Effects of 0.005% latanoprost on ocular anterior structures and ciliary body thickness.

PURPOSE: To assess the effects of 0.005% latanoprost on the anterior segment geometry and ciliary body thickness using ultrasound biomicroscopy. Intraocular pressure, refraction, visual acuity, and pupil size were also evaluated.

PATIENTS AND

METHODS

Thirty patients with untreated ocular hypertension or primary open-angle glaucoma (mean age: 59.3 +/- 9.9 years) were recruited into this prospective, controlled, open trial. Before and after 1 week of 0.005% latanoprost administration, the following parameters were tested: refraction, visual acuity, pupil diameter, intraocular pressure, 5 conventional ultrasonographic A-scan variables, 16 ultrasound biomicroscopy parameters, and the ultrasound biomicroscopy ciliary body thicknesses at a distance of 1500 microns (CBT1), 2000 microns (CBT2), and 2500 microns (CBT3) from the scleral spur.

RESULTS

Latanoprost 0.005% caused a marked intraocular pressure-lowering effect in all patients (from 22.8 +/- 3.1 mm Hg to 14.1 +/- 2.9 mmHg; -38%, P < 0.0001), without any refractive, visual acuity, or pupillary alterations. The A-scan echobiometry variables were unchanged, while ultrasound biomicroscopy confirmed a significant posttreatment increase of CBT2 (from 434 +/- 140 microns to 536 +/- 127 microns; +102 microns, P = 0.01) and CBT3 (from 319 +/- 103 microns to 412 +/- 100 microns; +93 microns, P = 0.003) compared with controls (CBT2: from 493 +/- 165 microns to 473 +/- 135 microns, -20 microns, P = NS; CBT3: from 388 +/- 130 microns to 365 +/- 87 microns, -23 microns, P = NS). None of the changes observed in the other UBM parameters was statistically significant. No significant correlation was detected between ciliary body thickness increase and intraocular pressure-lowering effect.

CONCLUSION

The increase of ciliary body thickness, which was measured in vivo by ultrasound biomicroscopy and associated with the intraocular pressure-lowering effect, indirectly supports the mechanism of uveoscleral outflow enhancement induced by latanoprost. These data are in agreement with the biochemical hypothesis of the passage of the aqueous flow through the extracellular spaces of the ciliary muscle.