a 72-year - old man underwent arthroscopy for symptoms of mechanical locking of his left knee . he had been taking amiodarone hydrochloride for the last 7 years for treatment of cardiac arrhythmia . he had areas of blue grey pigmentation on the face , forearms , hands , and legs ( fig . 1 ) . he did not have a storage disease and his only other medications were warfarin and aspirin . during knee arthroscopy , widespread pigmentation of the synovium similar to that on his skin was seen . 2 ) . the debrided meniscus and synovial tissue obtained during arthroscopy was sampled and sent for histopathological examination , which showed the presence of periodic acid  schiff - positive aggregates of yellowish brown granules within histiocytes consistent with the usual microscopic presentation of such deposits in the cornea and skin described by various authors previously.12 ) the histopathological examination ruled out any pigmented villonodular synovitis . considering the history , clinical picture and histological findings amiodarone hydrochloride is a coronary vasodilator used in the treatment of cardiac arrhythmias and can induce a blue - gray or violaceous pigmentation of the skin and yellow - brown stippling of the cornea.3 ) the pigmentation of the skin and cornea in patients on long - term amiodarone therapy is well established and usually develops after 6 months or more of the therapy.45 ) the cutaneous effects are more likely to manifest with longer durations of use and at doses greater than 400 mg per day.3 ) the pigmentation on the skin and cornea may slowly resolve months to years after withdrawal of the therapy , although it can be permanent.25 ) delage , a belgian ophthalmologist , was the first to report a gray pigmentation of the cornea secondary to amiodarone use.1 ) the pathogenesis of this side effect is poorly understood . in 1975 , delage et al.1 ) described light and electron microscopic findings of tissues affected by amiodarone as deposition of yellow - brown granules and lipofuscin within dermal macrophages . electron microscopy also demonstrated granules contained within intralysosomal laminated inclusion bodies , and they suggested a storage abnormality involving the drug or its metabolites as the mechanism.4 ) they also hypothesized that amiodarone accelerates normal cellular autophagocytosis resulting in increased production of lipofuscin which accumulates in lysosomes because of a deficiency in lipolytic enzymes and concluded that pigmentation in the skin and cornea may develop because the drug or its metabolites accumulate in the histiocytes between the collagen fibres . however , brazzelli et al.,6 ) in their article , suggested that the pathogenesis may be related to the action of the drug on cell membranes causing local metabolic damage , accumulation of the drug in the lysosomes , and acceleration of the physiological aging process . we think that drugs should be included in the differential diagnoses of pigmentation of the synovium and the arthroscopist should be aware of this condition .
an unusual grayish brown discoloration of the synovium was found during a knee arthroscopy of a 72-year - old man . 
 he also had similar pigmentation affecting the skin on the legs , arms , hands , and face . 
 it was found he had been taking 400 mg of amiodarone hydrochloride daily for last 7 years . 
 amiodarone is known to cause a slate grey pigmentation of skin and cornea , but we believe this is the first report of amiodarone - induced pigmentation of the synovium 
 . the arthroscopist should be aware of the possibility of drug - related synovial pigmentation and include this in differential diagnosis .