Abstract
Objectives
1) To evaluate the utility of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) for the diagnosis of giant cell arteritis (GCA) 2) to determine the frequency of normal ESR and CRP at diagnosis of GCA.
Methods
All patients undergoing temporal artery biopsy (TAB) between 2000 and 2008 were identified. Only subjects with both ESR and CRP at the time of TAB were included. The medical records of all patients were reviewed.
Results
We included 764 patients (65% women), mean age 72.7 (±9.27) years, who underwent TAB. Biopsy was consistent with GCA in 177 patients (23%). Elevated CRP and elevated ESR provided a sensitivity of 86.9% and 84.1% respectively, for a positive TAB. The odds ratio (OR) of a concordantly elevated ESR and CRP for positive TAB was 3.06 (95% CI 2.03, 4.62) while the OR for concordantly normal ESR and CRP was 0.49 (95% CI 0.29, 0.83).
Seven patients (4%) with a positive TAB for GCA had a normal ESR and CRP at diagnosis. Compared to GCA patients with elevated markers of inflammation, a greater proportion of these patients had polymyalgia rheumatica symptoms (p=0.008) while constitutional symptoms, anemia and thrombocytosis were observed less often (p<0.05).
Conclusions
CRP is a more sensitive marker than ESR for a positive TAB that is diagnostic of GCA. There may be clinical utility in obtaining both tests in the evaluation of patients with suspected GCA. A small proportion of patients with GCA may have normal inflammatory markers at diagnosis.
INTRODUCTION
Giant cell arteritis (GCA) is a granulomatous vasculitis involving the aorta and its primary and secondary branches (1). GCA is the most common form of systemic vasculitis in people over the age of 50 years, with an annual incidence of approximately 19 per 100,000 people aged 50 years and above (2). The lifetime risk for developing GCA is estimated at 1% for women and 0.5% for men (3). Vision loss due to ischemic optic neuropathy is a dreaded complication of GCA and therefore, prompt diagnosis and treatment are essential (1).
To date, there is no specific blood biomarker for GCA and histologic examination of a temporal artery biopsy (TAB) specimen is considered the gold standard diagnostic test. Laboratory findings in GCA are non-specific but most patients have elevated acute phase reactants at disease onset. An elevated erythrocyte sedimentation rate (ESR) has been considered a hallmark of this disease and is one of the ACR classification criteria for GCA (4). The C-reactive protein (CRP) is an acute phase reactant synthesized in the liver and is a sensitive marker of systemic inflammation. While CRP is often used in conjunction with the ESR for the initial evaluation of patients with suspected GCA, few studies have evaluated CRP performance in subjects undergoing TAB (5, 6).
We sought to evaluate the performance of ESR, CRP and a combination of the two tests for the diagnosis of GCA among all patients undergoing TAB. Secondly, we sought to evaluate the frequency of normal ESR and CRP at the time of GCA diagnosis in patients with a positive TAB, and describe the clinical characteristics of these patients.
PATIENTS AND METHODS
The study was approved by the Mayo Clinic Institutional Review Board. Using the Mayo Clinic database, a data retrieval specialist identified all patients who underwent TAB at our institution between January 1, 2000 and December 31, 2008.
Data collection
The medical records of all patients who underwent TAB were reviewed. Data regarding demographic information, date of biopsy and laboratory findings, including complete blood count (CBC), ESR and CRP prior to the biopsy were abstracted from the medical records. Pathology reports from all subjects undergoing TAB were reviewed to identify patients in whom TAB was interpreted as showing changes consistent with GCA. Patients with a positive TAB were all treated for GCA. In the subset of patients with biopsy-positive GCA, we also abstracted the date of first symptom onset, date of diagnosis of GCA, symptoms at disease onset, glucocorticoid use at the time of laboratory testing (if applicable) and use of non-steroidal anti-inflammatory medications at the time of laboratory testing.
