ABSTRACT
En el último tiempo, la inmunoterapia se ha convertido en una opción terapéutica para diversos tipos de neoplasias, aumentando la sobrevida en muchos casos, pero también los efectos adversos asociados. Existen tres tipos de inmunoterapia utilizados en cáncer: Terapia de células T con receptor de antígeno quimérico (CAR-T), destacando como reacciones adversas el síndrome liberador de citoquinas (CRS) y el síndrome de neurotoxicidad (ICANS); Anticuerpos monoclonales (AcM), cuyos efectos adversos más comunes están relacionados con reacciones de hipersensibilidad; y los Inhibidores de puntos de control inmunitario (ICI) con toxicidad pulmonar claramente reportada. Para un correcto manejo de estas reacciones adversas se requiere un alto índice de sospecha, un adecuado diagnóstico diferencial y un tratamiento oportuno, basado principalmente en corticoides y guiado por criterios de gravedad. Se presenta el caso de un paciente con reacción granulomatosa sarcoidea posterior al uso de Nivolumab.
In recent times, immunotherapy has emerged as a therapeutic option for various neoplasms, significantly improving survival rates in many cases, albeit with associated adverse effects. There are three types of immunotherapy commonly used in cancer treatment: Chimeric Antigen Receptor T-cell Therapy (CAR-T), notable for adverse reactions such as Cytokine Release Syndrome (CRS) and Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS); Monoclonal Antibodies (mAbs), with the most common adverse effects being hypersensitivity reactions; and Immune Checkpoint Inhibitors (ICI), with well-documented pulmonary toxicity. Adequate management of these adverse reactions requires a high index of suspicion, accurate differential diagnosis, and timely treatment, primarily based on corticosteroids and guided by severity criteria. We present a case of a patient with granulomatous sarcoid-like reaction following the use of Nivolumab.
Subject(s)
Humans , Male , Middle Aged , Nivolumab/adverse effects , Nivolumab/drug effects , Immune Checkpoint Inhibitors/adverse effects , Immunotherapy/adverse effects , Receptors, Chimeric Antigen/drug effects , Lung Neoplasms/therapy , Neoplasm StagingABSTRACT
Se presenta el caso de un paciente con diagnóstico de adenocarcinoma de pulmón metastásico que, luego de realizar cinco meses de tratamiento con pembrolizumab, presentó neumonitis grado 2, interpretada como toxicidad por pembrolizumab con buena respuesta y resolución de los infiltrados con la suspensión del inmunomodulador y la administración de corticoides(AU)
We present the case of a patient diagnosed with metastatic lung adenocarcinoma who, after five months of treatment with pembrolizumab, presented grade 2 pneumonitis, interpreted as pembrolizumab toxicity, with a good response and resolution of the infiltrates with the suspension of the immunomodulator and the administration of corticosteroids(AU)
Subject(s)
Adrenal Cortex HormonesABSTRACT
ABSTRACT 70-year-old male patient with chronic myeloid leukemia receiving treatment with dasatinib develops respiratory failure associated with pulmonary toxicity related to such drug.
RESUMEN Paciente de sexo masculino, 70 años, con leucemia mieloide crónica en tratamiento con dasatinib, desarrolla insuficiencia respiratoria asociada a toxicidad pulmonar por dicho fármaco.
ABSTRACT
Paciente de sexo masculino, 70 años, con leucemia mieloide crónica en tratamiento con dasatinib, desarrolla insuficiencia respiratoria asociada a toxicidad pulmonar por dicho fármaco.
70-year-old male patient with chronic myeloid leukemia receiving treatment with da satinib develops respiratory failure associated with pulmonary toxicity related to such drug.
