Ocular tissue neovascularization is an important clinical problem in ophthalmology. It results from an imbalance between the complex and exquisite angiogenic and antiangiogenic mechanisms.1 In all animal species, the crystalline lens does not have an intrinsic blood supply and intralenticular pathologic neovascularization rarely occurs.2
A 73-year-old woman presented with poor vision and leukocoria in the left eye. She had sustained a penetrating ocular injury with a wire about 20 years earlier. The entrance point was at the medial sclera, and the cornea was intact. She pulled the wire out and did not consult a doctor; the wound healed spontaneously. She had no problem seeing for a year after the injury, implying that only the sclera was penetrated and the lens capsule was intact. Thereafter, however, the lens became opaque, and her vision deteriorated. Two years previously, she was diagnosed with diabetes mellitus that was managed by dietary intervention. No other history of ocular symptoms, systemic disease, injury, or medication was noted.
Ocular examination of the left eye revealed hand motions visual acuity at 5.0 cm, a normal corneal appearance, a clear anterior chamber, and no rubeosis iridis. Fundus visualization was difficult because of the opaque media. Ophthalmic ultrasound showed a normal globe contour with no retinal detachment or vitreous hemorrhage. A dense cataract was present with posterior iris synechias at 11 o'clock. Slitlamp examination revealed intracapsular vascularization (Figure 1). The fundus in the right eye had no diabetic retinopathy and a normal appearance with the exception of mild drusen.
Because of phacomorphic distortion, intracapsular cataract extraction and intraocular lens implantation (model MTA3U0, Alcon) in the anterior chamber were performed on April 8, 1999. Bleeding occurred when the posterior synechias were lysed. This may imply that the angiogenic blood vessels were supplied through the synechias. Histologically, the lens had abundant stromal neovascularization (Figure 2). A fundus photograph of the left eye taken 1 day postoperatively showed macular drusen comparable to those in the right eye. At the final follow-up at 6 months, the visual acuity was 0.1.
Ocular angiogenesis is a complex pathophysiologic process. The influence of stimulating growth factors such as vascular endothelial growth factor and basic fibroblast growth factor is counterbalanced by antiproliferative agents.1 The net result of these opposing factors on the vascular endothelial cells determines angiogenic homeostasis. The lens has an antiangiogenic mechanism.3 The presence of an intact lens capsule may inhibit the development of neovascularization. Lens extracts can inhibit endothelial cell proliferation in a dose-dependent fashion.3 Therefore, neovascularization in the crystalline lens is rare even in cases of severe rubeosis iridis and neovascular glaucoma.
In this case, the lens capsule might be intact because the cataract occurred 1 year after the injury. The lens capsule may have weakened after cataract formation, however, possibly inducing inflammation caused by leakage of lens particles. In the presence of inflammation and capsule weakness, the angiogenic mechanisms may predominate over the antiangiogenic mechanisms of the crystalline lens.4
To the best of our knowledge, this is the first well-documented report of the presence of blood vessels in the crystalline lens. Our patient had a normal fundus except for mild drusen, and there was no angiogenic source in the retina. This case illustrates the differences that exist between the lens and other ocular tissues. Further investigation should be done to determine the exact antiangiogenesis mechanisms of the crystalline lens.
1. Casey R, Li WW. Factors controlling ocular angiogenesis. Am J Ophthalmol 1997; 124:521-529
2. Henkind P. Ocular neovascularization. Am J Ophthalmol 1978; 85:287-301
3. Williams GA, Eisenstein R, Shumacher B, et al. Inhibition of vascular endothelial cell growth in the lens. Am J Ophthalmol 1984; 97:366-371
4. Jackson JR, Seed MP, Kircher CH, et al. The codependence of angiogenesis and chronic inflammation. FASEB J 1997; 11:457-465