Relationship between amiodarone-induced subclinical lung toxicity and Th1/Th2 balance

Kuruma, Tadao; Maruyama, Toru; Hiramatsu, S; Yasuda, Yuichiro; Yasuda, Shin; Odashiro, Keita; Harada, Mine

doi:10.1016/j.ijcard.2008.02.027

Cited by 12 publications

(7 citation statements)

References 31 publications

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“…Three different mechanisms of amiodarone induced lung disease have been suggested: a direct toxic effect, an immune-mediated mechanism, the angiotensin enzyme system activation [9]. From the immunological perspective, Kuruma et al reported that the Th1/Th2 balance may influence amiodarone metabolism and may be a powerful indicator of amiodarone-induced subclinical lung toxicity [43]. …”

Section: Mechanisms Involved In Dildmentioning

confidence: 99%

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

Matsuno¹

2012

Respir Res

239

188

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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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Section: Mechanisms Involved In Dildmentioning

confidence: 99%

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

Matsuno¹

2012

Respir Res

239

188

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“…There are two different categories of pulmonary involvement following amiodarone assumption: asymptomatic lipid pneumonia and APT. In turn APT can be caused by two possible mechanisms: a direct cytotoxic effect or an immuno-mediated mechanism, supported by immunologic markers in the blood stream and lungs of patients and CD8 + lymphocytosis in bronchoalveolar lavage (BAL), with imbalance between T-helper type I and II subpopulations and cytokines [16,17]. APT is less common than thyroid, eye and skin toxicity, but it is the most dangerous one because it may occur as a subacute/chronic onsetting alveolar or interstitial pneumonia with vary degrees of fibrosis, as well as an acute respiratory distress with severe hypoxemia [18].…”

Section: Discussionmentioning

confidence: 99%

A Nontrivial Differential Diagnosis in COVID-19 Pandemic: A Case Report and Literary Review of amiodarone-induced Interstitial Pneumonia

et al. 2020

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Amiodarone is a drug commonly used to treat and prevent cardiac arrhythmias, but it is often associated with several adverse effects, the most serious of which is pulmonary toxicity. A 79-year-old man presented with respiratory failure due to interstitial pneumonia during coronavirus disease 2019 (COVID-19) pandemic. The viral etiology was nevertheless excluded by repeated nasopharyngeal swabs and serological tests and the final diagnosis was amiodarone induced organizing pneumonia. The clinical and computed tomography findings improved after amiodarone interruption and steroid therapy. Even during a pandemic, differential diagnosis should always be considered and pulmonary toxicity has to be taken into account in any patient taking amiodarone and who has new respiratory symptoms.

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“…Generally, cytotoxicity and immunological activation are considered to be the primary mechanisms leading to druginduced pulmonary toxicity. Amiodarone, which blocks the same channels as bepridil, has been reported to be cytotoxic to alveolar epithelial cells and fibroblasts [6], to induce an imbalance of TH1/Th2 lymphocytes [7], to induce TNF-alpha and-beta from alveolar macrophages [8] and to activate the angiotensin system [9], but the mechanism underlying the development of pulmonary toxicity due to bepridil are still unknown.…”

Section: Discussionmentioning

confidence: 99%

Incidence and outcomes of bepridil-induced interstitial pneumonia

Yamasaki

Yatera

Noguchi

et al. 2013

Respiratory Medicine

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Relationship between amiodarone-induced subclinical lung toxicity and Th1/Th2 balance

Cited by 12 publications

References 31 publications

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

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

A Nontrivial Differential Diagnosis in COVID-19 Pandemic: A Case Report and Literary Review of amiodarone-induced Interstitial Pneumonia

Incidence and outcomes of bepridil-induced interstitial pneumonia

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