梅毒性眼病患者C-反应蛋白和血沉与白细胞联合检测的价值

目的：探讨以眼病为主要表现的梅毒患者 C-反应蛋白( C-reactive protein, CRP )、血沉( erythrocyte sedimentation rate,ESR)和白细胞(white blood cell,WBC)联合检测的价值。方法：对2012-01/2015-12本院以眼部症状首诊的51例梅毒患者和50例正常对照者的快速血浆反应素环状卡片试验( RPR )及梅毒螺旋体血清凝集试验( TPPA )、CRP、ESR及WBC检测结果进行回顾性分析。
　　结果：梅毒性眼病患者CRP、WBC及ESR的阳性率分别为16%、18%和39%,明显高于正常对照组;ESR 阳性率分别与CRP、WBC 相比较,差异有统计学意义( P<0.05);CRP、WBC及ESR阳性率与RPR滴度无明显相关性。
　　结论：联合检测CRP、WBC和ESR,能更好地反映以眼病为主要症状的梅毒患者的感染情况,对病情评估及监测具有一定的辅助性作用。     

Giant cell arteritis in a neuro-ophthalmology clinic in Saskatoon, 1998-2003

Background: We present a retrospective review of all biopsy-positive cases of giant cell arteritis (GCA) presenting to a neuro-ophthalmology practice in Saskatoon, Saskatchewan.Methods: Records of 141 consecutive patients who underwent temporal artery biopsy at the Saskatoon Eye Centre from July 1998 through June 2003 were reviewed. Patients that were biopsy-positive for GCA were studied and an estimated regional incidence was calculated. Study variables included age at diagnosis, sex, ethnicity, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) level.Results: Of 141 patients, 37 (26%) had a positive biopsy result for GCA; 11 underwent a second biopsy for a total of 152 biopsies. The average age of the biopsy-positive patients was 76.5 (SD 8.2) years, and the female-to-male ratio was 2.4:1. There were 35 patients (95%) of European descent and 2 patients (5%) of Aboriginal descent. Twenty-three patients had both ESR and CRP testing done before starting steroids. The ESR was elevated in 19 (83%) and the CRP in 22 (96%). The estimated incidence of GCA for Saskatoon and area was 9.4 per 100 000 for people over the age of 50 years.Interpretation: GCA occurs primarily in people of European descent; however, it can affect North American people of Aboriginal descent. Sensitivity for the detection of GCA is higher in CRP than in ESR. The estimated incidence of GCA in Saskatoon and surrounding referral area is moderate compared with other northern areas.     

Management of ischemic optic neuropathies

Ischemic optic neuropathies (IONs) consist primarily of two types: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION comprises arteritic AION (A-AION: due to giant cell arteritis) and non-arteritic AION (NA-AION: due to other causes). PION consists of arteritic PION (A-PION: due to giant cell arteritis), non-arteritic PION (NA-PION: due to other causes), and surgical PION (a complication of several systemic surgical procedures). These five types of ION are distinct clinical entities etiologically, pathogenetically, clinically and from the management point of view. In the management of AION, the first crucial step with patients aged 50 and over is to identify immediately whether it is arteritic or not because A-AION is an ophthalmic emergency and requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones. Systemic risk factors, particularly nocturnal arterial hypotension, play major roles in the development of NA-AION; management of them is essential in its prevention and management. NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes. A-PION, like A-AION, requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.     

