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Table. LogMAR Visual Acuity and Mean Deviation of Standard Automated Perimetry
Table. LogMAR Visual Acuity and Mean Deviation of Standard Automated Perimetry
1.
Bengtsson BO. Incidence of manifest glaucoma.  Br J Ophthalmol. 1989;73(7):483-487PubMedArticle
2.
Johnson LN, Guy ME, Krohel GB, Madsen RW. Levodopa may improve vision loss in recent-onset, nonarteritic anterior ischemic optic neuropathy.  Ophthalmology. 2000;107(3):521-526PubMedArticle
3.
Quigley HA. Can diabetes be good for glaucoma? why can't we believe our own eyes (or data)?  Arch Ophthalmol. 2009;127(2):227-229PubMedArticle
4.
Gordon MO, Beiser JA, Brandt JD,  et al.  The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma.  Arch Ophthalmol. 2002;120(6):714-720PubMedArticle
5.
Gordon MO, Beiser JA, Kass MA.Ocular Hypertension Treatment Study Group.  Is a history of diabetes mellitus protective against developing primary open-angle glaucoma?  Arch Ophthalmol. 2008;126(2):280-281PubMedArticle
6.
Hayreh SS, Zimmerman MB. Nonarteritic anterior ischemic optic neuropathy: clinical characteristics in diabetic patients vs nondiabetic patients.  Ophthalmology. 2008;115(10):1818-1825PubMedArticle
Research Letters
Aug 2011

Early Diabetes Mellitus or Hypertension Is Not Significantly Associated With Severity of Vision Loss in Nonarteritic Anterior Ischemic Optic Neuropathy

Author Affiliations

Author Affiliations: Neuro-Ophthalmology Unit, Mason Eye Institute, University of Missouri–Columbia.

Arch Ophthalmol. 2011;129(8):1106-1107. doi:10.1001/archophthalmol.2011.209

Glaucoma is a progressive optic neuropathy with features similar to nonarteritic anterior ischemic optic neuropathy (NAION), the most common optic neuropathy causing acute vision loss. Glaucoma has an annual incidence rate of 240 per capita, while NAION has an annual incidence of 2.3 per capita among individuals older than 50 years.1,2 Early diabetes mellitus (DM)—defined as an absence of clinically visible diabetic retinopathy—may be associated with upregulation and downregulation of intraocular interferon, interleukins, and other cytokines promoting neuroprotection.3 The initial Ocular Hypertension Treatment Study report documented a protective effect of early DM in glaucoma development, but reanalysis showed no effect.4,5 Studies have shown DM to be a risk factor for NAION, but it is possible that early DM could have neuroprotective effects in NAION. Hayreh and Zimmerman6 had documented less severe visual field loss for diabetic patients with NAION. However, 11% of their participants had juvenile diabetes, 36% had diabetic retinopathy, and the investigators had used manual kinetic perimetry. To discern the role of early DM in NAION, we have studied patients aged 50 years or older without diabetic retinopathy using automated static perimetry.

Methods

We reviewed the records of all patients with NAION evaluated by the neuro-ophthalmology service between October 1990 and August 2009, after obtaining institutional review board approval. Criteria for NAION were similar to those used in past studies.2 Patients were excluded if they had significant cataract, presumed toxic causes of NAION such as amiodarone hydrochloride or erectile dysfunction drug use, perioperative NAION, diabetic retinopathy, temporal arteritis, or other disorders that could cause the vision loss. A standardized comprehensive medical history and comprehensive neuro-ophthalmologic examination were obtained for all patients, including best-corrected visual acuity, Humphrey automated perimetry program 24-2 or 30-2 Swedish interactive thresholding algorithm fast results, and dilated ophthalmoscopy.

Patients were classified as having DM with or without hypertension or not having DM with or without hypertension. Diabetes was identified if the patient had been diagnosed by the primary care physician as having DM or if the patient had been prescribed oral hypoglycemic medications or insulin prior to NAION. Patients with hypertension had been prescribed antihypertensive medications. Usable visual fields had less than 33% fixation loss, false-negative errors, and false-positive errors. Statistical analyses were performed with SAS version 9 statistical software (SAS Institute, Inc, Cary, North Carolina). We compared categorical variables such as sex with χ2 test, ordinal variables such as age with Wilcoxon rank sum test, and logMAR visual acuity and mean deviation on visual field with 2-sample t test and analyses of variance and covariance.

Results

A total of 206 patients (53 with DM [43 having hypertension] and 153 without DM [73 having hypertension]) who were aged 50 years or older (mean age, 65.1 years; male, 122 [59%]) qualified for the study. There were 176 usable visual fields (45 with DM and 131 without DM). There was no significant difference in logMAR visual acuity (P = .77) for DM (mean [SD], 0.81 [0.71]) and no DM (mean [SD], 0.84 [0.79]) or when accounting for the presence or absence of hypertension (P = .10) (Table). There was no significant difference in visual field mean deviation (P = .52) for DM (mean [SD], −18.5 [9.8] dB) and no DM (mean [SD], −17.5 [9.1] dB) or when accounting for the presence or absence of hypertension (P = .34). There was no trend for better (or worse) visual field for DM compared with no DM (Cochran-Armitage test, P = .79).

Comment

Among patients with NAION, those with early DM had a similar degree of visual acuity and visual field loss compared with those without DM. There was no trend for patients with early DM to have a better or worse visual field after NAION compared with patients without DM. Early DM is neither protective nor harmful in NAION with respect to the severity of vision loss.

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Article Information

Correspondence: Dr Johnson, Neuro-Ophthalmology Unit, Mason Eye Institute, University of Missouri–Columbia, 1 Hospital Dr, Columbia, MO 65212 (johnsonln@health.missouri.edu).

Financial Disclosure: None reported.

Funding/Support: This work was supported in part by an unrestricted grant from Research to Prevent Blindness, Inc, New York, New York, to the Department of Ophthalmology, University of Missouri–Columbia.

References
1.
Bengtsson BO. Incidence of manifest glaucoma.  Br J Ophthalmol. 1989;73(7):483-487PubMedArticle
2.
Johnson LN, Guy ME, Krohel GB, Madsen RW. Levodopa may improve vision loss in recent-onset, nonarteritic anterior ischemic optic neuropathy.  Ophthalmology. 2000;107(3):521-526PubMedArticle
3.
Quigley HA. Can diabetes be good for glaucoma? why can't we believe our own eyes (or data)?  Arch Ophthalmol. 2009;127(2):227-229PubMedArticle
4.
Gordon MO, Beiser JA, Brandt JD,  et al.  The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma.  Arch Ophthalmol. 2002;120(6):714-720PubMedArticle
5.
Gordon MO, Beiser JA, Kass MA.Ocular Hypertension Treatment Study Group.  Is a history of diabetes mellitus protective against developing primary open-angle glaucoma?  Arch Ophthalmol. 2008;126(2):280-281PubMedArticle
6.
Hayreh SS, Zimmerman MB. Nonarteritic anterior ischemic optic neuropathy: clinical characteristics in diabetic patients vs nondiabetic patients.  Ophthalmology. 2008;115(10):1818-1825PubMedArticle
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