Follow-up on the eye study
“Purpose: Diabetic retinopathy is characterised by morphological lesions secondary to retinal vascular impairment, and it is assumed that changes in the diameter regulation of retinal arterioles are involved in the disease pathogenesis. It has previously been shown that prostaglandin F2α can constrict retinal arterioles in vitro. In the present study, we investigated whether a similar effect could be achieved by topical administration in diabetic patients with dilated retinal arterioles and retinopathy.
Methods: Twenty-two type 1 diabetic patients with mild retinopathy and twenty-four matched normal controls were randomized to topical treatment with the prostaglandin F2α agonist latanoprost twice daily for 1 week, followed by similar treatment with the cyclo-oxygenase inhibitor diclofenac, or to receive the two medications in the reverse order. The Dynamic Vessel Analyzer was used to assess the effect of the interventions on the resting diameter of retinal vessels and on the diameter response of retinal arterioles to increased blood pressure (BP) induced by isometric exercise and flicker stimulation.
Results: Latanoprost reduced the resting diameter of retinal arterioles significantly in patients with diabetes (p = 0.01), but had no effect on normal persons. Diclofenac had no effect on the resting diameter of arterioles in either of the groups. The diameter responses to increased BP and flicker stimulation were not significantly changed by any of the treatments.
Conclusion: Long-term prospective studies are needed to study the effect of topical treatment with latanoprost on the consequences of retinal hyperperfusion in retinal vascular diseases such as diabetic retinopathy.”
So, to Plamus and others who might have no idea what I’m talking about, I participated in this study and wrote a couple of short posts about it back then. Only yesterday I incidentally asked Kathrine to send me the study and kindly enough she did – but I’ll not put it up here.
Diabetic retinopathy is a much feared complication to diabetes. It is ‘the most frequent cause of blindness of adults in the age of 20-74’ in Denmark. So far the usual approach to dealing with this complication has been (still is) to screen diabetics by taking pictures of their eyes at regular intervals (once every year) and then intervene when complications become significant enough to ‘merit attention’, so to speak – usually by means of surgical intervention. One of the main reasons why the screening protocol is implemented, in case you were wondering, is that patients will often have no symptoms even relatively late in the process – you basically don’t get any symptoms before you get bleeds in your eyes significant enough to cause potential vision loss. Katrine’s approach was to figure out if two extant and in other areas widely used pharmacological treatment options could help delay the progression of the damage to the eyes caused by diabetes.
To make a long story short, Latanoprost showed promise in the study, so now Toke Bek, Kathrine’s phd-advisor, has decided to do a long-term study using the drug. Unless I am currently greatly underestimating the long-term risks of complications from participating (have yet to read up on those), I’ll participate in that trial as well.
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