Ischaemic optic neuropathy

Ischaemic optic neuropathy is of two types: anterior (AION) and posterior (PION), the first involving the optic nerve head (ONH) and the second, the rest of the optic nerve. Pathogenetically AION and PION are very different diseases. AION represents an acute ischaemic disorder of the ONH supplied by the posterior ciliary artery (PCA), while PION has no specific location in the posterior part of the optic nerve and does not represent an ischaemic disorder of any definite artery. The most important step towards a logical understanding of the underlying causes, clinical features, pathogenesis and rational management of AION, is to understand the basic scientific issues involved; these are discussed in some detail. AION clinically is of two types: (1) that due to giant cell arteritis (arteritic AION: A-AION) and (2) non-arteritic AION (NA-AION). NA-AION, the more common of the two, is one of the most prevalent and visually crippling diseases in the middle-aged and elderly, and is potentially bilateral. NA-AION is a multifactorial disease, with many risk factors collectively contributing to its development. Although there is no known treatment for NA-AION, reduction of risk factors is important in decreasing chances of involvement of the second eye and of further episodes. Our studies have suggested that nocturnal arterial hypotension is an important risk factor for the development and progression of NA-AION. The role of nocturnal arterial hypotension in the pathogenesis of NA-AION and management of nocturnal hypotension is discussed. Potent antihypertensive drugs, when used aggressively and/or given at bedtime, are emerging as an important risk factor for nocturnal hypotension, and there is some evidence that NA-AION may be occurring as an iatrogenic disease in some individuals. A-AION, by contrast, is an ocular emergency and requires immediate treatment with systemic corticosteroids to prevent further visual loss. The clinical parameters which help to differentiate the two types of AION, and their respective management are discussed.     

Management of giant cell arteritis. Our 27-year clinical study: new light on old controversies

Giant cell arteritis (GCA) is the prime medical emergency in ophthalmology because of its dreaded complication of visual loss in one or both eyes, which is preventable if these patients are diagnosed early and treated immediately and aggressively with systemic corticosteroids. However, there is much controversy on diagnostic criteria and various aspects of steroid therapy to prevent visual loss. We discuss in detail the reasons for the controversy, clinical criteria to establish a definite early diagnosis of GCA, and its management. To provide new information on corticosteroid therapy in GCA, we also present our 27-year planned study on steroid therapy in GCA in 145 temporal artery biopsy-confirmed GCA patients (96 with and 49 without visual loss) seen and followed for 6 weeks or more in our clinic. The median follow-up time was 2.43 years, with interquartile range of 1-6 years (range 6 weeks to 20.2 years). Intravenous megadose steroid therapy was initially given to 33% followed by oral steroids, while the rest had only the oral therapy. The median starting oral prednisone dose was 80 mg/day, with 40% on >/=100 mg/day. We found that the most reliable and sensitive parameters to regulate and taper down steroid therapy were the levels of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) and NOT systemic symptoms. All patients were maintained at the high-dose prednisone till both the ESR and CRP had stabilized at low levels (that usually took 2-3 weeks), after which very gradual tapering of prednisone was started, guided by the ESR and CRP levels only. The median time to reach the lowest maintenance dose of prednisone at which the ESR and CRP stayed low and stable was 48.7 months (95% CI: 34.6, 71.4 months), and the median lowest prednisone dose achieved was 7 mg/day (interquartile range of 1-16 mg/day). A comparison of patients with and without visual loss showed no significant difference in the time to attain the lowest dose (p = 0.359). Our study showed that no generalization is possible for tapering down of prednisone and there is no set formula because of the infinite variation between individuals. Only 10 (7 without visual loss, 3 with visual loss) of 145 patients were able to stop the therapy and maintain stable ESR and CRP levels. We found that only 4% of GCA patients with visual loss showed any visual improvement with high-dose steroid therapy, and 4% developed further visual loss during the first 5 days of high-dose steroid therapy but none after that. Our studies found no evidence that intravenous megadose steroid therapy was more effective than oral therapy in improving vision or preventing visual deterioration due to GCA.     

