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Eosinophilic pneumonia induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
eosinophilia–myalgia syndrome occurred in the 1980s and was caused by a contaminant(s) found in L-tryptophan manufactured by a single company.31,32 At the time, L-tryptophan was commonly prescribed for insomnia and depression; it was also available in the United States without prescription and was often sold in health-food stores. In one series, approximately half of persons ingesting the contaminated drug developed acute peripheral blood eosinophilia accompanied by severe myalgias and multiple organ involvement.33 Respiratory findings occurred in more than 50 per cent of patients34 and included chest X-ray infiltrates, pleural effusions, dyspnoea, cough, pulmonary hypertension and respiratory muscle weakness. The IgE and creatine kinase levels were normal. Pulmonary function tests usually revealed a reduced diffusing capacity, often with restriction. Lung histology demonstrated interstitial infiltration by lymphocytes and eosinophils, alveolar eosinophils, and small to medium vessel vasculitis.35 Although pulmonary involvement was generally self-limited, patients frequently had lasting abnormalities of the musculoskeletal system, skin and nervous system.
Pulmonary Function Tests
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
Spirometers basically measure the respiratory volumes, or in the case of modern units, respiratory volume flow rate which is integrated to determine the volume. Some of the common parameters used in spirometry are: FVC (forced vital capacity): This is the total volume of air a patient can exhale after a maximum effort inspiration. Patients with restrictive lung disease (RLD) have a lower FVC than do patients with obstructive lung disease (OLD).FEV1 (forced expiratory volume in 1 s) (also, FEV1/2): The volume of air expired in the first second following the beginning of maximum expiratory effort. FEV1 is reduced from normal in both OLDs and RLDs, but for different reasons; increased airway resistance in OLD, and decreased vital capacity in RLD.FEV1/FVC: This ratio is about 0.7 in healthy subjects. It can be as low as 0.2–0.3 in patients with OLD. Patients with RLD have near-normal ratios.FEF (25%–75%) (forced mid-expiratory flow rate): The average rate of flow during the middle of the FVC maneuver.Reduced in both OLD and RLD.DLCO (diffusion capacity of the lung for carbon monoxide): The poison gas, CO, can be used to measure the diffusion capacity of the alveoli. The diffusion capacity of the lung is decreased in parenchymal diseases, such as emphysema. It is normal in asthma. (Other gases can be used.)FRC (functional residual capacity): The volume of air remaining in the lungs and trachea after an exhale in normal breathing.RV (residual volume): The volume of air left in the lungs after a maximum FVC exhale. It is the “dead space” of the respiratory system; mostly combined trachea and bronchial tube volumes. It cannot be measured directly.TV (tidal volume): The volume exchanged in normal, relaxed breathing.AV (alveolar volume): Total volume of all the minute alveoli in the lung parenchyma.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
In some early investigations, expected changes in pulmonary function were mostly absent despite indications that TS inhalation might lead to chronic bronchitis and emphysema. For example Park et al. (1977) and Wanner et al. (1973), demonstrated that TS inhalation using mask or “mouthpipe” exposures for 6 or 12 months yielded decreased tracheal mucous velocity, while alterations in pulmonary function parameters, including pulmonary resistance and dynamic compliance, lung diffusing capacity of carbon monoxide, arterial blood gases, or lung volumes were not apparent. Similar experiments using tracheostomy exposures for 10 months yielded mucus hypersecretion without a change in mucous velocity (King et al. 1989). No changes in ciliary beat frequency were noted (Park et al. 1977) suggesting TS-induced alterations in mucus viscosity played a role in protecting airway epithelium and parenchyma (King et al. 1989; Park et al. 1977). However, at least one study suggested that TS-induced mucus hypersecretion protected against nonspecific airway reactivity to inhaled methacholine (Desanctis et al. 1987).
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Chronic Beryllium Disease: Chronic Beryllium Disease (CBD) is a distinctive allergic condition of the lungs attributed to exposure to Be, which most frequently occurs in occupational settings. In 2009, it was estimated that over 800,000 workers are exposed to Be in the United States alone, and 2–5% of beryllium-exposed workers subsequently develop disease (Sood 2009). CBD is most common in workers employed in the aeronautics and transportation industry, Be manufacturing sector, and electronics and communications markets (Day et al. 2006; Forte, Petrucci, and Bocca 2008). CBD has been described as a form of granulomatous hypersensitivity pneumonitis that emerges following sensitization of susceptible individuals to Be. One of the unique aspects of this disease is that sensitization to the metal might occur following both inhalation exposure and dermal contact with Be (Tinkle et al. 2003). Irrespective of the exposure route involved, sensitization to Be involves the generation of metal-specific Th1-polarized CD4+ effector T-cells (McKee et al. 2015; Wade et al. 2018). Beryllium-specific T-cells are subsequently recruited to the airways, where their activity leads to inflammation of the alveolar spaces and formation of granulomas (Samuel and Maier 2008). Over time, CBD patients often develop decreases in lung volume and diffusing capacity, pulmonary fibrosis, and respiratory failure as a result of the disease (Sood 2009).
Approaches to improving exercise capacity in patients with left ventricular assist devices: an area requiring further investigation
Published in Expert Review of Medical Devices, 2019
Richard Severin, Ahmad Sabbahi, Cemal Ozemek, Shane Phillips, Ross Arena
Post-LVAD implant, patients demonstrate improved ventilation-perfusion coupling and ventilatory efficiency evident by reductions in the minute ventilation/carbon dioxide production (VE/VCO2) slope [14,29]. Junget al.l reported reductions in the VE/VCO2 slope with increasing pump speed during maximal exercise (41 ± 14.9–36 ± 11.7, p = 0.005) [26]. Apostoloet al.l also demonstrated that increasing LVAD pump speed improved ventilatory efficiency (−1.9 ± 3.1, p = 0.031) [25]. However, further reductions in alveolar-capillary gas diffusion measured by the diffusing capacity of the lungs for carbon monoxide (DLCO) and lung diffusing capacity for nitric oxide (DLNO) 16 h after changing LVAD speed were also reported [25]. This deterioration of lung diffusion was thought to be a consequence of higher left atrial pressures and lung fluid content [25]. These findings warrant further caution when suggesting free application of pump speeds during exercise.