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Eosinophilic pneumonia induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
In more severe or prolonged cases, simply discontinuing the drug may be insufficient and the addition of oral or parenteral corticosteroids may be necessary. In patients who are critically ill – for example with an acute eosinophilic pneumonia-like syndrome – and in patients who have vomiting, intravenous corticosteroids may be necessary. Although some patients with idiopathic acute eosinophilic pneumonia (and presumably drug-induced acute eosinophilic pneumonia) will recover without treatment, deaths have been reported, so corticosteroids are generally necessary. The optimal dose is uncertain, but patients with idiopathic acute eosinophilic pneumonia are often treated with 1–2 mg/kg of methylprednisolone every 6–12 hours. In patients with less severe reactions, doses of 0.25–1 mg/kg of prednisone (or equivalent oral corticosteroid) are generally effective. Fortunately, patients with drug-induced eosinophilic lung disease recover promptly and a short course of corticosteroids is usually sufficient. Once a causative drug is identified, patients should be warned to not use the drug or other drugs in the same category in the future.
Overview of HIV Infection
Published in Mark J. Rosen, James M. Beck, Human Immunodeficiency Virus and the Lung, 1998
The pathogenesis of acute eosinophilic pneumonia is unknown. Potential causes include medications, IgE-mediated hypersensitivity to unrecognized antigens, or HIV-induced activation of CD4+ eosinophils (13). Although several of the reported HIV-infected patients with eosinophilic pneumonia have been intravenous (iv) drug abusers, at the time of the pulmonary eosinophilia, iv drugs were not felt to be the cause (13).
Eosinophilic pneumonia: a case of daptomycin induced lung injury
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Vaishnavi Raman, Isha Chaudhary, Sean Shieh
This paper highlights a case of daptomycin-induced eosinophilic pneumonia (DAP-Induced EP) in a 71-year-old male. Eosinophilic pneumonia can be further subdivided into primary or secondary disorders, where a primary is typically idiopathic and secondary is due to the presence of an identifiable cause [1]. Acute eosinophilic pneumonia is a secondary disorder that can be caused by drugs, toxins, parasites and fungal infections [1,2,4]. In particular, drug-induced AEP has been reported to be associated with the use of daptomycin, mesalamine, sulfasalazine and minocycline. However, this condition is quite rare and thus the epidemiology is poorly understood. One large-scale literature review exploring drug-induced AEP found 228 cases reported between 1990 and 2017, with only 137 cases meeting their inclusion criteria. The demographics for these cases ranged from 18 to 82 years of age and affected males and females equally. Of these patients, 21% had an acute hypoxemic respiratory failure of which 19.8% required mechanical ventilation thus highlighting the severity of this condition. This study also found that daptomycin use accounted for one of the highest numbers of drug-induced AEP cases which emphasizes the need for a better understanding of this correlation [10,11].
Acute lung injury secondary to e-cigarettes or vaping
Published in Baylor University Medical Center Proceedings, 2020
Sarah Freathy, Nitin Kondapalli, Srikant Patlolla, Adan Mora, Clayton Trimmer
According to the recent Centers for Disease Control and Prevention report, EVALI remains a diagnosis of exclusion, with emphasis placed on first excluding entities such as influenza or bacterial pneumonia. Patients often present with respiratory symptoms including cough, dyspnea, and chest pain.4 The initial imaging workup should include a chest radiograph, which will often show bilateral infiltrates. On chest CT, findings consistent with acute eosinophilic pneumonia, hypersensitivity pneumonitis, diffuse alveolar damage, diffuse alveolar hemorrhage, organizing pneumonia, and lipoid pneumonia have been identified. Most patterns display diffuse ground-glass opacities and consolidation, predominantly in the basilar lobes, with subpleural sparing. Exceptions include hypersensitivity pneumonitis, which presents with a pattern of upper- and mid-lung–predominant ground-glass opacities and organizing pneumonia, which is typically more peripheral.5 Bronchial alveolar lavage can be performed on a case-by-case basis, along with staining for lipid-laden macrophages with Oil Red O or Sudan stain. Treatment typically includes broad-spectrum antibiotics until infection is ruled out and corticosteroids.4
The impact and toxicity of glyphosate and glyphosate-based herbicides on health and immunity
Published in Journal of Immunotoxicology, 2020
Cindy Peillex, Martin Pelletier
Some studies have reported a link between exposure to glyphosate and GBHs and the development of inflammatory diseases. For instance, de Raadt et al. (2015) described the case of a woman affected twice by acute eosinophilic pneumonia, each time a couple of weeks after an acute RoundUp® exposure, within a 4-year gap. Although the woman was a smoker, the authors suspect the herbicide was a causative agent for the disease. In epidemiological studies, Hoppin et al. (2008, 2017) found a correlation between GBH exposure and the development of allergic and non-allergic wheeze in male farmers, as well as atopic asthma in farm women. Those analyses suggested then that chronic GBH inhalation could promote various types of airway inflammation in the long-term. Moreover, a review reported that an accumulation of GBHs (more specifically RoundUp®) as a result of continual unintended ingestion might present a potential risk for the development of endometriosis since oxidative stress and estrogen pathway disruptions are each involved in this chronic inflammatory disease (Aris and Paris 2010). From the results presented above, it would seem that GBH exposure could play a part in the development of inflammatory syndromes, whether chronic or acute, in humans.