PURPOSE: To evaluate the relationship between initial postoperative overcorrection and long-term surgical success in exotropia patients. METHODS: The medical records of 46 patients who underwent surgery for intermittent exotropia after the age of 18 were enrolled. Enrolled patients also had at least 2 years of postoperative follow-up. Based on the initial postoperative deviation at distance measured by prism and the alternating cover test at 1 week, patients were assigned to one of the following groups: group A included patients who demonstrated any esodeviation, while group B included patients who showed orthophoria to exodeviation of 10 prism diopters. The records were analyzed to determine the preoperative deviation with stereoacuity and postoperative deviations with stereoacuity at the follow-up examinations at the following intervals: 1 week; 1, 3, and 6 months; and 1 and 2 years. A comparison between groups for demographic data and preoperative and postoperative angles of deviation was performed using analysis of variance. RESULTS: Of the 46 patients with intermittent exotropia included in this study, 18 (39%) belonged to group A, while 28 (73%) belonged to group B. The postoperative angle of deviation for distant fixation until 2 years of follow-up showed statistically significant differences in each group (p < 0.003 in all comparisons). The amount of exodrift until 2 years in group A (from −9.7 ± 6.1 to 1.6 ± 3.7) was greater than that in group B (from 2.0 ± 2.7 to 6.8 ± 5.6). The long-term surgical success rate within 2 years of surgery was significantly better in group A than in group B (p = 0.027). The number of patients with intermittent diplopia and the duration of diplopia were greater in group A (n = 8) than in group B (n = 2). CONCLUSIONS: Long-term surgical success was achieved in 89% of patients who were initially overcorrected. Overcorrection of an average of 10 prism diopters at the first postoperative week was found to be associated with a more favorable long-term surgical outcome.
Adult* ; Depth Perception ; Diplopia ; Esotropia ; Exotropia* ; Follow-Up Studies ; Humans ; Medical Records

BACKGROUND: High-fat diet-induced obesity is one of the major cause of chronic renal failure. This obesity-related renal failure is mainly caused by inflammatory processes. However, the role of the major anti-inflammatory cytokine interleukin (IL)-10 has not been researched intensively. METHODS: To evaluate the effect of IL-10 deficiency on obesity-related renal failure, the in vivo study was carried with four animal groups; (1) Low-fat dieted C57BL/6 mice, (2) Low-fat dieted IL-10 knockout (KO) mice, (3) High-fat dieted C57BL/6 mice and (4) High-fat dieted IL-10 KO mice group. The analysis was carried with blood/urine chemistry, H&E, Oil-Red-O, periodic acid-Schiff and Masson’s trichrome staining immunohistochemistry and real-time PCR methods. RESULTS: At week 12, high-fat dieted IL-10 KO mice showed 1) severe lipid accumulation in kidneys, cholesterol elevation (in total, serum kidney) and low-density lipoprotein increasion through the SCAP-SREBP2-LDLr pathway; (2) serious histopathologic alterations showing glomerulosclerosis, tubulointerstitial fibrosis and immune cell infiltration; (3) increased pro-inflammatory cytokines and chemokines expression; (4) enhanced renal fibrosis; and (5) serious functional failure with high serum creatinine and BUN and proteinuria excretion compared to other groups. CONCLUSION IL-10 deficiency aggravates renal inflammation, fibrosis and functional failure in high-fat dieted obese mice, thus IL-10 therapy could be applied to obesity-related chronic renal failure.

BACKGROUND: High-fat diet-induced obesity is one of the major cause of chronic renal failure. This obesity-related renal failure is mainly caused by inflammatory processes. However, the role of the major anti-inflammatory cytokine interleukin (IL)-10 has not been researched intensively. METHODS: To evaluate the effect of IL-10 deficiency on obesity-related renal failure, the in vivo study was carried with four animal groups; (1) Low-fat dieted C57BL/6 mice, (2) Low-fat dieted IL-10 knockout (KO) mice, (3) High-fat dieted C57BL/6 mice and (4) High-fat dieted IL-10 KO mice group. The analysis was carried with blood/urine chemistry, H&E, Oil-Red-O, periodic acid-Schiff and Masson’s trichrome staining immunohistochemistry and real-time PCR methods. RESULTS: At week 12, high-fat dieted IL-10 KO mice showed 1) severe lipid accumulation in kidneys, cholesterol elevation (in total, serum kidney) and low-density lipoprotein increasion through the SCAP-SREBP2-LDLr pathway; (2) serious histopathologic alterations showing glomerulosclerosis, tubulointerstitial fibrosis and immune cell infiltration; (3) increased pro-inflammatory cytokines and chemokines expression; (4) enhanced renal fibrosis; and (5) serious functional failure with high serum creatinine and BUN and proteinuria excretion compared to other groups. CONCLUSION IL-10 deficiency aggravates renal inflammation, fibrosis and functional failure in high-fat dieted obese mice, thus IL-10 therapy could be applied to obesity-related chronic renal failure.