Does levodopa improve vision in albinism? Results of a randomized, controlled clinical trial
Background Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safet...
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| Published in | Clinical & experimental ophthalmology Vol. 42; no. 8; pp. 713 - 721 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Australia
Blackwell Publishing Ltd
01.11.2014
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1442-6404 1442-9071 1442-9071 |
| DOI | 10.1111/ceo.12325 |
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| Abstract | Background
Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safety and effectiveness of levodopa on best‐corrected visual acuity in human subjects with albinism.
Design
Prospective, randomized, placebo‐controlled, double‐masked clinical trial conducted at the University of Minnesota.
Participants
Forty‐five subjects with albinism.
Methods
Subjects with albinism were randomly assigned to one of three treatment arms: levodopa 0.76 mg/kg with 25% carbidopa, levodopa 0.51 mg/kg with 25% carbidopa, or placebo and followed for 20 weeks, with best‐corrected visual acuity measured at enrollment, and at weeks 5, 10, 15, and 20 after enrollment. Side‐effects were recorded with a symptom survey. Blood was drawn for genotyping.
Main Outcome Measures
Side‐effects and best‐corrected visual acuity 20 weeks after enrolment.
Results
All subjects had at least one mutation found in a gene known to cause albinism. Mean age was 14.5 years (range: 3.5 to 57.8 years). Follow up was 100% and compliance was good. Minor side‐effects were reported; there were no serious adverse events. There was no statistically significant improvement in best‐corrected visual acuity after 20 weeks with either dose of levodopa.
Conclusions
Levodopa, in the doses used in this trial and for the time course of administration, did not improve visual acuity in subjects with albinism. |
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| AbstractList | Background
Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safety and effectiveness of levodopa on best‐corrected visual acuity in human subjects with albinism.
Design
Prospective, randomized, placebo‐controlled, double‐masked clinical trial conducted at the University of Minnesota.
Participants
Forty‐five subjects with albinism.
Methods
Subjects with albinism were randomly assigned to one of three treatment arms: levodopa 0.76 mg/kg with 25% carbidopa, levodopa 0.51 mg/kg with 25% carbidopa, or placebo and followed for 20 weeks, with best‐corrected visual acuity measured at enrollment, and at weeks 5, 10, 15, and 20 after enrollment. Side‐effects were recorded with a symptom survey. Blood was drawn for genotyping.
Main Outcome Measures
Side‐effects and best‐corrected visual acuity 20 weeks after enrolment.
Results
All subjects had at least one mutation found in a gene known to cause albinism. Mean age was 14.5 years (range: 3.5 to 57.8 years). Follow up was 100% and compliance was good. Minor side‐effects were reported; there were no serious adverse events. There was no statistically significant improvement in best‐corrected visual acuity after 20 weeks with either dose of levodopa.
Conclusions
Levodopa, in the doses used in this trial and for the time course of administration, did not improve visual acuity in subjects with albinism. Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safety and effectiveness of levodopa on best-corrected visual acuity in human subjects with albinism.BACKGROUNDDopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safety and effectiveness of levodopa on best-corrected visual acuity in human subjects with albinism.Prospective, randomized, placebo-controlled, double-masked clinical trial conducted at the University of Minnesota.DESIGNProspective, randomized, placebo-controlled, double-masked clinical trial conducted at the University of Minnesota.Forty-five subjects with albinism.PARTICIPANTSForty-five subjects with albinism.Subjects with albinism were randomly assigned to one of three treatment arms: levodopa 0.76 mg/kg with 25% carbidopa, levodopa 0.51 mg/kg with 25% carbidopa, or placebo and followed for 20 weeks, with best-corrected visual acuity measured at enrollment, and at weeks 5, 10, 15, and 20 after enrollment. Side-effects were recorded with a symptom survey. Blood was drawn for genotyping.METHODSSubjects with albinism were randomly assigned to one of three treatment arms: levodopa 0.76 mg/kg with 25% carbidopa, levodopa 0.51 mg/kg with 25% carbidopa, or placebo and followed for 20 weeks, with best-corrected visual acuity measured at enrollment, and at weeks 5, 10, 15, and 20 after enrollment. Side-effects were recorded with a symptom survey. Blood was drawn for genotyping.Side-effects and best-corrected visual acuity 20 weeks after enrolment.MAIN OUTCOME MEASURESSide-effects and best-corrected visual acuity 20 weeks after enrolment.All subjects had at least one mutation found in a gene known to cause albinism. Mean age was 14.5 years (range: 3.5 to 57.8 years). Follow up was 100% and compliance was good. Minor side-effects were reported; there were no serious adverse events. There was no statistically significant improvement in best-corrected visual acuity after 20 weeks with either dose of levodopa.RESULTSAll subjects had at least one mutation found in a gene known to cause albinism. Mean age was 14.5 years (range: 3.5 to 57.8 years). Follow up was 100% and compliance was good. Minor side-effects were reported; there were no serious adverse events. There was no statistically significant improvement in best-corrected visual acuity after 20 weeks with either dose of levodopa.Levodopa, in the doses used in this trial and for the time course of administration, did not improve visual acuity in subjects with albinism.CONCLUSIONSLevodopa, in the doses used in this trial and for the time course of administration, did not improve visual acuity in subjects with albinism. Background Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safety and effectiveness of levodopa on