ESR was measured by Westergren method. Based on Mayo Clinic clinical laboratory reporting, an ESR value of ≤22 mm/hour in men or ≤29 mm/hour in women was considered normal regardless of age. A normal CRP was defined as a value of ≤8 mg/L in all patients regardless of age.
Exclusions
Subjects who did not have both ESR and CRP testing available in the 6 weeks prior to TAB.
Statistical analysis
Descriptive statistics were used to summarize data. For the first portion of the study, sensitivity, specificity, positive and negative predictive value of ESR, CRP and the combination of the two for a positive TAB were calculated. Logistic regression was used to evaluate the association between the acute phase reactants and positive TAB. Receiver operator characteristic (ROC) curves were used to determine the optimal cutoff value for CRP.
In the second portion of the study, we compared the clinical features of patients with GCA confirmed by TAB who had normal ESR and CRP to those of patients with elevated markers at the time of diagnosis. We used Fisher’s exact test to compare categorical variables between patients with normal ESR and CRP at the time of diagnosis to patients with either test elevated. Rank sum tests were used to compare continuous variables between the two groups.
RESULTS
A total of 1,106 subjects underwent 1,174 TAB at our institution between January 1, 2000 and December 31, 2008. TAB findings were consistent with GCA in 242 patients (21.9%).
Performance of ESR and CRP among patients undergoing TAB
Of the 1,106 patients who underwent TAB, 764 (69.1%) had both ESR and CRP testing within 6 weeks before TAB and were included for this portion of the study. The study cohort therefore included 587 patients (77%) with a negative TAB and 177 patients (23%) with a positive TAB for GCA. Of the 177 patients with positive TAB, 165 patients (93.2%) met 1990 ACR Classification criteria for GCA. Twelve patients with positive TAB who did not meet 1990 ACR classification criteria included 8 patients with other cranial symptoms suspicious for GCA and 4 patients with symptoms of limb claudication and evidence of large-artery stenosis. We compared baseline demographics and the distribution of ESR and CRP in patients with a positive TAB for GCA to those with a negative TAB (Table 1). At baseline, patients with a positive TAB for GCA were on average, 2.4 years older than patients who had a negative TAB. The median ESR and CRP were also significantly higher in patients with a positive TAB compared to those with a negative biopsy. Additionally, a significantly greater proportion of patients with a positive TAB had a concordantly elevated ESR and CRP (81%) compared to subjects with a negative biopsy (59%).
Table 1.
Baseline and laboratory characteristics among 764 subjects undergoing a temporal artery biopsy (TAB)
| Variable | TAB negative | TAB positive | p-value |
|---|---|---|---|
| (N=587) | (N=177) | ||
| Mean Age (± SD), years | 72.1 (9.6) | 74.5 (7.8) | 0.008 |
| Female Sex, No. (%) | 371 (63.2) | 130(73.4) | 0.012 |
| Median ESR (IQR), mm/hour | 44.0 (25, 75) | 62.0 (36, 91) | <0.001 |
| Median CRP (IQR), mg/L | 24.0 (6, 73) | 52.0 (27, 95) | <0.001 |
| ESR elevated, No. (%) | 414(70.5) | 149 (84.2) | <0.001 |
| CRP elevated, No. (%) | 408 (69.5) | 153 (86.4) | <0.001 |
| Elevated ESR and CRP, No. (%) | 345 (58.8) | 143 (80.8) | <0.001 |
| Normal ESR and CRP, No. (%) | 110(18.7) | 18(10.2) | 0.006 |
data presented as median with 25th and 75th percentile values
SD=standard deviation; No.=number; ESR=erythrocyte sedimentation rate; CRP=C-reactive protein; IQR=interquartile range
The sensitivity, specificity, positive and negative predictive values of ESR, CRP and a combination of the two for a positive biopsy result are provided in Table 2. An elevated CRP provided a slightly higher sensitivity for a positive biopsy than an elevated ESR. The specificity of the ESR and CRP individually was low while the combination of elevated ESR and CRP provided modest specificity (41%). Both a normal ESR and normal CRP had excellent negative predictive values, with the CRP slightly outperforming the ESR. An elevated ESR was associated with increased odds ratio (OR) for a positive TAB (OR 2.22; 95%CI 1.43, 3.46) as was elevated CRP (OR 2.94; 95%CI 1.83, 4.71). The highest odds ratio for positive TAB was observed in subjects who had an elevation of both ESR and CRP (OR 3.06; 95% CI 2.03, 4.62). Conversely, if ESR and CRP were both normal the odds ratio for positive biopsy was reduced; OR 0.49 (95% CI 0.29, 0.83).
