Induction of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs correlates with outcome of acute experimental pseudomonal keratitis.

This study aimed to investigate expressions and sources of matrix metalloproteinases (MMP)-2 and MMP-9, and of tissue inhibitors of MMP (TIMP)-1 and TIMP-2 in experimental Pseudomonas aeruginosa keratitis in rabbits. Pseudomonal keratitis was induced in New Zealand white rabbits, and macroscopic and microscopic examinations were performed at appropriate time points (3, 9, 12, 18, 24, 72 h). Expressions and sources of MMP-2, 9, and TIMP-1, 2 were determined using immunohistochemistry, gelatin zymography, ELISA, and RT-PCR. A typical corneal ulcer with a ring abscess was observed 12-72 h post-infection (p.i.) with P. aeruginosa. In microscopic examinations, massive inflammatory cell (mostly polymorphonuclear leukocytes, PMNs) infiltration and liquefactive necrosis were characteristic features. MMP-2 was constitutively expressed in keratocytes, and its expression was not apparently enhanced after pseudomonal infection as evidenced by zymography, immunostaining, and RT-PCR. However, MMP-9 and its activated form were induced, and were significantly enhanced 12-24 h p.i. MMP-9 appeared to derive from PMNs rather than from resident corneal cells. TIMP-1 was expressed in PMNs, macrophages, and keratocytes, and its expression was enhanced 72 h p.i. Although TIMP-2 was constitutively expressed as seen by immunostaining and RT-PCR, its concentration was below detection limits during the experiments. We demonstrated that MMP-9 was one of the important factors for corneal tissue destruction, because it was induced and significantly expressed in keratocytes and inflammatory cells after pseudomonal infection. Although TIMP-1 was expressed in later stages of infection, enhancement and activation of MMP-9 were much faster and stronger than those of TIMP-1, thereby facilitating tissue destruction leading to corneal ulceration.

[Herpes simplex keratitis after ophthalmic surgery].

PURPOSE: We report 6 cases of herpes simplex keratitis after ophthalmic surgery, in eyes without clinical history of herpes simplex keratitis. CASES: These cases comprised 6 patients examined at our hospital between April 1992 and November 2001. Past operations were keratoplasty in 5 eyes and cataract surgery in 1 eye. Clinical findings and predisposing factors were evaluated retrospectively. The period between herpetic epithelial keratitis onset and ophthalmic surgery ranged from 1.5 to 79 months. Predisposing factors included corticosteroid therapy and operative wound. The herpetic epithelial lesions were dendritic ulcers in 2 eyes, geographic ulcer in 1 eye, and atypical epithelial lesions in 3 eyes; in all cases, herpes simplex virus (HSV)-DNA was detected by polymerase chain reaction (PCR) in tear fluid. All herpetic epithelial lesions healed with oral and topical acyclovir. CONCLUSIONS: When corticosteroids are used following ophthalmic surgery, physicians should be alert to the possibility of herpetic epithelial keratitis, even in patients with no clinical history of herpes simplex keratitis. PCR detection in tear fluid is helpful in diagnosing this disease.

[A case of corneal lactoferrin amyloidosis secondary to trichiasis].

PURPOSE: A case of corneal lactoferrin amyloidosis secondary to trichiasis is reported. CASE: A 30-year-old male suffered from trichiasis with an elevated gray whitish lesion just under the center of the cornea in his right eye. The lesion had an irregular surface. METHOD: We excised the corneal lesion, and studied the excised corneal lesion morphologically. RESULT: The deposit observed just under the corneal epithelial layer was positive for Congo red staining, and showed dichroism under polarizing microscopy. The deposit also showed a immunoreactivity against anti-human lactoferrin antibody. CONCLUSION: The morphological study proved that the deposits under the corneal lesion were derived from lactoferrin. Long term injury of the corneal surface by trichiasis may lead to the deposition and structural changes of lactoferrin originating from tears.

New surgical treatment for superior limbic keratoconjunctivitis and its association with conjunctivochalasis.

PURPOSE: To introduce a new surgical procedure for treating superior limbic keratoconjunctivitis (SLK) and to suggest the association of SLK with conjunctivochalasis. DESIGN: Interventional case series. METHODS: Six eyes of five patients with long-standing severe ocular irritation unresponsive to treatment with topical steroid and artificial tears were operated on using our new procedure. This technique consists of four steps as follows: (1) Rose bengal (RB) staining is used to localize the abnormal conjunctival area; (2) an arc-like conjunctival incision is placed from the 2 to the 10 o'clock position adjacent and distal to the RB-stained area; (3) the conjunctiva is resected to form a crescent using the arc-like incision as the base; the size of the resection is determined by conjunctival redundancy after removal of the subconjunctival connective tissue; and (4) the crescent conjunctival opening is closed with interrupted sutures. In two eyes, the new surgical procedure was performed together with surgery for inferior bulbar conjunctivochalasis. RESULTS: In all operated eyes, RB staining had disappeared by the end of the second postoperative week; recovery from symptoms and loss of inflammation were recorded by 1 month after treatment. In the case with the longest follow-up (14 months), there was cytologic evidence of goblet cell recovery at 3 months after the operation. In another, there was normalization of the nucleo/cytoplasmic ratio of conjunctival cells without the appearance of goblet cells. CONCLUSIONS: Our treatment very effectively resolved symptoms associated with SLK, even in eyes unresponsive to conventional therapy with eye drops. Considering that we did not address the diseased part of the conjunctiva but rather the adjacent conjunctival redundancy, we propose that superior bulbar conjunctivochalasis is involved in the pathogenesis of SLK.