Von Willebrand factor, endothelial damage and ocular disease

Plasma von Willebrand factor (vWF), a marker for vascular damage, was measured in patients with giant cell arteritis (GCA), central retinal vein occlusion (CRVO), and active intraocular inflammation (AII), vWF was highest in GCA (median 3.52 kIU/L) relative to age matched controls (1.08 kIU/L, p<0.0001), with elevated levels in 75% of patients, the highest values found at disease presentation. Longitudinal measurements showed prolonged elevation of vWF, and increased levels were also found in 50% of patients with clinically inactive disease. In CRVO, raised levels were found in 53% of patients (median 2.32 kIU/L, p = 0.0002), but could not differentiate between an ischaemic and non-ischaemic sub-group. There was no statistical difference between those patients with and without systemic disease. Although vWF was raised in 34% of patients with AII (median 1.26 kIU/L, p = 0.0114), it was not different in uveitis (median 1.26 kIU/L), as compared to retinal vasculitis (median 1.58 kIU/L) or in those patients with and without systemic disease. vWF did not correlate with C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) in any of the groups studied. It appears a sensitive test for detecting vascular damage in GCA and may have a role in monitoring the disease where either a prolonged elevation or alteration of vWF levels may be of importance, particularly if ESR and CRP levels are normal. vWF measurement may be limited to more widespread vascular disease, such as in GCA as it was unable to differentiate between different types of CRVO or AII.     

Thrombocytosis in patients with biopsy-proven giant cell arteritis

OBJECTIVE: To compare the platelet counts, complete blood counts, and Westergren sedimentation rates (WESR) of patients with a biopsy positive for giant cell arteritis (GCA) with those of patients with negative biopsies. DESIGN: Retrospective, case-control series. METHOD: The medical records of 91 consecutive patients who underwent temporal artery biopsy for possible GCA, over an 8-year period, were reviewed. MAIN OUTCOME MEASURES: Values obtained for the complete blood counts, including platelet counts, WESR, and biopsy results of 91 consecutive patients undergoing temporal artery biopsy were analyzed. RESULTS: The mean platelet count of 47 patients with positive temporal artery biopsies (433 x 10(3)/microl) was significantly higher than that of 44 patients with negative temporal artery biopsies (277 x 10(3)/microl), P < 0.0001. There was no statistically significant difference in the mean WESR between the biopsy-positive (82 mm/hour) and biopsy-negative (70 mm/hour) groups, P = 0.12. The sensitivity of an elevated WESR for biopsy-positive patients was greater (79%; 95% confidence interval [CI], 64%-89%) than that of an elevated platelet count (57%; 95% CI, 42%-72%). However, the specificity (91% [95% CI, 78%-97%] versus 27% [95% CI, 15%-43%]), positive predictive value (87% [95% CI, 70%-96%] versus 54% [95% CI, 41%-66%]), and negative predictive value (67% [95% CI, 53%-78%] versus 55% [95% CI, 32%-76%]) favored an elevated platelet count compared with WESR, or to the combination of platelets and WESR, as a better test for diagnosing GCA in the 91 patients studied. The area under the receiver operating characteristic function for platelets (0.72) was greater than that for WESR (0.59) or the combination of platelets and WESR (0.65). CONCLUSIONS: In patients suspected of having GCA, an elevated platelet count greater than 400 x 10(3)/microl is a useful marker of a positive temporal artery biopsy.     

总胆红素水平与糖尿病黄斑水肿发病及严重程度的相关性

目的 探讨总胆红素水平与糖尿病黄斑水肿(DME)发病及严重程度的相关性。方法 本研究共纳入82例2型糖尿病伴有糖尿病视网膜病变的患者。根据DME严重程度分级标准，将患者分为3组：无DME组22例(黄斑区中心凹厚度处于正常值范围)、早期DME组25例(黄斑区中心凹厚度高于正常上限值但等于或低于正常值上限130%)、晚期DME组35例(黄斑区中心凹厚度高于正常值上限130%以上)。患者眼底检查及荧光素眼底血管造影结果由2位经验丰富的眼底病专家独立进行分级。收集所有患者性别、年龄、糖尿病病程、体重指数(BMI)等基本参数，以及血液学指标——中性粒细胞数、系统免疫炎症指数[SII,(中性粒细胞数×血小板数)/淋巴细胞数]、空腹血糖、糖化血红蛋白(HbA1c)、总胆红素、尿酸等。使用Pearson相关分析探讨总胆红素水平与各种临床指标的相关性。采用多因素Logistic回归分析探索2型糖尿病患者DME的危险因素。建立受试者工作特征(ROC)曲线，计算曲线下面积(AUC),分析总胆红素对2型糖尿病患者DME的诊断效能。结果 无DME组、早期DME组及晚期DME组患者的糖尿病病程、BMI、中性粒细胞...     

