Abstract
Background
Despite corticosteroid treatment, patients with temporal arteritis may continue to lose vision. However, predictors of progressive visual loss are not known.
Methods
We retrospectively reviewed 341 consecutive patients with suspected temporal arteritis who underwent temporal artery biopsy. 90 patients with biopsy proven temporal arteritis were included in our study.
Results
Twenty‐one patients (23%) experienced continuous visual symptoms despite steroid therapy and 14 among these suffered persistent visual deterioration. Based on univariate analysis, visual loss on presentation was associated with disc swelling and a history of hypertension. Risk factors for progressive visual loss included older age, elevated C reactive protein and disc swelling.
Conclusion
Although corticosteroid therapy improves the visual prognosis in temporal arteritis, steroids may not stop the progression of visual loss. Our study reliably establishes the risk factors for visual loss in this serious condition. Whether addressing these risk factors early in their presentation can alter the visual outcome remains unknown. Individual risk anticipating treatment regimens and strategies might improve the visual prognosis in temporal arteritis in the future.
Left untreated, temporal arteritis (TA) frequently results in blindness. Treatment requires immediate high dose steroids. Risk factors for initial and progressive visual loss, despite appropriate treatment, have not been extensively characterised, making selection of patients at risk for progressive visual loss difficult.
We retrospectively reviewed clinical findings in patients with biopsy proven TA in order to assess risk factors for visual loss during the first days of steroid therapy.
Methods
A retrospective chart review of 341 patients with suspected TA undergoing temporal artery biopsy during 15 consecutive years at the National Hospital for Neurology and Neurosurgery, London, UK, was performed.
Biopsies were performed on the side of predominant symptoms. Biopsies were deemed positive for TA if the histological specimen demonstrated arteritis, characterised by mononuclear cell arterial wall infiltration and interruption of the internal lamina elastica. Additional evidence included media degeneration or intima thickening.1 Visual acuity was expressed as a decimal (20/20 = 1.00; finger counting = 0.012; hand motion = 0.006; light perception = 0.001; no light perception = 0).2 In order to compare steroids among patients, the doses in patients receiving a steroid other than hydrocortisone were converted according to the following dosing scheme: 1 mg dexamethasone = 30 mg hydrocortisone; 1 mg methylprednisolone = 5 mg hydrocortisone, 1 mg prednisone = 4 mg hydrocortisone.
SPSS10.0 was used for statistical analysis. A p value of <0.05 was considered statistically significant.
Results
Ninety‐three (27%) out of 341 biopsy results confirmed TA. Ninety patients (67 females; mean age 74.6 (SD 7.8); range 59–93) were included. The remaining three notes were lost.
Onset of symptoms prior to admission ranged from 2 days to 7 years (median 125 days). It took a median of 8 days (0–242 days) from referral until admission. Median duration of hospital stay was 11 days (0–53). Ninety‐one per cent of biopsies were performed within 5 days of admission; 71% were biopsied within 5 days after starting steroids. Five patients underwent temporal artery biopsy prior to initiation of steroids. All 90 biopsies were suggestive of TA. Fifty‐six (62%) biopsies showed giant cells.
Eighty‐nine patients received corticosteroids. One patient presented 3 weeks after blindness had occurred and was not treated. Thirty‐three patients initially received intravenous corticosteroid treatment (hydrocortisone, methylprednisolone or prednisolone). Fifty‐six patients were initially treated with prednisone by mouth. Doses were converted to hydrocortisone strength for comparison. The average initial corticosteroid dose consisted of 495 mg of hydrocortisone (range 0–5000). The average time until first dose taper was 21 days. In 31 patients, initial corticosteroid dose was increased in order to control symptoms completely.
Twenty‐one (23%) patients showed progressive visual symptoms despite corticosteroid therapy. A total of 20 patients suffered visual loss. Thirteen patients suffered persistent loss of acuity or field loss and one additional patient presented with a hemiparesis and diplopia (table 1). Deterioration occurred usually within the first days of treatment. Seven additional patients had transient visual impairment.
