G Duncker1, T Bredehorn. 1. Department of Ophthalmology, University of Kiel, Germany.
Abstract
BACKGROUND: The antimalarial and antirheumatic drug chloroquine is one of the most infamous amphiphilic cationic drugs in clinical ophthalmology. It is known to cause lipidosis and photoreceptor degeneration in the human and the rat retina. METHODS: We treated female albino Wistar rats (mean weight 200 g) orally with chloroquine (95 mg/kg body weight) for 12 weeks, followed by a period of 4 months with normal feed. After initial electroretinography in all rats, measurements were made after 4 and 12 weeks of treatment and 16 weeks after withdrawal. The rats were prepared for histological examination. RESULTS: Treatment of rats with chloroquine caused severe lipidosis in the neuroretina; photoreceptor cell degeneration was slight. After 12 weeks of treatment, the b-wave amplitude was reduced to 30% of the initial value; the a-wave amplitude was reduced, but remained within the range of normal values. After withdrawal of chloroquine the lipidosis remitted, but the degeneration of the photoreceptor cell layer continued to progress. Despite remission of lipidosis, electroretinography demonstrated functional disturbances, marked by reduction of the a- and b-wave amplitudes to 25% and 16% of initial values, respectively. CONCLUSIONS: Seen from the point of view of function, it is doubtful whether lipidosis is the primary cause of changes in the electroretinogram or of receptor cell degeneration.
BACKGROUND: The antimalarial and antirheumatic drug chloroquine is one of the most infamous amphiphilic cationic drugs in clinical ophthalmology. It is known to cause lipidosis and photoreceptor degeneration in the human and the rat retina. METHODS: We treated female albino Wistar rats (mean weight 200 g) orally with chloroquine (95 mg/kg body weight) for 12 weeks, followed by a period of 4 months with normal feed. After initial electroretinography in all rats, measurements were made after 4 and 12 weeks of treatment and 16 weeks after withdrawal. The rats were prepared for histological examination. RESULTS: Treatment of rats with chloroquine caused severe lipidosis in the neuroretina; photoreceptor cell degeneration was slight. After 12 weeks of treatment, the b-wave amplitude was reduced to 30% of the initial value; the a-wave amplitude was reduced, but remained within the range of normal values. After withdrawal of chloroquine the lipidosis remitted, but the degeneration of the photoreceptor cell layer continued to progress. Despite remission of lipidosis, electroretinography demonstrated functional disturbances, marked by reduction of the a- and b-wave amplitudes to 25% and 16% of initial values, respectively. CONCLUSIONS: Seen from the point of view of function, it is doubtful whether lipidosis is the primary cause of changes in the electroretinogram or of receptor cell degeneration.
Authors: A S Neubauer; K Samari-Kermani; U Schaller; U Welge-Lübetaen; G Rudolph; T Berninger Journal: Br J Ophthalmol Date: 2003-07 Impact factor: 4.638