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The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The authors have no proprietary interests in this report. Genead and Fishman, and Martin Lindeman, COMT, have presented a year-old man who was first seen in with good central vision and multiple yellowish flecks throughout the posterior pole of each eye, sparing each macula.
He had no night blindness or dyschromatopsia. Long term follow-up showed no significant progression of fundus abnormalities. Pennesi and Traboulsi have provided us with a differential diagnosis. Allowing for wide variation of phenotypes that can be associated with the same gene, the differential is as follows: I.
Gene Mutation A.
ABCA4 1. Fundus flavimaculatus B. PRPH2 1. ELOVL4 1. BEST1 1. Adult onset foveomacular vitelliform dystrophy 3. EFEMP1 1. Dominant drusen 3. Malattia Leventinese II. Other Flecked Retina Syndromes A. Benign flecked retinal detachment B.
Kjellin syndrome D. Fundus albipunctatus F. Retinitis punctata albescens Dr. Pennisi notes that the yellowish fleck lesions bore a resemblance to fundus flavimaculatus caused by ABCA4 mutations, but cautions that PRPH2 mutations have also been shown to cause fundus flavimaculatus-like dystrophies. At the end of the day, he feels this patient has a mutation in ABCA4 causing a fundus flavimaculatus appearance and preserved foveal function. Follow-up A blood sample was drawn and sent for genetic molecular analysis.
The genetic results, absence of a dark choroid on FA, absence of relative peripapillary sparing of pigmentary changes as noted in Stargardt disease , and the positive family history of a paternal central retinal pigmentary degeneration the latter suggestive of autosomal dominant disease , are collectively most consistent with the diagnosis of pattern dystrophy. Genead et al. Page 3 throughout the posterior pole and mid-peripheral retina which continued to spare the foveola.
The flecks were more extensive than those noted on prior exams. NIH-PA Author Manuscript At his most recent visit, which was 29 years after the initial visit, subjectively the patient still did not notice any changes in his central or peripheral vision, night vision or color vision.
The corneas and anterior chambers were clear while the lenses showed trace nuclear sclerosis in each eye. Dilated fundus examination showed diffuse flecks throughout the posterior pole and mid- peripheral retina with a relative sparing of the foveola.
The peripheral retina, optic discs, and retinal vessels were normal Figure 1A—B. Fundus autofluorescence AF testing was performed. AF images showed diffuse foci of hyper-autofluorescence scattered throughout the posterior pole and mid- peripheral retina associated with the fundus flecks. There were also scattered foci of hypo- autofluorescence within the posterior pole Figures 1C—F.
NIH-PA Author Manuscript The most recent visual field testing by Goldmann kinetic perimetry showed small paracentral scotomas to a IIe target which were not apparent on his prior visual field tests.
Additionally, the OCT scans showed focal areas of the photoreceptor layer disruption within the posterior pole of the fundus Figures 2A—F. Questions for Discussants 1. What would be the differential diagnosis of the ocular disease in this patient? What is the most likely diagnosis in this patient?
We asked several experts for their opinion. Mark Pennesi, Portland, Oregon In this case, we are presented with a year-old white male, who has good central visual acuity, mild visual disturbances as measured with an Amsler grid, and multiple yellowish-white fleck- like lesions in the posterior pole of each eye, which spare the fovea.
Twenty-nine years after the first visit, the patient still only manifests mild visual disturbances; in spite of the worsening of the flecks in the posterior pole. Pertinent negatives include a lack of photophobia, color vision defects, or nyctalopia.
The patient also has a notable family history for paternal grandparents who were first cousins and a father with perifoveal pigmentary changes with impaired central vision.
Page 4 The bilateral and symmetric nature of the disease and the family history is suggestive of a genetic cause for these findings. The history of consanguinity would raise the risk for a recessively inherited disease.
If we assume the patient indeed harbors the same mutation as his NIH-PA Author Manuscript father, then x-linked or mitochondrial inheritance can be ruled out. Two possibilities remain: dominant inheritance or autosomal recessive with pseudo-dominant inheritance. In the case of dominant inheritance, the patient's father would have a new mutation, which the patient received.
In pseudo-dominance, the patient's father would have received one recessive mutation from each parent and subsequently pass one copy to the patient. In addition, the patient's mother would have to be a carrier of the same recessive mutation, which was also passed on to the patient.
Several less common syndromes can also cause retinal flecks such as: benign fleck retina, flecks of Kandori, Kjellin syndrome, Alport syndrome, fundus albipunctatus, and retinitis punctata albescens.
Several of these can be ruled out based on the lack of systemic findings and appearance.
Benign fleck retina and flecks of Kandori present with flecks in the periphery and do not involve the macula as seen with this patient. Kjellin syndrome presents with the constellation of fleck lesions, spastic paraplegia, mental retardation, and amyotropia. Alport syndrome is usually X- linked, although a minority of cases can be inherited autosomal recessively.
The patient does have high frequency hear loss, which can be seen in Alport's, but we are led to believe that this NIH-PA Author Manuscript is secondary to his occupation. Furthermore, there is no evidence to support a history of nephritis or anterior lenticonus, which is typical in Alport syndrome.
The normal dark adaptation and the appearance of the flecks make fundus albipunctatus unlikely. The lack of peripheral visual field loss and nyctalopia also eliminate retinitis punctata albescens.
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