34.
Pharmacologic Vitreolysis – the First Decade
Jerry Sebag (Huntington Beach)
Concurrent weakening of vitreo-retinal adhesion and liquefaction of the gel results in posterior
vitreous detachment (PVD)1. Liquefaction without concurrent vitreo-retinal dehiscence
results in anomalous PVD2, where traction is exerted upon the retina and/or disrupts the posterior
vitreous cortex resulting in vitreoschisis2. In the periphery, retinal tears and detachments
result while at the macula there can be vitreo-macular traction syndrome, macular
holes, or macular pucker. Anomalous PVD also plays a role in diabetic vitreo-retinopathy3.
Thus, it would be desirable to develop new approaches to improve and facilitate vitreo-retinal
surgery, as well as to prevent anomalous PVD. To this end, several agents have been tested in
an attempt to alter the gel state of vitreous and separate the posterior vitreous cortex from the
retina. This approach is known as Pharmacologic Vitreolysis4, a term that was first introduced
in 1998.
During the past 10 years, the various agents being developed for Pharmacologic Vitreolysis can be grouped into two classes.
Those inducing liquefaction of the gel vitreous can be referred to as “liquefactants”, while those that cause dehiscence
at the vitreo-retinal interface and vitreo-retinal separation can be called interfactants”. Some agents are only liquefactants,
such as hyaluronidase, and some are only interfactants, such as dispase. Other agents are both, such as chondroitinase,
plasmin or microplasmin, and nattokinase.
No single agent available today may be able to achieve both of the desired components of pharmacologic vitreolysis; i.e.,
liquefaction of the gel and vitreoretinal dehiscence. Indeed, vitreous molecular morphology is so complex and there are so
many different changes that occur with aging and various diseases, that the future will probably see the use of a combination6,
7 of two or more agents whose relative concentrations will need to be adjusted depending upon the patient’s age, disease,
and the desired effect. It is important to note, however, that pharmacologic vitreolysis should begin by inducing vitreoretinal
dehiscence, followed by liquefaction of the gel vitreous. Reversing this sequence might induce iatrogenic anomalous
PVD and untoward sequelae.
1. Sebag J: The vitreous. In: Adler’s Physiology of the Eye (WM Hart, Jr, ed). Mosby, St. Louis, 1992, Pp 268-347.
2. Sebag J: Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease. Graefes Arch Clin Exp Ophthalmol 242:690-8,
2004.
3. Kroll P, Rodrigues E, Hoerle S: Pathogenesis and classificaton of proliferative diabetic vitreoretinopathy. Ophthalmologica. 2007; 221(2):78-94
4. Sebag J: Pharmacologic vitreolysis. Retina 18:1-3, 1998.
5. Sebag J: Is pharmacologic vitreolysis brewing? Retina 22:1-3, 2002.
6. Sebag J: Molecular biology of pharmacologic vitreolysis. Trans Am Ophthalmol Soc 103:473-494, 2005.