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The epidemiologic characteristics of giant cell arteritis (GCA) have been studied in large populations from the United States,1-4, United Kingdom,5, 6 Sweden,7-9 Denmark,10 Norway,11Israel12,13 and Saudi Arabia14 where incidences have been estimated mainly through retrospective study designs. These studies have demonstrated that GCA occurs more commonly in populations of Nordic descent,15 fluctuations in incidence with distinctive peaks were reported by some investigators;2,5,13,16-18 however this was not observed by others.16,19The epidemiologic characteristics of this disease have never been studied in Australasia. We present the first epidemiological study evaluating clinical and laboratory characteristics of biopsy proven GCA in the population of Otago, New Zealand; comparing the characteristics of the biopsy positive with the biopsy negative group and the annual incidence rate in Otago, New Zealand to internationally reported figures.Materials and Methods A retrospective analysis of the clinical presentation, management and postoperative course of 363 consecutive patients obtained from the surgical database at Dunedin Hospital, Otago, New Zealand between 1996-2005 was undertaken. All cases of suspected giant cell arteritis in the Otago region are referred to this centre for a temporal artery biopsy. Patients who underwent or were evaluated for a temporal artery biopsy (TAB) were included in the study, cases lacking sufficient medical information were excluded. Of a total of 369 cases, 6 cases had insufficient medical information and were excluded from this study. A total of 363 cases fulfilled the inclusion criteria. Variables documented from the medical records included demographic factors such as age and gender, and major symptoms and signs. An ophthalmic trainee or ophthalmologist evaluated all cases within 1 week of starting systemic steroids and temporal artery biopsies were conducted within 2 weeks of starting steroids. Inflammatory markers were requested for all cases at the time of referral. The decision to undertake a TAB was based on clinical criteria and raised inflammatory markers and / or platelet count. Trainees performed biopsies within 1 week of clinical assessment. A repeat biopsy was performed within 1 week in histologically negative cases if clinical features were judged to be sufficiently suggestive, inflammatory markers were raised inexplicably or the initial biopsy was shorter than 2 mm. An experienced pathologist examined all histological specimens. Temporal artery biopsies were processed and cut at 4-5 00b5m thickness from at least 3 levels. Hematoxylin and eosin stains slides were produced from each paraffin block. Cases with visual involvement were admitted to hospital and biopsy was performed within 24 hours and methylprednisone 1mg/kg/day was administered intravenously for 3 days. Follow-up within 1 week was arranged after the biopsy to ensure the improvement of symptoms, compliance with treatment and wound assessment. Major features assessed to determine the presence of GCA were giant cells in the intima and the media, lymphocytes and histiocytes in the media, reduplication/fragmentation of the internal elastic lamina and intimal thickening. Healed GCA was diagnosed in the presence of intimal fibrosis, media scarring with eccentric and segmented disruption of the internal elastic lamina or chronic media inflammation with neovascularisation. However, if one or more of these features were absent, healed arteritis or atherosclerosis was considered 20. Biopsy positive cases were placed on oral prednisone 1mg/kg/day immediately upon receiving the biopsy results. Statistical analysis was performed on the Statistical Package for the