Giant Cell (Temporal) Arteritis: The Rate and Clinical Predictors of Histopathological Diagnosis

doi:10.21203/rs.3.rs-896982/v1

Download PDF

Research Article

Giant Cell (Temporal) Arteritis: The Rate and Clinical Predictors of Histopathological Diagnosis

https://doi.org/10.21203/rs.3.rs-896982/v1

This work is licensed under a CC BY 4.0 License

Version 1

posted

You are reading this latest preprint version

Purpose

To determine the rate of histopathological diagnosis by temporal artery (TA) biopsy (TAB) and the predictive clinical features of TAB positivity in patients with giant cell arteritis (GCA).

Methods

The records of patients who underwent TAB with pre-diagnosis of GCA between January 2006 and May 2020 were retrospectively reviewed. The demographic characteristics, symptoms, clinical and laboratory findings, TAB data, and the medications of the patients were recorded. The patients were divided into two groups as TAB-negative and TAB-positive, and compared clinically. Factors affecting TAB positivity were determined.

Results

TAB confirmed the diagnosis of GCA in 48% of our cases. The median fixed TAB specimen length was 1.7 (0.5–4.0) mm. TAB positivity increased with age (74 vs. 66 years, p = 0.027) and was more common in women (91.7% vs. 38.5%, p = 0.019). Jaw claudication (66.7% vs. 15.4%, p = 0.027) and decreased pulse of the TA (58.3% vs. 7.7%, p = 0.022) were more in the TAB-positive group than in the TAB-negative. The median C-reactive protein (CRP) level was statistically higher in the TAB-positive group compared to the TAB-negative (37 mg/L vs. 12.6 mg/L, p = 0.039). The univariate logistic regression analysis revealed female gender [OR (95%CI): 2.9 (1.7-181.3), p = 0.016], presence of jaw claudication [OR (95%CI): 2.4 (1.6–75.5), p = 0.015], decreased TA pulse [OR (95%CI): 2.8 (1.6-174.5), p = 0.018], and erythrocyte sedimentation rate (ESR) [OR (95%CI): 0.03 (1.0-1.1), p = 0.049] as factors associated with TAB positivity.

Conclusion

The rate of TAB positivity was 48%. Older age, female gender, the presence of jaw claudication and decreased pulse of TA, high ESR and CRP values are predictive features of TAB positivity and GCA diagnosis.

Ophthalmology

Pathology

Giant cell arteritis

temporal arteritis

temporal artery biopsy

predictive factors

Giant cell arteritis (GCA) is a vasculitis in which granulomatous changes are seen in large and medium-sized vessels. The aorta and extracranial branches of the external carotid arteries are most commonly affected [1]. It is the most common form of systemic vasculitis seen in people over the age of 50 [2]. Although the exact etiology and pathogenesis of GCA are not fully understood, aging, genetics and infections are thought to play a role [3].

Patients with GCA have a wide range of symptoms and clinical findings related to the involved arteries [4, 5]. Headache, temporary and permanent vision loss, jaw claudication, scalp tenderness, and polymyalgia rheumatica are common symptoms [1, 5–7]. There may also be general complaints such as fatigue, fever and weight loss [1, 5]. Visual symptoms and signs may include unilateral or bilateral partial or complete vision loss, diplopia, amaurosis fugax, ischemic optic neuritis, and optic atrophy [1].

Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are usually high, but may be normal in a small number of patients. In addition, laboratory changes such as normochromic normocytic anemia, increased thrombocyte count, and elevated liver enzyme levels can be seen [8, 9].

Temporal artery biopsy (TAB) is the gold standard in the diagnosis of GCA, but may not always support the diagnosis because of the segmental involvement of the disease [10–12]. The characteristic TAB findings of GCA are vasculitis in which mononuclear cells predominate in the inner elastic lamina or segmental and focal panarteritis with granulomatous inflammation. Sometimes it can cause a blockage of the blood vessel or weakening of the vessel wall followed by rupture [1, 13].

Corticosteroids are very effective in the treatment of GCA [14, 15]. The recommended initial dose is 1 mg/kg of prednisone per day for 2 to 4 weeks, and then the dose is reduced [16]. Intravenous pulse methylprednisolone is recommended to reduce the risk of vision loss in patients with visual symptoms at the time of diagnosis [17]. Conventional immunosuppressive drugs can be used in patients whose diseases have relapsed and have serious side effects due to corticosteroids. For this purpose the most commonly used agent is methotrexate [15, 18].

