المؤلفون: Yan Li, Hailin Xu, Ying Wang, Yurou Zhu, Kun Xu, Zhu Yang, Yanbo Li, Caixia Guo

المصدر: Journal of Nanobiotechnology, Vol 22, Iss 1, Pp 1-18 (2024)

مصطلحات موضوعية: Silica nanoparticles, Pulmonary toxicity, Fibroblast activation, Epithelial-fibroblast communication, Exosomes, miR-494-3p, Biotechnology, TP248.13-248.65, Medical technology, R855-855.5

الوصف: Abstract Background In the context of increasing exposure to silica nanoparticles (SiNPs) and ensuing respiratory health risks, emerging evidence has suggested that SiNPs can cause a series of pathological lung injuries, including fibrotic lesions. However, the underlying mediators in the lung fibrogenesis caused by SiNPs have not yet been elucidated. Results The in vivo investigation verified that long-term inhalation exposure to SiNPs induced fibroblast activation and collagen deposition in the rat lungs. In vitro, the uptake of exosomes derived from SiNPs-stimulated lung epithelial cells (BEAS-2B) by fibroblasts (MRC-5) enhanced its proliferation, adhesion, and activation. In particular, the mechanistic investigation revealed SiNPs stimulated an increase of epithelium-secreted exosomal miR-494-3p and thereby disrupted the TGF-β/BMPR2/Smad pathway in fibroblasts via targeting bone morphogenetic protein receptor 2 (BMPR2), ultimately resulting in fibroblast activation and collagen deposition. Conversely, the inhibitor of exosomes, GW4869, can abolish the induction of upregulated miR-494-3p and fibroblast activation in MRC-5 cells by the SiNPs-treated supernatants of BEAS-2B. Besides, inhibiting miR-494-3p or overexpression of BMPR2 could ameliorate fibroblast activation by interfering with the TGF-β/BMPR2/Smad pathway. Conclusions Our data suggested pulmonary epithelium-derived exosomes serve an essential role in fibroblast activation and collagen deposition in the lungs upon SiNPs stimuli, in particular, attributing to exosomal miR-494-3p targeting BMPR2 to modulate TGF-β/BMPR2/Smad pathway. Hence, strategies targeting exosomes could be a new avenue in developing therapeutics against lung injury elicited by SiNPs. Graphical Abstract

وصف الملف: electronic resource

العلاقة: https://doaj.org/toc/1477-3155Test

الوصول الحر: https://doaj.org/article/9bbb9973c6304e249c7ec1488d7affabTest

المؤلفون: Ali Akbar, Rabia Azmat, Moazama Batool, Bader O. Almutairi, Mian Nadeem Riaz

المصدر: Journal of King Saud University: Science, Vol 36, Iss 5, Pp 103149- (2024)

مصطلحات موضوعية: Rhoifolin, Antioxidant, Cisplatin, Pulmonary toxicity, Oxidative stress, Science (General), Q1-390

الوصف: Cisplatin (CP) is a ubiquitous antineoplastic medicine that has been recognized to have sever toxic effects on different organs including lungs. Rhoifolin (RHO) is a therapeutic compound with significant pharmacological activities. The present study was designed to evaluate the protective effect of RHO against CP induced pulmonary toxicity. Twenty-four rats were randomly divided into 4 groups: control group, CP treated group (20 mgkg−1), CP + RHO treated group (20 mgkg−1 + 10 mgkg−1) and RHO supplemented group (10 mgkg−1). Following 30 days of administration, our results showed that CP treatment decreased the activity of antioxidant enzymes such as glutathione (GSH), glutathione reductase (GSR), glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT) while elevated the level of malondialdehyde (MDA) along with reactive oxygen species (ROS). Furthermore, levels of inflammatory cytokines involving interleukin-6 (IL-6), nuclear factor-kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α) and cyclo-oxygenase-2 (COX-2) activity were escalated. Besides, treatment with CP enhanced the activities of apoptotic proteins i.e., Bax, caspase-9 along with caspase-3 while reducing the activity of Bcl-2. Additionally, the histopathological examination revealed significant pulmonary tissue impairments in the CP exposed group. However, RHO treatment considerably (P

