Abstract

FR.20.06

Macular telangiectasia (MacTel) patterns of distribution of macular pigment and reaction on supplementation

Meike Brigitte Zeimer, Björn Padge, Georg Spital, Albrecht Lommatzsch, Daniel Pauleikhoff
Augenabteilung am St. Franziskus-Hospital, Münster

Objective
The distribution of macular pigment (MP) in type 2 idiopathic telangiectasia (IMT2) has been demonstrated to differ from the one of healthy subjects. Analyses of patterns of MP show different stages of changes which reflect the extent of telangiectatic changes. Can the amount and the pattern of MP be influenced by supplementation? Are there individual differences?
Methods
11 patients with IMT 2 were supplemented with 12mg Lutein (L) and 0.6mg Zeaxanthin (Z) (Ocuvite Lutein AMD). Every 3 months L- und Z- level in serum, visual acuity, fundus biomicroscopy, mikroperimetry, optic coherence tomography (OCT) and MP concentration via autofluorescence by use of two different extention wavelengths (488nm: good absorption by MP, 514: poor absorption by MP) were analysed. After 9 months supplementation was stopped and probands were investigated again 3months later.
Results
The reaction on supplementation was dependend on the baseline pattern of MP distribution: When central accumulation of MP similar to that in healthy subjects was present (with segment of reduced MP in the temporal fovea: MP class 1), supplementation was followed by enrichment of MP centrally at 0.5°, at 2° and peripherally at 5-6°. In MP class 2, with reduced concentration of MP centrally, accumulation at 2° peripherally, but not centrally was detectable. In MP Class 3 an oval-shaped effacement of MP in the center of the fovea and a surrounding oval shaped ring of MP at about 5- 7 degrees eccentricity supplementation with L and Z lead to an accumulation of MP only peripherally.
Conclusions
Solely in regions of MP presence before onset of supplementation concentration of MP increased. Degenerative processes leading to an impairment of transport and storage of L and Z may play a leading role in the pathogenesis of IMT 2.

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