|Year : 2017 | Volume
| Issue : 1 | Page : 22-27
Congenital and acquired colour vision deficiency among population in North Kordofan State of Sudan
Saif Hassan Alrasheed, Mohamed EL Hassan Ali EL Awad, Ahmed Alsedeeiq Abdulbagi, Mustafa Abdu
Department of Binocular Vision, Faculty of Optometry and Visual Sciences, Al-Neelain University, Khartoum, Sudan
|Date of Web Publication||19-Sep-2017|
Saif Hassan Alrasheed
Faculty of Optometry and Visual Sciences, Al-Neelain University, Khartoum
Source of Support: None, Conflict of Interest: None
Background: Congenital colour vision deficiency (CVD) is an x-linked chromosome disorders which, predominantly occurring in males. This disorder results from abnormalities in one or all three-cone type's photoreceptors. It is mainly affect long wavelength photopigments (red) and middle wavelength photopigments (green). However, the acquired CVD is due to ocular or general pathology as well as due to prolonged use of some medications, which is mostly affect short wavelength photopigments (blue). Objective: This study aimed to evaluate the prevalence of hereditary and acquired CVDs among Sudanese population in North Kordofan State. Materials and Methods: This is a population-based crossed-sectional study of 1100 subjects, their age ranged from 10 to 80 years, the mean age of subjects was 40.4 ± 16.6 (standard deviation) were selected from three districts and 110 subjects were selected from each set. Investigations included visual acuity using Snellen tumbling E-chart, refraction using retinoscopy, colour vision using Ishihara and City University colour vision tests, external eye using torch and magnifier and evaluation of internal eye and ocular media using direct ophthalmoscope. Results: A total of 1216 subjects were invited to participate in the study and 1100 were examined resulting in a participation rate of 91%. The findings revealed that 61 (5.5%) had CVD, 49 (9.0%) were males and 12 (2.2%) were females. The prevalence of congenital (red-green) CVD was 39 (3.5%) which was high in males 37 (6.8%) than females 2 (0.4%). The prevalence of congenital CVD was found associated with males (P < 0.001), but was not significantly correlated with females (P = 0.165). The prevalence of acquired CVD was 22 (2.0%) which was slightly higher among males 12 (2.2%) compared to 10 (1.8%) in females. The distribution of protanopia, deuteranopia and tritanopia among males was 12 (2.2%), 25 (4.6%) and 12 (2.2%), respectively, which was high compared to 1 (0.2%), protanopia, 1 (0.2%), deuteranopia, and 10 (1.8%), tritanopia in females. The main leading cause of acquired CVD was cataract change 8 (13.1%) followed by myopic degeneration 6 (9.8%). Conclusion: Congenital and acquired CVD affect the colour perception of individual. Thus, the early assessment and diagnosis of CVD is necessary to avoid disappointment and psychological trauma during study and career choices.
Keywords: Acquired colour vision defect, congenital colour vision defect, deuteranopia, protanopia, tritanopia
|How to cite this article:|
Alrasheed SH, EL Awad ME, Abdulbagi AA, Abdu M. Congenital and acquired colour vision deficiency among population in North Kordofan State of Sudan. Sudanese J Ophthalmol 2017;9:22-7
|How to cite this URL:|
Alrasheed SH, EL Awad ME, Abdulbagi AA, Abdu M. Congenital and acquired colour vision deficiency among population in North Kordofan State of Sudan. Sudanese J Ophthalmol [serial online] 2017 [cited 2022 Aug 9];9:22-7. Available from: https://www.sjopthal.net/text.asp?2017/9/1/22/215109
| Introduction|| |
Colour vision deficient (CVD) people have difficulties to perceive certain spectral hues. Normal human colour depends on three cone mechanisms for red, green, and blue lights (trichromatic). Congenital CVD is caused by inherited photopigments abnormalities in which the retina might be lacking one functional cone photoreceptors, or there may be only one or two cone photopigments. It is commonly affect the photopigments of Long wavelength (red) and middle wavelength (green). Red and green CVD which known as protanopia and deueranopia respectively, is a genetic condition has high prevalence among males population. Defective colour vision can be acquired due to ocular, neurological or systemic diseases. There are many conditions might be affecting the colour perception, such as diseases of ocular media, visual pathway, and pathology of visual cortex, it is mostly affecting the photopigments of Short wavelength (blue-yellow). There are three types of colour vision impairment, monochromacy, dichomacy, and anomalous trichromacy. Monochromatism is uncommon condition, people with this type of CVD are totally colour blind and occurs when two or all three of cone pigments are missing. Dichromatism occurs when only one of cone pigments is missing and divided into protanopia (red cones being absent) has normal green and blue cones, Deuteranopia (green cones being absent) has normal red and blue cones and tritanopia (blue cone being absent) has normal red and green cones., Anomalous trichromatism, involves the presence of abnormal red, green or blue sensitive photopigments respectively. Anomalous trichromatism divided into protanomaly, deuteranomaly and tritanomaly in these conditions the spectral sensitivity of the red, green, and blue cones receptors is altered.