This study was planned to evaluate the rate of histopathological diagnosis by TAB and its relation with symptoms and clinical findings in patients with GCA. Secondary aim was to evaluate the clinical characteristics, treatment results and mortality rates of the patients.

This study was approved by the local Research Ethics Committee and was performed according to the principles of Declaration of Helsinki. The records of patients who underwent TAB with pre-diagnosis of GCA at Ondokuz Mayıs University Medical Faculty Hospital between 01.01.2006 and 01.06.2020 were retrospectively reviewed.

Patients who were diagnosed as GCA with clinical and laboratory findings, who underwent TAB for the confirmation of GCA diagnosis, who were treated with the diagnosis of GCA, and who were followed up for at least 3 months after treatment were included in the study. Patients with the follow-up less than 3 months and patients with incomplete data were excluded from the study.

The demographic characteristics of the patients; complaints during the admission to the hospital; clinical findings and laboratory data during diagnosis and follow-up; imaging results, if any; TAB data; the applied medications were recorded. The presence of headache, vision loss, fever-fatigue, weight loss, polymyalgia rheumatica and jaw claudication were investigated among the symptoms of the patients. On examination, the presence of tenderness to palpation or decreased pulse of the temporal artery (TA) was investigated. The ophthalmological findings of patients with ischemic optic neuropathy at the presentation, after the treatment and at the follow-up were recorded. Among the blood tests, ESR, CRP, hemoglobin, white blood cells (WBCs), platelet, fasting plasma glucose (FPG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), blood urea nitrogen (BUN), creatinine, and fibrinogen values were recorded. The application time, macroscopic and microscopic findings of TAB were examined. The time of TAB was evaluated in 3 categories: before the initiation of the treatment, within the first 7 days after the initiation of the treatment and after the 7th day of the treatment. Initial doses, duration and side effects of steroid treatment and the need for additional therapeutic agent were recorded. Changes in findings after treatment were reviewed. Duration of follow-up, the rate and causes of mortality of patients were recorded.

The patients were divided into two groups as TAB-negative and TAB-positive, and compared clinically. Patients were classified as TAB-negative if they had no biopsy findings consistent with GCA and fulfilled the 1990 American College of Rheumatology (ACR) criteria for the classification of GCA (if there are 3 or more out of 5 criteria: 1- Development of symptoms or findings beginning at age 50 or older; 2- New onset of or new type of localized pain in the head; 3- TA tenderness to palpation or decreased pulsation, unrelated to arteriosclerosis of cervical arteries; 4- ESR ≥ 50 mm/h by the Westergren method; 5- Biopsy specimen with artery showing vasculitis characterized by a predominance of mononuclear cell infiltration or granulomatous inflammation, usually with multinucleated giant cells) [1]. Factors affecting TAB positivity were determined.

Statistical analysis

The statistical analysis was carried out using V22 Statistical Package for the Social Sciences software (SPSS Inc., Chicago, IL, USA). Non-parametric tests were used because the data are not normally distributed. The Mann–Whitney U test was used for continuous independent variables and Chi-square test used for categorical variables. For these tests, p values of < 0.05 were considered to be statistically significant. The results were given as median (minimum-maximum) and frequency (%). Univariate and multivariate regression analyzes were performed to determine the factors associated with TAB positivity.

Demographics

TAB had been performed in 41 patients with a pre-diagnosis of GCA at Ondokuz Mayis University Medical Faculty Hospital between 01.01.2006 and 01.06.2020. Data of 25 patients who met the inclusion and exclusion criteria of the study were analyzed. There were 16 (64%) females and 9 (36%) males with a median age of 70 (51–83) years in the study. It was determined that TAB positivity increased with age (74 years in TAB-positive group vs. 66 years in TAB-negative group, p = 0.027) and was more common in women (91.7% in TAB-positive group vs. 38.5% in TAB-negative group, p = 0.019) (Table 1). Eighteen (%72) patients had hypertension, 11 (44%) patients had diabetes mellitus, 9 (36%) patients had cardiovascular disease, 3 (12%) patients had chronic renal failure, and 2 (8%) patients had multiple myeloma.