Table 2.
Test characteristics of ESR, CRP and a combination of the two for positive temporal artery biopsy
| Sensitivity | Specificity | PPV | NPV | |
|---|---|---|---|---|
| ESR | 84.2% | 29.5% | 26.4% | 86.1% |
| 149/177 | 173/592 | 149/563 | 173/201 | |
| CRP | 86.4% | 30.5% | 27.2% | 88.6% |
| 153/177 | 179/587 | 153/561 | 179/202 | |
| ESR and CRP* | 80.8% | 41.2% | 29.3% | 87.7% |
| 143/177 | 242/587 | 143/488 | 242/276 |
evaluating subjects with both tests elevated
ESR=erythrocyte sedimentation rate; CRP=C-reactive protein; PPV=positive predictive value; NPV=negative predictive value
We performed a sensitivity analysis in which we included all subjects with TAB who had either ESR or CRP tested. The results of this analysis for ESR or CRP were similar to that reported in Table 2. When all subjects who had an ESR performed were included, elevated ESR had a sensitivity of 86% (193/225), specificity of 27% (217/810), positive predictive value of 25% (193/786) and negative predictive value of 87% (217/249). For CRP, the sensitivity of elevated CRP was 87% (155/178), specificity was 31% (183/599), positive predictive value was 27% (155/571) and negative predictive value was 89% (183/206). Based on estimates derived by modeling an ROC curve and including all subjects who underwent TAB and had CRP testing performed, the optimal cut-off value for CRP was 26.9 mg/L, yielding a sensitivity of 75% and specificity of 51% (Figure 1a). Similarly, estimates derived by modeling an ROC curve for all subjects with TAB and ESR testing, the optimal cut-off value for ESR was 53 (Figure 1b).
Figure 1.
Receiver operator characteristic curve of CRP (panel a) and ESR (panel b) in subjects undergoing temporal artery biopsy.
Based on estimates derived by modeling an ROC curve, the optimal cut-off value for CRP was 26.9 mg/L, yielding a sensitivity of 75% and specificity of 51% (Figure 1a). Similarly, estimates derived by modeling an ROC curve for all subjects with TAB and ESR testing, the optimal cut-off value for ESR was 53 mm/hour which gave a sensitivity of 66% and specificity of 55% (Figure 1b).
Normal ESR and CRP at diagnosis in GCA
The subset of 177 patients with GCA was used to evaluate the clinical characteristics of patients who had normal ESR and CRP at diagnosis. This included 130 women (73.4%) and 47 men (26.6%) with a mean age at diagnosis of 74.5 (±7.8) years. Table 3 summarizes the symptoms at diagnosis in all 177 patients.
Table 3.
