Topical mitomycin-C for subepithelial fibrosis after refractive corneal surgery.

OBJECTIVE: To determine the effectiveness of mitomycin-C (MMC), 0.02%, in preventing recurrence of corneal subepithelial fibrosis after debridement and/or keratectomy in patients who have undergone refractive corneal surgery. DESIGN: Noncomparative case series. PARTICIPANTS: Eight eyes of five patients with corneal subepithelial fibrosis who had previously undergone radial keratotomy (n = 4) or photorefractive keratectomy (n = 4). INTERVENTION: All eyes underwent epithelial debridement followed by a single intraoperative application of MMC (0.02%) for 2 minutes followed by saline irrigation. The eyes were then patched, or a bandage contact lens placed until epithelial healing was complete. MAIN OUTCOME MEASURES: Corneal clarity and best-corrected visual acuity (BCVA). RESULTS: In all cases, the cornea remained clear with no recurrence throughout the follow-up period (6-25 mos., mean, 13.8 mos). No adverse reactions were reported. BCVA improved in all cases. CONCLUSIONS: Subepithelial fibrosis can be a visually disabling condition after refractive corneal surgery. Topical application of MMC (0.02%) may be a successful method of preventing recurrence of subepithelial fibrosis after debridement.

Irreversible corneal decompensation in patients treated with topical dorzolamide.

PURPOSE: To describe irreversible corneal decompensation after topical dorzolamide hydrochloride (Trusopt; Merck and Co, Inc, West Point, Pennsylvania) therapy in nine patients who had histories consistent with corneal endothelial compromise. METHOD: Multicenter review of patients' charts. RESULTS: Nine eyes of nine patients developed overt corneal decompensation after starting topical dorzolamide, a condition that did not resolve with drug cessation. This occurred after 3 to 20 weeks (mean, 7.8) of therapy. All nine patients had undergone intraocular surgery. Eight patients had undergone cataract surgery; three were aphakic and three had posterior chamber intraocular lenses. Two patients had anterior chamber intraocular lenses and also had undergone trabeculectomies. Four patients had undergone penetrating keratoplasties, each case complicated by episodes of corneal allograft rejection that were successfully treated. Two patients had asymptomatic Fuchs endothelial dystrophy. Seven patients have since undergone successful penetrating keratoplasties. CONCLUSION: The reports suggest that dorzolamide can cause irreversible corneal edema in a subset of glaucoma patients with endothelial compromise. The findings suggest a rationale for research into the long-term effects of dorzolamide on the corneal endothelium.

Involvement of LFA-1 and ICAM-1 in the herpetic disease resulting from HSV-1 corneal infection.

Herpes simplex virus type 1 (HSV-1) corneal infection in immunologically normal mice results in a transient epithelial lesion followed in about 2 weeks by a potentially blinding inflammatory response in the corneal stroma, and a mild blepharitis. Similarly infected T cell-deficient mice do not develop corneal stromal inflammation, but exhibit severe periocular skin disease and succumb to viral encephalitis. The role of certain adhesion molecules in both T cell activation, and in the extravasation of inflammatory cells from the blood into inflammatory sites is now being established. These studies investigated the involvement of the adhesion pair LFA-1/ICAM-1 in the disease that results from HSV-1 corneal infection in mice. Treatment of mice with mAb to LFA-1 beginning 1 day before HSV-1 corneal infection resulted in a delay in the onset of stromal inflammation, but ultimately stromal inflammation developed to a normal extent. This treatment also caused a significant exacerbation of periocular skin disease, but did not render mice susceptible to encephalitis. Treatment with mAb to ICAM-1 beginning 1 day before HSV-1 corneal infection caused an acceleration of both stromal inflammation and periocular skin disease, and rendered mice uniformly susceptible to lethal encephalitis. Treatment with either mAb beginning 6 days after HSV-1 corneal infection did not significantly affect the clinical course of herpetic disease. Our findings suggest that LFA-1 may play a role in the early phase of corneal stromal inflammation following HSV-1 corneal infection. Both LFA-1 and ICAM-1 appear to be important for protection of the skin from HSV-1 infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Absence of normal keratan sulfate in the blood of patients with macular corneal dystrophy.

We measured levels of sulfated keratan sulfate in serum using a monoclonal antibody in an enzyme-linked immunosorbent assay. Sulfated keratan sulfate was not detected in the serum of 16 patients with macular corneal dystrophy, but was present at normal levels in 66 patients with other corneal diseases. There were no differences with respect to age, sex, and other ocular findings. This monoclonal antibody recognizes a sulfated carbohydrate epitope present in both corneal and skeletal keratan sulfate. Since most serum keratan sulfate is derived from the cartilages, the defect in keratan sulfate synthesis in macular corneal dystrophy may not be restricted to corneal cells. This assay should prove useful in the diagnosis of macular corneal dystrophy, particularly in children at risk before the appearance of opacification.

Anterior segment anomalies associated with the fetal alcohol syndrome.

Anterior segment anomalies were noted in eight children diagnosed as having the fetal alcohol syndrome. Peters' and Axenfeld's anomalies were among the specific defects noted. Four children have maintained clear corneal grafts. A teratogenic action of alcohol during a critical period of development of anterior chamber structures is suggested as an etiologic factor. It is proposed that the varied types and severity of abnormalities noted might result from differences in blood alcohol levels, timing of the insult, and genetic background of the fetus. The observation of various types of malformations thought to share a similar pathogenesis lends additional support to the assumption that there is an interrelationship among these types of congenital segment pathology.

Aspirin, cyclophosphamide, and dexamethasone effects on experimental secondary herpes simplex uveitis.

The effects of aspirin, cyclophosphamide, and dexamethasone on secondary herpes simplex uveitis were studied in rabbits. Neither daily treatment with aspirin (rectal suppositories, 650 mg begun 24 hours before challenge) nor cyclophosphamide injections every two days (80 mg begun eight days before challenge) had any effect on the severity of the uveitis, on the rise in intraocular pressure (IOP), or on the host's immune responses. As in the control animals, infectious herpes simplex virus (HSV) could not be isolated from iris tissues of either aspirin- or cyclophosphamide-treated rabbits. On the other hand, twice-daily treatment with topical dexamethasone (0.1% drops begun 24 hours before challenge) lessened the severity of the uveitis appreciably and suppressed the rise in IOP, but iris tissues yielded infectious HSV in two of ten eyes. Although the dexamethasone had no effect on the neutralizing-antibody or macrophage migration inhibition factor, it markedly suppressed the chemotactic activity of the aqueous humor for both polymorphonuclear leukocytes and macrophages.