Table 1

Clinical and laboratory findings of the patients.
	Total n = 25	Biopsy-positive n = 12	Biopsy-negative n = 13	p
Age Median (minimum-maximum), years	70 (51–83)	74 (53–83)	66 (51–80)	0.027^*
Gender Male / Female, n (%)	9 (36) / 19 (64)	1 (8.3) /11 (91.7)	8 (61.5) / 5 (38.5)	0.019^*
Headache Yes, n (%)	24 (96)	12 (100)	12 (92.3)	1.000
Vision loss Yes, n (%)	14 (56)	7 (58.3)	7 (53.8)	1.000
Fever-fatigue Yes, n (%)	5 (20)	3 (25)	2 (15.4)	0.920
Weight loss Yes, n (%)	3 (12)	1 (8.3)	2 (15.4)	1.000
Polymyalgia rheumatic Yes, n (%)	9 (36)	6 (50)	3 (23.1)	0.325
Jaw claudication Yes, n (%)	10 (40)	8 (66.7)	2 (15.4)	0.027^*
Tenderness to palpation of the TA Yes, n (%)	11 (44)	7 (58.3)	4 (30.8)	0.325
Decreased pulse of the TA Yes, n (%)	8 (32)	7 (58.3)	1 (7.7)	0.022^*
ESR High, n (%) Median, mm/h	23 (92) 77	12 (100) 88	11 (84.6) 74	0.497 0.053
CRP High, n (%) Median, mg/L	20 (80) 18.7	10 (83.3) 37	10 (76.9) 12.6	1.000 0.039^*
Hemogloglobin Low, n (%) Median, g/dL	21 (84) 11.20	11 (91.7) 11.05	10 (76.9) 11.20	0.647 0.624
WBCs High, n (%) Median, 10³/µL	9 (36) 8.28	5 (41.7) 9.06	4 (30.8) 8.0	0.891 0.446
Monocyte High, n (%) Median, 10³/µL	7 (28) 0.51	5 (41.7) 0.53	2 (15.4) 0.5	0.309 0.479
Neutrophil High, n (%) Median, 10³/µL	8 (32) 6.08	5 (41.7) 6.81	3 (23.1) 4.40	0.571 0.165
Platelet High, n (%) Median, 10³/µL	7 (28) 314	4 (33.3) 344	3 (23.1) 313	0.901 0.384
FPG High, n (%) Median, mg/dL	13 (52) 118	4 (33.3) 100.5	9 (69.2) 126.8	0.163 0.301
AST High, n (%) Median, U/L	1 (4) 20	0 22.6	1 (7.7) 18.6	1.000 0.724
ALT High, n (%) Median, U/L	3 (12) 16	2 (16.7) 18.5	1 (7.7) 14	0.941 0.399
ALP High, n (%) Median, U/L	5 (45.5)^α 115	4 (50) ^α 124	1 (33.3) ^α 100	1.000 0.683
BUN High, n (%) Median, mg/dL	7 (28) 19.6	3 (25) 17.6	4 (30.8) 19.7	1.000 0.414
Creatinine High, n (%) Median, mg/dL	7 (28) 0.84	3 (25) 0.80	4 (30.8) 0.84	1.000 0.496
Fibrinogen High, n (%) Median, mg/dL	4 (100)^α 648	3 (100) ^α 757	1 (100) ^α 587	- 0.180
TAB performing time n (%) Before thetreatment, In the first 7 days of the treatment After the 7th day of the treatment	12 (48) 8 (32) 5 (20)	4 (33.3) 5 (41.7) 3 (25)	8 (61.5) 3 (23.1) 2 (15.4)	0.369
TAB specimen length Median, mm	1.7	2.1	1.4	0.149
TA: Temporal artery; ESR: Erythrocyte sedimentation rate; CRP: C-reactive protein; WBCs: White blood cells; FPG: Fasting plasma glucose; AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; ALP: Alkaline phosphatase; BUN: Blood urea nitrogen; TAB: Temporal artery biopsy; ^α : Is the ratio within the patients who had test; ^*: Statistically significant result.

Complaints and signs

Headache was the most common complaint at presentation and was present in 24 (96%) patients. This was followed by vision loss in 14 (56%) patients, jaw claudication in 10 (40%), polymyalgia rheumatica in 9 (36%), fever and fatigue in 5 (20%), and weight loss in 3 (12%). On examination, tenderness to palpation of the TA was detected in 11 (44%) patients and decreased pulse of the TA in 8 (32%) patients. Jaw claudication (66.7% vs. 15.4%, p = 0.027) and decreased pulse of the TA (58.3% vs. 7.7%, p = 0.022) were more in the TAB-positive group than in the TAB-negative group. There was no statistically significant difference between the groups in terms of other complaints and signs (Table 1).