Subject(s)
Male , Toxicity Tests , Lung DiseasesABSTRACT
Objective: To investigate the protective and therapeutic role of ginseng against silicon dioxide nanoparticles (SiO
ABSTRACT
The present study was aimed to know the pulmonary toxicity by individual toxicities of cadmium, chlorpyrifos and their combination in albino wistar rats. The experiment was carried out for 28 days. Group 1 - Control. Group 2 - Cadmium chloride (Cd) @ 22.5 mg/ kg b.wt /per oral / day. Group 3 - Chlorpyrifos (CPF) @ 25 mg/ kg b.wt /per oral / day. Group 4 - Cadmium chloride (Cd) @22.5 mg + Chlorpyrifos (CPF) @ 25 mg/ kg b.wt /per oral / day. Lungs showed mild to moderate congestion in groups 2 and 3 and moderate to severe in group 4 on 15th and 29th day of the experiment. Lung sections of control rats showed normal architecture. Lung sections of group 2 rats on 15th day showed hemorrhages in the interstitium spaces with infiltration of lymphocytes, On 29th day, mild hyperplasia and desquamated bronchial epithelial cells, peri bronchial and peri vascular lymphoid aggregates were noticed. The sections of lung on 15th day of group 3 rats showed exudate and desquamated epithelial cells in the lumen of secondary bronchiole , on 29th day, emphysematous alveoli with loss of architecture of alveolar epithelium, interstitial edema with infiltration of lymphocytes, mild hyperplasia of bronchial epithelial cells were also noticed. In group 4 rats, similar lesions as described in groups 2 and 3 were observed with severe intensity on 15th and on 29th day of the experiment. In combined toxicity group, the severity of lesions were more thus suggesting synergistic effects of these components.
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Coumarin is an important class of natural organic compounds, which widely exists in a variety of plants and microorganisms. Coumarins have many biological activities and wide clinical applications, such as anti-tumor, anti-HIV, anti-bacterial, anti-inflammatory, anti-oxidation, anti-coagulation, but they have obvious toxic effects in rodents. It was found that the toxicity of coumarins in different animals and organs was significantly different, and high dose oral administration was more likely to produce toxic reactions. Based on the research and analysis of domestic and foreign literatures in recent 60 years, this paper mainly summarized the hepatotoxicity and pulmonary toxicity induced by coumarins, and probed into their possible mechanisms. It was found that the toxicity of coumarins had metabolic differences and species differences. The liver of rats and lungs of mice were more susceptible to coumarins. Toxic reactions occurred mainly in the second metabolic pathway of coumarin metabolism in vivo. In order to put forward safety considerations and evaluate the impact of coumarin on human body, it was found that coumarin is unlikely to produce hepatotoxicity at normal exposure level. It was also suggested that species differences due to different metabolic patterns in model animals should be carefully considered when assessing coumarin toxicity, in order to provide reference for clinical research and rational use of coumarins and improve the rational use of coumarins.
Subject(s)
Animals , Humans , Mice , Rats , Coumarins/toxicity , Liver/drug effects , Lung/drug effects , Metabolic Networks and Pathways , Species Specificity , Toxicity TestsABSTRACT
RESUMO Objetivo O objetivo deste estudo foi investigar os efeitos agudos e crônicos da vareniclina no tecido pulmonar em um estudo experimental. Métodos Um total de 34 ratos foi alocado aleatoriamente em grupos de estudo (vareniclina) e controle. Assim, os ratos foram divididos em dois grupos: (i) grupo controle e (ii) grupo vareniclina. A seguir, os ratos de cada grupo foram, por sua vez, subdivididos igualmente em agudos (C1; V1) e crônicos (C2; V2), e todos os ratos dos grupos agudos e crônicos foram sacrificados sob anestesia: no 45.º dia, para o grupo agudo [C1 (n=5) e V1 (n=12)], e no 90.º dia, para o grupo crônico [C2 (n=5) e V2 (n=12)], respectivamente. Em seguida, foram realizadas análises bioquímicas e histopatológicas. Resultados Trinta e quatro ratos completaram o estudo. Destes ratos, 24 estavam no grupo vareniclina e 10 no grupo controle. Na exposição crônica à vareniclina, os níveis de oxidante composto por malondialdeído (MDA) e mieloperoxidase (MPO) aumentaram, e os níveis de superóxido dismutase (SOD), catalase (CAT), glutationa (GSH) e glutationa peroxidase (GPx), nomeados como antioxidantes, diminuiram significativamente quando comparados com o grupo controle. Os níveis de MDA e MPO também foram significativamente mais elevados e os níveis de SOD, CAT, GPx e GSH foram significativamente mais baixos no grupo vareniclina crônico, quando comparado ao grupo vareniclina agudo. Estes achados também foram confirmados por observações histopatológicas. Conclusões Este é o primeiro estudo que avaliou os efeitos pulmonares da vareniclina experimentalmente em um modelo animal. Observamos que o tratamento crônico da vareniclina causa inflamação e lesão pulmonar.