Table 1 Fourteen patients with loss of visual acuity/fields despite corticosteroid therapy.
| Patient No | Sex | Age (years) | History of present illness | Visual acuities on admission | Therapy prior to deterioration | Outcome of visual acuities | Time after therapy started (days) | 2 eyes involved | |||
|---|---|---|---|---|---|---|---|---|---|---|---|
| OD | OS | OD | OS | ||||||||
| 1 | F | 78 | Visual loss OS since 2 days | 0.25 | 0.033 | 60 mg PD po | 0.012 | 0.006 | 5 | Yes | |
| 2 | F | 79 | Smeary vision OS since 4 days | 0.66 | 0.5 | 200 mg HC iv, 40 mg PD po | 0.66 | 0.006 | 1 | No | |
| 3 | F | 88 | Visual loss OS same day | 0.333 | 0.006 | 100 mg HC iv, 60 mg PD po | 0.333 | 0 | 1 | No | |
| 4 | F | 82 | Visual loss OS same day | 0.1 | 0.001 | 200 mg HC iv, 60 mg PD po | 0.1 | 0 | 2 | No | |
| 5 | F | 88 | Visual loss OU same day | 0 | 0.166 | 8 mg DM iv, 80 mg PD po | 0 | 0.001 | 1 | Yes | |
| 6 | F | 82 | Previous PMR 3 years ago, off steroids, OD blind 3 weeks ago, OS misty since 3 days | 0.001 | 0.001 | 200 mg HC iv, 500 mg MP iv x 3 days; then 80 mg PD po | 0 | 0 | 6 | Yes | |
| 7 | M | 64 | Sensory loss right forearm 3 weeks ago, double vision since 2 weeks, mild right hemiparesis since 1 day | 0.666 | 0.666 | 80 mg PD po | 0.333 | 0.666 | 2 | No | |
| 500 mg MP iv | 0.25 | 0.666 | 5 | ||||||||
| 120 mg PD po | 0.166 | 0.666 | 8 | ||||||||
| 80 mg PD po | Hemiparesis deteriorated | 12 | |||||||||
| 8 | F | 92 | Loss of vision OD 14 days ago | 0.001 | 0.666 | 60 mg PD po | 0 | 0.666 | 1 | No | |
| 9 | F | 75 | Visual loss OD since 1 day | 0.5 | 1.0 | 60 mg PD po | 0.001 | 1.0 | 2 | No | |
| 10 | M | 87 | Visual loss OD 6 days ago | 0.006 | 1.0 | 500 mg MP iv x 3 days; then 80 mg PD po | 0.001 | 0.012 | 3 | Yes | |
| 80 mg PD po | 0.012 | 0 | 9 | ||||||||
| 11 | F | 80 | Visual loss OD 2 weeks ago, blurred vision OS since 4 days | 0.001 | 0.666 | 500 mg MP iv x 3 days; then 80 mg PD po | 0.012 | 0.001 | 1 | Yes | |
| 80 mg PD po | 0 | 0 | 10 | Yes | |||||||
| 12 | F | 75 | OS blind 6 days ago, visual loss OD same day | 0.05 | 0 | 1000 mg MP iv x 3 days; then 80 mg PD po | 0 | 0 | 3 | Yes | |
| 13 | F | 59 | Black spot OS since 2 days, visual loss OS same day | 1.2 | 0.006 | 80 mg PD po | 0.666; scotoma | 0.012 | 2 | Yes | |
| 80 mg PD po | 0.666; enlarged scotoma | 0.012 | 27 | ||||||||
| 14 | F | 77 | PMR since 3.5 years, visual loss OS 6 months ago, visual loss OD 2 weeks ago | 0.016 | 0.166 | 1000 mg MP iv x 3 days; then 80 mg PD po | 0.012 | 0.1 | 7 | Yes | |
DM, Dexamethasone; HC, hydrocortisone; iv, intravenous; MP, methylprednisolone; OD, right eye; OS, left eye; OU, both eyes; PD, prednisolone; PMR, polymyalgia rheumatica; po, by mouth.
Of the seven patients with transient visual impairment despite corticosteroids, four patients had transient visual loss, one patient had an episode of left sided weakness and left visual loss, one patient complained about visual teichopsia and one patient developed disc swelling. All symptoms resolved after an increase in steroid dose.
The presence of disc swelling, history of hypertension and older age were significantly associated with visual loss on presentation. A trend of higher odds for initial visual loss was also seen in patients with polymyalgia, diabetes and jaw claudication (table 2). Patients with visual loss on presentation had a higher systolic blood pressure on presentation (table 3).