best-corrected visual acuity in human subjects with albinism. Design Prospective, randomized, placebo-controlled, double-masked clinical trial conducted at the University of Minnesota. Participants Forty-five subjects with albinism. Methods Subjects with albinism were randomly assigned to one of three treatment arms: levodopa 0.76mg/kg with 25% carbidopa, levodopa 0.51mg/kg with 25% carbidopa, or placebo and followed for 20 weeks, with best-corrected visual acuity measured at enrollment, and at weeks 5, 10, 15, and 20 after enrollment. Side-effects were recorded with a symptom survey. Blood was drawn for genotyping. Main Outcome Measures Side-effects and best-corrected visual acuity 20 weeks after enrolment. Results All subjects had at least one mutation found in a gene known to cause albinism. Mean age was 14.5 years (range: 3.5 to 57.8 years). Follow up was 100% and compliance was good. Minor side-effects were reported; there were no serious adverse events. There was no statistically significant improvement in best-corrected visual acuity after 20 weeks with either dose of levodopa. Conclusions Levodopa, in the doses used in this trial and for the time course of administration, did not improve visual acuity in subjects with albinism. Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a precursor to dopamine, levodopa, may improve visual acuity in albinism by enhancing neural networks. This study examines the safety and effectiveness of levodopa on best-corrected visual acuity in human subjects with albinism. Prospective, randomized, placebo-controlled, double-masked clinical trial conducted at the University of Minnesota. Forty-five subjects with albinism. Subjects with albinism were randomly assigned to one of three treatment arms: levodopa 0.76 mg/kg with 25% carbidopa, levodopa 0.51 mg/kg with 25% carbidopa, or placebo and followed for 20 weeks, with best-corrected visual acuity measured at enrollment, and at weeks 5, 10, 15, and 20 after enrollment. Side-effects were recorded with a symptom survey. Blood was drawn for genotyping. Side-effects and best-corrected visual acuity 20 weeks after enrolment. All subjects had at least one mutation found in a gene known to cause albinism. Mean age was 14.5 years (range: 3.5 to 57.8 years). Follow up was 100% and compliance was good. Minor side-effects were reported; there were no serious adverse events. There was no statistically significant improvement in best-corrected visual acuity after 20 weeks with either dose of levodopa. Levodopa, in the doses used in this trial and for the time course of administration, did not improve visual acuity in subjects with albinism. |
| Author | McKay, Brian S Holleschau, Ann M Connett, John E De Becker, Inge Brilliant, Murray H Summers, C Gail Anderson, Jennifer L |
| AuthorAffiliation | 2 Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA 6 Center for Human Genetics, Marshfield Clinic, Marshfield, WI, USA 5 Department of Ophthalmology and Vision Science, University of Arizona, Tucson, AZ, USA 3 School of Public Health, University of Minnesota, Minneapolis, MN, USA 4 Core Laboratory, Marshfield Clinic, Marshfield, WI, USA 1 Departments of Ophthalmology & Visual Neurosciences, University of Minnesota, Minneapolis, MN, USA |
| AuthorAffiliation_xml | – name: 6 Center for Human Genetics, Marshfield Clinic, Marshfield, WI, USA – name: 5 Department of Ophthalmology and Vision Science, University of Arizona, Tucson, AZ, USA – name: 1 Departments of Ophthalmology & Visual Neurosciences, University of Minnesota, Minneapolis, MN, USA – name: 3 School of Public Health, University of Minnesota, Minneapolis, MN, USA – name: 4 Core Laboratory, Marshfield Clinic, Marshfield, WI, USA – name: 2 Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA |
| Author_xml | – sequence: 1 givenname: C Gail surname: Summers fullname: Summers, C Gail email: summe001@umn.edu organization: Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, Minnesota, USA – sequence: 2 givenname: John E surname: Connett fullname: Connett, John E organization: School of Public Health, University of Minnesota, Minnesota, Minneapolis, USA – sequence: 3 givenname: Ann M surname: Holleschau fullname: Holleschau, Ann M organization: Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minnesota, Minneapolis, USA – sequence: 4 givenname: Jennifer L surname: Anderson fullname: Anderson, Jennifer L organization: Core Laboratory, Marshfield Clinic, Wisconsin, Marshfield, USA – sequence: 5 givenname: Inge surname: De Becker fullname: De Becker, Inge organization: Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minnesota, Minneapolis, USA – sequence: 6 givenname: Brian S surname: McKay fullname: McKay, Brian S organization: Department of Ophthalmology and Vision Science, University of Arizona, Arizona, Tucson, USA – sequence: 7 givenname: Murray H surname: Brilliant fullname: Brilliant, Murray H organization: Center for Human Genetics, Marshfield Clinic, Wisconsin, Marshfield, USA |
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Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that... Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that supplying a... Background Dopamine is an intermediate product in the biosynthesis of melanin pigment, which is absent or reduced in albinism. Animal research has shown that... |
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| SubjectTerms | Administration, Oral Adolescent Adult Albinism Albinism, Oculocutaneous - drug therapy Albinism, Oculocutaneous - genetics Albinism, Oculocutaneous - physiopathology Child Child, Preschool Clinical trials Dopamine Dopamine Agents - adverse effects Dopamine Agents - therapeutic use Double-Blind Method Female Humans levodopa Levodopa - adverse effects Levodopa - therapeutic use Male Middle Aged Neural networks Prospective Studies randomized controlled trial visual acuity Visual Acuity - drug effects Visual Acuity - physiology |
| Title | Does levodopa improve vision in albinism? Results of a randomized, controlled clinical trial |
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