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Bronchoalveolar Lavage Cell Count and Differential Are Not Reliable Indicators of Amiodarone-induced Pneumonitis
Section snippets
Patient Selection
Patients were enrolled in the study under a protocol reviewed and approved by the Institutional Review Board at St. Louis (Mo) University. Toxic, ILD, and sick patients were referred to the Division of Pulmonology and Pulmonary Occupational Medicine for definitive diagnosis and treatment. Nontoxic amiodarone-treated volunteers were recruited from the arrhythmia service outpatient clinic. Normal healthy hospital staff volunteers served as control subjects.
Amiodarone Treatment Protocol
Many of the amiodarone-treated patients
Patient Demographics and Number
Thirteen amiodarone-treated but clinically nontoxic patients volunteered to participate in this study. Seventeen amiodarone-treated referrals were evaluated for diagnosis and treatment of suspected amiodarone toxicity. Eleven of these fulfilled clinical and pathologic criteria for amiodarone toxicity. Six were diagnosed as having other pathologic processes affecting the lung. These included congestive heart failure (two), sarcoidosis (two), pneumonia (one), and anaphylaxis with noncardiogrenic
DISCUSSION
The purpose of this study was to determine if the diagnosis of amiodarone-induced pneumonitis could be made reliably with patient history, pulmonary function evaluation, and by examination of BAL fluid. We compared BAL fluid cells, pulmonary function variables, amiodarone dose, and duration of therapy in three groups of amiodarone-treated patients (toxic, sick but not toxic, nontoxic). BAL fluid cell counts and differential cell counts from the three amiodarone-treated groups were compared with
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Acute Amiodarone Pulmonary Toxicity
2021, Journal of Cardiothoracic and Vascular AnesthesiaCitation Excerpt :Inflammation and fibrosis may be nonlinear or possibly unrelated; in some instances, evidence of an antecedent inflammatory process is lacking, with nonspecific pulmonary fibrosis predominating.22 BAL total cell counts may be increased in AIPT but do not differ from those of nontoxic patients nor do absolute lymphocyte counts when compared with other causes of interstitial pneumonitis.15,27 Beyond the aforementioned features of lipoid pneumonia, no clear histopathologic distinctions can be made when comparing presumed acute AIPT-related ARDS with ARDS of alternative origins.15,28
Drug-induced pulmonary diseases
2019, Difficult to Diagnose Rare Diffuse Lung DiseaseCytopathology of Infectious and Inflammatory Diseases
2018, Diagnostic Pathology of Infectious DiseaseInitial characteristics and outcome of hospitalized patients with amiodarone pulmonary toxicity
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Supported in part by a grant from the Upjohn Co.