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• W2001938571 abstract "Purpose: Laser speckle flowgraphy (LSFG) can be used to non-invasively visualize the haemodynamics of choroidal circulation and the vascular pattern. The purpose of this study was to examine the ability of LSFG to quantitatively evaluate blood flow velocity at the macula in patients with Vogt–Koyanagi–Harada (VKH) disease before and after systemic corticosteroid therapy. Methods: Prednisolone (200 mg/day) was systemically administered in 10 VKH disease patients with serous retinal detachment at the macular area. The drug was gradually tapered to zero over a 6-month period. Laser speckle flowgraphy measurements were taken in the 20 eyes of these patients at their initial visit and at 1, 4 and 12 weeks after the onset of therapy. Square blur rate (SBR), a quantitative index of relative blood flow velocity, was calculated using LSFG. Results: Serous retinal detachment resolved within 4 weeks after treatment and visual acuities improved to > 1.0 in almost all cases. There were significant increases in average SBR at the macula at 4 weeks after treatment compared with at 1 week after treatment, and also at 12 weeks after treatment compared with at 4 weeks after treatment. Conclusions: These results suggest that systemic corticosteroid therapy improves inflammation-related impairment in choroidal blood flow velocity at the macula. Laser speckle flowgraphy can evaluate the effect of systemic corticosteroid therapy by enabling comparisons between measurements of blood flow velocity, which is considered to reflect inflammation activity in the choroid. Vogt–Koyanagi–Harada (VKH) disease is an immune-mediated inflammatory condition affecting choroidal and systemic melanocytes. In the eye, it can cause severe granulomatous uveitis. The choroid is the primary target in the posterior segment of the eye (Moorthy et al. 1995). Fluorescein angiography (FA) and indocyanine green (ICG) angiography have been used to evaluate chorioretinal findings in this disease (Oshima et al. 1996; Harada et al. 1997; Pece et al. 1997; Kohno et al. 1999; Bouchenaki & Herbort 2001). Moreover, ICG angiography can be used to quantitatively measure the velocity at which the choroid fills with dye in patients with VKH disease (Mawatari et al. 2006). Recently, laser speckle flowgraphy (LSFG; Kusyu Institute of Technology, Iizuka, Japan) has been used to investigate ocular blood flow distribution without the administration of contrast agents (Tamaki et al. 1995; Isono et al. 2003). This technique targets moving red blood cells in the eye. A diode laser (wavelength 830 nm) is used to illuminate the ocular fundus, and the reflected light from the ocular tissue produces a speckle pattern at the plane where the area sensor is focused. The reflected lights from the moving erythrocytes induce blurring within the speckle pattern. Square blur rate (SBR), a quantitative index of relative blood flow velocity, can be calculated from the variations noted in the blurring. In a previously published study, branch retinal artery occlusion was induced in monkey eyes. The comparison of panoramic maps taken before and after the occlusion indicated there was very little change in the vascular patterns. This suggested that blood flow velocity, as determined by LSFG, is mainly choroidal in origin (Isono et al. 2003). Therefore, LSFG may be useful in evaluating relative choroidal haemodynamics in various choroidal diseases. In the present study, we used LSFG in patients with VKH disease to evaluate blood flow velocity at the site of the macula before and after systemic corticosteroid therapy. The current study examined 20 eyes of 10 VKH disease patients (five men and five women; mean ± standard deviation [SD] age: 38.8 ± 11.4 years, range 20–53 years), who attended the Intraocular Inflammation Survey Clinic at Hokkaido University Hospital. The clinical features of the patients are summarized in Table 1. Vogt–Koyanagi–Harada disease was diagnosed according to the criteria of both Sugiura and the VKH Disease Committee (Sugiura 1978; Read et al. 2001). All patients were at an early stage of VKH, with serous retinal detachment (SRD) at the macula. None of the patients had any medical or ocular history, including systemic or ocular hypertension. Administration of prednisolone was started at 200 mg/day and gradually tapered to zero over a 6-month period in all patients. The tapering schedule for prednisolone required i.v. administrations of 200 mg/day, 150 mg/day and 100 mg/day, with each dose administered over a 2-day period. After the first 6 days of i.v. administration, tapering was continued using oral dosages as per the following schedule: 4 days