Symptoms at onset in 177 patients with GCA
| Variable | No. (%) |
|---|---|
| Median duration symptoms (IQR), days | 51.5 (18, 111.5) |
| Headache | 111 (62.7) |
| Jaw claudication | 78 (44.1) |
| Scalp sensitivity | 65 (36.7) |
| Transient vision loss | 37 (20.9) |
| Permanent vision loss | 18 (10.2) |
| Subjective fever | 3 9 (22.0) |
| Fatigue | 62 (35.0) |
| Anorexia | 21(11.9) |
| Subjective weight loss | 54 (30.5) |
| Polymyalgia rheumatica | 54 (30.5) |
GCA=giant cell arteritis; No.=number
The ESR and/or CRP were elevated in 159 (89.8%) patients while 18 patients (10.2%) had a normal ESR and CRP at the time of diagnosis. There was good concordance between ESR and CRP, as both were either elevated or normal in 163 patients (92.1%). However, 14 patients (7.9%) had discordant results; of these, CRP was elevated with a normal ESR in 9 patients.
Eleven of the 18 subjects with normal ESR and CRP were on glucocorticoids at the time of testing. Therefore, 7 (4%) patients had a normal ESR and CRP even in the absence of glucocorticoid use. Median ESR for these 7 patients was 13 mm/hour (range 3–25) with median CRP 4.4 mg/L (range 1.3–8.0 mg/L). While not statistically significant, the 7 patients with normal ESR and CRP tended to be younger, have a longer duration of symptoms and had fewer constitutional symptoms than the patients with elevated ESR and/or CRP (Table 4). Of concern, visual symptoms were present in 3 of the 7 patients (43%) with vision loss occurring in 1 patient (14.3%). A greater proportion of patients with normal ESR and CRP at the time of diagnosis had symptoms of polymyalgia rheumatica (Table 4). These patients also had a significantly lower platelet count and higher hemoglobin at the time of diagnosis compared to patients with an elevated ESR or CRP (Table 4).
Table 4.
Clinical manifestations of GCA patients with normal ESR and CRP to those with elevated ESR and/or CRP
| Clinical Variable | ESR and/or CRP elevated* N=138 |
ESR and CRP normal* N=7 |
p-value |
|---|---|---|---|
| Female gender, No. (%) | 98 (71) | 6 (85.7) | 0.40 |
| Age at diagnosis, Mean (±SD) years | 74.5 (8.0) | 70.0(5.9) | 0.11 |
| Symptom duration, Median (IQR)** days | 51(18, 101) | 112(16, 167) | 0.41 |
| New headache, No. (%) | 88 (63.8) | 4(57.1) | 0.72 |
| Jaw claudication, No. (%) | 65(47.1) | 2 (28.6) | 0.34 |
| Scalp tenderness, No. (%) | 50 (36.2) | 2 (28.6) | 0.68 |
| Transient vision loss, No. (%) | 30(21.7) | 2 (28.6) | 0.68 |
| Permanent vision loss, No. (%) | 13 (9.4) | 1 (14.3) | 0.67 |
| Fever, No. (%) | 33 (23.9) | 0(0) | 0.14 |
| Fatigue, No. (%) | 50 (36.2) | 0(0) | 0.05 |
| Anorexia, No. (%) | 17(12.3) | 0(0) | 0.32 |
| Weight loss, No. (%) | 43 (31.2) | 1 (14.3) | 0.34 |
| Polymyalgia rheumatica, No. (%) | 35 (25.4) | 5(71.4) | 0.008 |
| Anemia, No. (%) | 88 (68.8) | 0(0) | <0.001 |
| Hemoglobin, mean (±SD) g/dL | 11.6(1.53) | 13.4(0.99) | 0.002 |
| Thrombocytosis, No. (%) | 46 (36.2) | 0(0) | 0.05 |
| Platelet count, mean (±SD)x109/L | 424.2(135.2) | 270.9(56.79) | 0.001 |
Subjects on glucocorticoids were excluded
data presented as median with 25th and 75th percentile values
No=number; SD=standard deviation; IQR=interquartile ratio; NSAID=non-steroidal antiinflammatory drugs
DISCUSSION
Biomarkers of inflammation, particularly the ESR and CRP, are often used in the evaluation of patients suspected of having GCA. However, performance of both in the diagnosis of GCA is not well described (5, 6). To our knowledge, the current study is the largest to date that evaluates these markers of inflammation in a cohort of patients undergoing TAB for diagnosis of GCA. Additionally, we also assessed the frequency and clinical characteristics of patients with biopsy-positive GCA who had normal ESR and CRP.