The prevalence of inherited (red-green) CVD was reported by Anthony and Gunilla to be 8.0% and 0.5% among males and females respectively. They indicated that the inherited CVD is sex-linked it is located on the X chromosome in females (XX), resulting in prevalence of CVD in females approximately (0.08 × 0.08 = 0.0064) = 0.64%, however, in males (XY) this lead to prevalence of CVD approximately 8%. The prevalence of congenital (red-green) CVD has been reported to be 8% and 4% in males and females respectively among European Caucasian populations, and estimated about 4% and 6.5% in males of Chinese and Japanese ethnicity. In Iran the prevalence of CVD in male individuals has been reported to be 3.5%. The overall prevalence of congenital CVD among Nigerian secondary school students was 2.3% with prevalence of 3.8% and 0.9% in males and females respectively. Patients affected with disorders such as media opacities; macular diseases, peripheral retinal lesion, glaucoma, diabetic retinopathy, optic neuropathies, and squint amblyopia show high prevalence of acquired CVD, amblyopic children show the lowest prevalence of acquired CVD.
In Sudan, there is paucity of studies conducted to assess the hereditary and acquired colour vision defects. This study aimed to assess the prevalence and pattern of hereditary and acquired colour vision defects among population in North Kordofan State of Sudan.
| Materials and Methods|| |
Study design and population
This was a cross-sectional, population-based study of the prevalence of congenital and acquired colour vision defect among people from North Kordofan State of Sudan. North Kordofan State is located in central Sudan, it is covers an area of 244,700 square km with a population of approximately 2.9 million people.
The study sample was selected through random cluster sampling. The sample size for the study was calculated by using the formula for estimating a single population proportion.
Where N = minimum required sample size, Z = value of z statistic at 95% confidence level = 1.96, P = assumed prevalence of congenital colour vision defects = 8% for maximum sample size, C = maximum acceptable sampling error = 1.6%.
In addition, considering a 10% nonparticipant rate (111), the final sample size of this study was determined to be 1216 subjects. These subjects were invited to participate in the study from different districts of North Kordofan State. At the end of the study, 1100 subjects were screened giving a response rate of 91%. Three districts were chosen from nine districts in North Kordofan State, these districts were selected by random cluster sampling from different regions (north, south, and west) of El-Obid the capital of North Kordofan State. Thus, 1100 subjects their age ranged from 10 to 80 years were selected from three districts of North Kordofan State (Barra, Sheikan, and Umruaba), these districts were divided into 10 sets, 110 subjects were randomly selected from each position. Informed consent was obtained from all participants in this study to facilitate a better understanding of conditions of involvement in the study before data collection processes.
Distance visual acuity (VA) was assessed using Snellen tumbling E-chart with E's of standard size at a 6-meter distance. Near vision was also examined by Jagger test at 33cm. Monocular and binocular testing were performed for each subject to show the efficiency of vision functions. All the subjects underwent a penlight and low power hand magnifier examination to rule out any anterior segment abnormalities in the following: Eyelids, conjunctiva and cornea. The inner eye was examined by direct ophthalmoscope. These examinations were performed to show any ocular diseases that may be related to colour vision defects. The refractive state of each eye was measured by retinoscopy (Neitz RX, Japan) to determine the types of refractive errors as well as to differentiate reduction of vision from other ocular diseases.
Colour vision tests were used in this study to differentiate mainly between congenital and acquired CVD and to determine the different types of colour vision defects. All the subjects were screened using (Ishihara's 38 plates test, Ophthalmedex, Japan) to identify congenital defects mainly red-green defect. The test was performed at near reading distance 33 cm for each eye separated and binocular at natural daylight condition. Thereafter, City University colour vision test was performed to identify acquired colour vision defects at near reading distance 33 cm for each eye separately and binocular at natural day light condition. Finally, City University colour vision test was conducted to differentiate between protanopia (red defect), deuteranopia (green defect), and tritanopia (blue defect) for affected colour vision subjects.