Visual deterioration in giant cell arteritis patients while on high doses of corticosteroid therapy

PURPOSE: To report the incidence and extent of visual deterioration in patients with giant cell arteritis (GCA) on high doses of systemic corticosteroids during the early stages of treatment; the various factors that may influence the outcome; and whether intravenous megadose corticosteroid therapy is more effective than oral therapy. DESIGN: Noncomparative interventional case series. PARTICIPANTS: One hundred forty-four patients with GCA (271 eyes) seen initially with visual loss (91 patients) and without visual loss (53 patients). All patients had biopsy-confirmed GCA and were followed while on high doses of systemic corticosteroid therapy for at least 2 weeks. METHODS: Every patient at the initial visit had an ophthalmic evaluation, including visual acuity, visual fields, intraocular pressure, slit-lamp and ophthalmoscopic evaluation, erythrocyte sedimentation rate (ESR; Westergren) and C-reactive protein (CRP) estimation, and temporal artery biopsy as soon as possible. If GCA was either strongly suspected or confirmed by biopsy, they were immediately started in our clinic on high doses of oral (80-120 mg) prednisone daily or intravenous megadose systemic corticosteroids (usually 150 mg dexamethasone sodium phosphate every 8 hours for 1-3 days) followed by oral prednisone. At each visit they underwent all the initial ophthalmic evaluations and had an ESR and CRP evaluation done. Tapering of steroid therapy was not started until both ESR and CRP had reached their lowest stable levels. These showed marked interindividual variation and usually took approximately 2 weeks to stabilize. Then the steroid therapy was gradually tapered, guided primarily by the levels of ESR and CRP. No generalization is possible regarding the period required to achieve the maintenance dosage, because this also varied markedly from patient to patient. MAIN OUTCOME MEASURES: Visual acuity deterioration. RESULTS: While on high doses of steroid therapy during the initial stages of the treatment, only 9 (11 eyes) of the 91 patients seen initially with visual loss developed further visual acuity deterioration in one or both eyes within 5 days after the start of therapy (one of the eyes had normal vision initially), but none of the 53 patients initially seen without visual loss developed any visual deterioration. Six of the 48 patients (13%) who were on intravenous steroid therapy had visual deterioration compared with 3 of 97 patients (3%) who were only on oral steroid therapy (P = 0.060). CONCLUSIONS: Our study shows that although a few eyes can develop visual deterioration while on high doses of steroid therapy, early, adequate steroid therapy is effective in preventing further visual loss in most. When further visual deterioration occurred despite high doses of systemic corticosteroids, it almost invariably started within 5 days after the start of the high-dose steroid therapy. There was no evidence that intravenous megadose steroid therapy was more effective than oral therapy in preventing visual deterioration.     

Non-arteritic anterior ischemic optic neuropathy: role of systemic corticosteroid therapy