ABSTRACT Objective This study aimed to investigate acute and chronic effects of varenicline on lung tissue in an experimental study. Methods A total of 34 rats were randomly allocated into study (varenicline) and control groups. The rats were divided into two groups (i) control group, (ii) varenicline group. Then, the rats in the each group were sub-divided equally in turn as acute (C1; V1) and chronic (C2; V2) ; all rats of acute and chronic groups were sacrificed under the anesthesia on the 45th day for acute group [C1 (n=5) and V1 (n=12)] and the 90th day for chronic group [C2 (n=5) and V2 (n=12)], respectively. Thus, biochemical and histopathological analysis were carried out. Results Thirty four rats completed the study, 24 were in varenicline group and 10 were in control group. In chronic exposure to varenicline, oxidant levels comprising of malondialdehyde (MDA), and myeloperoxidase (MPO) increased and superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx) levels, named as antioxidants, decreased significantly when compared to the control group. MDA and MPO levels were also significantly higher and SOD, CAT, GPx, GSH levels were also significantly lower in chronic varenicline group when compared to acute varenicline group. These findings were also supported by histopathological observations. Conclusion This is the first study, which evaluated pulmonary effects of varenicline experimentally on an animal model. It was observed that chronic varenicline treatments cause inflammation and lung cell injury.
Subject(s)
Animals , Rats , Superoxide Dismutase/blood , Varenicline/pharmacology , Lung/drug effects , Catalase/blood , Oxidative Stress , Glutathione , Glutathione Peroxidase , Malondialdehyde/bloodABSTRACT
Se sabe que la amiodarona, un potente antiarrítmico, causa toxicidad pulmonar. La neumonitis intersticial crónica es la presentación más común. Sin embargo, la toxicidad pulmonar aguda es rara y provoca una mayor mortalidad. Se presenta un paciente de 61 años con fibrilación auricular persistente que, tras tratamiento por un mes con amiodarona vía oral a dosis baja de impregnación de 400 miligramos al día, desarrolló toxicidad pulmonar aguda secundaria al antiarrítmico confirmada por radiografía y tomografía. Su caso tuvo resolución después de la suspensión del fármaco y tratamiento con esteroides.
Amiodarone, considered a potent antiarrhythmic, is known to cause pulmonary toxicity. Chronic interstitial pneumonitis is the most common presentation. However, acute pulmonary toxicity is rare and has a higher case fatality rate. We present a 61-year-old patient with persistent atrial fibrillation who, after a one-month treatment with oral amiodarone at a low dose impregnation of 400 mg/day, develops acute pulmonary toxicity, with radiographic and tomographic resolution after antiarrhythmic suspension and steroid treatment.
