(1/403) Herpetic keratitis. Proctor Lecture.

Although much needs to be learned about the serious clinical problem of herpes infection of the cornea, we have come a long way. We now have effective topical antiviral drugs. We have animal models which, with a high degree of reliability, clearly predict the effect to be expected clinically in man, as well as the toxicity. We have systemically active drugs and the potential of getting highly active, potent, completely selective drugs, with the possibility that perhaps the source of viral reinfection can be eradicated. The biology of recurrent herpes and stromal disease is gradually being understood, and this understanding may result in new and better therapy of this devastating clinical disease.  (+info)

(2/403) Infectious keratitis in leprosy.

AIM: To describe leprosy characteristics, ocular features, and type of organisms that produce infective corneal ulcers in leprosy patients. METHOD: The records of all leprosy patients admitted for treatment of corneal ulcers between 1992 and 1997 were reviewed. RESULTS: 63 leprosy patients, 53 males and 10 females, are described. 16 were tuberculoid and 47 lepromatous. 25 patients had completed multidrug therapy. 10 patients had face patches, eight had type I reaction, and 10 had type II reaction. 43 (68%) patients had hand deformities. In 54% of patients pain was absent as a presenting symptom. 19 patients gave a history of trauma. In 15 patients ulcers had also occurred on the other eye, five of them having occurred during the study period and the rest before 1992. Of the 68 eyes with corneal ulcers, 28 had madarosis, 34 had lagophthalmos, nine had ectropion, three had trichiasis, six had blocked nasolacrimal ducts, and 39 decreased corneal sensation. In 14 eyes, a previous lagophthalmos surgery had been done. 16 patients were blind at presentation. 32% of ulcers were located centrally. After treatment only 18% of the eyes showed visual improvement. Five types of fungus were cultured, two of them rare ocular pathogens. CONCLUSIONS: Corneal ulcers occur more in males and in the lepromatous group of patients. Decreased corneal sensation, lagophthalmos and hand deformity are closely associated. Indigenous treatment and late presentations were notable in many patients. Visual outcome is not good. There is increased risk of developing an ulcer in the other eye. Fungal corneal ulcers are not uncommon.  (+info)

(3/403) Incidence of corneal melting in association with systemic disease in the Yorkshire Region, 1995-7.

AIMS: To estimate the incidence of corneal melting or necrotising keratitis in association with systemic disease in the Yorkshire Region and to determine the type and duration of the systemic association. METHODS: In a prospective study, vigorous attempts were made to identify all patients presenting with newly diagnosed corneal melting over a 3 year period. RESULTS: 27 patients were identified during the study period. Rheumatoid arthritis and Wegener's granulomatosis were the most common disease associations. Corneal melting was a late complication of rheumatoid arthritis, but usually occurred during early and overt systemic disease in patients with Wegener's granulomatosis. CONCLUSION: The annual incidence of corneal melting in the Yorkshire Region is 3.01/million/year (95% CI = 0.7-9.6).  (+info)

(4/403) Corneal epithelial-specific cytokeratin 3 is an autoantigen in Wegener's granulomatosis-associated peripheral ulcerative keratitis.

PURPOSE: In a previous investigation it was demonstrated that circulating antibodies to a 66-kDa corneal epithelial antigen (BCEA-A) are associated with peripheral ulcerative keratitis (PUK) in patients with Wegener's granulomatosis (WG). The aim of this study was to identify BCEA-A. METHODS: The 66-kDa antigen was purified from a bovine corneal epithelial protein extract, using DE52 ion exchange chromatography. Purified protein was used to raise rabbit polyclonal antibodies. These antibodies were used to screen a bovine corneal epithelial cDNA expression library. Positive clones were purified and sequenced. Clones were identified by DNA sequence homology searches of the GenBank DNA database. RESULTS: A cDNA clone that demonstrated strong binding to both the rabbit polyclonal antibody and patient sera, showed 85% homology to rabbit cytokeratin 3 (K3). K3 is a basic cytokeratin specific to corneal epithelium. No bovine DNA sequence for K3 is available. However, bovine K3 is larger than rabbit K3, with a molecular weight of 66 kDa. Immunofluorescence using both patient sera and the rabbit antibody demonstrated a cytoplasmic binding pattern on human corneal epithelium. CONCLUSIONS: This evidence suggests that the 66-kDa autoantigen (BCEA-A) associated with PUK in WG is cytokeratin 3, and this may form the basis of a diagnostic/prognostic test.  (+info)

(5/403) Fungal corneal ulcers of onion harvesters in southern Taiwan.

Fungal corneal ulcers related to agriculture has been reported throughout the world, especially in tropical areas. Most of them were sporadic and had histories of ocular trauma or use of topical corticosteroids and topical antibiotics. Five onion harvesters had fungal corneal ulcers during the same harvest period in Southern Taiwan. The authors think that this is the first report of a group occurrence relating to agricultural workers. Although all of the patients improved after medical and surgical management, their vision was greatly decreased. It is suggested that the tropical climate, the harvest procedure, the characteristic monsoon, and lack of eye protection were involved. Therefore, the importance of the eye protection, hygiene education, and improving medical care to reduce the occurrence of fungal corneal ulcer in agriculture workers must be emphasised.  (+info)

(6/403) Role of ocular matrix metalloproteinases in peripheral ulcerative keratitis.

