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Respiratory amiodarone

Respiratory Amiodarone pulmonary toxicity has been described after lung transplantation [28 ]. [Pg.381]

A 73-year-old man with acute respiratory failure, presumed to be secondary to amiodarone toxicity, developed sepsis and acute renal insufficiency, and required intermittent hemodialysis. Following a Herpes simplex labialis infection he was treated with oral aciclovir (400 mg tds). The next day he became sleepy, disoriented, and agitated. Over the next 48 hours his neurological condition deteriorated and he responded to pain... [Pg.29]

The commonest form of lung damage is an interstitial alveolitis, although pneumonitis and bronchiolitis obhter-ans have also been reported, as have sohtary localized fibrotic lesions, non-cardiac pulmonary edema, pleural effusions, acute respiratory failure, acute pleuritic chest pain, and adult respiratory distress syndrome (SEDA-17, 220) (SEDA-18, 201) (66-68). Amiodarone has also been reported to cause impairment of lung function, even in patients who do not develop pneumonitis (69), and preexisting impairment of lung function may constitute a contraindication to amiodarone. [Pg.153]

Adult respiratory distress syndrome occurred very rapidly in a 66-year-old man who took amiodarone 200 mg/day for a few weeks only (71). [Pg.153]

A 72-year-old man developed hypoxemic respiratory failure while taking amiodarone 300 mg/day (74). He had no history of lung disease. His CT scan was similar to that of the first patient. He responded to treatment with corticosteroids. [Pg.153]

A 77-year-old man who had taken amiodarone 400 mg/day for 11 months developed crackles at the lung bases and scattered respiratory wheeze (76). His leukocyte count was raised at 13.5 x 109/1 and he had progressive reduction in carbon monoxide diffusing capacity, serially measured. A chest X-ray showed bilateral opacities in the upper zones, peripheral in distribution, and a CT scan showed dense bilateral lung parenchjmal opacities. The symptoms of dyspnea on exertion, cough with minimal sputum, pleuritic chest pain, and low-grade fever abated after withdrawal, and the upper lobe densities resolved. [Pg.153]

Liverani E, Armuzzi A, Mormile F, Anti M, Gasbarrini G, GentUoni N. Amiodarone-induced adult respiratory... [Pg.168]

Miller B, Skupin A, Rubenfire M, Bigman O. Respiratory failure produced by severe procainamide intoxication in a patient with pre-existing peripheral neuropathy caused by amiodarone. Chest 1988 94(3) 663-5. [Pg.2927]

Burns KEA, Piliotis E, and Garcia BM (2000) Amiodarone pulmonary, neuromuscular and ophthalmological toxicity. Canadian Respiratory Journal 7 193-197. [Pg.99]

IAsu ].p-ANP(7-28). aminosuccinic acid aspartic acid, aminosultopride amisulpnde. amiodarone [ban, inn, usan) (Cordarone ) is a benzofuran derivative, a (Class III) antiarrhythmic used mainly to treat ventricular arrhythmias, amiphenazole [ban, inn] (DHA 245 amifenazole) is a phenylthiazole and has similar properties as doxapram as a CNS STIMULANT and RESPIRATORY STIMULANT. It was previously used intramuscularly to treat barbiturate and other CNS DEPRESSANT overdose. [Pg.15]

Fig. 16 Effects of amiodarone, perhexiline, and diethylaminoethoxyhexestrol (DEAEH) on mitochondrial function. After crossing the outer membrane, the uncharged secondary or tertiary amine (A) of amiodarone, perhexiline, or diethylaminoethoxyhexestrol (DEAEH) is protonated in the acidic intermembrane space. The positively charged molecule (AH ) is then electrophoretically pushed by the mitochondrial membrane potential into the matrix. High intramitochondrial concentrations inhibit both B-oxidation (causing steatosis) and oxidative phosphorylation, thus causing the accumulation of electrons in the respiratory chain and increasing the mitochondrial formation of ROS. The latter oxidize fat deposits, causing lipid peroxidation, which, together with ROS-induced cytokine production, could cause steatohepatitis. Fig. 16 Effects of amiodarone, perhexiline, and diethylaminoethoxyhexestrol (DEAEH) on mitochondrial function. After crossing the outer membrane, the uncharged secondary or tertiary amine (A) of amiodarone, perhexiline, or diethylaminoethoxyhexestrol (DEAEH) is protonated in the acidic intermembrane space. The positively charged molecule (AH ) is then electrophoretically pushed by the mitochondrial membrane potential into the matrix. High intramitochondrial concentrations inhibit both B-oxidation (causing steatosis) and oxidative phosphorylation, thus causing the accumulation of electrons in the respiratory chain and increasing the mitochondrial formation of ROS. The latter oxidize fat deposits, causing lipid peroxidation, which, together with ROS-induced cytokine production, could cause steatohepatitis.
Fromenty B, Fisch C, Berson A, Letteron P, Larrey D, Pessayre D (1990b) Dual effect of amiodarone on mitochondrial respiration. Initial protonophoric uncoupling effect followed by inhibition of the respiratory chain at the levels of complex I and complex II. J Pharmacol Exp Ther 255 1377-1384... [Pg.355]

High-dose oxygen may increase the risks of amiodarone-induced postoperative adult respiratory distress syndrome. [Pg.249]

Early-onset amiodarone toxicity due to diffuse alveolar hemorrhage, with respiratory distress, hemoptysis, severe hj oxia, and bilateral pulmonary infiltrates has been described in a 46-year-old man taking amiodarone [32" ]. [Pg.293]


See other pages where Respiratory amiodarone is mentioned: [Pg.259]    [Pg.259]    [Pg.154]    [Pg.164]    [Pg.587]    [Pg.91]    [Pg.249]    [Pg.622]    [Pg.292]    [Pg.293]    [Pg.136]    [Pg.1115]   
See also in sourсe #XX -- [ Pg.15 , Pg.168 ]




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