وصف الملف: electronic resource

العلاقة: http://www.sciencedirect.com/science/article/pii/S1018364724000612Test; https://doaj.org/toc/1018-3647Test

الوصول الحر: https://doaj.org/article/208e85bd33624b58af7c0ee43b6734afTest

المؤلفون: Johan F. Vansteenkiste, MD, PhD, Jarushka Naidoo, MB, BCH, MHS, Corinne Faivre-Finn, MD, PhD, Mustafa Özgüroğlu, MD, Augusto Villegas, MD, Davey Daniel, MD, Shuji Murakami, MD, Rina Hui, M.B.B.S., PhD, Ki Hyeong Lee, MD, Byoung Chul Cho, MD, PhD, Kaoru Kubota, MD, PhD, Helen Broadhurst, MSc, Catherine Wadsworth, BVSc, Michael Newton, PharmD, Piruntha Thiyagarajah, MD, Scott J. Antonia, MD

المصدر: JTO Clinical and Research Reports, Vol 5, Iss 3, Pp 100638- (2024)

مصطلحات موضوعية: Immunotherapy, Radiotherapy, Durvalumab, Pulmonary toxicity, Locally advanced NSCLC, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282

الوصف: Introduction: In the placebo-controlled, phase 3 PACIFIC trial, durvalumab significantly prolonged progression-free survival (PFS) (p < 0.0001) and overall survival (OS) (p = 0.00251) in patients with unresectable stage III NSCLC and no progression after platinum-based concurrent chemoradiotherapy (cCRT). Pneumonitis or radiation pneumonitis (PRP) was common in both arms. We report exploratory analyses evaluating the association of symptomatic (grade ≥2) PRP (G2+PRP) with baseline factors and clinical outcomes. Methods: Patients with WHO performance status of 0 or 1 were randomized (2:1) to 12 months of durvalumab or placebo, 1 to 42 days after cCRT. Associations between baseline factors and on-study G2+PRP in durvalumab-treated patients were investigated using univariate and multivariate logistic regression. PFS and OS were analyzed using Cox proportional hazards models adjusted for time-dependent G2+PRP plus covariates for randomization stratification factors without and with additional baseline factors. Results: On-study G2+PRP occurred in 94 of 475 (19.8%) and 33 of 234 patients (14.1%) on durvalumab and placebo, respectively (median follow-up, 25.2 mo); grade greater than or equal to 3 PRP was uncommon (4.6% and 4.7%, respectively). Time to onset and resolution of G2+PRP was similar with durvalumab and placebo. Univariate and multivariate analyses identified patients treated in Asia, those with stage IIIA disease, those with performance status of 1, and those who had not received induction chemotherapy as having a higher risk of G2+PRP. PFS and OS benefit favoring durvalumab versus placebo was maintained regardless of time-dependent G2+PRP. Conclusions: Factors associated with higher risk of G2+PRP with durvalumab after cCRT were identified. Clinical benefit was maintained regardless of on-study G2+PRP, suggesting the risk of this event should not deter the use of durvalumab in eligible patients with unresectable stage III NSCLC.

وصف الملف: electronic resource

العلاقة: http://www.sciencedirect.com/science/article/pii/S2666364324000080Test; https://doaj.org/toc/2666-3643Test

الوصول الحر: https://doaj.org/article/86197b668ce247a6aed1dbb164a76e9dTest

المؤلفون: Marco Umberto Scaramozzino, Giovanni Sapone, Ubaldo Romeo Plastina, Guido Levi, Mariacarmela Nucara

المصدر: Infermieristica Journal, Vol 2, Iss 3, Pp 123-129 (2023)

مصطلحات موضوعية: amiodarone-induced pulmonary toxicity, amiodarone, hyper-reactivity, ocs, ground glass opacity, Nursing, RT1-120

