Ocular demodicosis as a risk factor of pterygium recurrence

To evaluate ocular demodicosis as a potential risk factor in pterygium recurrence.

Cross-sectional study to correlate clinical findings with laboratory data.

We retrospectively reviewed 94 patients (43 with primary and 51 with recurrent pterygia), among whom 68 patients received surgical correction, and prospectively enrolled another 23 pterygium patients and 14 nonpterygium controls for measuring the tear level of interleukin (IL)-17.

All patients had microscopically confirmed ocular demodicosis. Statistical correlations were analyzed among age, sex, aqueous tear deficiency, dry eye, ocular demodicosis, follow-up period, surgical outcome, and tear levels of IL-17 measured by enzyme-linked immunosorbent assay.

Correlation between ocular demodicosis or IL-17 levels and pterygium recurrence.

Among 94 patients, ocular demodicosis was more prevalent in patients with recurrent pterygium than those with primary pterygium (P = 0.015). During follow-up of 16.5 ± 11.5 months, 68 postsurgical patients developed 7 corneal recurrences, which constituted 7.4% of primary and 12.2% of recurrent pterygium (P = 0.820). They also developed 8 conjunctival recurrences. Kaplan-Meier survival analysis showed combined (P = 0.000), corneal (P = 0.044), and conjunctival (P = 0.002) recurrence was significantly higher among patients with demodicosis than those without. Conjunctival recurrence occurred within 6 months in eyes without demodicosis but extended beyond 6 months in eyes with demodicosis. In 34 postsurgical patients with demodicosis, the mite count of 14 patients with recurrence was significantly higher than that of 20 without (P = 0.005). The IL-17 level was significantly higher in patients with either pterygium or demodicosis than controls (P = 0.049 and 0.040, respectively), and the IL-17 level was further elevated in patients with both pterygium and demodicosis (all P<0.05).

Ocular demodicosis is a risk factor for pterygium recurrence, especially for conjunctival recurrence, presumably by perpetuating chronic inflammation mediated by T-helper (Th)17 lymphocytes.