases are a heterogenous group of disorders that either directly or indirectly precipitate lung parenchyma pathology. Smoking has been directly implicated in 80% of chronic obstructive pulmonary disease (COPD) deaths [1–3]. Although COPD is by far the most common smoking-associated lung disease, other rare pulmonary diseases have been linked to smoking, including acute eosinophilic pneumonia (AEP), respiratory bronchiolitis interstitial lung disease (RB-ILD), desquamative interstitial pneumonitis (DIP), idiopathic pulmonary fibrosis (IPF), and combine pulmonary fibrosis emphysema (CPFE). These diseases encompass different pathological processes leading to a spectrum of airway changes and radiological findings [4]. Recently, the disease of E-cigarette or Vaping Related Lung Injury (EVALI) has become a public health emergency, prompting the CDC to release an updated guideline for the diagnosis and management of suspected EVALI [5]. The diagnostic challenge these conditions present to the clinician underscores the importance of a literature review on this topic.
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].