OBJECTIVE: To investigate systematically the role of systemic corticosteroid therapy in non-arteritic anterior ischemic optic neuropathy (NA-AION). METHODS: The study consists of a cohort of 613 consecutive patients (696 eyes), first seen in our clinic from 1973 to 2000. Of this cohort, 312 patients (364 eyes) voluntarily opted for systemic steroid therapy, and 301 (332 eyes) for no treatment. At first visit, all patients in both groups had a detailed ophthalmic and medical history, and comprehensive ophthalmic evaluation. Visual evaluation was done by recording Snellen visual acuity, and visual fields with a Goldmann perimeter. The same ophthalmic evaluation was performed at each follow-up visit. Patients in the steroid-treated group were initially given 80 mg Prednisone daily for 2 weeks, and then tapered down to 70 mg for 5 days, 60 mg for 5 days, and then cutting down by 5 mg every 5 days. Visual outcome in the two groups was compared RESULTS: Median follow-up was 3.8 years. At 6 months from onset of NA-AION, of the eyes with initial visual acuity 20/70 or worse and seen within 2 weeks of onset, there was visual acuity improvement in 69.8% (95% confidence interval (CI): 57.3%, 79.9%) in the treated group, compared to 40.5% (95% CI: 29.2%, 52.9%) in the untreated group (odds ratio of improvement: 3.39; 95% CI:1.62, 7.11; p = 0.001). Comparison of visual field defect at 6 months from onset of NA-AION, among those seen within 2 weeks of NA-AION onset with moderate to severe initial visual field defect, there was improvement in 40.1% (95% CI: 33.1%, 47.5%) of the treated group, and 24.5% (95% CI: 17.7%, 32.9%) of the untreated group (odds ratio: 2.06, 95% CI: 1.24, 3.40; p = 0.005). In both treated and untreated groups, the visual acuity and visual fields kept improving up to about 6 months from onset of NA-AION, and very little thereafter. CONCLUSION: This study suggested that NA-AION eyes treated during the acute phase with systemic corticosteroids resulted in a significantly higher probability of improvement in visual acuity (p = 0.001) and visual field (p = 0.005) than in the untreated group. Both visual acuity and visual fields improved up to 6 months after onset of NA-AION.     

Lower ocular pulse amplitude with dynamic contour tonometry is associated with biopsy-proven giant cell arteritis

Objectives

To determine the role of the ocular pulse amplitude (OPA) from Pascal dynamic contour tonometry in predicting the temporal artery biopsy (TABx) result in patients with suspected giant cell arteritis (GCA).

Ischemic optic neuropathy

Ischemic optic neuropathy is one of the major causes of blindness or seriously impaired vision, yet there is disagreement as to its pathogenesis, clinical features and especially its management. This is because ischemic optic neuropathy is not one disease but a spectrum of several different types, each with its own etiology, pathogenesis, clinical features and management. They cannot be lumped together. Ischemic optic neuropathy is primarily of two types: anterior (AION) and posterior (PION), involving the optic nerve head (ONH) and the rest of the optic nerve respectively. Furthermore, both AION and PION have different subtypes. AION comprises arteritic (A-AION – due to giant cell arteritis) and, non-arteritic (NA-AION – due to causes other than giant cell arteritis); NA-AION can be further classified into classical NA-AION and incipient NA-AION. PION consists of arteritic (A-PION – due to giant cell arteritis), non-arteritic (NA-PION – due to causes other than giant cell arteritis), and surgical (a complication of several systemic surgical procedures). Thus, ischemic optic neuropathy consists of six distinct types of clinical entities. NA-AION is by far the most common type and one of the most prevalent and visually crippling diseases in the middle-aged and elderly. A-AION, though less common, is an ocular emergency and requires early diagnosis and immediate treatment with systemic high dose corticosteroids to prevent further visual loss, which is entirely preventable.Controversy exists regarding the pathogenesis, clinical features and especially management of the various types of ischemic optic neuropathy because there are multiple misconceptions about its many fundamental aspects. Recently emerging information on the various factors that influence the optic nerve circulation, and also the various systemic and local risk factors which play important roles in the development of various types of ischemic optic neuropathy have given us a better understanding of their pathogeneses, clinical features and management. This knowledge should help us not only to manage them better but also to reduce their incidence. For example, clinically, the evidence that about 40% of NA-AION eyes experience spontaneous improvement in visual acuity and that systemic steroid therapy during early stages in both NA-AION and NA-PION has a significant beneficial effect for visual outcome are encouraging developments. This review discusses the current concepts on various issues related to various types of ischemic optic neuropathy.     

Ocular pulse amplitude as a diagnostic adjunct in giant cell arteritis

Background

To develop an algorithm based on the ocular pulse amplitude (OPA) to predict the probability of a positive temporal artery biopsy (TAB) result in the acute phase of suspected giant cell arteritis (GCA).