Social Sciences (SSPS) v16.0. The Exact method was used in calculating the confidence interval for the incidence of GCA. An independent-sample t-test was used to compare mean differences in clinical characteristics and laboratory findings between the GCA positive and negative groups. Annual age and gender specific incidence rates were calculated / 100,000 population aged 226550 years using the number of incident cases as the numerator and population estimates based on census counts as the denominator. Linear interpolation was used to estimate population size for intercensal years 21. Ninety five percent confidence intervals (95% CI) were computed for incidence rates. Results Patient demographicsThe population in Otago consists ethnically of Europeans (85.9%), M ori (7.1%), Pacific Islanders (1.8%), Asians (4.5%), Middle Eastern and African (0.7%). Over the 9 years of observation there was an estimated increase in total population numbers by 6265 (3.3%), an increase in the population age group 226550 years by 9484 (16.1%) and a decrease in the population <50 years by 3219 (2.4%). Temporal artery biopsies were performed on a total of 363 patients, of which 105 (29%) were males and 258 (71%) were females. The mean age of the population was 73.2 years (range 50-97 years, SD 9.3). The average follow up was 51.9 months (range 1-120, SD 24.9). A total of 70 (19%) patients with biopsy proven GCA (GCA+ve) were identified. The mean age at diagnosis was 72.8 years (range 57-91 years, SD 8.2). There were 52 (74%) females and 18 (26%) males giving a ratio of 2.9:1. The annual incidence of GCA/100,000 population aged 226550 years adjusted for gender and age is shown in Table 1, the mean annual incidence in the population 226550 years was 12.7/100,000 over the 9 years of observation. Table 1. Incidence of giant cell arteritis/100,000 population in the Otago region for the population age 226550 years. CI, confidence interval Variables Incidence /100,000 95% CI (P<0.5) All patients 12.7 11.7-14.3 Females 21.3 19.8-24.2 Males 8.8 8.3-10.2 Age 50-64 Age 65-74 Age 226575 21.0 144.3 342.7 20.9-21.5 143.2-146.4 340.2-347.3 The variation in annual incidence is shown in Figure 1. We observed a cyclic annual incidence with 2 peaks 5 years apart. Figure 1. Annual incidence of giant cell arteritis/100,000 population in the Otago region 1996-2005 for the population age 226550 years. The distribution is cyclic with a peak in 1998 and 2003 The incidence rates increased with age and there was a female: male ratio of 2.8:1. Seasonal variations were observed with more cases of GCA diagnosed in the spring 23 (32.8%) than the summer 17 (24.3%), autumn 16 (22.9%), and winter 14 (20%), however the difference between the seasons was not statistically significant (P<0.9). Among the biopsy positive cases 5 (1.4%) showed lesions consistent with healed giant cell arteritis. Unilateral biopsies were performed on 335 patients. These were positive in 67 cases (18.5%). In 28 cases bilateral sequential biopsies were performed of which 2/28 (7.2%) demonstrated active arteritic lesions and the other case was a lesion consistent with GCA. There were no reported postoperative complications from the procedure. A total of 293 (81%) patients were biopsy negative (GCA-ve). The mean age in this group was 73.4 years (range 50-97 years, SD 9.5). There were 88 (30%) males and 205 (70%) females. Discharge diagnoses included autoimmune conditions polymyalgia rheumatica, rheumatoid arthritis, systemic lupus erythematosus and other vasculitides in 54 (18.4%), optic neuropathies in 6 (2%), malignancies in 5 (1.7%), non-vasculitic cerebrovascular accident in 4 (1.4%), septicaemia in 3 (1.0%) and other diagnoses 15 (5.1%). No definite diagnosis was recorded in the medical notes