Reduced outflow facility implicated in IOP elevation in pigment dispersion syndrome

The authors conducted this study to investigate aqueous humor dynamics in patients with pigmentary dispersion syndrome (PDS).

They enrolled 71 patients in one of four age-matched groups: those with PDS with or without ocular hypertension and those without PDS with or without ocular hypertension. They found that patients with both PDS and ocular hypertension had higher intraocular pressures than ocular normotensive subjects with or without PDS (P < 0_.001). They also had higher episcleral venous pressure (P = 0.04) and lower outflow facility (P =0.01) than the group without PDS or ocular hypertension. And their anterior chamber volume was larger than among the other groups (P < 0.05 for all).

The authors conclude that the elevated IOP seen in patients with PDS is caused by reduced outflow facility. This differs from patients with ocular hypertension without PDS in which reductions in uveoscleral outflow and outflow facility have been reported.

The authors' findings show that patients in the early stages of PDS with normal IOP demonstrate normal trabecular outflow resistance and increased uveoscleral outflow. The authors propose that the increase in the uveoscleral outflow may be responsible for the normal IOP in this group. It would be interesting to determine how fluid regulation occurs in this scenario, with fluid being diverted towards the uveoscleral instead of the trabecular meshwork. The authors suggest that a low-grade inflammatory response to pigment release and deposition ciliary body may play a role in the increase in uveoscleral outflow. If this is the case, treating these patients with corticosteroids may make them more susceptible to IOP elevation.

The patients with PDS and high IOP demonstrated greater trabecular outflow resistance and deeper anterior chambers but normal uveoscleral outflow. This suggests that higher pigment loads or damage by pigment to the trabecular meshwork may lead to IOP elevation. It is intriguing that in the presence of increasing trabecular resistance, uveoscleral outflow normalizes. One would expect that if increased pigment deposition occurs in the trabecular meshwork as the disease advances, there would also be increased pigment deposition in the uveoscleral outflow pathway.

Another interesting finding reported in this paper is the significantly elevated episcleral venous pressure in patients with PDS and ocular hypertension compared with normal controls. This observation was not discussed by the authors and its cause remains unclear.