Management of scleral rupture during retinal detachment surgery: a case report.

PURPOSE: Rupture of the sclera occurring during retinal detachment surgery is generally associated with unfavourable anatomic and visual outcomes. Re-operation after a failed scleral buckle procedure and pre-existing scleral thinning are considered the main risk factors for scleral rupture. CASE REPORT: We describe the management and the favourable outcome of a case of scleral rupture in a 71-year-old woman during re-operation for retinal detachment. CONCLUSIONS: We managed this case of scleral rupture in accordance with current indications concerning the anatomical recovery, by scleral suture and patch graft, restoring IOP by gas tamponade. The positive outcome was partly related to the prompt closure of the retinal hole which led to reattachment, and partly to favourable events such as the moderate intensity of vitreous hemorrhage and the lack of any more serious intraoperative and postoperative complications.

Selective inhibition of NF-kB activation and TNF-alpha production in macrophages by red blood cell-mediated delivery of dexamethasone.

Glucocorticoids are a widely used class of anti-inflammatory and immunosuppressive drugs, but their therapeutic use is limited by endocrine and metabolic side effects that they produce when given systemically. Since cells of the monocyte/macrophage lineage play an important role in the pathogenesis of several autoimmune and inflammatory diseases, a drug-delivery system which targets phagocytic cells was studied. We had previously demonstrated that dexamethasone, a potent glucocorticoid analogue, can be encapsulated in erythrocytes and selectively delivered to macrophages. In addition, lipopolysaccharide (LPS) stimulation of dexamethasone-targeted macrophages results in the suppression of TNF-alpha secretion. In this paper we demonstrate that the administration of dexamethasone to macrophages by means of opsonized red blood cells allows efficient interference with NF-kB activation. This NF-kB repression was in part mediated by induction of IkBalpha gene transcription and, as a consequence, by an increased rate of IkBalpha protein synthesis. Furthermore, NF-kB inactivation correlated with downmodulation of TNF-alpha mRNA expression, demonstrating that suppression of TNF-alpha production in dexamethasone-targeted cells occurs at the transcriptional level.