Aims-To evaluate the clinical course and the characteristics of transient refractive error occurring during intensive glycaemic control of severe hyperglycaemia. Methods-28 eyes of patients with persistent diabetes were included in this prospective study. During the observation period, patients underwent general ophthalmological examination and A-mode scan ultrasonography was performed at each examination-at days 1, 3, and 7, and then once every week or every other week until recovery of hyperopia. Results-A transient hyperopic change occurred in all patients receiving improved control after hyperglycaemia. Hyperopic change developed a mean of 3.4 (SD 2.0) days after the onset of treatment, and reached a peak at 10.3 (6.1) days, where the maximum hyperopic change in an eye was 1.47 (0.87) D (range 0.50-3.75 D). Recovery of the previous refraction occurred between 14 and 84 days after the initial assessment. There was a positive correlation between the magnitude of the maximum hyperopic change and (1) the plasma glucose concentration on admission (p<0.01), (2) the HbA 1c level on admission (p<0.005), (3) the daily rate of plasma glucose reduction over the first 7 days of treatment (p<0.001), (4) the number of days required for hyperopia to reach its peak (p<0.001), and (5) the number of days required for the development and resolution of hyperopic changes (p<0.0001). There was a negative correlation between the maximum hyperopic change of an eye and baseline value of refraction (p<0.01). During transient hyperopia, no significant changes were observed in the radius of the anterior corneal curvature, axial length, lens thickness, or depth of anterior chamber. Conclusions-The degree of transient hyperopia associated with rapid correction of hyperglycaemia is highly dependent on the rate of reduction of the plasma glucose level. A reduction of refractive index in intraocular tissues, especially in lens, appears to be responsible for this hyperopic change. (Br J Ophthalmol 2000;84:1097-1102 Patients with diabetes mellitus (DM) can develop various ocular complications including cataract, optic neuropathy, uveitis, and keratopathy as well as retinopathy. In addition, transient refractive error occurs during the course of DM and is associated with treatment induced changes in the plasma glucose concentration.

Purpose: To determine the changes of corneal endothelium in pseudoexfoliation (PEX) syndrome and the relations between their changes and aqueous flare intensity. Methods: 26 eyes with PEX syndrome, 17 clinically unaffected fellow eyes and 27 normal age-matched eyes were studied. The corneal endothelium of the eyes was examined using a specular microscope, and the aqueous flare intensity of the eyes was measured using a laser flare cell meter. Results: The corneal endothelial density significantly decreased both in the eyes with PEX and in the clinically unaffected fellow eyes compared to the normal control eyes (p < 0.001, p < 0.01). The acqueous flare intensity significantly increased in PEX syndrome (p < 0.01). There was a significantly inverse correlation between the corneal endothelial cell density and the aqueous flare intensity in PEX. Conclusion: A decrease in corneal endothelial cells was quantitatively identified in PEX syndrome. This change might have a relationship with a disorder of the blood-aqueous barrier in this syndrome.

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. In order to investigate the effects of ET-1 on retinal vessels, ET-1 (1-1000 pmol) was injected into the posterior vitreous body in rabbits. A high dose of ET-1 induced transient complete obstruction of the retinal vessels. In this experimental model of transient complete obstruction of the retinal vessels, the effects of ET-1 on retinal function were further analyzed by means of electroretinograms. The scotopic a-wave was not affected, but the amplitude of the scotopic b-wave was significantly elevated. The amplitude of oscillatory potentials was significantly reduced. These phenomena suggested that retinal ischemia without choroidal ischemia was brought about due to severe vasoconstriction of the retinal arteries. These findings indicate that intravitreal injection of ET-1 causes a transient cessation of blood supply from retinal vessels and that oscillatory potentials in electroretinograms appear to be sensitive for detecting changes of retinal circulation. This new model of transient complete obstruction of retinal vessels might be useful for studying the pathophysiology of severe retinal ischemia.

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