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Pigmentary glaucoma (PG) is characterised by the liberation of pigment from the iris pigment epithelium and its deposition on various anterior segment structures.1 The accumulation of pigment in the aqueous outflow system can result in an increase in intraocular pressure (IOP) and eventual glaucoma. Campbell2 proposed that mechanical rubbing between the concave posterior iris surface and the zonular bundles is responsible for the release of pigment granules from the iris pigment epithelium. Laser iridotomy was proposed to eliminate the reverse papillary block mechanism of pigment dispersion syndrome (PDS).3 Using ultrasound biomicroscopy (UBM) laser iridotomy has been shown to alter the iris configuration in PDS patients.4,5 However, the effect of a laser iridotomy on IOP in PG is not clear. Here we present a case of PG with active pigment release, in which substantially lower IOPs were achieved for a short period following a yttrium-aluminium-garnet (YAG) laser iridotomy.
A 36 year old male patient was referred from an optometrist for high IOPs and visual field loss in 29 January 2001. We saw this young man on 6 February 2001. He denied any systemic disease or family history for blindness or glaucoma. The only medication taken was Propecia for treating hair loss for the past 1½12 years. His visual acuity was 20/25 +1 in the right eye and 20/20 in the left eye. IOPs were 54 mm Hg in the right eye and 52 mm Hg in the left by applanation. Slit lamp examination was remarkable for Krukenberg’s spindles; anterior chambers that were very deep with 3+ pigment debris; and irides demonstrating radial transillumination defects and posterior bowing. Gonioscopy revealed grade 4 anterior chamber angles with very heavy trabecular meshwork pigmentation and a Sampoelesi’s line in both eyes. Fundus examination showed cup:disc ratios of 0.8 bilaterally.
Combination timolol/trusopt and brimonidine were started in both eyes to lower the pressure. UBM examination on 9 March (Fig 1A) demonstrated posterior iris bowing and a relatively large zone of iris-lens contact. A YAG laser iridotomy was performed in the right eye 1 week afterwards and UBM examination showed a planar iris configuration following the laser iridotomy (Fig 1B). IOPs were 32 mm Hg in both eyes immediately before the laser. Three days later, IOPs were 17 mm Hg in the right eye and 34 mm Hg in the left. Examination revealed no anterior chamber pigment debris in the right eye and persistent pigment debris in the left. A YAG laser iridotomy was performed in the left eye on 16 March. One week later, IOPs were 25 mm Hg in the right and 18 mm Hg in the left with no pigment debris in the anterior chambers of both eyes. IOPs remained in the 20s in both eyes for several weeks. However, the IOP had risen to 28 mm Hg in the right eye and 24 mm Hg in the left on 4 April and bimatoprost was added to the glaucoma regimen of both eyes. Four months after laser therapy, the IOPs were 21 mm Hg in the right and 22 mm Hg in the left. On 4 September the IOPs were 27 mm Hg in the right eye and 23 mm Hg in the left. To prevent further increase in his IOP and optic nerve damage, Ahmed valve implantation combined with mitomycin C application was performed in the right eye on 16 November. Subconjunctival injections of 5-fluorouracil were given weekly for 6 weeks after the operation. Two months postoperatively, IOPs were 24 mm Hg in the right eye and 30 mm Hg in the left with only the left eye receiving glaucoma therapy. Filtering surgery is planned for the left eye.
In PDS, the accumulation of pigment can overwhelm the aqueous outflow system, causing trabecular occlusion and collapse, and an increase in IOP. An iridotomy may be effective in stabilising the iris configuration by reducing the IOP gradient between the anterior and the posterior chamber. Consequently, there would be a lower chance of iridozonular contact and pigment release. Using UBM, Potash et al4 and Lagreze and Funk5 showed the presence of iris concavity and iridozonular contact in PDS patients and demonstrated that laser iridotomy can restore a normal iris configuration. It has been suggested that an iridotomy might reduce the incidence of ocular hypertension in eyes affected by PDS.6
The ideal initial approach to treat PG is to eliminate the source of IOP elevation. Before YAG laser iridotomy, our patient had shown posterior iris bowing and constant pigment release, demonstrated by the 3+ pigment debris in the anterior chamber. After YAG laser iridotomy, he no longer had pigment debris in the anterior chamber. The iris moved forward to the planar position, which was clearly demonstrated by UBM imaging. The true mechanism for the pressure lowering is unknown. The iridotomy may reduce the pressure by ending the chronic irritation (and consequent inflammation) to the iris from the zonular rubbing and from the iris being stretched in the bowed position. Another possibility is that aqueous suppression has a role in the temporary improvement of IOP shortly following the iridotomy. A further mechanism may be that phagocytosis by the trabecular meshwork cells cleared much of the remaining pigment granules in the intertrabecular spaces. This may have temporarily reduced the outflow obstruction and lowered the IOPs. Our patient had shown lower IOPs for a short period following YAG laser iridotomy. In young patients who show constant active pigment release, laser iridotomy seems to have an effect on the short term IOP control and may have possible long term benefits.
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