الوصف: Amiodarone-induced pulmonary toxicity (AIPT) is among the most serious adverse effects and is one of the leading causes of death associated with its use. It is a clinical pathology that is conditioned by dose, patient’s age, and pre-existent pulmonary pathologies. Those effects reach a plateau at a cumulative dose bigger than 150g. Patient’s comorbidities; oxygen therapy, invasive procedures or surgical interventions can trigger the pulmonary symptoms induced by amiodarone toxicity. The increased risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dose and the duration of the intake. Despite significant advances in the understanding of AIPT, its aetiology and pathogenesis remain incompletely understood. The role of steroids in the management of pulmonary toxicity from amiodarone is debatable, however, most reports of improvement after amiodarone withdrawal di"er little from those in which concomitant steroid therapy was employed. Therefore, the addition of therapeutic doses of corticosteroids in amiodarone induced pneumopathy may be indicated. Typically, prednisone is started in doses of 40 to 60 mg/day orally and slowly reduced. Again, the pharmacodynamics of amiodarone dictate a treatment period of four to 12 months. The case report describes a patient with AIPT who after therapy with Prednisone at a dosage of 50mg/day by gradually scaling down the doses as reported in the above clinical studies, had a clinical, functional and CT radiological picture that was markedly improved with disappearance of most of the scattered ground glass areas and the previously reported thickening with associated bi-apical fibrotic outcomes.

وصف الملف: electronic resource

العلاقة: https://riviste.fupress.net/index.php/if/article/view/2066Test; https://doaj.org/toc/2785-7018Test

الوصول الحر: https://doaj.org/article/5c57ee8c757c4965a4a82757d4dff23dTest

المؤلفون: Tan C, Kumar P

المصدر: International Medical Case Reports Journal, Vol Volume 16, Pp 679-687 (2023)

مصطلحات موضوعية: amiodarone, amiodarone induced pulmonary toxicity, Medicine (General), R5-920

الوصف: Clement Tan, Pranav Kumar Department of Respiratory Medicine, Mackay Base Hospital, Mackay, Queensland, AustraliaCorrespondence: Clement Tan; Pranav Kumar, Email Clement.Tan@health.qld.gov.au; Pranav.Kumar@health.qld.gov.auAbstract: Amiodarone is a commonly prescribed antiarrhythmic drug. It can cause a myriad of complications associated with its long-term use, with amiodarone induced pulmonary toxicity being the worst. Amiodarone does this through its destructive properties and its’ ability to accumulate if taken for extended periods of time or in high cumulative doses. Albeit uncommon, the management of amiodarone induced pulmonary toxicity can be straightforward if recognized early. Otherwise, it can lead to severe respiratory failure causing death. In this case report, we aim to highlight the importance of vigilance with clinicians prescribing amiodarone and to spark interests into research for alternative management options of amiodarone induced pulmonary toxicity. This will be done through the description of a case of a 64-year-old male presenting with cough and dyspnoea, who has been on a large dose of amiodarone daily for the past 11 months. He was diagnosed too little, too late, which unfortunately culminated in his rapid fatality. This case is unique for two reasons. The diagnosis of amiodarone induced pulmonary toxicity was through the clinical picture – without the use of invasive investigations. In addition, the futile cessation of amiodarone and use of high dose systemic corticosteroids as a management – which to our knowledge is uncommon in literature.Keywords: amiodarone, amiodarone induced pulmonary toxicity

وصف الملف: electronic resource

العلاقة: https://www.dovepress.com/too-little-too-late-a-case-of-a-swift-fatal-culmination-of-amiodarone--peer-reviewed-fulltext-article-IMCRJTest; https://doaj.org/toc/1179-142XTest

الوصول الحر: https://doaj.org/article/04d21c82626444f5ace3323fb58995d0Test

المؤلفون: Takla, Andrew, Eid, Fahad, Ukrani, Hina, Mohamed, Moghniuddin, Lee, Elizabeth

