Sulfadiazine modified PDMS as a model material with the potential for the mitigation of posterior capsule opacification (PCO).

Cataract surgery, while the most common surgical procedure performed, leads to posterior capsule opacification in approximately 30% of cases. Transforming growth factor beta 2 (TGF-ß2) and matrix metalloproteinases (MMPs) have been shown to play important roles in the cellular processes leading to posterior capsule opacification. Delivery of inhibitors to MMPs may have the potential to inhibit the initial cascade of events that lead to PCO. However, delivery of these molecules via tethering has proven difficult. In this work, sulfadiazine was tethered to polydimethylsiloxane (PDMS) via a polyethylene glycol (PEG) spacer as a potential MMPI mimic. Surface characterization using a variety of methods demonstrated successful modification with the antibiotic. The surfaces were examined with lens epithelial cells to determine their effect on these cellular processes, including cell transdifferentiation and production of extracellular matrix components. The presence of TGF-ß2 in the cell culture media was found to stimulate the production of ECM components such as collagen, fibronectin, and laminin, as well as alpha smooth muscle actin (α-SMA), and the migration marker Rho by HLE-B3 and FHL124 cells. In all cases, these effects were decreased but not completely eradicated by the presence of sulfadiazine on the PDMS surfaces. While the level of inhibition necessary for inhibition of PCO in vivo is unknown, these results suggest that IOL surface modification with sulfadiazine has the potential to reduce cellular changes associated with PCO. Furthermore, the results demonstrate for the first time that changes consistent with inhibition of fibrosis may be elicited by surfaces modified with sulfadiazine.

The dilution of benzalkonium chloride (BAK) in the tear film.

The claim that benzalkonium chloride (BAK) synergistically enhances the antibiotic efficacy of gatifloxacin ophthalmic solution 0.3% (preserved with 0.005% BAK [50 microg/mL), Zymar; Allergan Inc., Irvine, Calif, USA) has been the subject of several studies. The purpose of this prospective clinical study was to test the hypothesis that BAK would be significantly diluted shortly after topical ocular administration and would thereafter have little or no effect on the enhancement of the antibiotic efficacy of commercial gatifloxacin on the ocular surface. This hypothesis was tested by investigators who measured the concentration of tear film BAK at successive time points after topical administration of commercial gatifloxacin. After subjects (N=10) received 5 separate instillations of a single 35-microL drop of gatifloxacin 0.3% ophthalmic solution in each eye, tear samples were collected at 30 sec, 1 min, 3 min, 5 min, and 20 min, with the use of graduated 5-microL glass microcapillaries. A validated high-performance liquid chromatography method was used to measure the concentration of BAK in each tear sample. The results showed rapid BAK dilution to 6.4 microg/mL, 3.2 microg/mL, 1.4 microg/mL, below the detection limit, and below the detection limit at 30 sec, 1 min, 3 min, 5 min, and 20 min after instillation of a single 35-microL drop of gatifloxacin. Because such rapid dilution reduces the concentration of BAK to near zero in minutes and does not allow the time (1 h) required for effective bacterial kill power, BAK is not expected to have a clinically significant effect on enhancement of the antimicrobial efficacy of gatifloxacin on the human ocular surface.