preservative-free ketorolac 0.5% (Acular PF [Allergan, Inc, Irvine, California, USA]), and carboxymethylcellulose sodium 0.5% (Refresh Plus FP [Allergan, Inc.]). The rats were sacrificed at 48 hours and 1 week. Matrix metalloproteinase-1, MMP-2 and MMP-8 were detected at 48 hours and 1 week in the debrided and intact epithelium groups treated with topical NSAID, in debrided groups treated with unpreserved artificial tears, but not in intact groups treated with unpreserved artificial tears. In intact corneas, the MMP-1 and MMP-8 levels were higher with diclofenac sodium than with ketorolac. This study suggests that topical application of some topical NSAIDs may induce the early expression of MMP-1, MMP-2, and MMP-8 in the cornea, thereby playing a role in the corneal cytotoxicity of some NSAIDs.—Michael D. Wagoner *Terence P. O’Brien, MD, Ocular Microbiology and Immunology Laboratory, The Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21093; e-mail:
[email protected]
●
Staphylococcus epidermidis adherence to human amniotic membrane and to human, rabbit and cat conjunctiva. John T,* Allen S, John AG, Lai CI, Carey RB. J Cataract Refract Surg 2003;29:1211–1218.
T
HE ADHERENCE OF STAPHYLOCOCCAL EPIDERMIDIS TO
human amniotic membrane (HAM) was determined and compared with S. epidermidis to human, rabbit, and cat conjunctiva in vitro. Commercially available HAM and conjunctival specimens from humans, rabbits, and cats were exposed to S. epidermidis (3⫻108 colony-forming units per milliliter) for 0, 5, 30 and 90 minutes, rinsed in sterile saline, then processed for light, scanning (SEM), and transmission (TEM) electron microscopy. Scanning electron microscopy (⫻2000) was used to quantify adherent bacteria/mm2 of tissue. Bacterial adherence occurred with HAM and human, rabbit and cat conjunctiva and increased over time. Adherence to HAM was similar to that of human conjunctiva at 0, 5, and 30 minutes but greater at 90 minutes (1.57⫻), although this difference was not statistically significant (P⬎.16). The authors conclude that caution must be taken to prevent possible ocular infection with the use of HAM for ocular surface transplantation.—Michael D. Wagoner *Thomas John, MD, Department of Ophthalmology, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153; e-mail:
[email protected]
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Schnabel cavernous degeneration. A vascular change of the aging eye. Giarelli L, Falconieri G,* Cameron JD, Pheley AM. Arch Pathol Lab Med 2003;127:1314 –1319.
VOL. 137, NO. 2
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CHNABEL CAVERNOUS DEGENERATION OF THE OPTIC
nerve occurs is a histologic finding in eyes consisting of atrophy with pools of glycosaminoglycan deposited in the areas of nerve fiber bundles. This finding had been attributed to chronically increased intraocular pressure, although the precise nature of the finding is unknown. In order to determine the basic cause of the formation of cavernous spaces in the proximal optic nerve and its clinical significance, a retrospective analysis of 4500 autopsy eyes processed for histologic evaluation between 1967 and 1991 was undertaken. Ninety-three (2.1%) of the eyes exhibited Schnabel cavernous degeneration. The majority of the eyes were from women (81%). The mean age of the entire group was 88 years (range, 54 –103 years). Severe vascular anomalies were present in 75% of the individuals. Cavernous degeneration was unilateral in 82% of the cases. Loss of ganglion cells and the nerve fiber layer, consistent with glaucoma, was found in only 23.7% of the individuals. Clinical information was available for 15 individuals (16%). Half of them were thought to have some clinical optic nerve damage; in the remainder, no specific optic disk abnormalities were noted. Histologic findings or arteriosclerosis in the optic nerve circulation were common. Schnabel cavernous optic atrophy appears to be a unilateral condition of elderly women with systemic vascular disease and few clinically characteristic ocular features. This study indicates that a chronic vascular occlusive disease of the proximal optic nerve is more likely involved with the pathogenesis of Schnabel cavernous atrophy than is a sustained increase of intraocular pressure.—Hans E. Grossniklaus
*Giovanni Falconieri, MD, Department of Pathology and Laboratory Medicine, Division of Anatomic Pathology, General Hospital “S. Maria della Misericordia”, I 33100 Udine UD, Italy; e-mail:falconieri.
