Showing papers by "Edward J. Holland published in 2007"

Nepafenac ophthalmic suspension 0.1% for the prevention and treatment of ocular inflammation associated with cataract surgery.

Abstract: Purpose To determine whether nepafenac ophthalmic suspension 0.1% decreases the incidence and severity of inflammation and pain after cataract surgery with posterior chamber intraocular lens implantation. Setting Twenty-one ophthalmology clinics in the United States. Methods A randomized double-blind vehicle-controlled trial was conducted in which adult patients were randomly assigned to receive nepafenac 0.1% or vehicle beginning 1 day before surgery and continuing on the day of surgery (day 0) for 14 days. Patients were evaluated on days 1, 3, 7, and 14. The primary efficacy variable was the percentage of patients cured at day 14 (cure defined as aqueous cells score + aqueous flare score=0). Other efficacy variables included percentage of patients who were pain free at all visits and aqueous cells, flare, and cells plus flare scores. Results The mean age of the 476 patients (243 nepafenac, 233 vehicle) was 70 years (range 27 to 93 years). At day 14, 152 patients (62.6%) in the nepafenac group and 40 (17.2%) in the vehicle group were cured ( P P P Conclusion Nepafenac ophthalmic suspension 0.1% was safe and effective for preventing and treating ocular inflammation and pain associated with cataract surgery.

Double-masked study of the effects of nepafenac 0.1% and ketorolac 0.4% on corneal epithelial wound healing and pain after photorefractive keratectomy.

Abstract: Two NSAIDs—nepafenac 0.1% and ketorolac tromethamine 0.4%—were compared in terms of their effects on corneal reepithelialization and pain after photorefractive keratectomy (PRK) in a randomized, double-masked, contralateral eye, multicenter study. A total of 40 healthy adult patients who were undergoing sequential bilateral PRK received nepafenac 0.1% and ketorolac 0.4% in contralateral eyes, 1 drop 3 times daily for 3 d after bandage contact lens insertion. Patients were assessed on postoperative days 1, 3, 4, 5, and 7. At each visit, patients provided a general rating of pain. Each patient also assessed the sensation of each eyedrop following instillation (after-drop pain, irritation, burning/stinging, and overall comfort). Starting on day 3, epithelial defect size was assessed. Mean epithelial defect size was similar between treatments at each postoperative visit (P > .05). The average time-to-healing was 4.18 d for nepafenac 0.1 % and 4.00 d for ketorolac 0.4% (P=.3134). No statistical difference was observed between nepafenac 0.1% and ketorolac 0.4% in mean postoperative pain scores (P > .05). On day 3, the nepafenac 0.1% group had significantly lower mean sensation scores than did the ketorolac 0.4% group for after-drop pain (P=.0090), irritation (P=.0007), and burning/ stinging (P=.0003). Mean overall comfort score was also significantly better for nepafenac 0.1% on day 3 (7.43 vs 6.41; P < .0001). Nepafenac 0.1% and ketorolac 0.4% provide postoperative pain relief after PRK surgery without associated adverse effects on corneal epithelial healing. Nepafenac 0.1 % treatment may offer greater comfort upon instillation in patients who have undergone PRK.

Resolution of Autoimmune Polyglandular Syndrome–Associated Keratopathy With Keratolimbal Stem Cell Transplantation: Case Report and Historical Literature Review

Abstract: In 1929, Thorpe and Handley1 described the case of a 4.5-year-old girl with chronic tetany secondary to parathyroid deficiency and chronic intractable oral mycelial infection. The authors also described “a slight opacity of both corneas” that later developed “large cornea ulcerations.” Since that time, the described syndrome has been well documented. However, the associated keratopathy has been poorly understood and not effectively treated. Autoimmune polyglandular syndrome type 1 (APS1) is a rare autosomal recessive polyendocrinopathy with variable combinations of mucocutaneous candidiasis, autoimmune destruction of endocrine glands, and ectodermal dystrophy. Specific endocrine dysfunction can include hypoparathyroidism, Addison disease, hypothyroidism, and diabetes. This syndrome is also known as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). Ocular manifestations are often disabling and include keratoconjunctivitis, dry eye, iridocyclitis, cataract, retinal detachment, and optic atrophy.2 Keratopathy has been associated with APS1 since its original description in 1929 and is considered to be an essential feature of the syndrome. In 1962, Gass published the first extensive review of APS1-associated keratoconjunctivitis.3 He reported that keratoconjunctivitis occurred in 50% of patients with APS1 and was often one of the earliest manifestations of the syndrome. The keratitis was thought to be phlyctenular and possibly related to monolithiasis. Two cases were suspected to be compatible with Salzmann nodular dystrophy. Visual acuity was as poor as 5/200 in 1 case. Since then, several reports have further described the keratopathy in APS1. Stieglitz et al4 described 2 cases that were later included in a case series by Wagman et al5 in 1987. Four of 16 patients with APS1 manifested a self-limited, bilateral keratitis. The age of onset ranged from 2 to 9 years. In 2 of the 4 patients, the keratitis preceded the onset of any endocrinopathy. Wagman et al did not believe that the keratitis was a hypersensitivity reaction to Candida. Instead, he suggested that the cause may be a defect in suppressor T-lymphocyte function. However, the laboratory studies of Wagman et al did not show an autoimmune etiology for the keratitis. These results corresponded well to a later long-term review of 69 patients with APS1 by Merenmies and Tarkkanen2 published in 2000. In this series, 17 patients (25%) had chronic bilateral keratitis. In 13 patients, the first symptoms occurred before the age of 4 years, and in 3 patients, keratitis was the presenting sign before any systemic disease. The final visual acuity of the better eye in the 17 patients with APS1-associated keratitis was 0.6 (20/80) or more in only one third of the patients. Keratitis was again not thought to be secondary to candidiasis, but no alternate etiology was proposed and remained unknown. Without a basic understanding of the cause of the keratopathy, previously attempted surgical treatments have had poor results. In this report, we discuss our hypothesis that APS1-associated keratopathy is secondary to limbal stem cell deficiency. In the past impression cytology has been used to show limbal stem cell deficiency in 2 patients with APS1.6 Furthermore, Tseng et al7 has reported the use of ex vivo expanded allogenic limbal stem cells on amniotic membrane to treat limbal stem cell deficiency in a patient with multiple endocrine deficiency. The following is the first case of bilateral APS1-associated keratopathy effectively treated with keratolimbal allograft (KLAL) stem cell transplantation and superficial keratectomy.