Retinal Vessel Diameter Changes in Relation to Dark Adaptation and Acute Hyperglycemia

The purpose of this experimental clinical study was to assess the effects of dark adaptation and acute changes in glycemia on retinal vessel diameters in men. The study included 14 patients (mean age 63 years, range 48–74 years) with type 2 diabetes mellitus and minimal or no diabetic retinopathy. Retinal vessel diameters were assessed using infrared photography before and after dark adaptation, first while fasting and then at peak hyperglycemia during an oral glucose tolerance test (OGTT). Dark adaptation was accompanied by retinal vasodilatation, both during fasting (mean glycemia 7.6 ± 1.7 mM) and postprandial hyperglycemia (15.7 ± 4.2 mM). When fasting, the increase in vein diameter during dark adaptation was 2.0% after 20 min (P=0.018) and 2.9% after 40 min (P=0.010). When subjects were hyperglycemic, the increase during dark adaptation was 2.8% for retinal vein diameters (P=0.027) and 2.0% for retinal artery diameters after 20 min (P=0.002) and 1.7% for retinal artery diameters after 40 min (P=0.022). For identical conditions of light/dark adaptation, retinal vessels were dilated when subjects were fasting compared to postprandial hyperglycemia. Thus, darkness and fasting were both associated with retinal vasodilation in this short-term experiment in patients with type 2 diabetes. Future studies should determine whether both the stimuli of vasodilation lead to retinal hyperperfusion, which would support that they may be involved in the aggravation of diabetic retinopathy

Evaluation of macular structure and function by OCT and electrophysiology in patients with vitelliform macular dystrophy due to mutations in BEST1

PURPOSE. To analyze retinal structure and function in vitelliform macular dystrophy (VMD) due to mutations in BEST1. METHODS. Patients from five Swedish and four Danish families were examined with electrooculography (EOG), full-field electroretinography (ffERG), multifocal ERG (mfERG), optical coherence tomography (OCT), and fundus autofluorescence photography (FAF). Genetic analysis of the BEST1 gene was performed by direct sequencing. RESULTS. Mutations in BEST1 have been reported previously in the Swedish families. In the Danish families, four disease-causing missense mutations were found, one of which is novel: c.936C>A (p.Asp312Glu). The mutation was homozygous in a 9-year-old boy and heterozygous in his father in a consanguineous family. ffERG rod response was reduced in the homozygous boy, but normal in the heterozygous father. EOG was reduced in all but two patients and did not correlate with the ffERG results. OCT ranged from normal to cystoid edema and thickening of the outer retina-choroid complex. Decreased mfERG amplitudes, increased mfERG latencies, and loss of integrity of the foveal photoreceptor inner/outer segment junction, correlated with decreased vision. FAF demonstrated hyperautofluorescence beyond the ophthalmoscopic changes in several patients. CONCLUSIONS. The finding of a homozygous dominant mutation in a patient with VMD and evidence of widespread retinal degeneration may imply that the pathogenesis of the generalized retinal degeneration differs from that of the macular degeneration. A relative agreement between hyperautofluorescence by FAF, reduced retinal function, and VMD implies that the hyperautofluorescence emanates from lipofuscin and A2E. A potential therapy for VMD, involving the inhibition of the retinoid cycle, is suggested. (Invest Ophthalmol Vis Sci. 2010;51:4754 - 4765) DOI:10.1167/iovs.10-515