المصدر: Advances in Clinical Medical Research and Healthcare Delivery

مصطلحات موضوعية: Amiodarone-induced Pulmonary Toxicity, Amiodarone Induced Pneumonitis, Diagnostic Dilemma, Diagnosis, Other Chemicals and Drugs, Therapeutics

الوصف: Amiodarone, a widely utilized antiarrhythmic drug, poses a significant risk of amiodarone-induced lung toxicity (ALT) in up to 10% of patients and can be fatal. This report presents the diagnostic challenges associated with ALT, given its non-specific clinical and radiological presentation. Clinicians should maintain a high index of suspicion for potential ALT, especially in patients with progressive respiratory failure despite optimization of other potential causes such as CHF. The mainstay of treatment is discontinuing amiodarone and initiating steroids. However, outcomes can remain unpredictable, emphasizing the need for heightened awareness and regular monitoring of patients on amiodarone therapy.

وصف الملف: application/pdf

العلاقة: https://scholar.rochesterregional.org/advances/vol4/iss2/4Test; https://scholar.rochesterregional.org/context/advances/article/1215/viewcontent/ACMRHD1215_proof.pdfTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/0/type/additional/viewcontent/Amiodarone.jpgTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/1/type/additional/viewcontent/1.pngTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/2/type/additional/viewcontent/2.pngTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/3/type/additional/viewcontent/Title_page.docxTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/4/type/additional/viewcontent/Separate_artwork1.pngTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/5/type/additional/viewcontent/Separate_artwork2.pngTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/6/type/additional/viewcontent/Captions.docxTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/7/type/additional/viewcontent/TNQ_response.docxTest; https://scholar.rochesterregional.org/context/advances/article/1215/filename/8/type/additional/viewcontent/TNQ_response.docxTest

الإتاحة: https://doi.org/10.53785/2769-2779.1215Test
https://scholar.rochesterregional.org/advances/vol4/iss2/4Test
https://scholar.rochesterregional.org/context/advances/article/1215/viewcontent/ACMRHD1215_proof.pdfTest
https://scholar.rochesterregional.org/context/advances/article/1215/filename/0/type/additional/viewcontent/Amiodarone.jpgTest
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https://scholar.rochesterregional.org/context/advances/article/1215/filename/3/type/additional/viewcontent/Title_page.docxTest
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https://scholar.rochesterregional.org/context/advances/article/1215/filename/5/type/additional/viewcontent/Separate_artwork2.pngTest
https://scholar.rochesterregional.org/context/advances/article/1215/filename/6/type/additional/viewcontent/Captions.docxTest

المؤلفون: Ömer Önder, Selin Ardalı Düzgün, Gamze Durhan, Orhan Macit Arıyürek

المصدر: Diagnostic and Interventional Radiology, Vol 30, Iss 1, Pp 28-29 (2024)

مصطلحات موضوعية: ct, chemotherapy, lung, pneumonitis, pulmonary toxicity, Medical physics. Medical radiology. Nuclear medicine, R895-920

العلاقة: http://www.dirjournal.org/archives/archive-detail/article-preview/centrilobular-ground-glass-nodule-pattern-in-acute/60311Test; https://doaj.org/toc/1305-3612Test; https://doaj.org/article/4b6d2a5a783c416ba4135d9b63fd92c3Test

الإتاحة: https://doi.org/10.4274/dir.2023.232217Test
https://doaj.org/article/4b6d2a5a783c416ba4135d9b63fd92c3Test

المؤلفون: Amani Sakineh, Mohammad Foad Noorbakhsh, Nasrollah Ahmadi, Nazifi Saeed, Barzan Behdokht

المصدر: Journal of Pharmacopuncture, Vol 26, Iss 2, Pp 184-191 (2023)

مصطلحات موضوعية: thymoquinone, pulmonary toxicity, citral, silymarin, methotrexate, Medicine, Miscellaneous systems and treatments, RZ409.7-999, Therapeutics. Pharmacology, RM1-950