Only two prior studies have evaluated the usefulness of CRP in the diagnosis of GCA among subjects undergoing TAB (5, 6). In a study evaluating the sensitivity and specificity of different laboratory markers for the diagnosis of GCA, CRP (>0.5 mg/dL) was more sensitive (sensitivity 100%) than ESR (sensitivity 97%) and the combination of the two provided the best specificity (97%) (6). However, the authors compared the test characteristics among patients with GCA to controls who were subjects seen in an ophthalmology practice for other conditions (6). Therefore, this study did not provide information on the performance of inflammatory markers in the setting of all-comers undergoing a TAB for suspected GCA. A more recent study evaluated the performance of ESR and CRP among subjects undergoing a TAB and also concluded that elevated CRP was a better predictor of a positive biopsy than ESR (5). However, while the latter study included 3,001 subjects undergoing TAB (459 with positive biopsy), the frequency of CRP testing was low and only available in 20% of the patients (98 patients with GCA and 493 subjects with a negative biopsy). In our study, 66% of patients who underwent TAB had both ESR and CRP measured at the time of the procedure.
We were able to evaluate the test characteristics of ESR or CRP alone and the combination of the two to determine which performed better and whether there is clinical utility to testing both. As in previous reports, we found that elevated CRP had a higher sensitivity than ESR for GCA (86.4%). However, the specificity of either ESR or CRP alone was low (approximately 30%). This improved modestly to 41% when a combination of ESR and CRP were used. While the combination of ESR and CRP did not improve sensitivity, the highest odds ratio for a positive TAB and the diagnosis of GCA was observed when both ESR and CRP were concordantly elevated. Conversely, the combination of normal ESR and CRP was associated with decreased odds of having a positive TAB.
While the majority of patients with GCA have elevated markers of inflammation at clinical presentation, normal ESR or CRP has been reported in a small proportion of patients at diagnosis. The frequency varies between 4–14% depending on the study and the definition of normal values (7–9). In one study, 22.5% subjects with polymyalgia rheumatica or GCA had a normal ESR at diagnosis (10). In a population-based study of newly diagnosed GCA, 5.3% of 167 patients had an ESR less than 40 mm/hour (7). A meta-analysis evaluating the diagnostic value of clinical findings among patients suspected of having GCA estimated that about 4% patients with GCA present with normal ESR (9). Few studies have evaluated normal CRP at diagnosis, with estimates ranging from 2% to 14% (8, 11–13). In one study of 119 patients with GCA, only 3 subjects (1.7%) had a normal CRP at the time of GCA diagnosis, of whom 1 subject (0.8%) had a normal ESR and CRP (8). Other studies which have evaluated CRP at diagnosis have included subjects with PMR and/or GCA, reporting a prevalence of normal CRP to be between 1.2% and 20% (11–13). However, since these studies also included patients with PMR, it is difficult to draw conclusions regarding the subset of patients with GCA.
In our study, the prevalence of normal ESR and CRP in the absence of glucocorticoid use was 4%. We used cut-off values defined by our laboratory for the normal ranges of these tests in our analysis, rather than other possible, generally higher, values for ESR and CRP. All of the patients with normal inflammatory markers underwent TAB because of clinical symptoms suggesting GCA.
