ABSTRACT.Purpose: Diabetes mellitus (DM) affects corneal biomechanical parameters. We compared analyses using ORA (Ocular response analyser) and Corvis ST to determine the influence of disease duration, hyperglycaemia and haemoglobin A1c (HbA1c) levels on these parameters. Methods: This observational, cross-sectional, observer-masked study assessed one eye of 94 consecutive DM patients and 41 healthy subjects. Two DM groups were analysed: the uncontrolled DM group (n = 54) (HbA1c ≥ 7%) and the controlled DM group (n = 40) (HbA1c < 7%). Central corneal thickness (CCT) was measured by ultrasonic pachymetry and intraocular pressure (IOP) by Goldmann applanation tonometry. ORA and Corvis ST analyses were performed to evaluate the changes. Results: Most of the Corvis ST parameters [Deformation amplitude (DA), A1 and A2 times, A1 velocity] in the uncontrolled DM group eyes were found to be significantly different to controls and controlled DM group eyes (p = 0.005, p = 0.001, p < 0.0001, p = 0.002, respectively). DA on the Corvis ST was correlated with blood glucose concentration (p = 0.004) and HbA1c percentage (p = 0.002). ORA corneal hysteresis was significantly lower in diabetic patients with elevated HbA1c than in control subjects (p = 0.001) and was affected by disease duration (p = 0.037), whereas the corneal resistance factor remained unaltered. Conclusions: A poor glucose control in DM affects corneal biomechanics measured by ORA and Corvis ST, which may cause high IOP measurements independent of CCT. The measurement of the corneal biomechanics should be taken into consideration in the clinical practice.
Obstructive sleep apnea-hypopnea syndrome (OSAHS) is becoming widely accepted as a risk factor for glaucoma. We discuss the proposed mechanism involved in the pathogenesis of glaucoma in OSAHS, and review the published data on the association between these two conditions, as well as papers regarding functional and structural tests related with glaucomatous damage. There is increasing evidence that the prevalence of glaucoma is higher in OSAHS patients, especially in those with severe disease with apnea-hypopnea index (AHI) >30, and also that sleep disorders may be more frequent in patients with glaucoma, especially in those with normal tension glaucoma (NTG). Several ophthalmic signs and symptoms have been associated with this condition. Raised intraocular pressure (IOP), possibly related to increased body mass index, thinning of retinal nerve fiber layer (RNFL), and alteration of visual field (VF) indices has been demonstrated in many studies, in patients with no history of glaucoma or evidence of glaucomatous changes in the ophthalmic examination. A correlation of AHI with RNFL and VF indices has been described in some studies. Finally, corneal thinning, suspicious glaucomatous disc changes and anomalies in electrophysiological tests such as multifocal visual evoked potential have been described in patients with OSAHS, even in patients with normal findings in the optic nerve and VF, suggesting subclinical optic nerve involvement not detectable in conventional ophthalmic examinations. The pathogenesis of optic nerve involvement has been related to vascular and mechanical factors. Vascular factors include recurrent hypoxia with increased vascular resistance, autonomic deregulation, oxidative stress and inflammation linked to hypoxia and subsequent reperfusion, decreased cerebral perfusion pressure and direct hypoxic damage to the optic nerve. Proposed mechanical factors include increased IOP at night related to supine position and obesity, raised intracranial pressure and elastic fiber depletion in the lamina cribosa and/or trabeculum. In conclusion, ophthalmic evaluation should be recommended in patients with severe OSAHS, and the presence of sleep disorders should be investigated in patients with glaucoma, especially in NTG patients and in those with progressive damage despite controlled IOP, as treatment with continuous positive airway pressure may contribute to stabilizing the progression of glaucomatous damage.
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