A case of phacolytic glaucoma with anterior lens capsule disruption identified by scanning electron microscopy.

BACKGROUND: Phacolytic glaucoma is induced by lens protein or macrophages that have leaked through a macroscopically intact anterior lens capsule. Here, we report a case of phacolytic glaucoma with anterior lens capsule disruptions visualized by scanning electron microscopy (SEM). CASE PRESENTATION: A 71-year-old man was referred to our institute for increased intraocular pressure (IOP) in the right eye. Slit-lamp biomicroscopic examination revealed corneal edema, the presence of inflammatory cells and iridescent crystalline in the anterior chamber, and a hypermature cataract in the right eye. Despite treatment with topical glaucoma medication (0.15% brimonidine, 1% brinzolamide/0.5% timolol, and 0.03% bimatoprost) and systemic mannitol, his IOP remained uncontrolled. Light microscopy was used to examine the aqueous humor obtained via anterior chamber paracentesis and the anterior lens capsule obtained via intracapsular cataract extraction (ICCE), which revealed that the anterior lens capsule was intact. However, SEM revealed full-thickness disruptions in the anterior lens. CONCLUSION: This is the first reported case of phacolytic glaucoma with disruptions of the anterior lens capsule confirmed by SEM.

First Described Case of Anterior and Posterior Segment Crystals in Phacolytic Glaucoma.

Phacolytic glaucoma is an open-angle glaucoma that occurs when lens proteins from hypermature cataracts seep through an intact anterior capsule and induce obstruction of the trabecular meshwork by inflammatory cells. We review the case of a 66-year-old man who presented with acute pain, a hypermature cataract, prominent anterior chamber crystals, and elevated intraocular pressure. After cataract surgery was performed, iridescent crystals were noted in the posterior chamber. Anterior chamber crystals have been associated with phacolytic glaucoma, but this is the first case demonstrating crystals in the posterior chamber as well.

Obstruction of aqueous outflow by lens particles and by heavy-molecular-weight soluble lens proteins.

Enucleated human eyes were perfused via the anterior chamber at 25 mm Hg pressure with lens particles (whole lens homogenates) in one series of experiments and with soluble lens proteins from human cataractous lenses in another series. Adding 1% of a homogenate of a single cataractous lens to the anterior chamber induced a 68% decrease in outflow. Perfusion with HMW soluble lens proteins (1 mg/ml; MW more than 150 million) caused a 60% decrease in outflow in 1 hr. In neither series was the obstruction to outflow relieved by subsequent irrigation of the anterior chamber with balanced salt solution or alpha-chymotrypsin. The results show that both lens particles and soluble lens proteins can directly obstruct the aqueous outflow pathways of human eyes. Such obstruction may be a significant factor in certain lens-induced glaucomas.

Phacolytic glaucoma--its treatment by planned extracapsular cataract extraction with posterior chamber intraocular lens implantation.

Phacolytic glaucoma has traditionally been treated with intracapsular lens extraction to avoid any anaphylaxis. Various mechanisms have been described for the rise of intraocular pressure in these cases. The present study was undertaken to evaluate the response of extracapsular cataract extraction (ECCE) with posterior chamber intraocular lens implantation (PC IOL) in five cases of phacolytic glaucoma that occurred between March 1989 and August 1990. A planned extracapsular cataract extraction with can-opener capsulectomy was done in all the cases with placement of a sulcus-fixated modified J-loop Sinskey design intraocular lens. With a mean follow-up period of two years, all patients (100%) maintained a normal postoperative intraocular pressure of less than 20 mm Hg without any additional medical therapy. The final best-corrected visual acuity in 4 cases (80%) was 6/12 or better, while in one case it was 6/24 due to a senile maculopathy. These results show that ECCE with PC IOL implantation is a safe and efficacious method of visual rehabilitation in cases of phacolytic glaucoma.

Polymorphism and higher order structures of protein nanofibers from crude mixtures of fish lens crystallins: toward useful materials.

Protein nanofibers are emerging as useful biological nanomaterials for a number of applications, but to realize these applications requires a cheap and readily available source of fibril-forming protein material. We have identified fish lens crystallins as a feedstock for the production of protein nanofibers and report optimized methods for their production. Altering the conditions of formation leads to individual protein nanofibers assembling into much larger structures. The ability to control the morphology and form higher order structures is a crucial step in bottom up assembly of bionanomaterials. Cell toxicity assays suggest no adverse impact of these structures on mammalian cell proliferation. There are many possible applications for protein nanofibers; here we illustrate their potential as templates for nanowire formation, with a simple gold plating process.

Pharmacological prevention of ocular inflammation induced by lens proteins.

Ocular inflammation was induced by lens protein to mimic the traumatic injury of the eyes. Pretreatment of the eyes with indomethacin resulted in marked reduction of this ocular inflammation in the early phase. Pretreatment of the eyes with phenidone and nordihydroguaiaretic acid (NDGA) on the other hand reduced ocular inflammation during both early and late phases. These results indicate that prostaglandins are involved in early phase of the inflammation which can be reduced with cyclooxygenase inhibitors such as indomethacin and leukotrienes are responsible primarily in the later phase because they are suppressed by lipoxygenase inhibitors such as phenidone and NDGA. Although histamine is implicated in the process of inflammation, the H1-antagonist, pyrilamine, had very little effect on ocular inflammation, whereas the H2-antagonist, cimetidine, exhibited no effect but rather enhanced the ocular inflammatory responses at the peak of inflammation. These results are not in accord with published findings.