Ophthalmic signs

Ischemic optic neuropathy was detected in 14 (56%) patients during ophthalmic examination. The right eye was involved in 8 (57.1%) patients, and the left eye in 6 (42.9%) patients. In the follow-up of 5 (35.7%) patients, it was observed that the second eye was also involved. While the initial median visual acuity (VA) was 0.005 (0.00-0.20) Snellen's line, it was found to be 0.03 (0.00–1.00) in the first ophthalmic examination after the initiation of treatment, and 0.05 (0.00–1.00) in the last ophthalmic examinations. Visual acuity was significantly increased with steroid therapy in patients with ischemic optic neuropathy (p = 0.012). During the follow-up, VA decreased in 1 (7.1%) patient, increased in 2 (14.3%) and remained stable in 11 (78.6%) patients. Visual field improvement was seen in 4 (57.1%) of 7 (16%) patients whose visual field could be tested. There was no difference between the TAB-positive and TAB-negative groups in terms of baseline VA (p = 0.844), post-treatment VA (p = 0.845), VA in the last visit (p = 0.620), change in VA (p = 0.947), and visual field improvement (p = 0.823).

Laboratory findings

The elevation of ESR was detected in 23 (92%) patients, in 19 (82.6%) of them ESR values decreased after the initiation of treatment. The elevation of CRP was detected in 20 (80%) patients, in 15 (75%) of them CRP values decreased after the initiation of treatment. Twenty-one (84%) patients had normocytic normochromic anemia. Nine (36%) patients had high WBC, of which 8 had an increase in neutrophils and 7 had an increase in monocytes. Platelet level was high in 7 (28%) patients, AST level in 1 (4%), and ALT level in 3 (12%). High FPG was found in 13 (52%) patients, 11 of whom were previously diabetic. High BUN and creatinine were found in 7 (28%) patients, 2 of whom had previous renal failure. ALP level was found to be high in 5 (45.5%) of 11 (44%) patients whose ALP was examined. Fibrinogen level was found to be high in all (100%) of the 4 (16%) patients whose fibrinogen was examined. The median CRP level was statistically higher in the TAB-positive group compared to the TAB-negative group (37 mg/L vs. 12.6 mg/L, p = 0.039). There was no significant difference between the groups in terms of the abnormality rate and levels of other laboratory findings (Table 1).

Biopsy findings

TABs were applied before the initiation of the treatment in 12 (48%) patients, within the first 7 days after the initiation of the treatment in 8 (32%), and after the 7th day of the treatment in 5 (20%). TABs were performed unilaterally from the side of the patient's complaint (headache, loss of vision, etc.). Median fixed TAB specimen length was 1.7 (0.5–4.0) mm. Although the median fixed TAB specimen length was longer in the TAB-positive group than the TAB-negative group, the difference was not statistically significant (2.1 vs. 1.4 mm, p = 0.149). TAB revealed normal TA in 4 (16%) patients, mononuclear cells infiltration with or without giant cells or fibrinoid necrosis in the vessel wall compatible with the GCA in 12 (48%) (Fig. 1), fibrointimal thickening in the vessel wall in 5 (20%), and medial calcific sclerosis in the vessel wall in 4 (16%).

Nine (36%) patients received TA ultrasonography, and an increase in arterial wall thickness consistent with GCA was detected in 3 (33.3%) of them.

Treatment and outcomes

Pulse and subsequent oral steroid treatment was administered to 8 (32%) patients, and only oral steroid therapy was administered to 17 (68%) patients. Median steroid usage period was 90 (35-1460) days. Treatment was changed in 10 (40%) patients due to steroid side effects or insufficient response to steroid treatment: Methotrexate was used in 7 (70%) patients, methotrexate + cyclophosphamide in 1 (10%), methotrexate + azathioprine in 1 (10%), and tocilizumab in 1 (10%). Side effects were detected in 13 (52%) patients. The most common side effect was increased FPG and was seen in 9 (69.2%) patients. Pneumonia occurred in 1 (7.7%) patient, reactivation of tuberculosis in 1 (7.7%), reactivation of tuberculosis and infective endocarditis in 1 (7.7%), and infective endocarditis and sepsis in 1 (7.7%). Mortality occurred in 3 (12%) patients during a median follow-up period of 9 (3-120) months. Deaths in three patients occurred at 3, 6, and 46 months after diagnosis. The cause of mortality was sepsis in 1 (33.3%) patient, and heart failure and cardiac arrest in 2 (66.7%) patients.

