American journal of ophthalmology · 2006
Smoking associated with damage to the lipid layer of the ocular surface.
Клиническое исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Altinors Dilek Dursun, Akça Sezin, Akova Yonca A, Bilezikçi Banu, Goto Eiki, Dogru Murat, Tsubota Kazuo
Аннотация
PURPOSE: To evaluate the effects of smoking on ocular surface.
DESIGN: Prospective, comparative, interventional case series.
METHODS: setting: Institutional. study population: Sixty smokers (33 men, 27 women) and 34 healthy subjects (18 men, 16 women) were enrolled into this study. Patients with associated ophthalmic or systemic diseases, and history of contact lens use and ocular surgery were excluded. The duration of average smoking was 13.1 years (range 5 to 35 years).
INTERVENTION: Ocular surface was evaluated by measuring corneal and conjunctival sensitivity, surface staining with fluorescein, tear film breakup time, Schirmer 1 test, and conjunctival impression cytology. Dry eye symptoms were scored by questionnaire. Kinetic analysis of sequential tear interference images obtained by a DR-1 tear lipid layer interferometry was used to investigate the precorneal lipid layer spread. Results were compared with a control group.
MAIN OUTCOME MEASURES: Comparison of subjective complaints with objective parameters in cigarette smokers and normal subjects.
RESULTS: In the smoker group, the mean Schirmer 1 test value was 10.8 mm (range 8 to 14 mm). The mean breakup time was 5.3 seconds (range 1 to 10 seconds), the average conjunctival sensitivity was 26.2 mm (range 0 to 45 mm), and the average central corneal sensitivity was 37.6 mm (range 5 to 60 mm). There was no statistically significant difference in goblet cell densities or in Schirmer 1 test values between smokers and controls (P > .05). Higher grades of lipid layer changes were observed in smokers by DR-1 interferometry kinetic analysis.
CONCLUSIONS: Smoking has deteriorating effects on the lipid layer of precorneal tear film.
DESIGN: Prospective, comparative, interventional case series.
METHODS: setting: Institutional. study population: Sixty smokers (33 men, 27 women) and 34 healthy subjects (18 men, 16 women) were enrolled into this study. Patients with associated ophthalmic or systemic diseases, and history of contact lens use and ocular surgery were excluded. The duration of average smoking was 13.1 years (range 5 to 35 years).
INTERVENTION: Ocular surface was evaluated by measuring corneal and conjunctival sensitivity, surface staining with fluorescein, tear film breakup time, Schirmer 1 test, and conjunctival impression cytology. Dry eye symptoms were scored by questionnaire. Kinetic analysis of sequential tear interference images obtained by a DR-1 tear lipid layer interferometry was used to investigate the precorneal lipid layer spread. Results were compared with a control group.
MAIN OUTCOME MEASURES: Comparison of subjective complaints with objective parameters in cigarette smokers and normal subjects.
RESULTS: In the smoker group, the mean Schirmer 1 test value was 10.8 mm (range 8 to 14 mm). The mean breakup time was 5.3 seconds (range 1 to 10 seconds), the average conjunctival sensitivity was 26.2 mm (range 0 to 45 mm), and the average central corneal sensitivity was 37.6 mm (range 5 to 60 mm). There was no statistically significant difference in goblet cell densities or in Schirmer 1 test values between smokers and controls (P > .05). Higher grades of lipid layer changes were observed in smokers by DR-1 interferometry kinetic analysis.
CONCLUSIONS: Smoking has deteriorating effects on the lipid layer of precorneal tear film.