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      A case report and literature review: previously excluded tuberculosis masked by amiodarone induced lung injury

      case-report

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          Abstract

          Background

          Amiodarone is an antiarrhythmic drug which is used to treat and prevent several dysrhythmias. This includes ventricular tachycardia and fibrillation, wide complex tachycardia, as well as atrial fibrillation (AF) and paroxysmal supraventricular tachycardia. Amiodarone may prove to be the agent of choice where the patient is hemodynamically unstable and unsuitable for direct current (DC) cardioversion. Although, it is not recommended for long-term use. The physician might encounter issues when differentiating amiodarone-induced lung toxicity with suspicion of interstitial lung disease, cancer or vasculitis. Adverse drug reactions are difficult to confirm and it leads to serious problems of pharmacotherapy.

          Case presentation

          A 78-year-old Caucasian male pensioner complaining of fever, dyspnea, malaise, non-productive cough, fatigue, weight loss, diagnosed with acute respiratory failure with a 16-year long history of amiodarone use and histologically confirmed temporal arteritis with long-term glucocorticosteroid (GCC) therapy.

          Patient was treated for temporal arteritis with GCC for ~ 1 year, then fever and dyspnea occurred, and the patient was hospitalized for treatment of bilateral pneumonia. Chest X-ray and chest high resolution computed tomography (HRCT) indicated several possible diagnoses: drug-induced interstitial lung disease, autoimmune interstitial lung disease, previously excluded pulmonary TB. Amiodarone was discontinued. Antibiotic therapy for bilateral pneumonia was started. Fiberoptic bronchoscopy with bronchial washings and brushings was performed. Acid fast bacilli (AFB) were found on Ziehl-Nielsen microscopy and tuberculosis (TB) was confirmed (later confirmed to be Mycobacterium tuberculosis in culture), initial treatment for TB was started. After a few months of treating for TB, patient was diagnosed with pneumonia and sepsis, empiric antibiotic therapy was prescribed.

          After reevaluation and M. Tuberculosis identification, the patient was referred to the Tuberculosis hospital for further treatment. After 6 months of TB treatment, pneumonia occurred which was complicated by sepsis. Despite the treatment, multiple organ dysfunction syndrome evolved and patient died. Probable cause of death: pneumonia and sepsis.

          Conclusions

          The current clinical case emphasizes issues that a physician may encounter in the differential diagnostics of amiodarone-induced lung toxicity with other lung diseases.

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          Most cited references 15

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          Drug-induced interstitial lung disease: mechanisms and best diagnostic approaches

           Osamu Matsuno (2012)
          Drug-induced interstitial lung disease (DILD) is not uncommon and has many clinical patterns, ranging from benign infiltrates to life-threatening acute respiratory distress syndrome. There are two mechanisms involved in DILD, which are probably interdependent: one is direct, dose-dependent toxicity and the other is immune-mediated. Cytotoxic lung injury may result from direct injury to pneumocytes or the alveolar capillary endothelium. Drugs can induce all types of immunological reactions described by Gell and Coombs; however, most reactions in immune-mediated DILD may be T cell-mediated. DILD can be difficult to diagnose; diagnosis is often possible by exclusion alone. Identifying the causative drug that induces an allergy or cytotoxicity is essential for preventing secondary reactions. One method to confirm the diagnosis of a drug-induced disease is re-exposure or re-test of the drug. However, clinicians are reluctant to place patients at further risk of illness, particularly in cases with severe drug-induced diseases. Assessment of cell-mediated immunity has recently increased, because verifying the presence or absence of drug-sensitized lymphocytes can aid in confirmation of drug-induced disease. Using peripheral blood samples from drug-allergic patients, the drug-induced lymphocyte stimulation test (DLST) and the leukocyte migration test (LMT) can detect the presence of drug-sensitized T cells. However, these tests do not have a definite role in the diagnosis of DILD. This study explores the potential of these new tests and other similar tests in the diagnosis of DILD and provides a review of the relevant literature on this topic.
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            2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

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              Meta-analysis of BACTEC MGIT 960 and BACTEC 460 TB, with or without solid media, for detection of mycobacteria.

              In a meta-analysis of 10 studies, the BACTEC 960/MGIT and BACTEC 460 systems showed a sensitivity and specificity in detecting mycobacteria (1,381 strains from 14,745 clinical specimens) of 81.5 and 99.6% and 85.8 and 99.9%, respectively. Combined with solid media, the sensitivity of the two systems increased to 87.7 and 89.7%, respectively.
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                Author and article information

                Contributors
                +37065823543 , egle.zlatkute@gmail.com
                silvijus.abramavicius@lsmuni.lt
                greta.musteikiene@lsmuni.lt
                edgaras.stankevicius@lsmuni.lt
                jurgita.zaveckiene@lsmuni.lt
                vidas.pilvinis@lsmuni.lt
                edmundas.kadusevicius@lsmuni.lt
                Journal
                BMC Pharmacol Toxicol
                BMC Pharmacol Toxicol
                BMC Pharmacology & Toxicology
                BioMed Central (London )
                2050-6511
                29 December 2018
                29 December 2018
                2018
                : 19
                Affiliations
                [1 ]ISNI 0000 0004 0432 6841, GRID grid.45083.3a, Institute of Physiology and Pharmacology, , Lithuanian University of Health Sciences, ; A. Mickeviciaus str. 9, 44307 Kaunas, LT Lithuania
                [2 ]ISNI 0000 0004 0432 6841, GRID grid.45083.3a, Department of Pulmonology, Medical Academy, , Lithuanian University of Health Sciences Kaunas Clinics, ; Kaunas, Lithuania
                [3 ]ISNI 0000 0004 0432 6841, GRID grid.45083.3a, Department of Radiology, Medical Academy, , Lithuanian University of Health Sciences Kaunas Clinics, ; Kaunas, Lithuania
                [4 ]ISNI 0000 0004 0432 6841, GRID grid.45083.3a, Department of Intensive Care, Medical Academy, , Lithuanian University of Health Sciences Kaunas Clinics, ; Kaunas, Lithuania
                [5 ]Intensive care unit, Republican Vilnius University Hospital, Vilnius, Lithuania
                Article
                279
                10.1186/s40360-018-0279-1
                6311077
                30594249
                ba86c60d-7768-4a62-aac4-121cc310a40f
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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                © The Author(s) 2018

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