at 60 mg/day; 10 days at 40 mg/day; 2 weeks at 30 mg/day; 1 month at 20 mg/day; 1 month at 15 mg/day; 1 month at 10 mg/day; 1 month at 7.5 mg/day, and 1 month at 5 mg/day. No other immunosuppressive medications were administered. Whenever possible, FA and ICG angiography were performed pretreatment and at 2 and 4 weeks after treatment. Optical coherence tomography (OCT Ophthalmoscope C7; Nidek Co., Ltd, Gamagori, Japan) was performed pretreatment, every week until 4 weeks after treatment, and then at 8 and 12 weeks after treatment. Foveal retinal thickness was measured in 14 eyes of seven patients. Laser speckle flowgraphy was measured pretreatment, and at 1, 4 and 12 weeks after the initiation of treatment (1, 2). This study followed the tenets of the Declaration of Helsinki. Informed consent was obtained from all subjects after the nature and possible consequences of the study had been explained. Composite colour map using the square blur rate (SBR) as measured by laser speckle flowgraphy (LSFG) at (A) the initial visit and (B) 1 week, (C) 4 weeks and (D) 12 weeks after systemic corticosteroid therapy in the right eye of case 4. The red colour indicates high SBR and the blue colour indicates low SBR. The SBR gradually increased at the macula during the 12-week treatment (square 1). (A) Fluorescein angiography and (B, C) composite colour maps using the square blur rate (SBR) as measured by laser speckle flowgraphy at the initial visit (A, B) and at 1 month (C) after systemic corticosteroid therapy in case 1. During treatment, the SBR increased at the macula (square 1) and in areas where there was no leakage of fluorescein dye (square 2). The mechanism of LSFG has been described elsewhere (Tamaki et al. 1995; Isono et al. 2003). The pupils of the subjects were dilated with 0.5% tropicamide and 0.5% phenylephrine hydrochloride. Eye movement in any direction during the measurement period was monitored using a previously described method (Tamaki et al. 1994). The measurement requires good fixation for three cardiac cycles, which occur approximately every 7 seconds. If good fixation during the measurement could not be obtained, the patient was excluded from the study. Consequently, 12 patients were screened and two were excluded. To evaluate the change in relative blood flow velocity at each site of the fundus, a square was set at the macula by excluding large retinal vessels in all eyes (1, 2, square 1). However, we did not exclude large choroidal vessels. In case 1, squares were also set in areas without SRD (Fig. 2, square 2). The average SBR was calculated for each square. Previous research has demonstrated that, within a certain range, the relationship between choroidal blood flow and ocular perfusion pressure (OPP) is linear (Riva et al. 1997). The patient’s blood pressure and intraocular pressure (IOP) were measured after each LSFG measurement. Mean blood pressure (mBP) was calculated from systolic blood pressure (sBP) and diastolic blood pressure (dBP), according to the following equation: mBP = dBP + 1/3(sBP − dBP) (Okuno et al. 2006). Ocular perfusion pressure was calculated using the following equation: OPP = 2/3mBP − IOP. Variations in IOP, mBP and OPP before and at 1 and 4 weeks after treatment in 17 eyes (nine right eyes, eight left eyes) of nine VKH patients were compared. Although the LSFG technique cannot determine absolute blood velocity, it is able to measure relative velocity. In addition, although we were not able to compare values between each of the patients, we were able to make comparisons between the values obtained during follow-up in one particular patient. The values were analysed using a non-parametric test, such as a Friedman test or a Wilcoxon signed ranks test, as previously described (Okuno et al. 2006). As the data for blood pressure, IOP and OPP showed approximately normal distributions, they were analysed using repeated analysis of variance (anova) and paired t-tests. In all tests, p < 0.05 was the criterion employed to declare statistical significance. All statistical analyses were performed for right and left eyes separately. Before treatment, SRD that was well documented by typical FA findings (e.g. multifocal pinpoint leakages and pooling of fluorescence within the subretinal fluid) was presented funduscopically at the macular area in all patients (Table 1). Indocyanine green angiography showed initial fuzzy choroidal vessels and late multiple hypofluorescent dark dots with diffuse hyperfluorescence, which is indicative of inflammatory vasculopathy of the choroidal vessels in VKH patients (Bouchenaki & Herbort 2001). SRD was markedly reduced 1 week after treatment, and was completely resolved at 12 weeks after treatment in