Table 2 Risk factors for initial visual loss: dichotomous variable.
| Dichotomous variable | Sign present (%) | Symptoms/sign absent (%) | χ2 p value | OR | CI |
|---|---|---|---|---|---|
| Disc swelling | 97.6 | 47.9 | 0.000 | 44.56 | 5.66–350.7 |
| Hypertension | 81.8 | 60.9 | 0.028 | 2.89 | 1.10–7.62 |
| Polymyalgia | 84.2 | 67.6 | 0.156 | 2.56 | 0.68–9.66 |
| Diabetes mellitus | 75 | 70.9 | 0.86 | 1.23 | 0.12–12.39 |
| Jaw claudication | 72.3 | 69.8 | 0.788 | 1.13 | 0.46–2.82 |
| Diplopia | 70 | 71.4 | 0.901 | 0.93 | 0.31–2.77 |
| Giant cells on biopsy | 69.6 | 73.5 | 0.693 | 0.83 | 0.32–2.14 |
| Cholesterol | 100 | 78.6 | 0.605 | 0.79 | 0.6–1.03 |
| Muscle tenderness | 67.6 | 73.6 | 0.535 | 0.75 | 0.30–1.88 |
| Male sex | 66.7 | 73.7 | 0.479 | 0.714 | 0.281–1.82 |
| Stroke | 60 | 71.8 | 0.573 | 0.59 | 0.09–3.76 |
| Systemic features | 63.6 | 78.3 | 0.126 | 0.49 | 0.19–1.23 |
| Temple tenderness | 63.6 | 78.3 | 0.126 | 0.49 | 0.19–1.23 |
| Smoker | 60.5 | 78.8 | 0.058 | 0.41 | 0.16–1.04 |
| Headache | 67.5 | 92.3 | 0.068 | 0.17 | 0.02–1.41 |
Table 3 Risk factors for initial visual loss: continuous variables.
| Continuous variable | Mean value in patients with visual loss (n) | Mean value in patients without visual loss (n) | t test p value | OR | CI |
|---|---|---|---|---|---|
| Blood glucose (mg/dl) | 160 (59) | 144 (22) | 0.272 | 1.22 | 1.02–1.46 |
| Age (y) | 76.6 (64) | 69.5 (26) | 0.000 | 1.15 | 1.07–1.24 |
| Systolic BP (mm Hg) | 156 (64) | 145 (26) | 0.056 | 1.02 | 1.0–1.04 |
| ESR at referral (mm) | 75 (54) | 66 (18) | 0.213 | 1.01 | 0.99–1.04 |
| Onset (days) | 140 (63) | 88 (26) | 0.51 | 1.0 | 0.998–1.00 |
| Platelets at presentation | 457 (50) | 448 (17) | 0.831 | 1.0 | 0.997–1.0 |
| Corticosteroid dose (mg HC) | 672 (64) | 245 (26) | 0.004 | 1 | 1.00–1.00 |
| Time referral to admission (days) | 9 (61) | 6 (24) | 0.289 | 1.00 | 0.98–1.02 |
| ESR at presentation (mm/h) | 70 (26) | 68 (63) | 0.779 | 0.996 | 0.98–1.01 |
| Diastolic BP (mm Hg) | 82 (64) | 84 (26) | 0.422 | 0.99 | 0.95–1.03 |
| Duration of hospital stay | 12 (64) | 9 (26) | 0.363 | 1.03 | 0.97–1.09 |
BP, blood pressure; ESR, erythrocyte sedimentation rate; HC, hydrocortisone.
Risk factors for progressive visual loss included older age, elevated C reactive protein (CRP) and disc swelling (tables 4 and 5). Fourteen patients with early progressive visual loss despite corticosteroid therapy were, on average, 79.4 years old. Seventy‐six patients without progressive visual loss were, on average, 73.7 years old and therefore significantly younger (p<0.05, t test value 2.2). The CRP of patients with progressive visual loss was, on average, significantly higher (57.4; n = 7) than that of patients without visual loss (22.1; n = 12; p<0.02, t test value −3.0). Other factors significantly (p<0.05) associated with progressive visual loss were disc swelling (odds ratio (OR) 5.3 (95% CI 1.4 to 20.7)) and administration of steroids intravenously (OR 5.6 (95% CI 1.6 to 19.9)) (tables 4 and 5). Men had reduced odds of visual loss progression (OR 0.24 (95% CI 0.05 to 1.2)), approaching statistical significance (p = 0.06) (tables 4 and 5).