of 206 (70%) cases. Clinical and laboratory differences between the biopsy positive and negative groupsThere was no difference in mean age between the GCA +ve and -ve groups (p<0.2) or gender (p<0.6). The major presenting symptoms and signs are summarised in Tables 2 and 3 respectively. Headache was the commonest symptom occurring in 198 (54.5%) patients. Fever was the commonest sign occurring in 38 (10.5%) of patients. In analysing the clinical difference in the GCA +ve and -ve groups, jaw claudication, anorexia and scalp tenderness were the most significant discriminating symptoms (Table 2). Table 2. Major symptoms in the study population Symptom GCA +ve cases GCA -ve cases Total cases (%) P value Headache PMR symptoms Jaw claudication Scalp tenderness Malaise Anorexia Weight loss Permanent visual loss Transient visual loss 47 (67.1%) 22 (31.4%) 17 (24.3%) 16 (22.9%) 12 (17.1) 10 (14.3%) 9 (12.9%) 10 (14.3%) 7 (10%) 156 (53.2%) 69 (23.5%) 17 (5.8%) 39 (13.3%) 39 (13.3%) 22 (7.5%) 30 (10.2%) 31 (10.6%) 24 (8.2%) 198 (54.5%) 91 (25%) 34 (9.4%) 55 (15.2%) 51 (14.1%) 32 (8.8%) 39 (10.7%) 41 (11.3%) 31 (8.5%) 0.1 0.1 0.0001 0.003 0.4 0.005 0.6 0.3 0.7 PMR=Polymyalgia rheumatica, GCA+ve= patients with giant cell arteritis, GCA-ve=patients without giant cell arteritis. The P value indicates the statistical significance of the difference in the prevalence of the symptom in the biopsy positive versus the biopsy negative population. Among the signs abnormalities of the superficial temporal arteries, a clinical diagnosis of arteritic anterior ischemic optic neuropathy (AAION) and raised inflammatory markers without suggestive clinical symptoms and signs were significant discriminators (Table 3). Table 3. Major signs in the study population Signs GCA +ve cases GCA -ve cases Total cases (%) P value Fever 9 (12.9%) 29 (9.9%) 38 (10.5%) 0.4 STA tenderness 9 (12.9%) 18 (6.1%) 27 (7.4%) 0.002 STA reduced pulse 6 (8.6%) 1 (0.3%) 7 (1.9%) 0.001 CVA 4 (5.7%) 11 (3.8%) 15 (4.1%) 0.3 Anemia 2 (2.9%) 4 (1.4%) 6 (1.7%) 0.2 Raised inflammatory markers without suggestive clinical symptoms and signs 1 (1.4%) 14 (4.8%) 15 (4.1%) 0.004 STA=superficial temporal artery, AAION=arteritic anterior ischemic optic neuropathy, CVA=cerebrovascular accident, GCA+ve= patients with giant cell arteritis, GCA-ve= patients without giant cell arteritis. The P value indicates the statistical significance of the difference in the prevalence of the sign in the biopsy positive versus the biopsy negative population. Table 4. The distribution of inflammatory markers in the study population ESR mm/hr GCA +ve cases GCA -ve cases 226420 21-70 71-120 121-170 2265171 3 (4.3%) 31 (44.3%) 30 (42.9%) 6 (8.6%) 3 (4.3%) 34 (11.6%) 160 (54.6%) 84 (28.7%) 14 (4.8%) 1 (0.3%) Total 70 293 CRP mg/dl 22645 6-50 51-95 96-140 2265141 3 (4.3%) 18 (25.7%) 31 (44.3%) 10 (14.3%) 8 (11.4%) 43 (14.7%) 64 (21.8%) 150 (51.2%)\r\n

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

Hauser WA, Ferguson RH, Holley KE, Kurland LT. Temporal arteritis in Rochester, Minnesota, 1951 to 1967. Mayo Clin Proc. 1971 Sep;46(9):597-602.Salvarani C, Crowson CS, O'Fallon WM, et al. Reappraisal of the epidemiology of giant cell arteritis in Olmsted County, Minnesota, over a fifty-year period. Arthritis Rheum. 2004 Apr 15;51(2):264-8.Machado EB, Michet CJ, Ballard DJ, et al. Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota, 1950-1985. Arthritis Rheum. 1988 Jun;31(6):745-9.Smith CA, Fidler WJ, Pinals RS. The epidemiology of giant cell arteritis. Report of a ten-year study in Shelby County, Tennessee. Arthritis Rheum. 