Pneumonitis after amiodarone therapy.

Olson, L. Karl; Forrest, John V.; Friedman, P. J.; Kiser, Pamela E.; Henschke, Claudia I.

doi:10.1148/radiology.150.2.6691083

Cited by 27 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies indicated that the toxic effect was related to a daily dose of amiodarone. [15][16][17] However, Ott et al showed that low-dose amiodarone (200 mg/day) could increase the risk for pulmonary toxicity, 18 which is consistent with the results in our study. The risk of amiodarone-induced pulmonary toxicity cor relates better with the total cumulative dose than with the daily dose and plasma concentrations.…”

Section: Discussionsupporting

confidence: 92%

Amiodarone-induced pulmonary toxicity

et al. 2011

View full text Add to dashboard Cite

Amiodarone-induced pulmonary toxicity is a critical and potentially fatal side effect of amiodarone. Our study was designed to reveal its clinical features, including KL-6, as an interstitial marker. The medical records of eight patients (five men and three women) with amiodarone-induced pulmonary toxicity, who had been referred to our hospital, were examined. The mean age at the initiation of amiodarone was 48 years (range, 54-87 years) and mean duration of medication prior to the development of pulmonary toxicity was 18 months (range, 7-33 months). Serum KL-6 was elevated in six of the eight patients with a range of 525-2915 U/mL. Chest computed tomography (CT) findings showed non-segmental consolidation and/or ground glass opacity. Foamy macrophages were found in bronchoalveolar lavage (BAL) fluids of all examined patients and in transbronchial lung biopsy (TBLB) specimens in half of the examined patients. We concluded that serum KL-6, chest CT findings, and foamy macrophages in BAL fluids and TBLB specimens will be helpful for the diagnosis of amiodarone-induced pulmonary toxicity

show abstract

Section: Discussionsupporting

confidence: 92%

Amiodarone-induced pulmonary toxicity

et al. 2011

View full text Add to dashboard Cite

show abstract

“…The most serious adverse effect has been pulmonary toxicity, affecting 3 to 18% (1-4, 6,7,[11][12][13][14][15][16]. This generally presents as a pneumonitis with or without pulmonary interstitial fibrosis, causing progressive dyspnea and cough (3,(11)(12)(13)(14)(15)(16), and is fatal in up to 10% of cases (13). Other toxicity includes biochemical and clinical evidence of hypo-and hyperthyroidism ( 17, 35-38), cutaneous photosensitivity and skin discoloration (1 1, 39-41 1.…”

Section: Discussionmentioning

confidence: 99%

Amiodarone hepatotoxicity: Prevalence and clinicopathologic correlations among 104 patients

et al. 1989

View full text Add to dashboard Cite

The prevalence of apparent amiodarone-related hepatic injury in 104 patients followed prospectively is compared to that reported in the literature. Asymptomatic elevation of serum aminotransferase levels was detected in approximately one-fourth of the patients, a figure similar to the average of reported cases. The frequency of extrahepatic organ toxicity was increased in patients with elevated levels. Symptomatic "hepatitis" developed in 3% of this series and in less than 1% of cases in the literature. Evidence of hepatic phospholipidosis and the development of pseudoalcoholic liver injury is most likely due to the biochemical effects of the drug and to possible metabolic idiosyncrasy, respectively. Serial blood enzyme measurements, as recommended by the manufacturer, may offer some protection against the development of more serious liver injury. However, levels of amiodarone may persist in various tissues for weeks to months following withdrawal, and stopping the drug does not guarantee the prompt reversal of any organ toxicity. Accordingly, the risks posed and benefits offered by amiodarone should be carefully weighed prior to discontinuing the drug, as the risk of sudden cardiac death may outweigh the hazards of ongoing hepatic, pulmonary or other toxicity.

show abstract

“…Recent findings suggest that the dramatic hydrothermal vent communities may represent only a small fraction of Earth's high-pressure life. Microbes have been isolated from numerous deep crustal environments, including oil reservoirs [9,10], deep terrestrial aquifers [11,12], oceanic sediments [13,14], terrestrial sedimentary rocks [15][16][17], granite [18], and basalt [19]. It now appears possible that life is ubiquitous anywhere on Earth that water persists in liquid form [20][21][22].…”

Section: High-pressure Lifementioning

confidence: 99%

High pressure and the origin of life

Hazen¹,

Boctor²,

Brandes³

et al. 2002

J. Phys.: Condens. Matter

View full text Add to dashboard Cite

Three lines of experimental research suggest that high pressure may have played a significant role in the origin of life. Discoveries of abundant life in high-pressure environments, including deep oceans, hydrothermal vents, and crustal rocks, point to the adaptation of life to a variety of aqueous habitats. Cultures of microbes at high pressure display both barotolerant and barophilic behaviour. And studies of high-pressure hydrothermal organic synthesis reveal unexpectedly facile reaction mechanisms for the production of a variety of requisite biomolecules.

show abstract

Pneumonitis after amiodarone therapy.

Cited by 27 publications

References 0 publications

Amiodarone-induced pulmonary toxicity

Amiodarone-induced pulmonary toxicity

Amiodarone hepatotoxicity: Prevalence and clinicopathologic correlations among 104 patients

High pressure and the origin of life

Contact Info

Product

Resources

About