Subject(s)
Humans , Male , Middle Aged , Amiodarone/adverse effects , Lung Diseases/chemically induced , Anti-Arrhythmia Agents/adverse effects , Atrial Fibrillation/drug therapy , Acute Disease , Dose-Response Relationship, Drug , Amiodarone/administration & dosage , Anti-Arrhythmia Agents/administration & dosageABSTRACT
Background: Diesel vehicles exhaust contains toxic nanoparticles that drastically affect lung tissue due to their direct cytotoxic effects, induction of oxidative stress, inflammatory signaling pathways and DNA damage. Mesenchymal stem cells (MSCs) exhibit anti-inflammatory effects and efficient regenerative capacity in chronic lung diseases. Objectives: Evaluation of the effects of MSCs and MSCs-derived micro vesicles (MSCs-MVs) on pulmonary toxicity induced by diesel exhaust nanoparticles (DENPs). Materials and Methods: Sixty male rats were equally divided into: Group I (Control rats), Group II (DENPs group) received repeated doses of DENPs (180μg/rat) intratracheally every other day for 6 days, Group III (MSCs group) received MSCs intravenously (3×106 cells) after the last dose of DENPs and Group IV (MSCs-MVs group) received MSCs-MVs (0.5 mg/mL) intravenously after the last dose of DENPs. Lung tissue were subjected to histological and immunohistochemical assessment. Inflammatory cytokines and bronchoalveolar lavage fluid (BALF) contents of inflammatory cells, albumin, LDH and total proteins were evaluated. Results: Histological picture of lung tissue in DENPs group showed numerous collapsed alveoli, thick interalveolar septa and marked cellular infiltration. Elastic fibers were markedly decreased by DENPs. Increased optical density of NF-κB/p65 immunoreactivity. Bronchoalveolar lavage fluid showed significant elevation of inflammatory cytokines (TNF-a, IL-6), polymorphonuclear leukocytes (PMN), neutrophils, macrophages, LDH, total proteins and albumin. Treatment with either MSCs or MSCs-MVs led to a significant amelioration of all of the aforementioned studied parameters. Conclusion: MSCs-MVs and MSCs showed significant therapeutic effects against DENPs damaging effects on the lung tissues via their regenerative capacity and anti-inflammatory effects.
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En el tratamiento del cáncer de mama, son varias las técnicas que se describen en materia de radioterapia oncológica. Objetivo: La investigación pretendió analizar la técnica de mama prona en cuanto a beneficio para las pacientes con cáncer de mama estadios I y II en el servicio de radioterapia oncológica y medicina nuclear del Hospital Universitario de Caracas. Métodos: Se trata de un estudio descriptivo, prospectivo y comparativo con una muestra conformada por 20 pacientes. Los casos se registraron en el instrumento de recolección de datos del paciente. Para este estudio se emplearon las técnicas de la estadística descriptiva. Resultados: La frecuencia de pacientes atendidas tuvo un aumento interanual entre 35 % y 40 %. El 60 % de las pacientes presentaron estadio IB, 25 % IA y 15 % con estadio IIA. Conclusión: La posición prona es una técnica reproducible que beneficia principalmente a las pacientes con mamas grandes y/o péndulas, permite protección del corazón excluyendo el haz del rayo a nivel cardiaco(AU)
In the treatment of breast cancer, there are several techniques that are described in terms of radiation therapy. Objetive: The research aimed to analyze the prone breast technique in terms of benefit for patients with stage I and II breast cancer in the oncological radiotherapy and nuclear medicine service of the University Hospital of Caracas. Methods: This is a descriptive, prospective and comparative study with a sample consisting of 20 patients. The cases were recorded in the patient data collection instrument. For this study, the techniques of descriptive statistics were used. Results: the frequency of patients attended had an interannual increase between 35 % and 40 %. 60 % of the patients presented stage IB, 25 % IA and 15 % with stage IIA. Conclusion: The prone position is a reproducible technique that mainly benefits the patients with large breasts and / or pendulums, allows protection of the heart excluding the beam of the ray at cardiac level(AU)
Subject(s)
Humans , Female , Middle Aged , Breast Neoplasms/pathology , Breast Neoplasms/radiotherapy , Prone Position , Dosimetry , Medical OncologyABSTRACT
Monotherapy of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) serves as the first-line treatment for non-small cell lung cancer (NSCLC) patients with EGFR mutation. Pre-clinical studies confirmed that TKIs can increase radiation sensitiv-ity. Clinical studies confirmed that EGFR-TKI combined with radiotherapy may improve survival of patients and can be used as alterna-tive to chemoradiotherapy. Pulmonary toxicity induced by EGFR-TKIs monotherapy features low incidence rate but high mortality rate, and the incidence rate raries when TKIs is combined with radiotherapy. In this review, we summarise related literature on pulmonary toxicity in EGFR-TKI monotherapy or its combination with radiotherapy for advanced NSCLC. This study can serve as reference for safe-ty of this combined therapy.
