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PubMed · 9081941

[Amiodarone pigmentation].

Abstract

Amiodarone can occasionally lead to a slate-coloured pigmentation in chronically UV-expose skin. A 63 year old patient presented with a pruritic bluish-purple pigmentation of the face 2 years after taking 400 mg of amiodarone daily for 2 years. During the 24 months after the dose was reduced to 200 mg daily, the pigmentation remained unchanged. Amiodarone pigmentation is caused by the UV-induced accumulation of lipofuscin in dermal macrophages, depending on both the daily dose and the duration of therapy. In the differential diagnosis, pigmentation caused by other drugs is the main consideration. Cessation of therapy eventually leads to complete normalization of skin colour.

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BibTeXRIS

R Ammann, L R Braathen. 1996. [Amiodarone pigmentation].. https://doi.org/10.1007/s001050050534

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Amiodarone protects cardiac myocytes against oxidative injury by its free radical scavenging action.

BACKGROUND: Oxidative stress plays an important role in the pathophysiology of ischemic heart disease and heart failure, and antioxidants might be beneficial in the treatment of these patients. This study was performed to determine the scavenging effects of amiodarone on oxygen free radicals and its protective effects against oxygen radical-mediated injury in cardiac myocytes. METHODS AND RESULTS: The formation of the radical spin adduct with hydroxy radical (.OH) in the presence of H(2)O(2) (10 mmol/L) and Fe(3+)-nitrilotriacetate (20 micromol/L) was monitored by electron paramagnetic resonance spectroscopy combined with a spin trapping agent, 5,5-dimethyl pyrroline-N-oxide (DMPO). Amiodarone decreased the intensity of the DMPO-OH signals in a dose-dependent manner (0.1 to 100 micromol/L), whereas other antiarrhythmia drugs such as disopyramide and atenolol had no such effects. Furthermore, amiodarone (10 micromol/L) protected intact adult canine cardiac myocytes against.OH-mediated myocyte injury, as assessed by the degree of morphological change from rod shape to the irreversible hypercontracture state during the exposure of cells to H(2)O(2) and Fe(3+) in vitro. CONCLUSIONS: Amiodarone can protect cardiac myocytes against oxidative stress-mediated injury by directly scavenging oxygen free radicals. Antioxidant action of amiodarone might potentially contribute to the beneficial effects of this drug in the treatment of patients with ischemic heart disease and congestive heart failure.

Amiodarone