AIM: Peripheral ulcerative keratitis (PUK) is an ocular manifestation of rheumatoid arthritis and other similar systemic diseases. The purpose of this inquiry was to investigate the involvement of matrix metalloproteinases (MMPs) in the induction and/or maintenance of PUK. METHODS: Substrate gel electrophoresis was used to characterise the MMP activities secreted by primary cultures of keratocytes derived from normal and perforated pathological corneal specimens, and those present in tears of normal subjects and patients with PUK. Substrate specificity and the in vivo activity status of the secreted MMPs was assessed by SDS-polyacrylamide gel electrophoresis of standard collagens incubated in the presence or absence of the various enzyme preparations. RESULTS: In addition to MMP-2 of M(r) 66,000, cultured keratocytes derived from perforated corneas of patients with PUK abnormally produce the MMP-2 of apparent M(r) 62,000. Other MMPs and in particular MMP-9 of M(r) 92,000, also occur in the tears of these patients. Their visualisation on substrate polyacrylamide gels correlated with clinical manifestations of disease activity; during periods of disease quiescence they were barely detectable. The steroid prednisolone, frequently used in systemic therapy, had no effect on the in vitro activity of MMP-2, or on its production by cultured corneal keratocytes. Although the in vitro activity of MMP-2 was inhibited by both Cu(2+) and Zn(2+), Cu(2+) apparently induced the keratocytes to produce activated enzyme and Zn(2+) irreversibly inhibited their production of MMP-2. CONCLUSION: Overexpression of corneal MMP-2 and tear film MMP-9 are characteristic features of patients with PUK and their activation may be a crucial facet of disease initiation or progression. Although effective in systemic therapy for PUK, prednisolone had no direct control over corneal MMP-2 production or activity. Zn(2+) on the other hand inhibited both MMP-2 production and MMP-2 activity and may, therefore, be of therapeutic value if suitably formulated and used in conjunction with systemic steroid treatment.  (+info)

(7/403) Evidence for TIMP-1 protection against P. aeruginosa-induced corneal ulceration and perforation.

PURPOSE: To determine the biological significance of individual endogenous tissue inhibitors of metalloproteinases (TIMPs) in protection against tissue destruction using a Pseudomonas aeruginosa-induced model of corneal ulceration. METHODS: Corneal TIMP-1, -2, and -3 mRNA levels were compared between young adult (resistant) and aged (susceptible) mice challenged with P. aeruginosa. Resistant mice that demonstrated greater amounts of an individual TIMP were treated with polyclonal antibody (pAb) to that TIMP. To determine whether TIMP neutralization exacerbated P. aeruginosa-induced corneal disease, TIMP pAb- and normal rabbit serum (NRS)- (control) treated mice were examined macroscopically and histopathologically after infection. Corneal neutrophil (PMN) myeloperoxidase (MPO) levels also were examined in these mice. RESULTS: Greater amounts of TIMP-1 mRNA only were found in corneas of resistant versus suscep tible mice after P. aeruginosa challenge. Systemic treatment of resistant mice with TIMP-1 pAb resulted in corneal perforation by 5 to 7 days after infection (PI). Histopathologic evaluation of corneal tissues from TIMP-1 pAb- versus NRS-treated mice confirmed that TIMP-1 pAb treatment resulted in extensive stromal dissolution. This treatment also was associated with loss of epithelium within the central cornea. Both the histopathology and PMN MPO enzyme assays also showed an increase in corneal PMN number following TIMP-1 pAb treatment. CONCLUSIONS: These studies provide evidence that, after P. aeruginosa infection, adequate endogenous expression of TIMP-1 in cornea protects against extensive corneal tissue destruction. The protective effects of TIMP-1 may be multifactorial. In addition to directly protecting extracellular matrix components from active matrix metalloproteinases, TIMP-1 may either directly or indirectly influence recruitment of PMNs into infected cornea. Finally, TIMP-1 also may affect wound healing and resurfacing of the corneal epithelium.  (+info)

(8/403) Peripheral ulcerative keratitis 'corneal melt' and rheumatoid arthritis: a case series.

OBJECTIVES: (1) To review the visual and systemic outcomes of patients who developed rheumatoid arthritis (RA)-associated peripheral ulcerative keratitis (PUK). (2) To describe the clinical and serological characteristics of the patients' arthropathy at the time of presentation of this rare condition. (3) To review the aetiology and management of RA-associated PUK. Patients and methods. A case series is given of all nine patients within our unit who have developed RA-associated PUK since 1996. Details of the patients' arthropathy and the serological characteristics of the RA at presentation of PUK were noted. The patients' visual outcomes and the development of any significant systemic complications were recorded. RESULTS: All patients had long-standing seropositive, erosive RA. PUK was associated with a poor visual outcome in most patients, five requiring emergency corneal surgery to prevent perforation of the globe. Two patients developed systemic vasculitis within 1 month of PUK onset, one of whom died. CONCLUSION: RA-associated PUK often has a poor visual outcome and its appearance may herald the transformation of a patient's RA into the systemic vasculitic phase. RA-associated PUK should be managed with aggressive immunosuppression if the associated morbidity and mortality are to be avoided. Cell-mediated mechanisms appear to be important in the aetiopathogenesis of PUK and a combination of corticosteroids and cyclosporin is therefore probably the regimen of choice.  (+info)