{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T15:29:15Z","timestamp":1787758155770,"version":"build-2784847793"},"reference-count":28,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Wilson's disease (WD) is an autosomal recessive disorder of copper metabolism. We aimed to study the abnormalities in the retinal layers in patients with WD using optical coherence tomography (OCT).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>The study is a chart review of 16 patients with WD (six females) who underwent OCT at our hospital during follow-up visits. Spectral-domain OCT was performed in all subjects to assess the thickness of macula and retinal nerve fiber layer (RNFL) and the data was compared with 14 healthy controls (three females).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      The mean age of the patients was 20.81 \u00b1 7.47 years and controls was 26.86 \u00b1 9.95 years. The mean age at the onset of the illness was 16.25 \u00b1 5.57 years (range 11\u201328 years) with the mean duration of illness being 4.81 \u00b1 3.31 years at the final follow-up examination. The mean macular thickness was found to be significantly reduced in patients (232.13 \u00b1 19.39) when compared to controls (271.30 \u00b1 17.32 \u03bcm;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.01). There was a significant difference in the ganglion cell and inner plexiform (GCIP) layer between the patients (86.83 \u00b1 8.20 \u03bcm) and controls (97.72 \u00b1 5.31 \u03bcm;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.01). In addition, the outer nuclear layer with the photoreceptor layer (ONL + PRL) thickness was also reduced in WD (93.90 \u00b1 10.23 \u03bcm vs. 108.43 \u00b1 10.00 \u03bcm;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.01) There was no change in the RNFL thickness, between the two groups (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.53).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Abnormalities of the retinal layers were observed in the patients with WD. OCT is a non-invasive tool to identify and quantify the abnormalities of the retinal layers.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.4103\/aian.aian_865_21","type":"journal-article","created":{"date-parts":[[2022,7,14]],"date-time":"2022-07-14T06:52:00Z","timestamp":1657781520000},"page":"852-857","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":2,"title":["Retinal Degeneration in Patients with Wilson's Disease"],"prefix":"10.4103","volume":"25","author":[{"given":"Amitabh","family":"Bhattacharya","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Albert","family":"Stezin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nitish","family":"Kamble","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PM","family":"Mohammed Shereef","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bakula","family":"Kashyap","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pramod Kumar","family":"Pal","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-18-20240828","doi-asserted-by":"crossref","first-page":"344","DOI":"10.1038\/ng1293-344","article-title":"The Wilson disease gene is a copper transporting ATPase with homology to the Menkes disease gene","volume":"5","author":"Tanzi","year":"1993","journal-title":"Nat Genet"},{"key":"R2-18-20240828","doi-asserted-by":"crossref","first-page":"639","DOI":"10.1016\/j.parkreldis.2010.07.007","article-title":"Genetics of Wilsons disease","volume":"16","author":"Behari","year":"2010","journal-title":"Parkinsonism Relat Disord"},{"key":"R4-18-20240828","doi-asserted-by":"crossref","first-page":"21","DOI":"10.1038\/s41572-018-0018-3","article-title":"Wilson disease","volume":"4","author":"Cz\u0142onkowska","year":"2018","journal-title":"Nat Rev Dis Primers"},{"key":"R5-18-20240828","doi-asserted-by":"crossref","first-page":"165","DOI":"10.1016\/S0168-8278(00)00028-3","article-title":"The Wilson's disease gene and phenotypic diversity","volume":"34","author":"Riordan","year":"2001","journal-title":"J Hepatol"},{"key":"R6-18-20240828","doi-asserted-by":"crossref","first-page":"1234","DOI":"10.1002\/hep.1840120526","article-title":"Perspectives on Wilson's disease","volume":"12","author":"Sternlieb","year":"1990","journal-title":"Hepatology"},{"key":"R7-18-20240828","doi-asserted-by":"crossref","first-page":"103","DOI":"10.1016\/S1474-4422(14)70190-5","article-title":"Wilson's disease and other neurological copper disorders","volume":"14","author":"Bandmann","year":"2015","journal-title":"Lancet Neurol"},{"key":"R8-18-20240828","doi-asserted-by":"crossref","first-page":"794","DOI":"10.1136\/bjo.54.12.794","article-title":"Kayser-Fleischer ring. 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