Table 4 Odds ratios for progressive visual loss: dichotomous symptoms.
| Symptom (dichotomous) | Symptom in patients with progressive loss (%) | Symptom in patients without progressive visual loss (%) | χ2 p value | OR | 95% CI |
|---|---|---|---|---|---|
| IV steroids | 30.3 | 7.1 | 0.004 | 5.65 | 1.6–19.91 |
| Disc swelling | 26.2 | 6.3 | 0.009 | 5.32 | 1.37–20.66 |
| Stroke | 40 | 14.1 | 0.121 | 4.06 | 0.61–26.86 |
| Headache | 16.9 | 7.7 | 0.398 | 2.44 | 0.29–20.42 |
| Scalp tenderness | 20.5 | 10.9 | 0.21 | 2.11 | 0.65–6.81 |
| Diabetes mellitus | 25 | 15.1 | 0.498* | 1.87 | 0.18–19.41 |
| Systemic symptoms | 18.2 | 13.0 | 0.501 | 1.48 | 0.47–4.68 |
| Hypertension | 18.2 | 13 | 0.501 | 1.48 | 0.47–4.68 |
| Muscle tenderness | 16.2 | 15.1 | 0.885 | 1.09 | 0.34–3.45 |
| Polymyalgia | 15.8 | 15.5 | 0.609* | 1.02 | 0.25–4.11 |
| Cholesterol by history | 0 | 14.3 | 0.867* | 0.86 | 0.69–1.06 |
| Giant cells on biopsy | 14.3 | 17.6 | 0.67 | 0.78 | 0.24–2.47 |
| Jaw claudication | 12.8 | 18.6 | 0.445 | 0.64 | 0.2–2.02 |
| Diplopia | 10 | 17.1 | 0.35* | 0.537 | 0.11–2.63 |
| Smoker | 7.9 | 21.2 | 0.086 | 0.32 | 0.08–1.24 |
| Male sex | 6.1 | 21.1 | 0.059 | 0.242 | 0.051–1.16 |
*Fisher's exact test.
Table 5 Odds ratios for progressive visual loss: continuous symptoms.
| Symptom (continuous) | Mean value in patients with progressive loss (n) | Mean value in patients without progressive visual loss (n) | t test p value | OR | 95% CI |
|---|---|---|---|---|---|
| CRP on presentation | 57.43 (7) | 22.17 (12) | 0.016 | ||
| Age (y) | 79.41 (14) | 73.7 (76) | 0.042 | 1.1147 | 1.0208–1.2171 |
| Glucose (mg/dl) | 155.8 (14) | 154.5 (67) | 0.297 | 1.0699 | 0.9009–1.2707 |
| Diastolic BP (mm Hg) | 86.79 (14) | 82.25 (76) | 0.066 | 1.0371 | 0.9839–1.0932 |
| Systolic BP (mm Hg) | 159.64 (14) | 152.15 (76) | 0.305 | 1.0118 | 0.9894–1.0347 |
| ESR at referral (mm/h) | 77.92 (13) | 71.90 (59) | 0.466 | 1.01 | 0.99–1.03 |
| Time referral to admission (days) | 18.29 (14) | 6.18 (71) | 0.497 | 1.0093 | 0.9941–1.0247 |
| ESR at presentation (mm/h) | 70.79 (14) | 67.70 (76) | 0.671 | 1.0044 | 0.9830–1.0263 |
| Platelets at presentation | 463.36 (11) | 453.79 (56) | 0.854 | 1.0004 | 0.9962–1.0047 |
| Steroid dose (mg HC) | 780 (14) | 479.21 (76) | 0.437 | 1.0002 | 0.9998–1.0007 |
| Onset of symptoms (days) | 109.36 (14) | 128.35 (75) | 0.681 | 0.9997 | 0.9975–1.0020 |
| Length of hospital stay | 21.57 (14) | 9.13 (76) | 0.005 | 1.1044 | 1.0403–1.1725 |
BP, blood pressure; CRP, C reactive protein; ESR, erythrocyte sedimentation rate; HC, hydrocortisone.
*Fisher's exact test.
