Malignant glaucoma due to drug-related angioedema.

PURPOSE: To report postsurgery angioedema resulting in malignant glaucoma. Interventional case report. METHODS: Three hours after uncomplicated cataract surgery on the right eye, a 61-year-old woman developed angioedema with swelling of the parapharyngeal tissue. Visual acuity deteriorated, and tonometry revealed an intraocular pressure of 60 mm Hg, with shallow anterior chambers, in both eyes. RESULTS: Ultrasound showed choroidal effusion on both eyes. Intraocular pressure could only be controlled surgically by procedure to deepen the anterior chamber. The angioedema regressed after withdrawal of candesartan, an angiotensin II antagonist that the patient had taken for 1 year. CONCLUSIONS: Angioedema without urticaria is well documented in patients receiving angiotensine-converting enzyme inhibitors or angiotensin II antagonists. Drug-related angioedema may lead to a choroidal effusion syndrome with malignant glaucoma. Surgical intervention may trigger angioedema. Most important in treatment is withdrawal from the implicated medication and control of intraocular pressure.

Lysine residues of Epstein-Barr virus-encoded nuclear antigen 2 do not confer secondary modifications via ubiquitin or SUMO-like proteins but modulate transcriptional activation.

Epstein-Barr virus nuclear antigen 2 (EBNA2) is essential for transformation through activation of viral and cellular genes. Within 487 residues, EBNA2 contains six lysine (K) residues (positions 335, 357, 359, 363, 366 and 480), which were mutated to arginine (R) residues, either individually or in combination, and tested for subcellular localization, mobility by SDS-PAGE and transactivation of three promoters. All mutants featuring the K(480)R mutation within the nuclear localization signal were partially cytoplasmic with a reduced level of transactivation of the latent membrane protein 1 (LMP1) promoter (-327 to +40). The K(366)R mutation also showed a decrease in transactivation of a promoter consisting only of 12 recombination signal-binding protein-Jkappa-binding sites, while all mutants with the K(335)R exchange showed a markedly elevated transactivation with the -327 to +40 construct and all mutants showed slightly reduced transactivation with a -634 to +40 LMP1 promoter. None of the mutants exhibited altered migration in SDS-PAGE, excluding secondary modification, i.e. through SUMO-like proteins.