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Progress in diabetic maculopathy
  1. Tennent Institute of Ophthalmology, Gartnavel General Hospital, Glasgow G12 0YN

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    With an ever increasing prevalence of type II diabetes, diabetic maculopathy will continue to pose a large problem for ophthalmologists. Laser photocoagulation is often disappointing both for the patient and the doctor, and there seems to have been little in the way of progress for some years now.

    Whitelocke and colleagues’ paper1 classified maculopathy into focal, exudative, and ischaemic types and they highlighted their different prognoses. Although treatment of focal maculopathy is reasonable, the scope for improving vision in established exudative and ischaemic maculopathy is very limited and despite treatment this group of patients must account for a large percentage of the blind and partially sighted registrations attributed to diabetes, especially in the over 65 age group. Some of the medical factors predisposing to maculopathy are starting to be identified, with the EUCLID study2 identifying systemic hypertension at levels previously not thought to be significant, particularly in the development of ischaemic maculopathy.

    It is particularly encouraging therefore to read in this issue of theBJO (p 12) the possible role of vitrectomy in diabetic maculopathy. The role of the vitreous in the development of macular oedema secondary to aphakia, uveitis, and retinitis pigmentosa has been known for some time,3 and more recently considerable attention has been given to the role of vitreous traction on the development of macular holes.4 Because in all types of diabetic maculopathy there are such obvious changes in the retinal vasculature it is easy to see why so little attention was given to the possible role of the vitreous.

    Nasrallah et al5 were among the first to suggest the possible role of the vitreous in the development of diabetic maculopathy, and in 1992 Lewiset al6 described diabetic macular oedema associated with a taut premacular posterior hyaloid membrane and demonstrated that surgical removal of this membrane could result in significant improvement in vision. Similar encouraging results were obtained by Harbour et al,7 but this type of vitreous configuration seems most uncommon and the influence of surgery on this group would seem unlikely to affect the overall results of treatment of diabetic maculopathy. Interestingly, and perhaps not surprisingly, it was the diffuse type of diabetic maculopathy that was most often associated with the premacular membrane, and Harbour et al emphasise the difficulty of assessing the exact vitreomacular relation when there is no obvious taut premacular membrane visible.

    Ikeda and colleagues are therefore to be commended for their initiative in considering vitreous surgery in diabetic maculopathy without obvious signs of vitreomacular traction, and show encouraging results, albeit with small numbers. Given the limitations of laser treatment for diabetic maculopathy, it is likely that further studies will be undertaken to help identify features which influence the prognosis, and it may well be that vitrectomy may have a considerable influence on our ability to treat this common condition.

    Looking further ahead, work has been reported on the enzymatic creation of a posterior vitreous detachment8 9 and, while this is primarily for the treatment of proliferative diabetic retinopathy, it is tempting to speculate if this might have a similar effect on relieving the type of anomalous vitreomacular traction which may contribute to the development of diabetic maculopathy.

    Only a decade or so ago, little attention was being paid to the interrelation between the vitreous and the macula, but over this period not only has our understanding improved considerably, but also our ability to treat a variety of related conditions and now, hopefully, diabetic maculopathy may be added to this list.


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