The Relationship of Macular Pigment Optical Density to Serum Lutein in Retinitis Pigmentosa

The Berman-Gund Laboratory for the Study of Retinal Degenerations, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114, USA.
Investigative ophthalmology & visual science (Impact Factor: 3.43). 09/2009; 51(2):1086-91. DOI: 10.1167/iovs.09-3396
Source: PubMed

ABSTRACT To determine whether macular pigment optical density (MPOD) is related to serum lutein or serum zeaxanthin in patients with retinitis pigmentosa.
The authors measured MPOD with heterochromatic flicker photometry, serum lutein and serum zeaxanthin by high performance liquid chromatography, and central foveal retinal thickness by optical coherence tomography (OCT) in 176 patients (age range, 18-68 years) with typical forms of retinitis pigmentosa; 37 (21%) of these patients had cystoid macular edema (CME) by OCT. The authors performed multiple regression analysis with MPOD as the dependent variable and with log(e) serum lutein and log(e) serum zeaxanthin as independent variables adjusting for age, sex, iris color, central foveal retinal thickness, and, in some analyses, serum total cholesterol.
MPOD increased with increasing serum lutein (P = 0.0017) and decreased with increasing serum total cholesterol (P = 0.0025) but was unrelated to serum zeaxanthin. MPOD was higher in patients with brown irides than in patients with lighter irides (P = 0.014) and was nonmonotonically related to central foveal retinal thickness (P < 0.0001), being lower in eyes with more photoreceptor cell loss and in eyes with moderate to marked CME.
MPOD is independently related to serum lutein, serum total cholesterol, iris color, and central foveal retinal thickness in patients with retinitis pigmentosa.

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    ABSTRACT: Introduction: Retinitis pigmentosa (RP), which occurs about 1 in 4,000 people worldwide, is a hereditary retinal degeneration that leads to legal blindness. The condition is characterized by a degeneration of the photoreceptors caused by a variety of responsible genes. Investigations of photoreceptor cell death in RP have provided clues on potential therapeutic targets. In this review, our current understanding of the mechanisms responsible for photoreceptor cell death is briefly summarized and strategies for preventing or retarding the progression of RP are discussed by specifically focusing on its putative therapeutic options. Areas covered: The clinical features, genetic backgrounds and molecular basis for photoreceptor cell death in RP are presented. Since the mechanisms for retinal degeneration appear to be extremely complicated, a variety of possible therapeutic targets have been proposed, with some having been applied clinically. Expert Opinion: Because RP is genetically heterogeneous, mechanisms for photoreceptor cell death are known to be complicated, partially depending on the individual causative genes. These pathways include oxygen stress, endoplasmic reticulum (ER) stress, increased Ca2+ uptake by photoreceptor cells, caspase-dependent and/or -independent pathways of apoptosis, parthanatos (poly-ADP-ribose polymerase-1-dependent cell death), epigenetic factors, neurotrophic factors and autophagy, among others. In order to effectively achieve photoreceptor protection therapy, it is necessary to develop proper combinations of various treatment methods, in addition to creating new gene therapy and cell or tissue replacement strategies.
    11/2013; 2(1). DOI:10.1517/21678707.2014.858596
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    ABSTRACT: PURPOSE: To assess the range of macular pigment optical density (MPOD) in a healthy group of young adults of South Asian origin; to investigate whether any dietary factors or personal characteristics were related to inter-subject variations in MPOD; and to compare the mean MPOD of the South Asian group with the mean MPOD of a white group. METHODS: Heterochromatic flicker photometry was used to measure the MP levels of 169 healthy volunteers, of which 117 were Asian and 52 were white. In addition, the Asian participants completed a questionnaire pertaining to the various physical, ocular, lifestyle, dietary and environmental factors that may be associated with MPOD or age-related macular degeneration (AMD). RESULTS: The mean MPOD of the Asian subjects was 0.43±0.14. The male participants had a higher mean MPOD than the females (0.47±0.13 vs 0.41±0.14, p<0.01). Possible associations also emerged between MPOD and form of refractive correction, and iris colour. No MPOD associations were found for the other variables examined in the questionnaire. The mean MPOD of the white subject group was 0.33±0.13, which was significantly lower than the Asian group (p<0.0005). CONCLUSIONS: This study adds to the currently limited information on MPOD in South Asians, and while a comparison between Asians and Whites was not the main focus here, highly significant differences between these two ethnicities were revealed. This provokes the possibility that South Asian individuals could have a lower risk for AMD, and it warrants further study.
    Investigative ophthalmology & visual science 03/2013; 54(4). DOI:10.1167/iovs.12-10957 · 3.43 Impact Factor
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    Investigative ophthalmology & visual science 08/2012; 53(10):6178-86. DOI:10.1167/iovs.12-10275 · 3.43 Impact Factor


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