Median follow‐up duration was 7 months (range 11 days to 16 years). Two year follow‐up was available for 28 patients. Four patients without previous visual symptoms had visual loss (unilateral permanent visual loss in two and unilateral temporary visual loss in two). Visual loss occurred, on average, 24 months after initial presentation. All four patients were on a tapering dose of oral prednisone at that time (on average 14 mg daily).
Discussion
Continuous visual symptoms despite steroid therapy were seen in 23% of patients, and 16% suffered visual deterioration during therapy. Risk factors for visual loss on presentation were disc swelling and hypertension. Risk factors for progressive visual loss included older age, elevated CRP and disc swelling.
Fifty‐eight patients (3.1%) with visual loss after initiation of corticosteroid therapy were found among 1296 patients with TA in the literature (table 6) ranging from 0%3 to 38.9% in prospective series.4 In a meta‐analysis of 39 retrospective4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24 and prospective studies (table 6), we found a highly significant correlation (Pearson's correlation coefficient 0.604; p<0.0001) between the percentage of patients with visual loss on presentation and visual loss under corticosteroid therapy (fig 1). Visual loss on presentation may therefore predict visual deterioration under corticosteroid therapy, as also seen in our patients.
Table 6 Visual loss during corticosteroid therapy (prospective studies).
| Author | Year | Study design (cases) | n | Positive biopsy | Patients with visual loss (%) | Patients with ocular deterioration during therapy (%) |
|---|---|---|---|---|---|---|
| Birkhead33 | 1957 | Prospective | 55 | 55 (100%) | 21 (38%) | 2 (3.6%) |
| Palm34 | 1958 | Prospective | 31 | 13 (21%) | 31 (100%) | 4 (12.9%) |
| Parsons‐Smith35 | 1958 | Prospective | 50 (13 treated) | NR | 13/55; all 13 treated (24%) | 1 (7.7%) |
| Russell36 | 1959 | Retrospective (8) | 35 (21 treated) | 11 (31%) | 16/35 with visual symptoms (46%) | 6 (28.6%) |
| Prospective (27) | ||||||
| Mosher4 | 1959 | Retrospective | 32 (18 treated) | 23 (72%) | 20 with eye symptoms (62.5%) | 7 (38.9%) |
| Whitfield37 | 1963 | Prospective | 72 | NR | 40 (55%) | 1 (1.4%) |
| Cullen38 | 1967 | Prospective | 25 | 25 (100%) | 25 (100%) | 1 (4%) |
| Fauchald39 | 1972 | Prospective | 94 | 61 (65%) | 5 ocular symptoms (5%) | 1 (1.1%) |
| Hunder40 | 1975 | Prospective | 60 | 60 (100%) | 3 (5%) | 0 (0%) |
| Bengtsson41 | 1981 | Prospective | 27 | 17 (63%) | NR | 2 (7.4%) |
| Jones42 | 1981 | Prospective | 85 | 22 (26%) | 6/22 (27%) permanent | 1 (1.2%) |
| Behn3 | 1983 | Prospective | 68 | 25 (37%) | 10 (15%) | 0 (0%) |
| Boesen43 | 1987 | Prospective | 21 | 11 (52%) | NR | 0 (0%) |
| Caselli44 | 1988 | Prospective | 166 | 166 (100%) | 14 permanent (8.4%) | 1 (0.6%) |
| 17 transient | ||||||
| 8 scotoma | ||||||
| Kyle45 | 1989 | Prospective | 35 | NR | NR | 1 (2.9%) |
| Myles46 | 1992 | Prospective | 96 TA | 48/78 (61.5%) | NR | 4/96 (4%) |
| 210 PMR | NR | 3/210 PMR (1.4%) | ||||
| Aiello47 | 1993 | Prospective | 245 | 204 (83%) | 34 (14%) | 5 (1.6%) |
| Duhaut48 | 1999 | Prospective | 292 | 207 (71%) | 31 (55%) | 14 (6.8%) |
| Kupersmith49 | 1999 | Prospective | 22 | 19 (86%) | 7 (32%) | 2 (9%) |
| Chevalet50 | 2000 | Prospective | 164 | 128 (78%) | NR | 1 amaurosis (0.6%) |
| Kupersmith 2 | 2001 | Prospective | 20 | 20 (100%) | 4 (20%) | 0 (0%) |
| Liozon29 | 2001 | Prospective | 174 | 147 (85%) | 48 (28%) visual symptoms; | 4 (2.3%) |
| 23 (13%) permanent | ||||||
| Danesh‐Meyer25 | 2005 | Prospective | 34 | 34 (100%) | 34 (100%) | (27% of eyes during the first 6 days) |
| SUM | 1838 | 1296 (70.5%) | 362 (19.7%) | 58 (3.1%) |
GC, Giant cells; NR, not reported; PMR, polymyalgia rheumatica; TA, temporal arteritis.