Methods

Unilateral TAB was performed and ipsilateral OPA measurements were taken by Dynamic Contour Tonometry. Among the clinical signs and laboratory findings tested in univariate analyses, OPA, Erythrocyte Sedimentation Rate (ESR) and thrombocyte count showed a strong association with a positive TAB result. Algorithm parameters were categorized into three groups (OPA >3.5, 2.5–3.5, and <2.5 mm Hg; ESR <25, 25–60, and >60 mm/h; thrombocyte count <250''000, 250''000–500''000, and >500''000/μl). Score values (0, 1, and 2) were attributed to each group, resulting in a total score range from 0 to 6. A univariate logistic regression analysis using the GCA diagnosis as the dependent and the total score as the independent variate was fitted and probability estimates were calculated.

Results

Thirty-one patients with suspected GCA undergoing TAB during an eighteen-month observation period were enrolled. Twenty patients showed histologically proven GCA. Four patients had score values ≤2, fourteen between 3 and 4, and thirteen of ≥5. The corresponding estimated probabilities of GCA were<7, 52.6, and >95%.

Conclusion

The present study confirms previous findings of reduced OPA levels, elevated ESR, and elevated thrombocyte counts in GCA. It indicates that a sum score based on OPA, ESR, and thrombocyte count can be helpful in predicting TAB results, especially at the upper and the lower end of the sum score range.     

血清淀粉样蛋白A检测对感染性眼内炎诊断的临床价值

目的：探讨血清淀粉样蛋白A(SAA)在感染性眼内炎诊断中的临床应用价值。

方法：收集2016-06/2019-03我院就诊的270例患者,其中116例感染性眼内炎患者作为研究组,154例非感染性患者作为对照组。采用胶体金免疫层析法检测SAA水平,用受试者工作特征(ROC)曲线分析诊断效能。

结果：感染性眼内炎患者和对照组SAA值中位数分别为14.98、2.56mg/L,两组比较有差异(P<0.001); CRP值和WBC值中位数两组比较均有差异(P<0.001)。SAA、CRP和WBC计数诊断感染性眼内炎的ROC曲线下面积分别为0.772、0.638、0.618,SAA检测取Youden指数最大值所对应的最佳临界值为6.975mg/L,其灵敏度为63.79%,特异度为84.42%。

结论：SAA联合CRP和WBC计数有助于提高感染性眼内炎的诊断效能。SAA可为感染性眼内炎的辅助诊断提供有用的参考信息。     

Anterior ischemic optic neuropathy due to giant cell arteritis with normal inflammatory markers

Background In anterior ischemic optic neuropathy (AION), it is important not to miss the diagnosis of giant cell arteritis (GCA) because this requires immediate steroid treatment to prevent involvement of the second eye and possible blindness. A missed diagnosis also might lead to fatal systemic complications. Materials and Methods Observational case report. Results A 79-year-old woman noticed decreased visual and visual field loss in the right eye. At presentation, right visual acuity was 10/20 (ETDRS chart 2000). There was a right relative afferent pupillary defect of 0.6 log units. Asked for symptoms of GCA she complained about temporal and occipital headache, jaw claudication combined with malaise, and myalgia of the upper limbs. Laboratory tests showed normal inflammatory markers. Repeated tests confirmed ESR and CRP to be within the normal range. GCA being suspected, ultrasound of the superficial temporal arteries and temporal artery biopsy were performed unilaterally on the right side. Histology showed a chronic inflammatory cell infiltrate consistent with active GCA. The patient was treated with high-dose corticosteroids (250 mg methylprednisolone, three times/day, initially) and symptoms rapidly resolved, but visual loss remained unchanged. Conclusion The case presented here proves that GCA with typical related visual loss (AION) is possible even when both ESR and CRP are in the normal range. Therefore, in the presence of typical symptoms, the clinician must not rely solely on laboratory testing, but start steroid therapy immediately and order a temporal artery biopsy. None of the authors has a financial or property interest in any material or method mentioned.     

