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目的检测Vogt-小柳原田(VKH)综合征患者不同病期血-房水屏障功能变化,为临床治疗提供依据。方法VKH综合征患者77例(144只眼)根据临床特点将其分为后葡萄膜炎期组10例(20只眼)、前葡萄膜受累期组27例(50只眼)、前葡萄膜炎反复发作期组23例(41只眼)和消退期组17例(33只眼)。对照组50例(100只眼)。应用激光前房蛋白细胞测定仪(LFCM)和裂隙灯显微镜检测各期患者前房闪辉和前房细胞数。结果后葡萄膜炎期患者裂隙灯检查前房细胞和前房闪辉均为0级(20只眼),LFCM检测前房细胞数为(0.9±0.6)/0.5mm3,与正常对照组(0.8±0.6)/0.5mm3的差异无统计学意义(P=0.899),前房闪辉值为(9.7±3.4)pc/ms,高于对照组(5.3±2.3)pc/ms,具有统计学意义(P<0.001)。前葡萄膜受累期患者裂隙灯前房细胞为25只眼(1+)、19只眼(2+)和6只眼(3+),前房闪辉为27只眼(1+)和23只眼(2+),LFCM前房细胞数分别为(13.7±6.5)/0.5mm3、(40.8±17.6)/0.5mm3、(75.7±25.5)/0.5mm3、前房闪辉值分别为(31.4±12.8)pc/ms、(133.4±59.5)pc/ms。前葡萄膜炎反复发作期患者裂隙灯前房细胞为19只眼(1+)、15只眼(2+)、7只眼(3+),前房闪辉为24只眼(1+)、17只眼(2+),LFCM前房细胞数分别为(11.2±5.4)/0.5mm3,(29.6±14.4)/0.5mm3、(69.3±22.2)/0.5mm3,前房闪辉值分别为(34.9±14.3)pc/ms、(150.9±83.3)pc/ms,前葡萄膜受累期和前葡萄膜炎反复发作期患者前房闪辉值和前房细胞数均高于对照组,具有统计学意义(P<0.001)。消退期患者裂隙灯前房细胞为0级(33只眼),前房闪辉为0(15只眼)和18只眼(1+),LFCM前房细胞数为(1.0±0.7)/0.5mm3,与对照组的差异无统计学意义(P=0.310),前房闪辉值分别为(9.5±4.8)pc/ms、(30.0±12.3)pc/ms,均高于对照组,具有统计学意义(P<0.001)。结论VKH综合征各期均有不同程度血-房水屏障的破坏,但并非各期均有炎症细胞存在,此结果对VKH综合征临床治疗有重要指导意义。
Objective To detect the changes of blood-aqueous barrier function in patients with Vogt-Koyanagi-Harada (VKH) syndrome during different stages of disease, and provide the basis for clinical treatment. Methods Totally 77 patients (144 eyes) with VKH syndrome were divided into 10 cases (20 eyes) in the posterior uveitis group, 27 cases (50 eyes) in the anterior uveal involvement group, the anterior uveal membrane Twenty three patients (41 eyes) with recurrent episodes of inflammation and 17 patients (33 eyes) with extinction groups. Control group, 50 cases (100 eyes). The anterior chamber glomerulus and anterior chamber cells were detected by LFCM and slit lamp microscope. Results The number of anterior chamber cells and anterior chamber were 0 (20 eyes) in slit lamp examination and (0.9 ± 0.6) /0.5 mm3 in LFCM, respectively. Compared with normal control group (0.8 ± 0.6) /0.5mm3 was not statistically significant (P = 0.899), the value of anterior chamber was (9.7 ± 3.4) pc / ms, higher than that of the control group (5.3 ± 2.3) pc / ms, with statistical significance (P <0.001). Patients with anterior uveal involvement included 25 eyes (1 +), 19 eyes (2+) and 6 eyes (3+), anterior chamber was 27 eyes (1+) and 23 The number of LFCM anterior chamber cells was (13.7 ± 6.5) /0.5mm3, (40.8 ± 17.6) /0.5mm3 and (75.7 ± 25.5) /0.5mm3 in the eyes (2 + ± 12.8) pc / ms, (133.4 ± 59.5) pc / ms. The anterior chamber cells of slit lamp in patients with recurrent anterior uveitis were 19 eyes (1 +), 15 eyes (2 +), 7 eyes (3+), anterior chamber glint was 24 eyes (1+) , 17 eyes (2 +) and LFCM were (11.2 ± 5.4) /0.5mm3, (29.6 ± 14.4) /0.5mm3 and (69.3 ± 22.2) /0.5mm3, respectively (34.9 ± 14.3) pc / ms and (150.9 ± 83.3) pc / ms, respectively. The anterior chamber and the number of anterior chamber cells in patients with anterior uveal and recurrent anterior uveitis were significantly higher than those in the control group Significance (P <0.001). The number of anterior chamber cells in patients with remission was 0 (33 eyes), the anterior chamber was 0 (15 eyes) and 18 eyes (1 +), the number of LFCM anterior chamber cells was (1.0 ± 0.7) /0.5 mm3, respectively. There was no significant difference between the control group and the control group (P = 0.310). The values of anterior chamber glint were (9.5 ± 4.8) pc / ms and (30.0 ± 12.3) pc / Significance (P <0.001). Conclusions VKH syndromes have different degrees of blood-aqueous barrier damage in all stages, but not all of them have inflammatory cells in all stages. This result has important guiding significance for the clinical treatment of VKH syndrome.