Figure 1 Visual deterioration in relationship to visual loss on presentation, in per cent, based on retrospective and prospective series with complete data from the literature.
Visual deterioration occurs in two peaks. The first peak manifests as progression of the ongoing flare on an unchanged steroid dose, typically during the first 6 days.25 The second peak occurs after weeks or months of tapering treatment. Relapses increase with reduction of corticosteroid therapy and were seen in 19% of patients within 1 year.26
Reasons for progression of visual loss despite treatment may include hypoperfusion of the optic disc, treatment delay, inadequate steroid dose, quick taper or hypercoagulability with retinal artery infarction, possibly due to steroid therapy. Continuation of arteritis despite adequate corticosteroid dose may be considered part of the spectrum of TA or may even be a separate disease entity.
Differential diagnoses mimicking TA include systemic lupus erythematodes, Sjögren's syndrome, rheumatoid arthritits, Behcet's disease, antiphospholipid antibody syndrome, polyarteritis nodosa, Churg–Strauss syndrome, Wegener's granulomatosis and other rheumatic conditions presenting with granulomatous vasculitis such as Takyasu arteritis.27 Sarcoid, primary angiitis of the central nervous system, non‐arteritic AION, neoplastic conditions as well as viral infections (varicella zoster, human parvo virus B19, human herpes virus 6, herpes simplex) and nocardiosis should also be considered.
Risk factors for initial visual loss include transient visual ischaemic symptoms, increased platelet count, jaw claudication and HLA‐DRB1 phenotype.20,28 Constitutional symptoms and elevated liver enzymes are associated with a lower risk of visual loss.28,29 Risk factors for permanent visual loss include amaurosis fugax and cerebrovascular accidents.20
Risk factors for progressive visual loss may include occlusive strokes, possibly due to steroid therapy itself.30 Late recurrence of visual loss was associated with female sex, older age, worse initial visual acuity, oral (as compared to intravenous) initial steroid treatment and higher erythrocyte sedimentation rate.24 HLA DRB1 alleles were also associated with progressive symptoms.31
Intravenous or high dose oral corticosteroids remain the standard of care for patients at risk for visual loss.25 A retrospective review of 166 patients demonstrated better outcome in patients on low dose aspirin at the time of symptom onset.32 Aspirin may therefore decrease the rate of visual loss and strokes in patients with TA. Further research is on the way to determine effectiveness. Some authors also use heparin, in particular in patients with progressive visual loss.25 Additional steroid sparing agents during the long term treatment period have been tried but no positive randomised placebo controlled prospective trials are available.
Limitations of our study include the retrospective design and referral bias at a tertiary treatment centre. Our literature review attempted to compensate for these variations by comparing our data with previous studies in different settings.
The 1990 American College of Rheumatology (ACR) Criteria for the Classification of Giant Cell (Temporal) Arteritis1 were not applied to all 341 patients seen in our clinic because of the retrospective study design. We limited our study population to the gold standard of diagnosis prior to establishment of these criteria, a positive temporal artery biopsy. Nevertheless, all included patients met the 1990 ACR criteria. By making the positive biopsy a prerequisite, we likely applied more sensitive inclusion criteria. Stricter inclusion criteria may also have led to a selection bias towards more active cases. Our data are therefore valid for patients over 50 years old and in whom the biopsy is positive and at least one additional diagnostic ACR criterion is present. A prospective study on progressive visual loss according to ACR standards is needed.
Conclusion
Progression of visual loss despite steroid therapy occurs in a significant minority of patients with TA. In most patients, deterioration occurs within the first 3 days after initiation of steroid therapy. Individual risk anticipating treatment strategies might improve visual prognosis in TA.
Abbreviations
ACR - American College of Rheumatology
CRP - C reactive protein
TA - temporal arteritis
Footnotes
Competing interests: None.
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