Macular pigment optical density in central serous chorioretinopathy
Sunday, October 24, 2010
Low macular pigment optical density (MPOD) may be a risk factor for chronic central serous chorioretinopathy (CSC), according to a new study.
Macular pigment is composed of three carotenoids (i.e., lutein, zeaxanthin, and meso-zeaxanthin). Lutein and zeaxanthin can be obtained only from food, and meso-zeaxanthin is synthesized mainly from retinal lutein.
Macular pigment has light-absorbing properties and is thought to filter blue light, which is toxic to the photoreceptors. In addition, macular pigment itself has an antioxidant effect. It quenches excited triplet states, reacts with singlet oxygen and free radicals, and inhibits peroxidation of long-chain polyunsaturated fatty acids. Thus, it helps retard some destructive processes in the retina and the retinal pigment epithelium (RPE), which may lead to macular diseases such as age-related macular degeneration (AMD).
Some investigators have tried to determine the amount of macular pigment and elucidate factors affecting macular pigment. However, whether macular pigment optical density (MPOD) is affected by aging, sex, and smoking is still controversial. In those studies, several clinical methods of measuring MPOD were used, including heterochromatic flickering photometry, motion detection photometry, fundus reflectance spectroscopy, Raman spectrometry, and autofluorescence spectrometry. Among them, autofluorescence spectrometry using a two-wavelength method is independent of the psychophysical methods and is considered to have the highest reproducibility.
Central serous chorioretinopathy (CSC) is characterized by serous detachment of the neural retina, which also can affect the macula and develop bilaterally. Associations with a type A personality, the use of corticosteroids, and pregnancy have been suggested, but the pathogenesis is still unknown. MPOD in eyes with CSC has not been previously evaluated.
Methods and Results
In the present study, the researchers measured MPOD and compared results in Japanese patients with CSC with those in normal subjects. MPOD was measured by autofluorescence spectrometry by using a two-wavelength. Central retinal thickness (CRT) was measured with optical coherence tomography. Statistical analyses were performed to determine factors associated with MPOD.
Ninety-four eyes of 94 normal control subjects, 123 eyes of 70 patients with chronic CSC, and 74 eyes of 41 patients with acute CSC were included. The mean MPOD was 0.548 density unit (DU) in the control group. Stepwise regression analysis of the control group showed that CRT was associated positively with MPOD. The mean MPOD was 0.386 DU in the eyes with chronic CSC, 0.443 DU in fellow eyes with chronic CSC, 0.542 DU in affected eyes with acute CSC, and 0.528 DU in fellow eyes with acute CSC. Stepwise regression analysis showed a significant association between eyes with a lower MPOD and affected eyes with chronic CSC (P = 0.0126) and fellow eyes with chronic CSC (P = 0.0023) and a thinner central retina (P = 0.0016).
Discussion and Conclusions
This study used autofluorescence spectrometry to evaluate MPOD in a control group and in two groups of patients with CSC. Among the several methods of estimating MPOD, autofluorescence spectrometry is considered to have the highest reproducibility.
The researchers found that MPOD at an eccentricity of 0.5° was 0.548 DU in normal subjects. CRT was moderately positively correlated with MPOD in normal subjects.
The investigators then evaluated the association between MPOD and CSC. The mean MPOD in all eyes with CSC was 0.456 DU, which differed significantly from the control eyes. Among the characteristics in affected eyes, the CRT correlated positively with MPOD in the affected eyes with chronic CSC, as seen in normal subjects.
When it was compared between the control group and the CSC subgroups, MPOD in the affected and fellow eyes with chronic CSC was significantly lower than in the control eyes (FIGURE). The central retina in eyes with chronic CSC is thin and correlates with disease duration based on OCT studies. The present study also showed that the central retina in eyes with chronic and acute CSC was significantly thinner than in normal subjects. Therefore, a thinner central retina may result in a low MPOD in the affected eyes with chronic CSC for the same reason as in normal eyes.
The duration of the SRD also was considered to be associated with lower MPOD, independent of the morphologic retinal changes in eyes with chronic CSC. The long-term persistence of subretinal fluid may disrupt the macular pigment supply from the RPE–choroid complex and cause a shortage in the retina. These possibilities suggest that the lower MPOD in CSC eyes is the result of the disease.
The results of regression analysis showed that the affected and fellow eyes with chronic CSC had significantly lower MPOD independent of CRT. This suggests that eyes with low MPOD are likely to develop chronic CSC. This hypothesis is supported by the finding of lower MPOD in fellow eyes with chronic CSC, although the CRT was maintained.
In conclusion, low MPOD may be a risk factor for the development of chronic CSC, and a decrease in MPOD may be accelerated by a thinning central retina. The exact relationship between low MPOD and development of chronic CSC is unknown; however, this study suggests the possibility that the supplementation of macular pigment suppresses the development or progression of chronic CSC.
WHAT IT MEANS TO YOU: The cause of CSC is not clearly understood, but there is good evidence that CSC is primarily a disease of the choroid. Imaging technology has revealed abnormal fluid leakage from choroidal blood vessels in patients with CSC. However, breakdown in retinal pigment epithelial (RPE) function may also play a role in the development of CSC. It is unclear whether (or how) MPOD deficiencies might contribute to this disease. It is possible that low MPOD might be an effect, rather than a cause of the disease. This is the first study to examine the possible relation between MPOD and CS, and as is so often the case, it raises more questions than it answers.
