Long-term visual outcomes in patients with successful macular hole surgery.

OBJECTIVE: The purpose of the study is to determine the long-term visual outcomes in patients undergoing successful macular hole surgery. DESIGN: A consecutive series of eyes with an anatomically successful macular hole surgical result and at least 1 year postoperative follow-up information was identified and studied. Preoperative and postoperative visual acuities were measured in accordance with the Early Treatment Diabetic Retinopathy Study protocol. MAIN OUTCOME MEASURES: Visual acuity, improvement of visual acuity, and rate of final visual greater than or equal to 20/40 were measured. RESULTS: The median visual acuity increased from 20/125 before surgery to 20/50 1 year after surgery (93 eyes) and to 20/30 at 36 months after surgery (68 eyes). The trend for improvement in visual acuity after 1 year after surgery was statistically significant. The postoperative visual acuity was greater than or equal to 20/40 in 15 (17%) eyes at 3 months and 53 (78%) at 36 months. Before surgery, 12 (13%) eyes were pseudophakic, and 77 (83%) were pseudophakic at 36 months. Median visual acuity in the fellow eye was 20/32 at baseline and 20/32 at 36 months. The visual acuity in the study eye was better than in the fellow eye in 36 (39%) patients at 36 months after surgery. CONCLUSIONS: Visual acuity in patients after anatomically successful macular hole surgery continues to improve even beyond 1 year after surgery. Although substantial improvement occurs soon after cataract extraction, further improvement in visual acuity continues for 2 years thereafter.

Iritis and hypotony after treatment with intravenous cidofovir for cytomegalovirus retinitis.

OBJECTIVE: To describe intraocular inflammation due to treatment with intravenous cidofovir dihydrate for cytomegalovirus retinitis. DESIGN: Retrospective cohort. SETTING: Three university outpatient ophthalmology clinics. PATIENTS: All patients treated with intravenous cidofovir therapy before October 31, 1996. INTERVENTION: Treatment with intravenous cidofovir was given according to standardized protocols. Intraocular inflammation was treated according to the best medical judgment. MAIN OUTCOME MEASURES: The presence of new intraocular inflammation, the severity of inflammation, visual acuity, and intraocular pressure. RESULTS: Eleven cases of iritis (26%) occurred among 43 patients. In 6 cases, the iritis was bilateral. Patients who experienced iritis were more likely to have been previously treated for cytomegalovirus retinitis (P = .03), to be diabetic (P = .05), or to be receiving protease inhibitors (P < .001). Four patients and 15 control subjects had also taken rifabutin (P = .70). The onset of iritis occurred at a mean (+/-SD) of 4.9 +/- 1.8 days after a cidofovir dose and after a mean (+/-SD) of 4.2 +/- 1.6 doses of cidofovir. Six eyes of 4 patients had hypotony. Five eyes of 5 patients had a persistent decrease in visual acuity of at least 2 Snellen lines. CONCLUSIONS: Acute intraocular inflammation may occur with or without hypotony after intravenous cidofovir therapy, similar to the reactions seen after intravitreous administration. Although the manifestations may be severe, they are manageable with topical corticosteroid therapy in most cases. Cidofovir therapy can be continued in some patients if medical necessity warrants, but recurrent inflammation or permanent hypotony may occur.

Visual acuity and macular hole size after unsuccessful macular hole closure.

PURPOSE: To evaluate the visual acuity, change in macular hole size, and change in subretinal fluid cuff size after unsuccessful macular hole closure. METHODS: Forty-two consecutive eyes with macular hole and unsuccessful surgery for macular hole were studied. Preoperative and postoperative best-corrected visual acuities were tested according to the Early Treatment Diabetic Retinopathy Study (ETDRS) protocol, and changes were compared. Preoperative and postoperative fundus photographs were analyzed on a photograph documenter for changes in diameter of the macular hole and surrounding subretinal fluid cuff. RESULTS: Mean visual acuity decreased from 20/133 preoperatively to 20/154 postoperatively (mean loss, 0.79 ETDRS line). Mean diameter of the macular hole enlarged 22%; mean diameter of the visible surrounding subretinal fluid cuff enlarged 36%. A decrease in best-corrected visual acuity postoperatively was correlated with better preoperative visual acuity, earlier macular hole stage, and shorter duration. Enlargement in the diameter of the macular hole and fluid cuff did not correlate with better preoperative best-corrected visual acuity, earlier macular hole stage, or shorter duration. In 23 eyes that had failed previous surgery, macular hole surgery was anatomically successful in 17 (65%) (mean improvement, 3.7 ETDRS lines; mean best-corrected final visual acuity, 20/74). CONCLUSION: After macular hole surgery, anatomically unsuccessful closure of the hole correlates with small enlargements in the diameter of the macular hole and its surrounding subretinal fluid cuff, and with a slight decrease in visual acuity. Macular hole closure after repeat surgery improves visual acuity outcome in the majority of retreated eyes.

Structural elements in the N-terminal half of transcription factor IIIA required for factor binding to the 5S RNA gene internal control region.

Zinc binding domains and the conserved Thr-Gly-Glu-Lys (TGEK) tetrapeptide in the N-terminal half of transcription factor IIIA (TFIIIA) were subjected to in vitro mutagenesis to biochemically assess their role in factor interaction with the 5S gene internal control region (ICR). TFIIIA containing a Leu in place of His33 in the Cys2His2 zinc binding site of finger I lost the ability to protect the entire 5S RNA gene ICR (nucleotides +96 to +43) from DNase I digestion. Thus, mutation of one potential zinc ligand in the N-terminal finger inhibited specific DNA binding by the N-terminal as well as downstream fingers. Cooperativity apparently exists among TFIIIA zinc fingers in metal binding/finger folding and DNA binding. Substituting a Ser for Gly69 or a Glu for Lys 71 in the conserved TGEK tetrapeptide in finger II of TFIIIA resulted in the loss of DNA binding. A Gly-dependent bend structure and a terminal positive charge in this tetrapeptide are important for TFIIIA interaction with DNA. Whereas TFIIIA with a Ser substituted for Cys20 in finger I (proposed zinc ligand) did not protect the ICR from DNase I digestion, TFIIIA containing a Ser substituted for Cys35 (not a proposed zinc ligand) retained the ability to bind the ICR. When Cys112 or Cys 164 (proposed zinc ligands in fingers IV and VI) were replaced by Ser, the DNase I footprint patterns afforded by the respective mutant proteins were similar, protection on the ICR from about nucleotides +96 up to +78. A similar pattern was obtained with a TFIIIA mutant in which fingers V, VI, VII, and a portion of VIII were deleted. Maintenance of zinc coordination spheres in necessary for DNA binding by downstream fingers. The six fingers comprising the N-terminal half of TFIIIA appear to act in two groups of three with binding of the second group dependent upon initial binding of the N-terminal group to the +90 to +80 region of the 5S gene ICR.