No study has so far evaluated the impact of coffee drinking on ocular wavefront aberration (OWA) measurements. This study presents novel findings regarding the OWA of the eye following coffee intake. We aimed to evaluate the acute changes in pupil size and OWA of the eye after single administration of coffee. A total of 30 otherwise healthy participants were included in this prospective study. All subjects drank a cup of coffee containing 57 mg caffeine. Measurements of pupil size, total coma (TC), total trefoil (TF), total spherical aberration (TSA), and total higher order aberration (HOA) were performed before and at 5 minutes, at 30 minutes, and at 4 hours after coffee drinking using a wavefront aberrometer device (Irx3, Imagine Eyes, Orsay, France). The mean age of the study population was 20.30 ± 2.74 years. Pupil size did not show a significant change during the measurements (p > 0.05). A significant increase was observed in TF and HOA measurements following coffee intake (p = 0.029 and p = 0.009, resp.). Single administration of coffee results in significant increase in TF and total HOAs in healthy subjects without any effect on pupil diameter. Ultrastructural changes in the cornea following coffee intake might be of relevance to the alterations in ocular aberrations in healthy subjects.
To investigate the malondialdehyde (MDA) levels, paraoxonase1 (PON1) activity and 8-hydroxy 2-deoxyguanosine (8-OHdG) levels in the primary open angle glaucoma (POAG) patient. Blood samples from 52 healthy individuals and 53 patients with POAG were analyzed for MDA and 8-OHdG by HPLC (high-performance liquid chromatography) and PON1 by spectrophotometry. The data obtained were analyzed statistically. MDA levels were 10.46±8.4 and 4.70±1.79 µmol; PON1 levels were 121±39.55 and 161.62±60.22 U/mL; and 8-OHdG values were 1.32±0.53/10 dG and 0.47±0.27/10 dG in the POAG patients and the control group, respectively. The difference was significant in MDA levels, 8-OHdG levels and PON1 activity in POAG patients in comparison with controls (<0.001). We concluded that the observed increase in MDA and 8-OHdG levels may be correlated with decreased PON1 activity. Oxidative stress plays an important role in glaucoma development.
When used in conjunction with eyelid hygiene, topical administration of NAC appears to be as effective as a topical steroid-antibiotic combination, betamethasone-sulfacetamide sodium therapy in patients with MGD.
Purpose:The aim was to evaluate central corneal thickness in patients with meibomian gland dysfunction. Methods: The study group was made up of 40 eyes of 20 patients with meibomian gland dysfunction (mean age, 40.55 Ϯ 10.7 years). Forty eyes of 20 healthy individuals (mean age, 39.25 Ϯ 11.1 years) without any ophthalmic or systemic pathology were used as a control group. The central corneal thickness was measured with ultrasonic pachymetry. Results: The mean central corneal thickness was 541.45 Ϯ 24.68 mm in the study group and 544.30 Ϯ 22.16 mm in the control group. There was no statistically significant difference in the mean central corneal thickness measurements in the meibomian gland dysfunction group in comparison with the control group (p > 0.05). Conclusion: Central corneal thickness measurements do not differ in patients with meibomian gland dysfunction compared with healthy control subjects. Key words: blepharitis, central corneal thickness, cornea, corneal pachymetry, meibomian gland dysfunction Meibomian gland dysfunction (MGD), a major form of blepharitis, is an extremely common, chronic condition of the eyelids. Hom and colleagues 1 reported the prevalence of meibomian gland dysfunction to be 38.9 per cent in apparently normal patients presenting for routine visual examinations. It increases in prevalence to nearly 68 per cent in patients over 60 years of age.2 MGD is characterised by inflammatory changes at the lid margins and changes in the anatomy of orifices and the character of secretions of the meibomian glands.The importance of meibomian gland function has been emphasised because lipids secreted by these glands combine with the outer layers of the tear film to suppress evaporation of tear fluid and to form a hydrophobic barrier at the lid margin to prevent loss of tears. In MGD, a reduction in the quantity and changes in the composition of meibomian gland secretions result in instability and thinning of the tear film. As the aqueous component of tears evaporates, the tear osmolarity rises, and aqueous tear flow and volume decrease, initiating an inflammatory cycle.3-10 The compromised preocular tear film leads to dry eye, which also interferes with the ocular surface.
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