Purchase this article with an account.
T. Missotten, J.A. M. van Laar, T. van der Loos, P.M. van Hagen, G.S. Baarsma; Treatment of Uveitic Chronic Macular Edema with Octreotide . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1527.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
to report the efficacy of the somatostatin analogue octreotide, in the treatment of uveitic chronic macular edema (CME). As a major inhibitory hormone, somatostatin has immuno–suppressive and anti–angiogenic properties. Somatostatin analogues have been reported to have CME reducing effects in diabetic maculopathy, retinal dystrophies and uveitis. CME is the main reason of poor visual outcome in uveitis.
Retrospective non–controlled study. In 15 patients, a total of 27 episodes of recurrent CME during quiescent uveitis were treated with subcutaneous octreotide injections (20mg sc, monthly). Patients were selected for the study if CME control with acetazolamide or periocular steroid had failed during previous CME episodes.
CME changes during and after treatment were measured by Stratus–OCT in 20 episodes. Total macular volume as calculated by OCT was the parameter followed and analyzed. In 7 older CME episodes Stratus–OCT mapping was absent, and CME was classified as increased, stable or decreased by biomicroscopy and fluoroscein angiography (FA). .
chronic anterior uveitis was the cause of CME in 5, intermediate uveitis in 4, birdshot retinopathy in 5 and vasculitis in 13 episodes of CME. The included CME episodes occured 8.2 ± 5.3 years post onset of uveitis. Start of octreotide treatment was 3.5 ± 2.9 months after diagnosis of recurrent CME. Treatment was continued 16.4 ± 4.6 months. Overal VA change (VA prior to treatment – VA last day of treatment) was an increase of 0.07 ± 0.15 snellen lines. This corresponded to an increase in VA in 13 episodes (48.2%), stable VA in 11 episodes (40.7%) and deterioration of VA during 3 episodes (11.1%).
CME as measured by OCT (n = 20) or FA (n=7) reduced in 59.3% of episodes during treatment.
In 5 of 14 cases where succesful treatment was ceased, CME was absent over 1 year. In the others CME recurred instantly (5/14) or within 3 months (4/14) after the end of treatment.
During 2 episodes octreotide treatment had to be stopped : because of deteriorated serum liver tests (1) and glycemia deregulation (1).
Octreotide has a CME reducing effect in 59.3% of recurrent CME episodes in this study. This corresponded to an improvement of VA in 48.2% of episodes. In 11.1% of episodes, the anatomical improvement was not reflected in a functional benefit. In 64.3% of episodes, the arrest of octreotide therapy resulted in a swift recurrence of CME. This advocates a long–term treatment in patient who respond to octreotide, during which glycemia and serum liver tests should be followed closely.
This PDF is available to Subscribers Only