The epidemiology of giant cell arteritis : a 12-year retrospective study

OBJECTIVE: To study the incidence of biopsy-proven giant cell arteritis (GCA) in a Hispanic population with clinical features suggestive of GCA. DESIGN: Retrospective review. PARTICIPANTS: Records of 121 consecutive patients who underwent temporal artery biopsy at the Doheny Eye Institute and the Los Angeles County/University of Southern California Hospital from January 1986 through April 1998 were reviewed. MAIN OUTCOME MEASURES: The incidence of biopsy-proven GCA was determined, and the biopsy-positive group was compared with the biopsy-negative group. Study variables included age at diagnosis, gender, erythrocyte sedimentation rate (ESR), and ethnic background. RESULTS: Among these 121 patients who underwent temporal artery biopsy, the mean age of those in the biopsy-positive group (75.2 +/- 5.0 years) was higher than that of those in the biopsy-negative group (69.1 +/- 9.2 years; P < 0.0001). There was no statistical correlation between biopsy-positive and biopsy-negative groups for gender or ESR level, but ESR was statistically significant for whites when we controlled for race. Nineteen of 66 white patients (29%) had positive biopsy results, whereas only 1 of the 9 Asian patients (11%) none of the 40 Hispanic patients (0%; P < 0.0001) and none of the 6 African American patients (0%) had positive biopsy results. CONCLUSIONS: Giant cell arteritis occurs primarily in the white population. None of the Hispanic patients in our study was found to have positive biopsy results. Hispanic persons may have unknown factors that protect them from this disease. Further study is necessary to examine the genetic predisposition.     

Risk factors associated with retinal neovasculari-zation of diabetic retinopathy in type 2 diabetes mellitus

AIM: To evaluate the risk factors associated with retinal neovascularization of diabetic retinopathy in northern Chinese Han patients with type 2 diabetes mellitus (T2DM). METHODS: The clinical characteristics of 200 patients with proliferative diabetic retinopathy (PDR) and 100 age-matched healthy individuals were compared. The univariate and multivariate logistic regression analysis were performed in the patients with PDR. RESULTS: Fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), blood urea nitrogen (BUN), uric acid (UA), white blood cell count (WBC), absolute neutrophil count, hematocrit (HCT) and mean platelet volume (MPV) and mean platelet volume (MPV) were all significantly higher in patients with PDR than in the control group (P<0.05). The univariate and multivariate logistic regression analysis showed that risk factors independently associated with retinal neovascularization of DR were duration of diabetes mellitus (OR=1.112; P =0.000), BUN (OR=1.277; P=0.000), smoking (OR=3.967; P=0.000) and MPV(OR=2.472; P=0.000). On the other hand, panretinal photocoagulation was associated with reduced risk of retinal neovascularization (OR=0.983; P=0.000). CONCLUSION: Preventing and controlling T2DM in terms of risk factors, including duration of diabetes, BUN, smoking and MPV, might offer novel approaches to prevent or delay the onset of retinal neovascularization in patients with PDR.     

Anterior segment ischaemia with giant cell arteritis

CASE REPORT: A 69-year-old male presented with bilateral blurred vision, left periocular pain, and headache. Ocular examination revealed a right optic neuropathy and left anterior segment ischaemia. An elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) raised suspicion of giant cell arteritis (GCA), which was confirmed by temporal artery biopsy. Treatment with intravenous methylprednisolone followed by a gradually reducing dose of oral prednisolone improved vision in both eyes. COMMENTS: GCA typically affects large- and medium-sized vessels. It is a recognised cause of anterior ischaemic optic neuropathy. Anterior segment ischaemia is usually caused by disease of the anterior ciliary arteries not typically affected by GCA. This case illustrates that GCA can rarely cause anterior segment ischaemia, without posterior segment involvement in the same eye.     