Regression analyzes

In the univariate logistic regression analysis, female gender [OR (95%CI): 2.9 (1.7-181.3), p = 0.016], presence of jaw claudication [OR (95%CI): 2.4 (1.6–75.5), p = 0.015], decreased pulse of TA [OR (95%CI): 2.8 (1.6-174.5), p = 0.018], and ESR [OR (95%CI): 0.03 (1.0-1.1), p = 0.049] were determined as factors associated with the TAB positivity. The relationship of these factors with TAB positivity could not be confirmed by multivariate logistic regression analysis.

Histopathological findings considered as TAB-positive GCA (mononuclear cells infiltration with or without giant cells or fibrinoid necrosis in the vessel wall) was detected in 48% of cases in our study. Although this rate is low, there are studies reporting TAB positivity below 20% in the literature [11, 19]. A meta-analysis by Rubenstein et al. showed that the rate of TAB positivity in GCA cases ranged between 50% and 95%, and the overall pooled rate was 77.3% [20]. We found that the median fixed TAB specimen length was 1.7 (0.5–4.0) mm, and was longer in the TAB-positive group than in the TAB-negative group, although this was not statistically significant. Mahr et al. reported that a fixed TAB specimen length of at least 0.5 cm may be sufficient for histopathological diagnosis of GCA [11]. In the diagnosis of GCA, it is also thought that the length of the TAB specimens does not have an important impact on positivity [11, 20, 21]. In 80% of our patients, the time for TAB administration was before the treatment or within the first 7 days after the initiation of the treatment. It has also been reported that delaying the TAB for 14 days or longer may not affect the accuracy of the biopsy result [22]. TAB was not performed later than 14 days in any of our patients.

We determined that TAB positivity increases with age and is more common in women. Similar to our observation, there are studies reporting a higher mean age in TAB-positive patients than in TAB-negative patients, and that ≤ 70 years should downgrade the level of suspicion for GCA [23, 24]. On the contrary, there are publications in the literature reporting that age is not associated with TAB positivity [25, 26]. It has been reported that women are 2 or 3 times more likely to have positive TABs than men [26]. We also found that the probability of TAB positivity in women was 2.9 times higher. Headache was present in 96% of our patients and was the most common symptom at presentation. Although headache is reported in the temporal region with a rate of 70–80%, it is important in prompting suspicion rather than its diagnostic value in GCA [24, 27]. A recent meta-analysis suggested that jaw claudication, limb claudication, temporal artery abnormalities, and anterior ischemic optic neuropathy are the features that should raise the level of suspicion for GCA [24]. We found that the presence of jaw claudication and decreased pulse of the TA on examination were more in TAB-positive patients than in TAB-negative patients. Ischemic optic neuropathy was observed in 56% of our patients. Visual manifestations can be found in 9.6–61.1% of patients with GCA [20]. However, we did not find a relationship between TAB positivity and ischemic optic neuropathy. Gonzalez-Gay et al. determined that a history of constitutional syndrome, presence of visual problems, and an abnormal temporal artery on examination may predict TAB abnormality [25]. Selby et al. stated that scalp tenderness is a significant predictor of a positive TAB [26]. We showed that the factors associated with TAB positivity were female gender, the presence of jaw claudication, and decreased pulse of TA by univariate logistic regression analysis.

In recent study, high ESR was detected in 92% of the patients and high CRP in 80%. In addition, 84% of the patients had normocytic normochromic anemia, 36% of the patients had leukocytosis, and 28% of the patients had thrombocytosis. Of these laboratory findings, only the CRP level was higher in TAB positive patients. In addition, ESR was also determined to be associated with TAB positivity in univariate logistic regression analysis. Anemia, leukocytosis, thrombocytosis, high CRP and ESR levels are frequently detected in laboratory examinations of patients with GCA. However, inflammatory markers may be normal in some patients with GCA [9, 14]. A recent systematic review and meta-analysis revealed that presence of a platelet count of > 400 × 10³/µL and an ESR > 60 mm/h in laboratory findings are features that should raise the level of suspicion for GCA [24]. Selby et al. found that CRP and platelets were significant predictors of a positive TAB in a veteran population [26]. Kermani et al. stated that CRP is a more sensitive marker than ESR for a positive TAB in patients with GCA, but it would be useful to evaluate both tests together in the evaluation of patients with suspected GCA [8].