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OBJECTIVE:To summarize general regularity and characteristics of amiodarone-induced pulmonary toxicity,and to provide reference for rational use of amiodarone and avoiding the occurrence of ADR. METHODS:Retrieved from CNKI,VIP and Wanfang database,individual case report literatures about amiodarone-induced pulmonary toxicity were collected during 1990-2016. The included cases were analyzed statistically. RESULTS:A total of 19 related literatures were collected,involving 20 cases of amiodarone-induced pulmonary toxicity. Among them,the patients older than 60 years old accounted for 75.0% with ratio of male to female 3:1. 75.0% patients had used medicine more than 1 month when pulmonary toxicity occurred. The dose of amiod-arone in 17 patients ranged 200-400 mg/d. Six patients died,accounting for 30.0%. CONCLUSIONS:Pulmonary toxicity induced by amiodarone may be related to patients'gender,age,dose and medication time. The mortality of it is in relative high level. Med-ical staff should pay attention to it,regularly monitor and process it timely.
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<p><b>OBJECTIVE</b>The effect of the silica nanoparticles (SNs) on lungs injury in rats was investigated to evaluate the toxicity and possible mechanisms for SNs.</p><p><b>METHODS</b>Male Wistar rats were instilled intratracheally with 1 mL of saline containing 6.25, 12.5, and 25.0 mg of SNs or 25.0 mg of microscale SiO2 particles suspensions for 30 d, were then sacrificed. Histopathological and ultrastructural change in lungs, and chemical components in the urine excretions were investigated by light microscope, TEM and EDS. MDA, NO and hydroxyproline (Hyp) in lung homogenates were quantified by spectrophotometry. Contents of TNF-α, TGF-β1, IL-1β, and MMP-2 in lung tissue were determined by immunohistochemistry staining.</p><p><b>RESULTS</b>There is massive excretion of Si substance in urine. The SNs lead pulmonary lesions of rise in lung/body coefficients, lung inflammation, damaged alveoli, granuloma nodules formation, and collagen metabolized perturbation, and lung tissue damage is milder than those of microscale SiO2 particles. The SNs also cause increase lipid peroxidation and high expression of cytokines.</p><p><b>CONCLUSION</b>The SNs result into pulmonary fibrosis by means of increase lipid peroxidation and high expression of cytokines. Milder effect of the SNs on pulmonary fibrosis comparing to microscale SiO2 particles is contributed to its elimination from urine due to their ultrafine particle size.</p>
Subject(s)
Animals , Male , Rats , Air Pollutants , Toxicity , Dose-Response Relationship, Drug , Lung , Pathology , Microscopy, Electron, Transmission , Nanoparticles , Toxicity , Pulmonary Fibrosis , Metabolism , Pathology , Random Allocation , Rats, Wistar , Silicon Dioxide , Toxicity , Specific Pathogen-Free Organisms , Spectrometry, X-Ray Emission , Urine , ChemistryABSTRACT
Objective To systematically study the pulmonary toxicity of single-wall carbon nanotubes (SWCNTs) and to explore the related cytotoxicity mechanism, so as to provide a theoretical basis for the safe productionandapplication of SWCNTs. Methods A549 cells were cultured in the media containing 0, 25, 50, 100, 150, and 200 μg/mL SWCNTs for 24 h, and then the cell viability and degree of cell membrane damage were assessed by CCK-8 and lactate dehydrogenase (LDH) release assay kit, respectively; the ultrastructural alteration of A549 cells was detected by transmission electron microscope (TEM). The oxidative stress response was evaluated by assessing reactive oxygen species (ROS), glutathione (GSH) and superoxide dismutase (SOD). The rats were exposed to SWCNTs by intratracheal inhalation, and then the animals were sacrificed 3 days later and