Objective To investigate the clinical features of tuberculous meningoencephalitis.Methods The clinical characteristics and laboratory results of 126 cases who were diagnosed as tuberculous meningoencephalitis fromJanuary 2000 to April 2009 were analyzed retrospectively. Results The clinical manifestations of tuberculous meningoencephalitis included fever, headache, vomitting, hemiparalysis,paraplegia, mental anomaly, hypopsia, deafness, diplopia, muscular spasms, coma, and incomplete oculomotor palsy, etc. Vomitting which was characteristic symptom of tuberculous meningoencephalitis was found in 25 cases( 19. 8% ) . The diagnosis was confirmed more than eightweeks after the onset of the disease in 31 cases ( 24. 6% ) . The inhospital mortality rate of tuberculous meningoencephalitis was 14. 3% ( 18 /126) . The inhospital mortality rate of re-treatment patients was 42. 9% ( 6 /14) . In 41 patients with poor prognosis ( death or therapy failure) , 68. 3% ( 28/41) cases were complicated with military tuberculosis, which was higher than the overall occurrence of 41. 3% ( 52/126) . Conclusions Strict diagnostic criteria and atypicalsymptoms lead to delayed diagnosis, delayed treatment, and high mortality in patients with tuberculous meningoencephalitis, particularly in patients with military tuberculosis and re-treatment patients. There is still no effective treatment which have a significant impact on the prognosis.
Objective To observe the spectral domain optical coherence tomography (SD-OCT) features of acute Vogt-Koyanagi-Harada (VKH) eyes before and after treatment.Methods Twenty-eight patients (56 eyes) with acute VKH diagnosed by slitlamp microscopy, B mode ultrasound and fundus fluorescein angiography (FFA) were enrolled in this study. All the patients were treated with steroid after diagnosis. SD-OCT was performed in all the patients before and after treatment. The follow-up was ranged from 12 to 32 weeks with a mean of (21.30plusmn;8.53) weeks. The foveal retinal detachment height, inner and outer segments (IS/OS) of photoreceptors, and the changes in retinal structure within the vascular arcades before and after treatment were comparatively analyzed. Results OCT examination results showed that before treatment, all eyes had retinal neural epithelial detachment. The average neural epithelial detachment height in the fovea was (635.44plusmn;340.04) mu;m. Forty-three eyes (76.8%) had different types of subretinal exudates; 41 eyes (73.2%) had b granular reflection in the subretinal space. Twenty-two eyes (39.3%) had paraforveal outer nuclear layer (ONL) thickening with finger-like protrusions attached with membrane-like structure. Thirty-three eyes (58.9%) had wavy lines of the retinal pigment epithelium (RPE). After the treatment, these exudates dissolved within one week and RPE line became straight. The retina reattached after (2.33plusmn;0.82) weeks. In most patients external limiting membrane and IS/OS became intact after (5.01plusmn;6.71) weeks and (11.40plusmn;7.89) weeks respectively. However, at the end of follow-up, 46 eyes (82.1%) still had focal areas of IS/OS defect and 11 eyes (19.6%) had focal ONL thinning. Conclusions Before the treatment, the OCT features of acute VKH are serous retinal detachment at fovea, different types of subretinal exudates and wavy RPE. After the treatment, the OCT features of acute VKH are exudates dissolving, straight RPE line and early recovery of external limiting membrane.