In only 33.3% of our patients who underwent TA ultrasonography, an increase in arterial wall thickness consistent with GCA was found. This rate was lower than the rate of TAB positivity. Therefore, it was thought that TA ultrasonography was not an alternative to biopsy in the diagnosis of GCA. It has been emphasized in the literature that the advantage of TA ultrasonography may be that it provides cost and time savings and reduces the number of TABs [28].

Glucocorticoid treatment was applied to all of our patients. Methotrexate was used in 9 (36%) cases and tocilizumab was used in 1 (4%) case due to steroid side effects or insufficient response to steroid treatment. In GCA, the use of MTX is recommended to reduce the relapse rate and to lower the cumulative glucocorticoid doses [15,29,30)]. It has been reported that tocilizumab, an anti-IL-6 receptor, is beneficial in reducing the cumulative glucocorticoid doses and the relapse rate, and in refractory disease in patients with GCA [15]. One of the biggest problems with the treatment of GCA is the morbidity associated with glucocorticoids. If patients remain untreated, they may have a poor prognosis due to blindness, stroke or myocardial infarction (MI). Approximately 1–3% of patients with GCA die from stroke or MI [13, 31]. Mortality rate was 12% in our patients during the follow-up period. Causes of mortality were sepsis, heart failure, and cardiac arrest. Patients with GCA have a high risk of hospitalization due to cardiovascular comorbidities such as atherosclerotic disease, heart failure and cardiac arrhythmia [32]. A study from Sweden suggested that the mortality risk increased significantly within the first 2 years after the diagnosis of GCA, but then returned to normal [33]. Deaths occurred in the first 6 months in two of our patients, and in the fourth year in one.

The limitations of the study are its retrospective nature and a relatively small sample of patients that admitted to a single tertiary referral center, although we have scanned for a period of approximately 15 years. However, this study provides useful information for clinical practice by detecting clinical and laboratory features associated with TAB positivity in patients with GCA. It can be predicted in which patients the probability of positive TAB is increased and GCA diagnosis is more likely to be made. According to the results of our study, older age, female gender, the presence of jaw claudication and decreased pulse of TA, high ESR and CRP values are predictive features for TAB positivity and GCA diagnosis.

Compliance with Ethical Standards:This study was approved by the Ondokuz Mayis University Clinical Research Ethics Committee.

Funding: There is no funding for this study.

Conflict of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Acknowledgments: The authors would like to thank Ozlem Terzi, M.D. for her assistance with the statistical analyses. The authors report no conflicts of interest. There is no funding for this research.

