**6. Conclusion**

membranous lamellar bodies in extraocular muscle fibers, corneal epithelium, stromal and endothelial cells, conjunctival epithelium, scleral cells, lens epithelium, iris, ciliary body, choroid, retinal pigment epithelium, ganglion cells, large diameter axons of the optic nerve, the endothelium of ocular blood vessels and basal cells of corneal epithelium. Lamellar bodies in these cells contained iodine [53, 59]. Deposits were observed in the corneal epithelium of Amiodarone treated patients [59] about one week after the initiation of treatment with Amiodarone [59], keratopathy, unilateral and bilateral anterior ischemic optic neuropathy are also occurred [60, 61]. The corneal deposits are caused by secretion of Amiodarone from lacrimal gland on corneal surface. These deposits are brown and have been described as resembling cat's whiskers [57, 58]. Amiodarone- induced ocular side effects are time and dose-dependent. The changes are reversible after stopping Amiodar‐ one treatment. Amiodarone-related optic neuropathy has been reported after 4 month duration of treatment with unilateral or bilateral visual loss that can progress to blind‐ ness [62, 63]. Microscopic studies showed the accumulation of lamellar inclusions in the

Dermatologic, gastrointestinal, neurologic and genitourinary changes are the other side effects of chronic use of Amiodarone. Photosensitivity and less frequently phototoxicity are important dermatological side effects. Photosensitivity is quite common and there is a wide spectrum of skin reactions, ranging from an increased propensity to suntan to intense burning and erythema and swelling of the exposed area [64, 65]. Phototoxicity induces blue-gray skin hyperpigmentation of predominantly sun exposed areas. It develops in <10% of patients, preferentially affecting men. It was mainly observed after an average of 20 months of contin‐ uous Amiodarone treatment and a minimal cumulative dose of 160 g [64, 66]. Histopatholog‐ ically, Amiodarone-induced phototoxicity has been related to lysosomal dermal lipofuscin deposits. The only treatment is reduction or cessation of therapy, upon which skin changes may slowly abate [64, 66]. However, skin discoloration is likely to persist for years. The intensity of these reactions could be alleviated by a reduction in dosage or by application of a protective sunscreen. Patients should be instructed to avoid exposure to the sun or use

Peripheral neuropathy has been observed in 3–30% of patients on long-term high dosage (generally over 400mg/day) regimen which include tremor, ataxia and sleep disturbances. Histologically, inclusion bodies and segmental demyelination of the nerve fibers have been demonstrated in peripheral nerve fibers. After discontinuation of the medicine, the neurolog‐

A significant association was found between the development of epididymitis and high-dose Amiodarone treatment for a long time. Genitourinary effects include sterile epididymitis with

axons of the optic nerve because of drug induced lipidosis [57, 63].

**5. Other side effects of Amiodarone**

124 Abnormal Heart Rhythms

protective measures during therapy [64–66].

pain and swelling in the scrotum [68].

ical complication is slowly and incompletely resolved [65, 67].

Side effects occur more frequently with long-term administration of the drug, e.g. more than 6 months and is related to total dose of the drug administered; therefore the effectiveness of Amiodarone in long-term treatment of patients with heart arrhythmia is limited because of the development of its adverse side effects.