Source:
Invest Ophthalmol Vis Sci. 2010 Oct;51(10):5219-25. Epub 2010 May 5.
http://www.ncbi.nlm.nih.gov/pubmed/20445108
Macular pigment is composed of three carotenoids (i.e., lutein, zeaxanthin, and meso-zeaxanthin). Lutein and zeaxanthin can be obtained only from food, and meso-zeaxanthin is synthesized mainly from retinal lutein.
Macular pigment has light-absorbing properties and is thought to filter blue light, which is toxic to the photoreceptors. In addition, macular pigment itself has an antioxidant effect. It quenches excited triplet states, reacts with singlet oxygen and free radicals, and inhibits peroxidation of long-chain polyunsaturated fatty acids. Thus, it helps retard some destructive processes in the retina and the retinal pigment epithelium (RPE), which may lead to macular diseases such as age-related macular degeneration (AMD).
Some investigators have tried to determine the amount of macular pigment and elucidate factors affecting macular pigment. However, whether macular pigment optical density (MPOD) is affected by aging, sex, and smoking is still controversial. In those studies, several clinical methods of measuring MPOD were used, including heterochromatic flickering photometry, motion detection photometry, fundus reflectance spectroscopy, Raman spectrometry, and autofluorescence spectrometry. Among them, autofluorescence spectrometry using a two-wavelength method is independent of the psychophysical methods and is considered to have the highest reproducibility.
Central serous chorioretinopathy (CSC) is characterized by serous detachment of the neural retina, which also can affect the macula and develop bilaterally. Associations with a type A personality, the use of corticosteroids, and pregnancy have been suggested, but the pathogenesis is still unknown. MPOD in eyes with CSC has not been previously evaluated.
Methods and Results
In the present study, the researchers measured MPOD and compared results in Japanese patients with CSC with those in normal subjects. MPOD was measured by autofluorescence spectrometry by using a two-wavelength. Central retinal thickness (CRT) was measured with optical coherence tomography. Statistical analyses were performed to determine factors associated with MPOD.
Ninety-four eyes of 94 normal control subjects, 123 eyes of 70 patients with chronic CSC, and 74 eyes of 41 patients with acute CSC were included. The mean MPOD was 0.548 density unit (DU) in the control group. Stepwise regression analysis of the control group showed that CRT was associated positively with MPOD. The mean MPOD was 0.386 DU in the eyes with chronic CSC, 0.443 DU in fellow eyes with chronic CSC, 0.542 DU in affected eyes with acute CSC, and 0.528 DU in fellow eyes with acute CSC. Stepwise regression analysis showed a significant association between eyes with a lower MPOD and affected eyes with chronic CSC (P = 0.0126) and fellow eyes with chronic CSC (P = 0.0023) and a thinner central retina (P = 0.0016).
Discussion and Conclusions
This study used autofluorescence spectrometry to evaluate MPOD in a control group and in two groups of patients with CSC. Among the several methods of estimating MPOD, autofluorescence spectrometry is considered to have the highest reproducibility. The researchers found that MPOD at an eccentricity of 0.5° was 0.548 DU in normal subjects. CRT was moderately positively correlated with MPOD in normal subjects.
The investigators then evaluated the association between MPOD and CSC. The mean MPOD in all eyes with CSC was 0.456 DU, which differed significantly from the control eyes. Among the characteristics in affected eyes, the CRT correlated positively with MPOD in the affected eyes with chronic CSC, as seen in normal subjects.
When it was compared between the control group and the CSC subgroups, MPOD in the affected and fellow eyes with chronic CSC was significantly lower than in the control eyes (FIGURE). The central retina in eyes with chronic CSC is thin and correlates with disease duration based on OCT studies. The present study also showed that the central retina in eyes with chronic and acute CSC was significantly thinner than in normal subjects. Therefore, a thinner central retina may result in a low MPOD in the affected eyes with chronic CSC for the same reason as in normal eyes.
The duration of the SRD also was considered to be associated with lower MPOD, independent of the morphologic retinal changes in eyes with chronic CSC. The long-term persistence of subretinal fluid may disrupt the macular pigment supply from the RPE–choroid complex and cause a shortage in the retina. These possibilities suggest that the lower MPOD in CSC eyes is the result of the disease.
The results of regression analysis showed that the affected and fellow eyes with chronic CSC had significantly lower MPOD independent of CRT. This suggests that eyes with low MPOD are likely to develop chronic CSC. This hypothesis is supported by the finding of lower MPOD in fellow eyes with chronic CSC, although the CRT was maintained.
In conclusion, low MPOD may be a risk factor for the development of chronic CSC, and a decrease in MPOD may be accelerated by a thinning central retina. The exact relationship between low MPOD and development of chronic CSC is unknown; however, this study suggests the possibility that the supplementation of macular pigment suppresses the development or progression of chronic CSC.
WHAT IT MEANS TO YOU: The cause of CSC is not clearly understood, but there is good evidence that CSC is primarily a disease of the choroid. Imaging technology has revealed abnormal fluid leakage from choroidal blood vessels in patients with CSC. However, breakdown in retinal pigment epithelial (RPE) function may also play a role in the development of CSC. It is unclear whether (or how) MPOD deficiencies might contribute to this disease. It is possible that low MPOD might be an effect, rather than a cause of the disease. This is the first study to examine the possible relation between MPOD and CS, and as is so often the case, it raises more questions than it answers.
Source:
Invest Ophthalmol Vis Sci. 2010 Oct;51(10):5219-25. Epub 2010 May 5.
http://www.ncbi.nlm.nih.gov/pubmed/20445108