Comment on ‘Vitreomacular traction syndrome: a comparison of treatment with intravitreal plasmin enzyme vs spontaneous vitreous separation without treatment’

Sir,

In some patients, incomplete posterior vitreous detachment leads to symptomatic vitreomacular adhesion or vitreomacular traction syndrome. This is a medico-surgical problem in which new therapy is interesting due to the potential prognosis of the untreated disease and its only actual therapy being surgery. Several studies^{1, 2}, have reported the use of intravitreal proteases such as plasmin, which is able to degrade biochemical glue composed of proteoglycans, including laminin and fibrinectin. The microplasmin is a truncated derivative of plasmin. The product thus obtained has a significantly reduced size and maintains native proteolytic activity. Stalmans et al.¹ report that intravitreal injection of microplasmin was superior to injection of placebo in altering the vitreoretinal interface significantly, with the resolution of more vitreomacular tractions and the closure of more macular holes, than that accomplished by placebo treatment of the affected eyes. Therefore, Codenotti et al³ should wait longer to conclude that ‘a single intravitreal APE (autologous plasmin enzyme) injection seems insufficient to induce a complete posterior vitreous detachment in these patients’. In previous studies, there was no statistically significant difference between placebo and microplasmin before 7 days, but it was significant for all comparisons after 7 days, especially as there seemed to be a marked difference during surgery in the adhesion of the posterior hyaloid between autologous plasmin enzyme and placebo treatment in their study.³