Hematologic abnormalities associated with various types of retinal vein occlusion

BACKGROUND: The objective of this study was two-fold: (1) to investigate hematologic abnormalities associated with various types of retinal vein occlusion (RVO) and comparison of their prevalence among those various types of RVO; (2) to review the conflicting literature on the subject, to place the information in perspective. METHODS: In patients with various types of RVO seen in our clinic since 1973, we conducted planned prospective studies on the prevalence of: (1) routine hematologic tests (535 patients) and (2) certain special hematologic parameters (platelet aggregation, antithrombin III, and proportional, variant(2) globulin in 110, 81 and 91 patients, respectively). Patients were categorized into six types of RVO, based on defined criteria: non-ischemic and ischemic central RVO (CRVO), non-ischemic and ischemic hemi-CRVO (HCRVO), and major and macular branch RVO (BRVO). The patients had a detailed ophthalmic, systemic and hematologic evaluation. The data were abstracted and analyzed retrospectively from the detailed information originally collected prospectively in the patients' records. For data analysis, patients were divided into young, middle-aged and elderly. Observed prevalence rates of hematologic abnormalities were estimated. Logistic regression, adjusting for age and gender, was used to compare the observed prevalence of hematologic abnormalities among the various types of RVO. RESULTS: No generalizations about the prevalence of hematologic disorders in all six types of RVO are possible. Ischemic CRVO showed a significantly higher prevalence of abnormal hematocrit ( P=0.044), hemoglobin ( P=0.018), and blood urea nitrogen ( P=0.025) than non-ischemic CRVO, while a significantly higher prevalence of abnormal antinuclear antibody (ANA; P=0.049) was seen in non-ischemic CRVO than in ischemic CRVO. There was a significant ( P=0.011) difference in the prevalence of abnormal uric acid among the three main RVO groups (CRVO, HCRVO, BRVO), highest in BRVO and lowest in HCRVO. There was a higher prevalence of abnormal glucose ( P=0.069) and ANA ( P=0.071) in CRVO+HCRVO than in BRVO. Results of special hematologic studies are given. CONCLUSIONS: Our study showed that a variety of hematologic abnormalities may be seen in association with different types of RVO, and any generalization about these disorders applied to all RVO patients may be misleading. The evidence of our study and in the literature indicates that there is no good reason why all patients with RVO should be subjected to extensive, expensive, special hematologic and hypercoagulability investigations, unless, of course, there is some clear indication; the routine, inexpensive hematologic evaluation is usually sufficient for RVO patients. Treatment with anticoagulants or platelet anti-aggregating agents may adversely influence the visual outcome, without any evidence of protective or beneficial effect.     

Familial non-arteritic anterior ischemic optic neuropathy

PURPOSE: Primary objective was to investigate clinical characteristics of nonarteritic anterior ischemic optic neuropathy (NA-AION) in three families; secondarily, to test these families for a previously detected mitochondrial mutation in a pedigree with familial NA-AION. METHODS: Study comprised three families where more than one member developed NA-AION. All patients with NA-AION had a detailed ophthalmic, medical and family history, and comprehensive ophthalmic evaluation at initial visit and on follow-up. One patient from family 1, one from family 2, 41 non-familial NA-AION patients, 97 control subjects and 1,488 patients with suspected Leber hereditary optic neuropathy (LHON) were tested for the presence of mitochondrial mutation (G4132A) in a previously reported genetic study of family 3. RESULTS: Familial NA-AION was found in seven individuals of family 1, four of family 2 and six of family 3. Symptoms, signs and clinical findings of familial NA-AION were similar to classical NA-AION, with two exceptions: familial NA-AION had an earlier onset (47.3 + 8.6 years versus 60.1 + 13.6 years) and a higher frequency of bilateral disease. The G4132A mitochondrial variant was not detected outside family 3. None of the three major mutations associated with LHON (G3460A, G11778A, T14484C) was found among Familial NA-AION patients. CONCLUSIONS: The only difference in clinical features between familial NA-AION and classical NA-AION is that the former has an earlier onset and a higher frequency of bilateral disease. The G4132A mutation is not commonly associated with familial NA-AION, and was not detected in patients with non-familial NA-AION. The role of hereditary factors in familial NA-AION remains largely unknown.