We conducted a retrospective study of 30 penetrating keratoplasties (30 patients) for corneal opacity due to herpes simplex keratitis from Jan. 1980 to Dec. 1989 at St. Mary's Hospital. The follow-up periods ranged from 1.3 years to 11 years (mean; 4.8 years). Overall, 23 out of the 30 transplants (76.7%) remained clear grafted cornea and 18 eyes (60%) achieved good to excellent visual acuities (0.3 or better). Herpes simplex keratitis was inactive at the time of corneal transplantation in 27 eyes (90%) and the recurrent rate after surgery was 18.5%. Patients with active ulceration or perforation, had particularly poor success rates. The overall rate of recurrent herpetic keratitis after transplantation for herpes was 26.6% Preoperative corneal neovascularization was not a statistically significant prognostic factor with regard to final visual outcome, graft clarity, graft rejection or recurrent herpetic keratitis.
Cornea ; Corneal Neovascularization ; Corneal Opacity ; Corneal Transplantation* ; Follow-Up Studies ; Graft Rejection ; Herpes Simplex* ; Humans ; Keratitis, Herpetic* ; Keratoplasty, Penetrating ; Recurrence* ; Retrospective Studies ; Transplants ; Ulcer ; Visual Acuity

We conducted a retrospective study of 30 penetrating keratoplasties (30 patients) for corneal opacity due to herpes simplex keratitis from Jan. 1980 to Dec. 1989 at St. Mary's Hospital. The follow-up periods ranged from 1.3 years to 11 years (mean; 4.8 years). Overall, 23 out of the 30 transplants (76.7%) remained clear grafted cornea and 18 eyes (60%) achieved good to excellent visual acuities (0.3 or better). Herpes simplex keratitis was inactive at the time of corneal transplantation in 27 eyes (90%) and the recurrent rate after surgery was 18.5%. Patients with active ulceration or perforation, had particularly poor success rates. The overall rate of recurrent herpetic keratitis after transplantation for herpes was 26.6% Preoperative corneal neovascularization was not a statistically significant prognostic factor with regard to final visual outcome, graft clarity, graft rejection or recurrent herpetic keratitis.
Cornea ; Corneal Neovascularization ; Corneal Opacity ; Corneal Transplantation* ; Follow-Up Studies ; Graft Rejection ; Herpes Simplex* ; Humans ; Keratitis, Herpetic* ; Keratoplasty, Penetrating ; Recurrence* ; Retrospective Studies ; Transplants ; Ulcer ; Visual Acuity

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.