the pathological sections of lung tissue were examined. Results SWCNTs showed considerable toxicity to A549 cells, decreasing cell viability, causing severe damage of cell membrane and ultrastructure, increasing the intracellular ROS level, and decreasing GSH content and SOD activity. It was found that oxidative stress is the main mechanism of SWCNTs toxicity on A549 cells. In vivo toxicity results showed that SWCNTs accumulated in the lung tissue # causing alveolar wall edema. Conclusion In vitro and in vivo toxicity results have found that SWCNTs possess a significant pulmonary toxicity # with its main toxicity mechanismbeing oxidative stress.
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BACKGROUND/AIMS: Amiodarone is one of the most widely used antiarrhythmic agents; however, amiodarone-induced pulmonary toxicity (APT) can be irreversible and sometimes fatal. The aim of this study was to evaluate the feasibility of chest computed tomography (CT) as a diagnostic tool for APT and to assess the utility of the CT APT score as an index for predicting the severity of APT. METHODS: Patients underwent amiodarone treatment for various reasons, most often atrial fibrillation, for more than 2 years, and those that received a cumulative dose > 100 g were enrolled. A total of 34 patients who underwent chest CT between December 2011 and June 2012 were enrolled, whether or not they had clinical symptoms. The APT CT score was defined as the number of involved regions in the lung, which was divided into 18 regions (right and left, upper, middle, and lower, and central, middle, and peripheral). The CT findings were evaluated according to the total dose and duration of amiodarone treatment and the results of a pulmonary function test. Clinical symptoms and outcomes were also evaluated according to APT CT scores. RESULTS: Seven patients had positive APT CT scores (interstitial fibrosis in five, organizing pneumonia in one, and mixed interstitial fibrosis and organizing pneumonia in one), and these patients exhibited significantly lower diffusion capacity for carbon monoxide in the lungs compared with patients without an increased APT CT score (70.2% +/- 6.9% vs. 89.7% +/- 19.4%; p = 0.011). Three of the seven patients experienced overt APT that required hospital admission. CONCLUSIONS: Chest CT is a useful diagnostic tool for APT, and the APT CT score might be a useful index for assessing the severity of APT.
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Amiodarone/adverse effects , Anti-Arrhythmia Agents/adverse effects , Atrial Fibrillation/diagnosis , Cross-Sectional Studies , Cryptogenic Organizing Pneumonia/chemically induced , Feasibility Studies , Forced Expiratory Volume , Hospitalization , Lung/drug effects , Predictive Value of Tests , Prospective Studies , Pulmonary Diffusing Capacity , Pulmonary Fibrosis/chemically induced , Respiratory Function Tests , Risk Factors , Time Factors , Tomography, X-Ray Computed , Vital CapacityABSTRACT
Amiodarone is an antiarrhythmic drug known to have adverse effects on multiple organs. Most studies have reported the side effects of the drug, which may result from rapid administrations or from long-term, high dosage administrations. However, toxicity issues have also been reported from patients administered with low doses of the drug for a long period of time. Here we report a case of an 82-year-old female who had shown symptoms and signs of pulmonary, hepatic, and neurotoxicity after taking amiodarone for 14 months in order to treat her atrial fibrillation without regular outpatient follow-up. We highlight the importance of the recommended evaluations, including lung, liver, and thyroid functions, as well as the neurological examinations in patients treated with amiodarone for a long period of time during regular follow-up.
