Rosiglitazone and macular edema

As noted in Box 1 in the article by Claire Kendall and Eric Wooltorton,¹ long-standing diabetes mellitus, poor diabetes control and insulin therapy are by themselves risk factors for macular edema. Furthermore, only 1 of the 9 cases of visual impairment reported in Canada for patients taking rosiglitazone was clearly associated with macular edema, and in that case the problem was resolved by discontinuation. The questions thus arise of whether macular edema (especially if it is asymptomatic) is an absolute contraindication to rosiglitazone therapy and whether every patient with diabetes must be subjected to ophthalmologic evaluation before starting this drug.

Although adverse symptoms may diminish upon discontinuation of rosiglitazone, the potential for loss of glycemic control must also be considered. In such situations, what is the risk-benefit ratio for continuation of rosiglitazone therapy, especially if good glycemic control has been achieved?

Perhaps there is a role for “drug holidays” with rosiglitazone. In this regard, macular edema induced by latanoprost, echothiophate iodide or nicotinic acid is usually reversible upon discontinuation of the drug,² which can be reintroduced later.

Systemic factors that may contribute to the progression of diabetic macular edema are blood glucose control, hypertension, nephropathy and proteinuria. It has been suggested that use of an angiotensin-converting enzyme (ACE) inhibitor be considered for patients with diabetic retinopathy and nephropathy.³ ACE inhibitors are already indicated for microalbuminuria of diabetes, but it is not known whether they would be beneficial in preventing macular edema as well.