الوصف: Objectives: Several studies have reported that methotrexate is an anti-cancer and immunosuppressive drug leading to lung injury. Therefore, the present study aimed to investigate the protective effects of silymarin, citral, and thymoquinone on methotrexate-induced pulmonary toxicity.Methods: Forty-eight rats were divided into six groups, including healthy, Methotrexate, and drug carrier control groups and silymarin, citral, and thymoquinone treatment groups. At the end of the experiment, the studied rats were anesthetized and sacrificed by CO2. Lung tissue samples were isolated to measure the antioxidant activity and histopathological evaluation.Results: In the thymoquinone treatment group, the concentration of total antioxidant capacity and Malondialdehyde increased and decreased significantly, respectively, compared to the methotrexate group. The histopathological evaluation of the lung of the methotrexate group showed hemorrhage and congestion, the nodule-like accumulation of mononuclear inflammatory lymphocytes around the blood vessel, a small number of neutrophils around the blood vessel, and the inflammatory cells around the small vessels. However, no significant pathological alterations were observed in the treatment groups, especially the thymoquinone treatment group.Conclusion: Thymoquinone has the greatest protective effect on methotrexate-induced lung injury, probably due to its antioxidant effect.

وصف الملف: electronic resource

العلاقة: http://www.journal-jop.org/journal/view.html?doi=10.3831/KPI.2023.26.2.184Test; https://doaj.org/toc/2093-6966Test

الوصول الحر: https://doaj.org/article/584415a7ae2944009f9480e6078a687fTest

المؤلفون: Christopher S Dossett MD, Kelli Kosako Yost MD, Christopher Lau MD, Nafis Shamsid-Deen MD

المصدر: Southwest Journal of Pulmonary and Critical Care, Vol 26, Iss 6, Pp 90-96 (2023)

مصطلحات موضوعية: bleomycin, pulmonary fibrosis, treatment, pulmonary function tests, corticosteroids, ct scan, etoposide, case presentation, bleomycin-induced lung injury, bleomycin pulmonary toxicity, General works, R5-130.5, Medical emergencies. Critical care. Intensive care. First aid, RC86-88.9

الوصف: Bleomycin is a common chemotherapy agent used to treat germinative tumors. Bleomycin-induced lung injury (BILI) is an uncommon but devastating adverse effect of its use. It occurs in 10-20% of patients receiving bleomycin, and the initial diagnosis is usually made by new-onset respiratory symptoms and reduced diffusing capacity for carbon monoxide (DLCO). Mainstay treatment includes discontinuing bleomycin, corticosteroids, and supplemental oxygen if needed. We present a case of a 38-year-old male who was found to have a severe presentation of bleomycin-induced lung injury after chemotherapy for metastatic mixed germ cell testicular cancer. During his course, he was treated with the standard of care regimen of corticosteroids and salvage therapy with infliximab but ultimately died from complications of his illness. This case report is noteworthy because our patient had progressive bleomycin-induced lung injury, despite discontinuing bleomycin many months prior, consistent high-dose corticosteroid treatment, and even salvage therapy. In all patients on bleomycin, pulmonary function monitoring is essential, and any complaints of dyspnea should prompt concern for bleomycin-induced lung injury. If initial treatment does not improve their condition, more aggressive measures may be necessary.

وصف الملف: electronic resource

العلاقة: https://www.swjpcc.comTest/pulmonary/2023/6/10/a-case-of-progressive-bleomycin-lung-toxicity-refractory-to.html; https://doaj.org/toc/2160-6773Test

الوصول الحر: https://doaj.org/article/57b658f4ac864510a431942ee795735eTest

المؤلفون: Chinatsu Nishida, Hidenori Higashi, Yasuo Morimoto, 東 秀憲, 森本 泰夫, 西田 千夏

المصدر: エアロゾル研究 / Earozoru Kenkyu. 2023, 38(4):248