Data forms were reviewed for accuracy and completeness prior to data capture. The data entry was performed by the principal investigator, using the Statistical Package of Social Sciences software version 22 (SPSS version 22, Armonk, NY: IBM Corp USA). The data was checked for data entry errors before data analysis. The data for each subject were analysed descriptively using standard deviations (SDs), mode and percentages. The relationship between measures was determined using Person's coefficient correlation. For all statistical determinations, significance levels were established at P < 0.05.
| Results|| |
A total of 1216 subjects from three selected districts in North Kordofan Setae were invited to participate in this study. A total of 1100 subjects were presented at the sets on the examination days resulting in a participation rate of 91%. Thus, the results of those subjects were analysed as follows:
Sociodemographic characteristics of participants
The age of the subjects ranged from 10 to 80 years with mean of 40.4 ± 15.6 years (SD). There were 556 females representing 50.5% and 544 males representing 49.5% of the sample.
Anterior segment examination
Anterior segment examination revealed that, a total of 742 (67.5%) (95% confidence interval [CI], 65.9–69.1) of subjects had no significant abnormalities detected, followed by 153 (13.9%) (95% CI, 12.3–15.4) of subjects had allergic conjunctivitis. Other eye conditions were conjunctivitis (bacterial and viral), cataract, corneal opacity and pteryginm at 104 (9.4%) (95% CI, 7.8–10.9), 73 (6.6%) (95% CI, 5.0–8.2), 15 (1.4) (95% CI, 0.2–3.0) and 13 (1.2%) (95% CI, 0.4–2.8) respectively. The distributions of external eye diseases are presented in [Table 1].
Distribution of congenital and acquirer colour vision deficiency among subjects
The findings of congenital and acquired CVD among the 1100 subjects were shown in [Table 2]. The overall prevalence of congenital and acquired CVD among subjects was 61 (5.5%) (95% CI, 3.9–7.1). Prevalence was higher among males 49 (9.0%) (95% CI, 7.4–10.6) subjects than females 12 (2.2%) (95% CI, 0.6–3.8), and significantly more among aged group 41–50 and 51–60 years which was 16 (9.4%) (95% CI, 7.8–11.0) and 15 (9.1%) (95% CI, 7.5–10.6) respectively, compared to 6 (4.0%) (95% CI, 2.4–5.6) and 1 (0.9%) (95% CI, 0.7–2.5) in those age groups 10–20 and 71–80 years, respectively. The prevalence of congenital and acquired CVD was statistically significant for the association with age (P = 0.008) and gender (P < 0.001).
|Table 2: The prevalance of congental and aquried colour vision impairment according to age and gender|
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Prevalence of congenital colour vision defects
The findings of congenital CVD among the 1100 subjects were shown in [Table 3]. The prevalence of congenital (red-green) CVD was 39 (3.5%) (95% CI, 1.9–5.1) which was high in males 37 (6.8%) (95% CI, 5.2–8.4) than females 2 (0.6%) (95% CI, 1.0–2.2). The prevalence of congenital (red-green) CVD were associated with males (P < 0.001), but was not significantly associated with females (P = 0.165). The prevalence of protanopia and deueranopia was 13 (1.2%) and 26 (2.4%), respectively. The prevalence of protanopia and deuteranopia among males was 12 (2.2%) and 25 (4.6%) respectively, which was high compared to 1 (0.2%) protanopia and 1 (0.2%), deuteranopia in females, was statistically significant (P < 0.001).
|Table 3: The prevalance of congenital colour vision impairment according to age and gender|
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Prevalence acquired colour vision defects
The findings of acquired CVD among the 1100 subjects were shown in [Table 4]. The prevalence of acquired (blue-yellow) CVD was 22 (2.0%) (95% CI, 0.4–1.4) which was slightly high among males 12 (2.2%) (95% CI, 0.6–3.8) compared to 10 (1.8%) (95% CI, 0.2–3.4) in females. The prevalence of acquired CVD were more among aged group 51–60 years which was 8 (4.9%) (95% CI, 3.3–6.4) compared to 4 (2.3%) (95% CI, 0.7–3.9) and 1 (0.9%) (95% CI, 0.7–2.5) in those age groups 41–50 and 10–20 years, respectively.
|Table 4: The prevalance of aquried colour vision impairment according to age and gender|
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Causes of colour vision defect among subjects
The causes of colour vision defect among participants in one eye or both eyes are presented in [Table 5]. A total of 39 (63.9%) (95% CI, 62.3–65.5) of congenital CVD (red-green) had no abnormalities detected. Cataract changes was the main cause of acquired CVD (blue) in 8 (13.1%) (95% CI, 11.5–14.7) of the affected subjects followed by myopic degeneration in 6 (9.8%) (95% CI, 8.2–11.4). Retinal disorders (retinal degeneration, retinitis pigmentosa and age related macular degeneration) were the cause of acquired CVD (blue) in 4 (6.6%) (95% CI, 5.0–8.2) subjects. Albinisms accounted for 3 (4.9%) (95% CI, 3.3–6.5) subjects. Glaucoma was the cause of acquired CVD in 1 (1.6%) (95% CI, 0.0–3.2) subject.