Hunder GG, Bloch DA, Michel BA, Stevens MB, Arend WP, Calabrese LH, Edworthy SM, Fauci AS, Leavitt RY, Lie JT, Lightfoot RW, Masi AT, McShane DJ, Mills JA, Wallace SL, Zvaifler NJ (1990) The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum 33(8):1122–1128. doi:10.1002/art.1780330810
Watts RA, Robson J (2018) Introduction, epidemiology and classification of vasculitis. Best Pract Res Clin Rheumatol 32(1):3–20. doi:10.1016/j.berh.2018.10.003
Samson M, Corbera-Bellalta M, Audia S, Planas-Rigol E, Martin L, Cid MC, Bonnotte B (2017) Recent advances in our understanding of giant cell arteritis pathogenesis. Autoimmun Rev 16(8):833–844. doi:10.1016/j.autrev.2017.05.014
Machado EBV, Michet CJ, Ballard DJ, Hunder GG, Beard CM, Chu C-P, O’Fallon WM (1988) Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota, 1950–1985. Arthritis Rheum 31:745–749. doi:10.1002/art.1780310607
Pradeep S, Smith JH (2018) Giant Cell Arteritis: Practical Pearls and Updates. Curr Pain Headache Rep 22(1):2. doi:10.1007/s11916-018-0655-y
Caselli RJ, Hunder GG, Whisnant JP (1988) Neurologic disease in biopsy proven giant cell (temporal) arteritis. Neurology 38(3):352–359. doi:10.1212/wnl.38.3.352
Aiello PD, Trautmann JC, McPhee TJ, Kunselman AR, Hunder GG (1993) Visual prognosis in giant cell arteritis. Ophthalmology 100(4):550–555. doi:10.1016/s0161-6420(93)31608-8
Kermani TA, Schmidt J, Crowson CS, Ytterberg SR, Hunder GG, Matteson EL, Warrington KJ (2012) Utility of erythrocyte sedimentation rate and C-reactive protein for the diagnosis of giant cell arteritis. Semin Arthritis Rheum 41(6):866–871. doi:10.1016/j.semarthrit.2011.10.005
Gonzalez-Gay MA, Lopez-Diaz MJ, Barros S, Garcia-Porrua C, Sanchez-Andrade A, Paz-Carreira J, Martin J, Llorca J 82005) Giant cell arteritis: laboratory tests at the time of diagnosis in a series of 240 patients. Medicine (Baltimore) 84(5):277–90. doi: 10.1097/01.md.0000180043.19285.54
Oh LJ, Wong E, Gill AJ, McCluskey P, Smith JEH (2018) Value of temporal artery biopsy length in diagnosing giant cell arteritis. ANZ J Surg 88(3):191–195. doi:10.1111/ans.13822
Mahr A, Saba M, Kambouchner M, Polivka M, Baudrimont M, Brochériou I, Coste J, Guillevin L (2006) Temporal artery biopsy for diagnosing giant cell arteritis: the longer, the better? Ann Rheum Dis 65(6):826–828. doi:10.1136/ard.2005.042770
Varma D, O'Neill D (2004) Quantification of the role of temporal artery biopsy in diagnosing clinically suspected giant cell arteritis. Eye (Lond) 18(4):384–388. doi:10.1038/sj.eye.6700677
Ameer MA, Peterfy RJ, Bansal P, Khazaeni B (2020) Temporal (Giant Cell) Arteritis. StatPearls [Internet]. StatPearls Publishing, Treasure Island (FL). https://www.ncbi.nlm.nih.gov/books/NBK459376/
Rinden T, Miller E, Nasr R (2019) Giant cell arteritis: An updated review of an old disease. Cleve Clin J Med 86(7):465–472. doi:10.3949/ccjm.86a.18103
González-Gay M, Pina T, Prieto-Peña D, Calderon-Goercke M, Gualillo O, Castañeda S (2019) Treatment of giant cell arteritis. Biochem Pharmacol 165:230–239. doi:10.1016/j.bcp.2019.04.027
Bienvenu B, Ly KH, Lambert M, Agard C, André M, Benhamou Y, Bonnotte B, de Boysson H, Espitia O, Fau G, Fauchais AL, Galateau-Sallé F, Haroche J, Héron E, Lapébie FX, Liozon E, Luong Nguyen LB, Magnant J, Manrique A, Matt M, de Menthon M, Mouthon L, Puéchal X, Pugnet G, Quemeneur T, Régent A, Saadoun D, Samson M, Sène D, Smets P, Yelnik C, Sailler L, Mahr A; Groupe d’Étude Français des Artérites des gros Vaisseaux, under the Aegis of the Filière des Maladies Auto-Immunes et Auto-Inflammatoires Rares (2016) Management of giant cell arteritis: recommendations of the French Study Group for Large Vessel Vasculitis (GEFA). Rev Med Interne 37(3):154 – 65. doi:10.1016/j.revmed.2015.12.015
Hayreh SS, Biousse V (2012) Treatment of acute visual loss in giant cell arteritis: should we prescribe high-dose intravenous steroids or just oral steroids? J Neuroophthalmol 32(3):278–287. doi:10.1097/WNO.0b013e3182688218
Mukhtyar C, Guillevin L, Cid MC, Dasgupta B, de Groot K, Gross W, Hauser T, Hellmich B, Jayne D, Kallenberg CG, Merkel PA, Raspe H, Salvarani C, Scott DG, Stegeman C, Watts R, Westman K, Witter J, Yazici H, Luqmani R, European Vasculitis Study Group (2009) EULAR recommendations for the management of large vessel vasculitis. Ann Rheum Dis 68(3):318–323. doi:10.1136/ard.2008.088351