Compared to patients with elevated acute phase reactants and biopsy-confirmed GCA, the patients with normal markers had fewer constitutional symptoms. Additionally, other laboratory abnormalities including anemia and thrombocytosis were also less prevalent in those with normal ESR/CRP, suggesting an overall muted inflammatory response. This finding is similar to what has been reported in a population-based study evaluating low ESR (<40 mm/hour) at diagnosis (7). In that study, patients with a low ESR had fewer systemic symptoms (11%) than patients with GCA and elevated ESR (57%), p=0.02 (7). Results from another study revealed a trend toward less anemia and less fever in patients with GCA who had an ESR of <50 mm/hour compared to those with elevated ESR (14). While not statistically significant, we found that the duration of symptoms antecedent to TAB and diagnosis of GCA was longer in patients with normal ESR and CRP compared to patients with elevated acute phase reactants. This likely reflects a delay in diagnosis in these patients with atypical findings. Of concern is that vision loss (transient or permanent) occurred in 3 of 7 patients with normal acute phase reactants. Previous studies have shown that a strong inflammatory response may be protective against cranial ischemic complications including vision loss, possibly because of increased alertness to the potential for visual loss in these patients on the part of the managing physician (15). It is important to recognize that in the presence of clinical symptoms or findings of ischemic eye disease, GCA should be considered even in the absence of elevated markers of inflammation.
While our study includes a large cohort of subjects, several limitations need to be considered. This study was conducted at a tertiary care referral center. We only included cases with biopsy-positive GCA and therefore these results may not be applicable to all patients with GCA. There may also have been patients with clinically diagnosed GCA who had a negative TAB and were therefore misclassified. Given our research question of interest, we only included patients with both ESR and CRP testing available at the time of diagnosis. Also, the estimates for sensitivity and specificity of ESR and CRP are only applicable to patients in whom a decision has been made to perform a TAB. Given the referral nature of our practice, the prevalence of normal ESR and CRP in GCA patients may be higher than would be expected in the general population. Additionally, there may be greater vigilance for GCA at our center, leading to TAB even in atypical cases where markers of inflammation are normal.
CONCLUSIONS
In this study, CRP was a more sensitive marker than ESR for GCA among subjects undergoing TAB. The combination of elevated ESR and CRP provided better specificity than either test alone and was associated with greater odds of a positive TAB. Among GCA patients with a positive biopsy, normal ESR and CRP was observed in 4% of cases. These patients tended to have an overall muted inflammatory response but more frequently had PMR symptoms. Our findings highlight that absence of a systemic inflammatory response as reflected in the currently routinely used ESR and CRP does not exclude GCA. TAB should be pursued in all patients where clinical suspicion of GCA is high. While ESR and CRP are often helpful for the diagnosis of GCA, they are nonspecific and better diagnostic markers are needed.
ACKNOWLEDGEMENTS
Grant Supports: Dr. Kermani was supported by the Vasculitis Clinical Research Consortium (VCRC) which has received support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (U54AR057319), the National Center for Research Resources (U54 RR019497), and the Office of Rare Diseases Research. The VCRC is part of the Rare Diseases Clinical Research Network (RDCRN).
Footnotes
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ROLE OF THE FUNDING SOURCE: The funding source had no involvement in the study design, data collection, analysis and interpretation of data, manuscript preparation or decision to submit the manuscript.