Visual acuity and colour vision defect
The findings of presenting VA and type of colour vision defect among defective colour vision are shown in [Table 6]. A total of 34 (55.7%) of congenital CVD (red-green) had normal VA of 6/6, there are two protanopia subjects and one deuteranopia subject had VA of 6/9. The remaining colour vision defect the acquired type defects (blue-yellow) were associated with reduced VA ranged from 6/9 to 6/60.
|Table 6: Correlation between vision among subjects and types of colour vision defects|
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Uncorrected refractive error and colour vision defects
The results of the refractive conditions and types of colour vision defect among participants are demonstrated in [Table 7]. A total of 29 (47.5) (95% CI, 45.9–49.0) of congenital CVD (red-green) had normal refractive conditions. About 19 (31.2%) (95% CI, 29.6–32.7) of acquired CVD (blue-yellow) had myopic refractive conditions, which was statistical significant (P < 0.001).
|Table 7: Association between refractive condition among partcipants and types of colour visin defect|
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| Discussion|| |
Congenital colour vision defects
The prevalence of congenital colour vision in the present study (3.5%) was slightly higher compared to previous studies, which were conducted in some African countries, for example, in Libyan and Nigerian population, which reported to be 2.2% and 2.3% respectively. However, studies conducted among European Caucasian and Asian populations reported higher prevalence of congenital colour vision defect (8%–6.5%). The variation in the prevalence of colour vision defects could be attributed to racial differences.
In the current study, male subjects had a higher prevalence of congenial CVD 6.8% than females 0.6%, and the findings were comparable to that reported among females in KSA 0.35% and Ethiopian males and females which was 4.2% and 0.2% respectively. This may be attributed to the X-linked inheritance deficiency; the males have one X chromosome and females two. Thus, the males have higher prevalence of Congenital CVD than females. In this study, males more affected with CVD than females, so the association between gender and congenital CVD was statistical significant (P < 0.001).
Acquired colour vision defects
The prevalence of acquired colour vision defects in this study was 22 (2.0%), which was slightly higher among males12 (2.2%) than females 10 (1.8%). This could be attributed to males are more working in outdoors conditions than females resulting development of cataract, this lead to change of colour of crystalline lens from transparent to yellow which was acts as filtering and affect the shot-wavelength. This clear in this study, the leading cause of acquired colour vision defect tritanopia (blue-yellow) cataract change which was responsible for 8 (13.1%) of affected subjects. Pacheco-Cutillas et al. indicated that the acquired colour vision defects are equally distributed between males and females, because these types of colour vision defects are due to secondary causes. Moreover, Anthony and Gunilla they reported that there are three mechanism of acquired colour vision defects; absorption (filtering) this occur with excessive yellowing of crystalline lens; or red-filtering effect of a vitreous hemorrhage; alteration result of absorption spectra of the photopigments are altered and reduction results when a pigment is lost.
The second leading cause of acquired colour vision defects was myopic degeneration account in 6 (9.8%) for affected subjects. Mäntyjärvi and Tuppurainen they reported that the myopic refractive cause blue-yellow colour vision defects, they concluded that “the stretching of the posterior pole of the eye might explain this minimal impairment of photoreceptors layer of the retina.” In this study, acquired colour vision defects (tritanopia) was associated with myopic refractive error, which was statistical significant (P < 0.00 1). Retinal disorders also affected the colour perception in our study sample, this result agree with Heon et al. they reported that the retinal disorders lead to colour vision defects. In the current study, the acquired CVD was found in patients with glaucoma and an albino, which is similar to other studies., The present study had some limitations; the sample included in this study was small, because the assessment of congenital and acquired colour vision defects need the large populations sample and colour vision tests, which were used in this study Ishihara, and city university, cannot differentiate between dichromatism and anomalous trichromatism.
| Conclusion|| |
The prevalence of congenital CVD among males and females was 6.8% and 0.6% respectively. However, the prevalence of acquired CVD 2.0% similar among males and females. The findings of the current study revealed that there is high proportion of congenital and acquired colour vision defects among population of North Kordofan State of Sudan. Thus, early assessment and counselling of colour vision defects could be beneficial for affected subjects as well as to avoided disappointment and trauma during profession choices.
We are grateful to the staff of faculty of optometry and visual sciences Al-Neelain University for their help in data collection. We would also like to thanks all the people who participated in this study.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]