[email protected]
● Refractive changes in pregnancy. Pizzarello LD.* Graefes Arch Clin Exp Ophthalmol 2003;241:484 – 488.
T
O DETERMINE THE CAUSES OF ANY VISION CHANGE
reported during pregnancy, 240 pregnant women were asked whether they had any alteration in vision. Those who agreed to participate in the survey (83) and who complained of vision changes (12) were matched with asymptomatic pregnant women. All patients underwent a complete ophthalmic examination, including refraction. Those who had alterations in vision status were again evaluated after delivery. All women who complained of visual changes were found to have experienced a myopic shift from pre-pregnancy vision [0.87⫾0.3 diopters in the right eye (P⬍.0001) and 0.98⫾0.3 diopters in the left eye (P⬍.0001). Post partum, all subjects returned to near pre-pregnancy levels of myopia. Worsening of myopia occurs during pregnancy in some patients. The cause of
ABSTRACTS
393
this myopic shift is not readily evident.—Hans E. Grossniklaus
*Bjarni A. Agnarson, MD, Department of Pathology, University Hospital, PO Box 1465, 121 Reykjavik, Iceland; e-mail:
[email protected]
*L. D. Pizzarello, 137 Hampton Road, Southampton, NY 11968; e-mail:
[email protected]
● Repositioning of a dislocated intraocular lens during a roller-coaster ride. Bosch MM, Landau K, Thiel MA.* N Eng J Med 2003;249:1094 –1096.
●
Lymphoid tumours of the ocular adnexa: a morphologic and genotypic study of 15 cases. Sigurdardottir M, Sigurdsson H, Bjo¨ rk Bakardottir R, Kristjandottir S, Agnarsson AB.* Acta Ophthalmol Scan 2003;81:299 – 303.
A
T
LL LYMPHOPROLIFERATIVE LESIONS OF THE OCULAR
adnexa diagnosed in Iceland during 1983 and 2000 were examined in order to determine whether polymerase chain reaction (PCR) methods to determine clonality are helpful in characterizing these lesions. Fifteen cases were identified. Seven were classified as inflammatory pseudotumor, one as lymphoid hyperplasia, four as atypical lymphoid hyperplasia an three as lymphoma. Of 12 cases examined by PCR, three were monoclonal for B-cells (one lymphoma, one inflammatory pseudotumor, and one atypical lymphoid hyperplasia) while the remaining lesions (including two lymphomas) appeared polyclonal. The results of this study suggest that analysis of clonality by PCR methods may be of limited use in classifying lymphoproliferative lesions of the ocular adnexa as benign or malignant. These results underscore the importance of using several techniques when determining clonality.—Hans E. Grossniklaus
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AMERICAN JOURNAL
HE AUTHORS REPORT OF A BOY WHO AT THE AGE OF 8
years had undergone implantation of a posteriorchamber intraocular lens (IOL) and a peripheral iridectomy for a traumatic cataract. At the age of 19 years, he noticed an irregularly shaped pupil after being struck in his right eye. Examination showed that the optic of the IOL had dislocated into the anterior chamber and the haptic remained behind the iris. Mydriatic drops were administered while the patient lay in a supine position in order to reposition the IOL. The optic partially repositioned into the posterior chamber and the patient was scheduled for surgical repositioning. Prior to surgery, the patient had three consecutive rides on one of the largest roller coasters in Europe. Hours later, the patient noticed that his right pupil had become round. Examination showed complete repositioning of the IOL optic into the posterior chamber. Reposition of the IOL optic was attributed to sympathomimetic dilation of the pupil during the first steep descent followed by acceleration on the curved track. The centripetal force and deceleration of the upward slope forced the optic into the posterior chamber.—Hans E. Grossniklaus *Michael A. Thiel, MD, PhD, University of Zurich, 8091 Zurich, Switzerland; e-mail:
[email protected]
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OPHTHALMOLOGY
FEBRUARY 2004