COMPETING INTERESTS: None
REFERENCES
- 1.Salvarani C, Cantini F, Hunder GG. Polymyalgia rheumatica and giant-cell arteritis. Lancet. 2008;372:234–245. doi: 10.1016/S0140-6736(08)61077-6. [DOI] [PubMed] [Google Scholar]
- 2.Kermani TA, Schafer VS, Crowson CS, Hunder GG, Gabriel SE, Matteson EL, et al. Increase in age at onset of giant cell arteritis: a population-based study. Ann Rheum Dis. 2010;69:780–781. doi: 10.1136/ard.2009.111005. [DOI] [PubMed] [Google Scholar]
- 3.Crowson CS, Matteson EL, Myasoedova E, Michet CJ, Ernste FC, Warrington KJ, et al. The lifetime risk of adult-onset rheumatoid arthritis and other inflammatory autoimmune rheumatic diseases. Arthritis Rheum. 2011;63:633–639. doi: 10.1002/art.30155. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Hunder GG, Bloch DA, Michel BA, Stevens MB, Arend WP, Calabrese LH, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum. 1990;33:1122–1128. doi: 10.1002/art.1780330810. [DOI] [PubMed] [Google Scholar]
- 5.Walvick MD, Walvick MP. Giant Cell Arteritis: Laboratory Predictors of a Positive Temporal Artery Biopsy. Ophthalmology. 2011 doi: 10.1016/j.ophtha.2010.10.002. [DOI] [PubMed] [Google Scholar]
- 6.Hayreh SS, Podhajsky PA, Raman R, Zimmerman B. Giant cell arteritis: validity and reliability of various diagnostic criteria. Am J Ophthalmol. 1997;123:285–296. doi: 10.1016/s0002-9394(14)70123-0. [DOI] [PubMed] [Google Scholar]
- 7.Salvarani C, Hunder GG. Giant cell arteritis with low erythrocyte sedimentation rate: frequency of occurence in a population-based study. Arthritis Rheum. 2001;45:140–145. doi: 10.1002/1529-0131(200104)45:2<140::AID-ANR166>3.0.CO;2-2. [DOI] [PubMed] [Google Scholar]
- 8.Parikh M, Miller NR, Lee AG, Savino PJ, Vacarezza MN, Cornblath W, et al. Prevalence of a normal C-reactive protein with an elevated erythrocyte sedimentation rate in biopsy-proven giant cell arteritis. Ophthalmology. 2006;113:1842–1845. doi: 10.1016/j.ophtha.2006.05.020. [DOI] [PubMed] [Google Scholar]
- 9.Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA. 2002;287:92–101. doi: 10.1001/jama.287.1.92. [DOI] [PubMed] [Google Scholar]
- 10.Ellis ME, Ralston S. The ESR in the diagnosis and management of the polymyalgia rheumatica/giant cell arteritis syndrome. Ann Rheum Dis. 1983;42:168–170. doi: 10.1136/ard.42.2.168. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Kyle V, Cawston TE, Hazleman BL. Erythrocyte sedimentation rate and C reactive protein in the assessment of polymyalgia rheumatica/giant cell arteritis on presentation and during follow up. Ann Rheum Dis. 1989;48:667–671. doi: 10.1136/ard.48.8.667. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Pountain GD, Calvin J, Hazleman BL. Alpha 1-antichymotrypsin, C-reactive protein and erythrocyte sedimentation rate in polymyalgia rheumatica and giant cell arteritis. Br J Rheumatol. 1994;33:550–554. doi: 10.1093/rheumatology/33.6.550. [DOI] [PubMed] [Google Scholar]
- 13.Myklebust G, Gran JT. A prospective study of 287 patients with polymyalgia rheumatica and temporal arteritis: clinical and laboratory manifestations at onset of disease and at the time of diagnosis. Br J Rheumatol. 1996;35:1161–1168. doi: 10.1093/rheumatology/35.11.1161. [DOI] [PubMed] [Google Scholar]
- 14.Martinez-Taboada VM, Blanco R, Armona J, Uriarte E, Figueroa M, Gonzalez-Gay MA, et al. Giant cell arteritis with an erythrocyte sedimentation rate lower than 50. Clin Rheumatol. 2000;19:73–75. doi: 10.1007/s100670050017. [DOI] [PubMed] [Google Scholar]
- 15.Cid MC, Font C, Oristrell J, de la Sierra A, Coll-Vinent B, Lopez-Soto A, et al. Association between strong inflammatory response and low risk of developing visual loss and other cranial ischemic complications in giant cell (temporal) arteritis. Arthritis Rheum. 1998;41:26–32. doi: 10.1002/1529-0131(199801)41:1<26::AID-ART4>3.0.CO;2-0. [DOI] [PubMed] [Google Scholar]