all eyes. As measured by OCT ophthalmoscope, mean ± SD foveal retinal thickness in right eyes was 870.3 ± 567.2 μm before treatment, and 269.0 ± 114.0 μm at 1 week, 134.8 ± 40.4 μm at 4 weeks and 121.8 ± 16.9 μm at 12 weeks after treatment. Equivalent measurements in left eyes were 591.6 ± 304.3 μm before treatment, 274.1 ± 109.4 μm at 1 week, 118.2 ± 37.1 μm at 4 weeks and 122.8 ± 16.1 μm at 12 weeks after treatment. There were significant differences between the pretreatment and 1-week-after-treatment results (right eyes: p = 0.022; left eyes: p = 0.016; paired t-test). After treatment, FA showed resolution of dye leakage and the number of hypofluorescent spots in ICG angiography decreased in all eyes. Visual acuity (VA) improved to > 1.0 at 12 weeks after treatment in almost all eyes. Average logMAR VA in right eyes was 0.63 ± 0.55 (mean ± SD) before treatment, 0.31 ± 0.32 at 1 week, 0.06 ± 0.14 at 4 weeks and − 0.08 ± 0.10 at 12 weeks after treatment. Average logMAR values in left eyes were 0.46 ± 0.49 before treatment, 0.27 ± 0.31 at 1 week, 0.005 ± 0.14 at 4 weeks and − 0.05 ± 0.10 at 12 weeks after treatment. There were significant differences between the pretreatment and 4-weeks-after-treatment results (right eyes: p = 0.005; left eyes: p = 0.01; paired t-test). For the LSFG composite pseudo-colour map, SBR at the macula gradually increased during systemic corticosteroid therapy in almost all eyes (1, 2, square 1). Changes in the average SBR observed at the macular area during the period of systemic corticosteroid therapy are shown in Fig. 3. At 4 weeks after treatment, average SBR was significantly increased (Friedman test; right eyes: p = 0.00002; left eyes: p = 0.0003) compared with that seen at 1 week after treatment (Wilcoxon signed rank test; right eyes: p = 0.0010; left eyes: p = 0.0092). In addition, at 12 weeks after treatment, average SBR was significantly increased compared with that seen at 4 weeks after treatment (Wilcoxon signed rank test; right eyes: p = 0.0038; left eyes: p = 0.0322). The average SBR set in areas without SRD was 4.9 at 1 week after treatment, 5.2 at 4 weeks after treatment and 6.2 at 12 weeks after treatment. Changes in the average square blur rate (SBR) at the macula during systemic corticosteroid therapy in (A) right eyes and (B) left eyes. Compared with values obtained at 1 week after the start of treatment, there was a significant increase in SBR (Friedman test; right eyes: p = 0.00002; left eyes: p = 0.0003) after 4 weeks of treatment (Wilcoxon signed rank test; right eyes: p = 0.0010; left eyes: p = 0.0092), and at 12 weeks after treatment compared with 4 weeks after treatment (Wilcoxon signed rank test; right eyes: p = 0.0038; left eyes: p = 0.0322). Numbers refer to individual cases. Mean BP, IOP and OPP results are shown in Table 2. No significant differences were noted for IOP in left eyes (repeated ANOVA, p = 0.140). However, significant differences were identified in IOP in right eyes (repeated anova, p = 0.02), with IOP at 4 weeks after treatment significantly higher than at 1 week post-treatment (paired t-test, p = 0.036) and before treatment (paired t-test, p = 0.036). There were no significant differences noted for either mBP (repeated ANOVA, p = 0.464) or OPP (repeated ANOVA; right eyes: p = 0.240; left eyes: p = 0.135) between results obtained before and at 1 and 4 weeks after treatment. As choroidal blood flow exceeds the retinal flow by approximately 96% in areas outside the fovea (Alm & Bill 1973) and as there are no large retinal vessels at the fovea (Schatz 1994), SBR calculations at the square of the macula we set in this study when using LSFG are considered to reflect choroidal flow velocity. In the current study, we used LSFG to quantitatively examine blood flow velocity in VKH disease. After treatment, funduscopic and angiographic findings revealed that foveal retinal thickness, as well as VA, improved in proportion to the elevation of the SBR in the macula. These results suggest that systemic corticosteroid therapy improves impaired choroidal blood flow velocity at the macula. Because no significant differences in OPP were noted between pre- and post-treatment results, the elevation of SBR was possibly caused by a decrease in choroidal vascular resistance. The primary pathological feature of the acute phase of VKH is the diffuse thickening of the uveal tract caused by a non-necrotizing granulomatous inflammation with infiltration of lymphocytes, epithelioid and giant cells, especially in the choroidal stroma (Inomata & Rao 2001; Rao 2007). This thickening is more prominent in the posterior part of the uvea and the juxtapapillary choroid. The thickening gradually decreases towards the equator