] Diub Camp 1993;7:63-64

LETTER TO THE EDITOR

Rapid1 Progressing Diabetic Retinopathy Upon mproved Metabolic Control P

The case-control study by Agardh et a1.i appears to confirm that improving glycemia drastically in poorly controlled diabetic patients (transiently) deteriorates pre-existing diabetic retinopathy.’ However, the im- provement in glycemia in the cases as demonstrated by a decline in HbA1, from a mean of 10.8% to a mean of 9.6% over 6 months is far from being drastical; such monthly 0.2% decline is less than one-tenth of what has been described as being the maximum possible decay rate of I-I~AI,.~ Unfortunately, Agardh et al.* fail to provide data on the incidence of hypoglycemia4 and of macular edema,5,6 although both phenomena have been linked to the appearance of rapidly pro- gressive diabetic retinopathy. We recently reported7 on patients in whom severe macular edema and pro- liferative retinopathy developed when HbAI, was lowered from 11.6%-12.3% to 5.2%-6.4% within 8-12 weeks with frequent episodes of light hypogly- cemias. All of these patients were females, they were young (20-41 years) and had diabetes for only 6-17 years. They had incipient diabetic nephropathy and painful neuropathy, and few of them had peripheral edema and amenorrhoea. As in the study by Agardh et al.,’ the deterioration of retinopathy could not be reverted by lasercoagulation, whereas neuropathy and proteinuria improved upon re-entry to near-nor- moglycaemia.

Lowered provision of nutrient substrates to the reti- nal tissues’ might be involved in the progression of diabetic retinal damage: in the presence of persistent hyperglycemia, the retina may reduce glucose uptake from the bloodstream, as the brain’ does; this reduced glucose transport cannot speed up appropriately dur- ing hypoglycemia. The normal retina is further pro- tected (as is brain’) against hypoglycemia by increas- ing blood flow. lo Retinal vasculature is dilated,‘l,12 however, and retinal blood flow is already at its maxi- mum in diabetic retinopathy; hence, this protective mechanism is unlikely to function during acute hypo- glycemia in severe diabetes. Thus, retinoglycopenia

0 1993 Iournal of Diabetes and Its Complications

may ensue as well as acute lack of fuel causing the immediate breakdown of tissue membrane functions and the formation of edema. Retinal edema is a pre- dominant finding in patients with rapidly progressing diabetic retinopathy. 5*6*13~14 In high-risk patients with Mauriac’s syndrome, 5 restoration of the effects of sex- ual hormones15 by improved diabetes control might further aggravate diabetic retinopathy, in conjunction with the edema-promoting effects of insulin itself.16 The deleterious consequences of severe retinal edema are manyfold.

In conclusion, in accordance with Frier and Hilsted,17 a very slow reduction of extreme hypergly- cemia and avoidance of hypoglycemia is proposed in patients with chronic poor control. This strategy may also be preferred in patients with relatively short-term glycemic deterioration, because edematous intracta- ble retinopathy has also been observed some months after manifestation of, and initiation of insulin treat- ment for insulin-dependent diabetes mellitus.‘3,*4

Ernst Chantelau, M.D. Diabetesambulanz MNR-Klinik

Dusseldorf, Germany

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2. Wang PH, Chalmers TC: Intensive glycemic control reduces the progression of late diabetic complications in IDDM [Abstract]. Diabetes 1992;41(suppl 1):175A.

3. Chantelau E: Decay of haemoglobin Ale upon return to normoglycaemia [Letter]. DiubefoZogia 1992;35:191.

4. Dahl-Jorgensen K, Brinchmann-Hansen 0, Hanssen KF, Sandvik L, Aagenaes 0, Aker Diabetes Group: Rapid tightening of blood glucose control leads to tran- sient deterioration of retinopathy in insulin-dependent diabetes mellitus: The Oslo study. BMJ 1985;290: 811-815.

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11. Brinchmann-Hansen 0, Dahl-Jorgensen K, Hanssen

KF, Sandvik L: Effects of intensified insulin treatment on retinal vessels in diabetic patients. BY J Ophthalmol 1988;72:666-673.

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15. Williams JR, Rowold E, Change K, Marvel J, Tomlin- son M, Sherman WR, Ackermann KE, Berger RA, Kilo C: Sex steroid dependency of diabetes-induced changes in polyol metabolism, vascular permeability, and collage cross-linking. Diabetes 1985;35:20-27.

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