Objective To investigate the genetic interaction of HLA-DQB1 promoter and coding alleles in the pathogenesis of Vogt-Koyanagi-Harada syndrome (VKH). Methods Eighty-eight Chinese Han patients with VKH and eighty-eight non-VKH normal controls were enrolled in this study. DNA was extracted from white blood cells of the subjects by phenolchloroform method. Thirteen alleles were genotyped by polymerase chain reaction-sequence-specific primers (PCR-SSP), polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and clone-sequencing was applied to determine the polymorphisms of the promoter and coding regions of HLA-DQB1 gene. Chromas and Bioedit software were used to analyze the sequences of the promoter of HLA-DQB1. Chi-square test and Fisher exact test were the statistical methods. Relationships among single nucleotide polymorphism (SNP) in the promoter and coding region were analyzed. Results Twelve of thirteen already known HLA-DQB1 alleles were genotyped by PCR-SSP in VKH patients. The most frequent allele in VKH patients was HLA-DQB10401 (0.318, 56∶176) which was significantly higher in patients than that in normal controls (0.045, 8∶176) (chi;2＝44.00, P＝0.000, OR＝9.8). So was for HLA-DQB10303 (0.068 vs. 0.006, chi;2＝9.67, P＝0.002, OR＝12.81). In contrast, the frequency of HLA-DQB10601 (0.017 vs.0.096, chi;2＝10.39, P＝0.001, OR＝0.16) and HLA-DQB10302 (0.062 vs. 0.193,chi;2＝13.48, P＝0.000, OR＝0.28) in VKH patients were significantly lower than normal controls. Twelve SNP were found in all subjects. The frequency of C allele at position -189C/A in VKH patients was significantly higher than that in controls (0.324 vs. 0.074, chi;2＝45.92, P＝0.000). However, the frequency of G allele at position -227G/A in VKH patients was significantly lower than that in the normal controls (0.011 vs. 0.108, chi;2＝15.63,P＝0.000). The frequency of combination of susceptible alleles in promoter and coding area （-189C and HLA-DQB10401） in VKH patients was statistically higher than that in controls, the frequency of combination of resistant alleles in control (-227G and HLA-DQB10601) was higher than that in VKH patients. Conclusions The specific interactions of SNP in the promoter and coding alleles of HLA-DQB1 are associated with the pathogenesis of VKH.
Objective To observe the proportion changes of CD4+CD25+FOXP3+ T cells in peripheral blood of patients with VogtKoyanagiHarada disease (VKH) before and after one month of treatment. Methods he peripheral blood samples from 15 patients with VKH disease before and after one month of treatment by glucocorticoid, and from 15 healthy volunteers were collected，and lymphocytes were separated from them. CD4+CD25+ regulatory T cells were labeled by antibodies of cell surface marker CD4、CD25 and transcription factor FOXP3. The proportion of CD4+CD25+FOXP3+ T cells were detected by flow cytometry. Results Before the treatment, the percentage of CD4+CD25+FOXP3+ T cells in periphery blood was（0.30plusmn;0.19）% of CD4+ cell in VKH patients, and（1.41plusmn;0.52）% in control group, the difference was statistically significant（t=7.665,Plt;0.01）; after one month of treatment, the VKH patients group was（1.28plusmn;0.54）% which close to the control group. However there were two patients whose CD4+CD25+ T cells increased extraordinarily after one month of treatment. Conclusions The proportion of CD4+CD25+ FOCP3+ T cells in periphery blood in VKH patients were lower than control group obviously before treatment, but were close to control group after treatment. Those results indicated that VKH diseases may be associated with the decreased proportion of CD4+CD25+ regulatory T cells.
Objective To observe the clinical features of choroidal folds in Vogt-Koyanagi-Harada disease. Methods The clinical data of 112 patients with choroidal folds in Vogt-Koyanagi-Harada disease were retrospectively analyzed. All patients were examined by fundus color photography and fundus fluorescein angiography (FFA). 8 patients underwent indocyanine green angiography (ICGA) and 7 patients received optical coherence tomography (OCT) meanwhile. Results Of the 112 patients, 16 patients (14.3%) had choroidal folds. on FFA, there are 10 to 15 hypofluorescenct bands radiating from the optic disk which were similar to the large retinal vessels in shape and number(choroidal fine folds). On ICGA the choroidal folds showed obvious hyperfluorescence at the late stage. On OCT the reflective bands of Bruch membrane and retinal pigment epithelium (RPE) showed the wavy folds. Conclusions Choroidal folds in Vogt-Koyanagi-Harada disease are characterized by fine folds radiating from the optic disk which is not uncommon in Vogt-Koyanagi-Harada disease.
Objective To study choroidal vascular abnormal characterisitics in Harada is disease using indocyanine green angiography (ICGA)． Methods Twenty-six cases(52 eyes)of Harada is disease were examined with fundus fluorescein angiography(FFA) and ICGA． Results ICGA findings in Harada is disease were as follows:(1)choroidal hypofluorescence with edema in the early phase;(2)choroidal filling defects;(3)dilatation of choroidal vessels and vortex veins;(4)choroidal hyperpermeability in late period;(5)multifocal lower fluorescence in the midperiphery and posterior pole of the fundus in the late phase. Conclusions ICGA can find lesions of the choroidal vessels i．e． hypofluorescence with edema,disturbances of choroidal circulation，dilatation of choroidal vessels and vortex veins and the lower fluorescence maculation in the early phase and choroidal hyperpermeability in the late phase． (Chin J Ocul Fundus Dis,20000,16:12-13)