Gerard A Lutty
Hyperglycemia has toxic effects on almost all cells inthe body.
Ophthalmic complications of hyperglycemia are mostprofound in retina. Diabetic retinopathy (DR) is themost common cause of blindness in people over theage of 50. There is accumulating evidence that DR is aninflammatory disease. There are high systemic levels ofcytokines like TNF? and IL1-?. The initial events inanimal models of DR are increased vascular permeabil-ity and leukostasis. This binding of leukocytes to theendothelium results from an increase in ICAM-1 onthe retinal capillary endothelium (EC) and expressionof CD11/CD18 on the surface of the activated leuko-cyte. We have observed polymorphonuclear leuko-cytes (PMNs) at sites of EC vascular dysfunction inboth diabetic retinas well as choroid. NeutralizingICAM-1 or CD18, prevents leukostasios in diabeticanimals. Anti-inflammatory drugs like Etanercept,aspirin, or Meloxicam reduce leukostasis and ECdeath. Future therapies may include repopulation of the acellular capillaries after EC and pericyte deathwith vascular progenitors made from the patient’s ownblood cells.
COMPARISON OF RANIBIZUMAB AND AFLIBERCEPT IN PATIENTS WITH NEOVASCULAR AGE-RELATED MACULAR DEGENERATION TREATED FOLLOWING A ?TREAT AND EXTEND? PROTOCOL: EFFICACY VARIABLES FROM THE PRE-SPECIFIED 12- MONTH INTERIM ANALYSIS OF THE RIVAL STUDY