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Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor

Patient: Female, 63 Final Diagnosis: Diabetic macular edema Symptoms: Visual disturbance Medication: — Clinical Procedure: Treatment with sodium glucose transporter 2 inhibitor Specialty: Ophthalmology OBJECTIVE: Unusual or unexpected effect of treatment BACKGROUND: Diabetic macular edema (DME) caus...

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Autores principales: Yoshizumi, Hideyuki, Ejima, Tetsushi, Nagao, Tetsuhiko, Wakisaka, Masanori
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928754/
https://www.ncbi.nlm.nih.gov/pubmed/29670074
http://dx.doi.org/10.12659/AJCR.909708
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author Yoshizumi, Hideyuki
Ejima, Tetsushi
Nagao, Tetsuhiko
Wakisaka, Masanori
author_facet Yoshizumi, Hideyuki
Ejima, Tetsushi
Nagao, Tetsuhiko
Wakisaka, Masanori
author_sort Yoshizumi, Hideyuki
collection PubMed
description Patient: Female, 63 Final Diagnosis: Diabetic macular edema Symptoms: Visual disturbance Medication: — Clinical Procedure: Treatment with sodium glucose transporter 2 inhibitor Specialty: Ophthalmology OBJECTIVE: Unusual or unexpected effect of treatment BACKGROUND: Diabetic macular edema (DME) causes serious visual impairments in diabetic patients. The standard treatments of DME are intra-vitreous injections of corticosteroids or anti-vascular endothelial growth factor antibodies and pan-photocoagulation. These treatments are unsatisfactory in their effects and impose considerable physical and economic burdens on the patients. CASE REPORT: A 63-year-old woman was diagnosed as type 2 diabetes with retinopathy 7 years ago. Before the initiation of an SGLT2 inhibitor, the dipeptidyl peptidase-4 inhibitor, sitagliptin (50 mg daily), and metformin (250 mg daily) were used for her glycemic control. The level of her hemoglobin A1c had been controlled around 7%. She began to feel decreased visual acuity and blurred vision of her left eye 8 months before the visit to our clinic. She was diagnosed as DME, which turned out to be corticosteroid-resistant. Her visual acuity further decreased to 20/50. Metformin was changed to ipragliflozin (25mg/day). Her left visual acuity started to improve after 4 weeks of treatment with ipragliflozin and improved to 20/22 after 24 weeks. The macular edema did not change until 12 weeks of the treatment, however, it decreased prominently after 16 weeks. CONCLUSIONS: In our patient with steroid-resistant DME, her visual symptoms and macular edema recovered after the initiation of an SGLT2 inhibitor. SGLT2 inhibitors might be a potential candidate for the DME treatment.
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spelling pubmed-59287542018-05-01 Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor Yoshizumi, Hideyuki Ejima, Tetsushi Nagao, Tetsuhiko Wakisaka, Masanori Am J Case Rep Articles Patient: Female, 63 Final Diagnosis: Diabetic macular edema Symptoms: Visual disturbance Medication: — Clinical Procedure: Treatment with sodium glucose transporter 2 inhibitor Specialty: Ophthalmology OBJECTIVE: Unusual or unexpected effect of treatment BACKGROUND: Diabetic macular edema (DME) causes serious visual impairments in diabetic patients. The standard treatments of DME are intra-vitreous injections of corticosteroids or anti-vascular endothelial growth factor antibodies and pan-photocoagulation. These treatments are unsatisfactory in their effects and impose considerable physical and economic burdens on the patients. CASE REPORT: A 63-year-old woman was diagnosed as type 2 diabetes with retinopathy 7 years ago. Before the initiation of an SGLT2 inhibitor, the dipeptidyl peptidase-4 inhibitor, sitagliptin (50 mg daily), and metformin (250 mg daily) were used for her glycemic control. The level of her hemoglobin A1c had been controlled around 7%. She began to feel decreased visual acuity and blurred vision of her left eye 8 months before the visit to our clinic. She was diagnosed as DME, which turned out to be corticosteroid-resistant. Her visual acuity further decreased to 20/50. Metformin was changed to ipragliflozin (25mg/day). Her left visual acuity started to improve after 4 weeks of treatment with ipragliflozin and improved to 20/22 after 24 weeks. The macular edema did not change until 12 weeks of the treatment, however, it decreased prominently after 16 weeks. CONCLUSIONS: In our patient with steroid-resistant DME, her visual symptoms and macular edema recovered after the initiation of an SGLT2 inhibitor. SGLT2 inhibitors might be a potential candidate for the DME treatment. International Scientific Literature, Inc. 2018-04-19 /pmc/articles/PMC5928754/ /pubmed/29670074 http://dx.doi.org/10.12659/AJCR.909708 Text en © Am J Case Rep, 2018 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Articles
Yoshizumi, Hideyuki
Ejima, Tetsushi
Nagao, Tetsuhiko
Wakisaka, Masanori
Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor
title Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor
title_full Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor
title_fullStr Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor
title_full_unstemmed Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor
title_short Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor
title_sort recovery from diabetic macular edema in a diabetic patient after minimal dose of a sodium glucose co-transporter 2 inhibitor
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928754/
https://www.ncbi.nlm.nih.gov/pubmed/29670074
http://dx.doi.org/10.12659/AJCR.909708
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