and peripheral choroid. These changes are considered to lead to choroidal stromal oedema, which, in turn, compresses the vessels in choroidal stroma (Rao 2007) and, consequently, decreases choroidal blood flow. If the granulomatous inflammation can be relieved, these changes are reversible, as the inflammatory cell infiltration does not involve the choriocapillaris (Inomata & Rao 2001; Rao 2007). Therefore, blood flow velocity in the posterior part of the choroid is considered to directly reflect inflammatory activity in the choroid. The exudative retinal detachment typically seen during the uveitic stage of VKH indicates alterations in the retinal pigment epithelium (RPE). Serous retinal detachment is the secondary reaction that results from impairment of the RPE caused by inflammatory changes in the choroid. Therefore, SRD does not directly reflect the activity of VKH disease. Although FA or optical OCT can detect and quantitate SRD, these procedures cannot quantitate initial inflammatory activity in the choroid. Laser speckle flowgraphy has limitations similar to those of laser Doppler flowmetry techniques, in that the procedures can only provide unambiguous information on flow changes if the optical properties of the sampled tissue do not vary between successive measurements. During the acute uveitic stage prior to systemic corticosteroid therapy in VKH disease, SRD in the macula, along with extensive choroidal diffuse cell infiltration, may be able to influence the scattering properties. Therefore, we decided to omit the pretreatment data. As a consequence of deleting this data, the SBR at the macula continued to increase even after the SRD had almost resolved. In addition, we also noted increases in the SBR at sites without any SRD. These results suggest that the measured change noted for choroidal blood flow velocity was not simply an effect of changes in the anatomical properties of the measured tissue, but was related to an improvement in blood flow velocity at the macula. Although a marked reduction in average macular retinal thickness was noted at 1 week after treatment, it is unlikely that this decreased retinal thickness had an effect on the SBR, as transparent tissue does not normally influence the laser speckle pattern (H. Fujii, personal communication, 2007). However, we cannot completely exclude the possibility that the results reflected an effect of the scattering properties of the tissue change that occurred over time or with treatment, as expected in oedema of the RPE, and which will resolve under steroid therapy. The coefficients of reproducibility of the SBR measurements at 1-min intervals (Tamaki et al. 1997) were 2.1 ± 0.4%. These represent an index of physiological fluctuations in the fundus tissue circulation, as well as an index of the error of measurement. The current results indicate the stability of the measured SBR and suggest that LSFG is well suited for monitoring changes in fundus tissue circulation. In patients with VKH disease, multiple hypofluorescent spots are the most constant and easily recordable signs noted during ICG angiography and, when observed, suggest the presence of choroidal granuloma (Bouchenaki & Herbort 2001; Herbort et al. 2007). Because such findings indicate choroidal stromal scarring as well as active choroidal inflammation, it can be difficult to assess the activity of choroidal inflammation based on just the number of hypofluorescent spots, especially during the recurrent or protracted stages. However, ICG angiography with image analysis software has been reported to be able to document the significant improvement in choroidal filling velocity that occurs after systemic corticosteroid treatment (Mawatari et al. 2006). Furthermore, the quantitative assessment of choroidal circulation provides an important indicator of VKH treatment efficacy. Therefore, because it is able to compare the extent of any change in choroidal blood flow velocity before and after treatment in patients with VKH disease, LSFG may be an effective method for evaluating the effect of systemic corticosteroid therapy. Its other benefits include the fact that it is not an invasive procedure and that it can provide results within 60 seconds without requiring the administration of contrast agents. This work was supported by the 21st Century Center of Excellence Programme ‘Topological Science and Technology’, Ministry of Education, Culture, Sports, Science and Technology of Japan." @default.
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• W2001938571 title "Elevated choroidal blood flow velocity during systemic corticosteroid therapy in Vogt-Koyanagi-Harada disease" @default.
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