Corneal Pigment Opacity From Face-Down Positioning After Pars Plana Vitrectomy, Treated With Descemet Stripping Only Technique.

PURPOSE: The purpose of this study was to report a case of corneal opacity resulting from pigment deposition after face-down positioning, which was treated with Descemet stripping only (DSO) to enable concurrent pars plana vitrectomy (PPV) for retinal detachment repair. METHODS: A 79-year-old man with a history of Fuchs endothelial dystrophy and retinal detachment presented for the repair of recurrent retinal detachment and evaluation of a central corneal opacity. RESULTS: The patient was found to have significant corneal endothelial pigment deposition obscuring the view to the fundus. A repeat macula-involving retinal detachment was visualized on limited fundoscopic examination and confirmed using ultrasonography. The patient subsequently underwent combination scleral buckle, DSO, and PPV. DSO achieved corneal clarity for the entire duration of the PPV and allowed for the necessary postoperative face-down positioning. Immunohistochemistry of the corneal specimen revealed deposition of retinal pigment epithelium as the origin of the pigment opacity. The corneal edema cleared at postoperative month 4, and the retina remained attached, resulting in an improvement of visual acuity from counting fingers preoperatively to 20/70. DISCUSSION: This is, to the best of our knowledge, the first case describing the formation of a corneal endothelial opacity because of retinal pigment epithelium deposition associated with face-down positioning after PPV for retinal detachment. DSO is a minimally invasive, viable alternative to endothelial keratoplasty or temporary keratoprosthesis placement for the clearance of focal corneal endothelial opacities for PPV.

Changes in testicular gene expression following reduced estradiol synthesis: A complex pathway to increased porcine Sertoli cell proliferation.

Porcine Sertoli cell number including number present at puberty is increased if testicular estradiol synthesis is reduced during the neonatal interval. Evaluating the changes in gene expression during the crucial interval of suppressed estradiol that leads to the increased Sertoli cell population will increase our understanding of Sertoli cell biology but this evaluation first required a more precise determination of the critical interval for treatment and timing of a detectable response. Previously, reduced testicular estrogens from 1 week of age were accompanied by increased Sertoli cell number at 6.5 weeks of age but the age at which Sertoli cell numbers were initially increased was unknown, one of the current objectives. Additional experiments were designed to further delineate the essential timing of treatment for the Sertoli cell response. Finally, changes in gene expression induced by the reduced estradiol synthesis were evaluated to elucidate molecular mechanisms. Experimental design typically consisted of one member of littermate pairs of boars treated with the aromatase inhibitor, letrozole, beginning at 1 week of age and the remaining member treated with canola oil vehicle. Weekly treatments continued through 5 weeks of age or tissue collection, whichever came first. Increases in Sertoli cell numbers were not detectable prior to 6.5 weeks of age and persistent treatment through 5 weeks of age was required to induce the increase in Sertoli cell numbers. This increase resulted from prolonging the first interval of Sertoli cell proliferation in the treated animals. Few genes exhibited dramatically altered transcription and similarities in pathway analysis or principal modified genes were quite limited in 2, 3, and 5-week-old boars. The critical timing and prolonged treatment required and the sequential changes in gene expression suggest a complex mechanism is involved in this model of increased proliferation of Sertoli cells.