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Eleven patients with leukemia refractory to conventional therapy were treated with high doses of cytarabine (3 g/m2intravenously every 12 hours for six days) followed by daunorubicin (30 mg/m2/day intravenously for three days). Each patient received, in a double-masked, randomized manner, either 1% prednisolone phosphate or placebo eyedrops in each eye 12 hours before and along with the cytarabine so that we could determine whether a topical corticosteroid prevents corneal toxicity from systemic cytarabine. Ten of the 11 patients had a significant reduction in the intensity and duration of the symptoms and signs of corneal toxicity in the corticosteroid-treated eye (P<.0005). In the placebo-treated eye, pain, photophobia, and tearing occurred at a median time of 6.5 days after initiation of therapy but resolved in approximately one week.

Forty-one human conjunctival papillomas were histopathologically examined for koilocytosis and papillomavirus common antigen with a peroxidase-antiperoxidase technique immunospecific for genus-specific papillomavirus antigen. Koilocytotic cells, typically found in other papillomavirus-induced tumors, were present in 24 of the 41 specimens. Two of the 41 specimens were positive for viral antigen. The positive reactions were intranuclear within the superficial layers of the epithelium.

In a double-masked, randomized fashion, 11 patients with hematologic malignancies received 13 courses of high-dose cytarabine therapy, intravenously (3 g/m2every 12 hours for five to six days). Each patient received topical prednisolone phosphate 1% in one eye and 2-deoxycytidine 100 μM in the other eye every six hours. Topical therapy was initiated 12 hours before the first cytarabine dose and continued for up to ten days (until four to five days after completion of cytarabine therapy). Slit-lamp biomicroscopy was performed before therapy and then weekly for one month. 2-Deoxycytidine was equally as effective as the topical corticosteroid therapy in reducing photophobia and pain, microcysts, and punctate epithelial erosions, and each treatment gave results significantly better when compared historically to placebo-treated eyes.

Two histologically proven conjunctival papillomas (one from a 33-month-old boy and the other from a 28-year-old woman) were examined for the presence of papillomavirus by DNA molecular hybridization. The first case, a recurrent tumor known to be positive for papillomavirus structural antigen, demonstrated human papillomavirus DNA sequences that cross-hybridized to a human papillomavirus type 11 DNA probe. The second case, an initial tumor, which was negative for papillomavirus structural antigen, demonstrated no viral DNA sequences by hybridization.

Seven patients with type I diabetes mellitus (Group 1), seven with normoglycemic cystic fibrosis (Group 2), seven with hyperglycemic cystic fibrosis (Group 3), and ten age-matched control subjects underwent corneal fluorophotometry and quantitative specular microscopy. Group 1 had background microangiopathic retinopathy but no evidence of proliferative disease by fluorescein angiography. Significant increases in mean corneal endothelial permeability and mean pump rate occurred in Group 1, indicating a defect in the endothelial barrier function early in type I diabetes mellitus. Similar significant increases in mean corneal endothelial permeability and mean pump rate occurred in both cystic fibrosis groups. The greatest increase was found in Group 3, suggesting a primary defect in the endothelial barrier function in cystic fibrosis, aggravated by the hyperglycemic state. No morphologic abnormalities were noted in Group 1, but both cystic fibrosis groups had smaller mean cell areas than did the control group. There were significant differences in the morphologic and functional correlations between Groups 1 and 3, suggesting different mechanisms for the increased endothelial permeability in these two disorders.

Five patients with multiple, recurrent conjunctival papillomas underwent surgical excision of their tumor and then received interferon alpha-N1, 5 × 106units/m2(5 Mu/m2), intramuscularly daily for one month. A similar dose was given two to three times per week for the next six months and tapered off or discontinued thereafter. The follow-up period varied from one to four years. Two patients have had no recurrence of tumor. The other three patients have had recurrences of lesser severity upon tapering or discontinuing the interferon, and repeat surgical or laser excision of these lesions has been performed. The presence of koilocytosis and human papillomavirus type 11a DNA sequences was noted in all specimens large enough to examine, whereas papillomavirus structural antigens were detected in only two of five specimens. A regimen of interferon therapy appears to be tumor suppressive, but not curative.