Subject(s)
Aged, 80 and over , Female , Humans , Amiodarone , Atrial Fibrillation , Cardiomyopathy, Hypertrophic , Follow-Up Studies , Liver , Lung , Neurologic Examination , Outpatients , Thyroid GlandABSTRACT
The purpose of this study was to determine the acute pulmonary toxicity of metallic silver nanoparticles (MSNPs, 20.30 nm in diameter). Acute pulmonary toxicity and body distribution of inhaled MSNPs in mice were evaluated using a nose-only exposure chamber (NOEC) system. Bronchoalveolar lavage (BAL) fluid analysis, Western blotting, histopathological changes, and silver burdens in various organs were determined in mice. Mice were exposed to MSNPs for 6 hrs. The mean concentration, total surface area, volume and mass concentrations in the NOEC were maintained at 1.93 x 10(7) particles/cm3, 1.09 x 10(10) nm2/cm3, 2.72 x 10(11) nm3/cm3, and 2854.62 microg/m3, respectively. Inhalation of MSPNs caused mild pulmonary toxicity with distribution of silver in various organs but the silver burdens decreased rapidly at 24-hrs post-exposure in the lung. Furthermore, inhaled MSNPs induced activation of mitogen-activated protein kinase (MAPK) signaling in the lung. In summary, single inhaled MSNPs caused mild pulmonary toxicity, which was associated with activated MAPK signaling. Taken together, our results suggest that the inhalation toxicity of MSNPs should be carefully considered at the molecular level.
Subject(s)
Animals , Mice , Blotting, Western , Bronchoalveolar Lavage , Inhalation , Lung , Nanoparticles , Protein Kinases , SilverABSTRACT
Amiodarone is one of the most commonly prescribed antiarrhythmic drug for almost all atrial or ventricular arrythmias. Amiodarone-induced pulmonary toxicity (APT) was first described in 1980 and has potentially serious side effects that are believed to develop in 5% of patients. In general, APT occurs only when high amiodarone doses are used for a long time. However, during short-term therapy of amiodarone, APT is rarely reported. In this report, we describe a case of amiodarone-induced pulmonary toxicity after a short course of amiodarone therapy for atrial fibrillation.
Subject(s)
Humans , Amiodarone , Arrhythmias, Cardiac , Atrial Fibrillation , DimapritABSTRACT
Background. To study the clinical presentation, pulmonary functions and outcomes in subjects who were accidentally exposed to chlorine gas. Methods. Prospective observational study of 64 patients who sustained acute accidental exposure to chlorine gas during a leak in the chlorination system of the public bathing pool of a temple. Results. The major presenting symptoms and signs included acute dyspnoea (100%), chest discomfort (100%), cough (97%), eye irritation (88%), giddiness (72%), vomiting (46%), and heaviness in the head (44%); tachycardia (100%), tachypnoea (96%) and polyphonic wheezing (28%). All patients were managed in the emergency room with humidified oxygen inhalation and beta-2 agonist nebulisation and 52 were discharged within six hours. Twelve patients were severely affected and required hospitalisation; three of them were admitted into the intensive care unit. Three patients developed pulmonary oedema six to eight hours following admission. Pulmonary function testing (n=12) at presentation revealed obstructive defect in eight and mixed obstructive-cum-restrictive defect in four patients. The mean duration of hospital stay was 5.1±2.1 days. None of the patients died. Reactive airway dysfunction syndrome (RADS) was observed in three of the 12 hospitalised patients, who complained of manifested persistent cough that lasted for three months period following discharge. Serial pulmonary functions recovered to normal range by the end of the six months in all patients and remained so at one-year follow-up. Conclusion. Acute exposure to chlorine gas is an uncommon, but important public health hazard and can cause RADS, acute lung injury and pulmonary function abnormalities , which are reversible on prompt and appropriate management.