Kent RB, Thomas L (1990) Temporal artery biopsy. Am Surg 56:16–21
Rubenstein E, Maldini C, Gonzalez-Chiappe S, Chevret S, Mahr A (2020) Sensitivity of temporal artery biopsy in the diagnosis of giant cell arteritis: a systematic literature review and meta-analysis. Rheumatology 59(5):1011–1020. doi:10.1093/rheumatology/kez385
Papadakis M, Kaptanis S, Kokkori-Steinbrecher A, Floros N, Schuster F, Hübner G (2018) Temporal artery biopsy in the diagnosis of giant cell arteritis: bigger is not always better. Am J Surg 215:647–650. doi:10.1016/j.amjsurg.2017.08.020
Daily B, Dassow P, Haynes J, Nashelsky J (2017) Giant cell arteritis: biopsy after corticosteroid initiation. Am Fam Physician 95(2):116–117
Aghdam KA, Sanjari MS, Manafi N, Khorramdel S, Alemzadeh SA, Navahi RAA (2020) Temporal Artery Biopsy for Diagnosing Giant Cell Arteritis: A Ten-year Review. J Ophthalmic Vis Res 15(2):201–209. doi:10.18502/jovr.v15i2.6738
van der Geest KSM, Sandovici M, Brouwer E, Mackie SL (2020) Diagnostic Accuracy of Symptoms, Physical Signs, and Laboratory Tests for Giant Cell Arteritis: A Systematic Review and Meta-analysis. JAMA Intern Med 180(10):1295–1304. doi:10.1001/jamainternmed.2020.3050
Gonzalez-Gay MA, Garcia-Porrua C, Llorca J, Gonzalez-Louzao C, Rodriguez-Ledo P (2001) Biopsy-negative giant cell arteritis: clinical spectrum and predictive factors for positive temporal artery biopsy. Semin Arthritis Rheum 30(4):249–256. doi:10.1053/sarh.2001.16650
Selby LD, Park-Egan BAM, Winges KM (2020) Temporal Artery Biopsy in the Workup of Giant Cell Arteritis: Diagnostic Considerations in a Veterans Administration Cohort. J Neuroophthalmol 40(4):450–456. doi:10.1097/WNO.0000000000001040
Winkler A, True D (2018) Giant Cell Arteritis: 2018 Review. Mo Med 115(5):468–470
Ching J, Smith SM, Dasgupta B, Damato EM (2020) The role of vascular ultrasound in managing giant cell arteritis in ophthalmology. Surv Ophthalmol 65(2):218–226. doi:10.1016/j.survophthal.2019.11.004
Mahr AD, Jover JA, Spiera RF, Hernández-García C, Fernández-Gutiérrez B, Lavalley MP, Merkel PA (2007) Adjunctive methotrexate for treatment of giant cell arteritis: an individual patient data meta-analysis. Arthritis Rheum 56(8):2789–2797. doi:10.1002/art.22754
Hoffman GS, Cid MC, Hellmann DB, Guillevin L, Stone JH, Schousboe J, Cohen P, Calabrese LH, Dickler H, Merkel PA, Fortin P, Flynn JA, Locker GA, Easley KA, Schned E, Hunder GG, Sneller MC, Tuggle C, Swanson H, Hernández-Rodríguez J, Lopez-Soto A, Bork D, Hoffman DB, Kalunian K, Klashman D, Wilke WS, Scheetz RJ, Mandell BF, Fessler BJ, Kosmorsky G, Prayson R, Luqmani RA, Nuki G, McRorie E, Sherrer Y, Baca S, Walsh B, Ferland D, Soubrier M, Choi HK, Gross W, Segal AM, Ludivico C, Puechal X, International Network for the Study of Systemic Vasculitides (2002) A multicenter, randomized, double-blind, placebo-controlled trial of adjuvant methotrexate treatment for giant cell arteritis. Arthritis Rheum 46(5):1309–1318. doi:10.1002/art.10262
Koster MJ, Matteson EL, Warrington KJ (2018) Large-vessel giant cell arteritis: diagnosis, monitoring and management. Rheumatology 57(suppl_2):ii32–ii42. doi:10.1093/rheumatology/kex424
Pugnet G, Sailler L, Fournier JP, Bourrel R, Montastruc JL, Lapeyre-Mestre M (2016) Predictors of Cardiovascular Hospitalization in Giant Cell Arteritis: Effect of Statin Exposure. A French Population-based Study. J Rheumatol 43(12):2162–2170. doi:10.3899/jrheum.151500
Mohammad AJ, Nilsson J-Å, Jacobsson LT, Merkel PA, Turesson C (2015) Incidence and mortality rates of biopsy-proven giant cell arteritis in southern Sweden. Ann Rheum Dis 74(6):993e7. doi:10.1136/annrheumdis-2013-204652

Download PDF

Version 1

posted

You are reading this latest preprint version

Giant Cell (Temporal) Arteritis: The Rate and Clinical Predictors of Histopathological Diagnosis

Status:

Version 1

Abstract

Purpose

Methods

Results

Conclusion

Figures

Introduction

Methods

Statistical analysis

Results

Demographics

Complaints and signs

Ophthalmic signs

Laboratory findings

Biopsy findings

Treatment and outcomes

Regression analyzes

Discussion

Declarations

References

Status:

Version 1