1983 Oct;26(10):1214-9.Smeeth L, Cook C, Hall AJ. Incidence of diagnosed polymyalgia rheumatica and temporal arteritis in the United Kingdom, 1990-2001. Ann Rheum Dis. 2006 Aug;65(8):1093-8.Jonasson F, Cullen JF, Elton RA. Temporal arteritis. A 14-year epidemiological, clinical and prognostic study. Scott Med J. 1979 Apr;24(2):111-7.Bengtsson BA, Malmvall BE. The epidemiology of giant cell arteritis including temporal arteritis and polymyalgia rheumatica. Incidences of different clinical presentations and eye complications. Arthritis Rheum. 1981 Jul;24(7):899-904.Nordborg E, Bengtsson BA. Epidemiology of biopsy-proven giant cell arteritis (GCA). J Intern Med. 1990 Apr;227(4):233-6.Ostberg G. Temporal arteritis in a large necropsy series. Ann Rheum Dis. 1971 May;30(3):224-35.Boesen P, Sorensen SF. Giant cell arteritis, temporal arteritis, and polymyalgia rheumatica in a Danish county. A prospective investigation, 1982-1985. Arthritis Rheum. 1987 Mar;30(3):294-9.Haugeberg G, Paulsen PQ, Bie RB. Temporal arteritis in Vest Agder County in southern Norway: incidence and clinical findings. J Rheumatol. 2000 Nov;27(11):2624-7.Friedman G, Friedman B, Benbassat J. Epidemiology of temporal arteritis in Israel. Isr J Med Sci. 1982 Feb;18(2):241-4.Sonnenblick M, Nesher G, Friedlander Y, Rubinow A. Giant cell arteritis in Jerusalem: a 12-year epidemiological study. Br J Rheumatol. 1994 Oct;33(10):938-41.Chaudhry IA, Shamsi FA, Elzaridi E, et al. Epidemiology of giant-cell arteritis in an Arab population: a 22-year study. Br J Ophthalmol. 2007 Jun;91(6):715-8.Lane SE, Watts R, Scott DG. Epidemiology of systemic vasculitis. Curr Rheumatol Rep. 2005 Aug;7(4):270-5.Petursdottir V, Johansson H, Nordborg E, Nordborg C. The epidemiology of biopsy-positive giant cell arteritis: special reference to cyclic fluctuations. Rheumatology (Oxford). 1999 Dec;38(12):1208-12.Elling P, Olsson AT, Elling H. Synchronous variations of the incidence of temporal arteritis and polymyalgia rheumatica in different regions of Denmark; association with epidemics of Mycoplasma pneumoniae infection. J Rheumatol. 1996 Jan;23(1):112-9.Bas-Lando M, Breuer GS, Berkun Y, et al. The incidence of giant cell arteritis in Jerusalem over a 25-year period: annual and seasonal fluctuations. Clin Exp Rheumatol. 2007 Jan-Feb;25(1 Suppl 44):S15-7.Gonzalez-Gay MA, Garcia-Porrua C, Rivas MJ, et al. Epidemiology of biopsy proven giant cell arteritis in northwestern Spain: trend over an 18 year period. Ann Rheum Dis. 2001 Apr;60(4):367-71.Ray-Chaudhuri N, Kine DA, Tijani SO, et al. Effect of prior steroid treatment on temporal artery biopsy findings in giant cell arteritis. Br J Ophthalmol. 2002 May;86(5):530-2.Statistics NZ. Statistics New Zealand; 2006 Population Census Data. 2006. http://www.stats.govt.nz/census/default.htmSalvarani C, Gabriel SE, O'Fallon WM, Hunder GG. The incidence of giant cell arteritis in Olmsted County, Minnesota: apparent fluctuations in a cyclic pattern. Ann Intern Med. 1995 Aug 1;123(3):192-4.Elling P, Olsson AT, Elling H. Synchronous variations in the incidence of temporal arteritis and polymyalgia rheumatica in Danish counties. Association with epidemics of Mycoplasma pneumonia infection. Ugeskr Laeger. 1997 Jun 23;159(26):4123-8.Llorca J, Bringas-Bollada M, Amor-Dorado JC, et al. Lack of association between altitude and incidence of giant cell arteritis in Northwest Spain. Clin Exp Rheumatol. 2004 Mar-Apr;22(2):270.Gonzalez-Gay MA, Miranda-Filloy JA, Lopez-Diaz MJ, et al. Giant cell arteritis in northwestern Spain: a 25-year epidemiologic study. Medicine (Baltimore). 2007 Mar;86(2):61-8.Narvaez J, Clavaguera MT, Nolla-Sole JM, et al. Lack of association between infection and onset of polymyalgia rheumatica. J Rheumatol. 2000 Apr;27(4):953-7.Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA. 2002 Jan 2;287(1):92-101.Gonzalez-Gay MA, Barros S, Lopez-Diaz MJ, et al. Giant cell arteritis: disease patterns of clinical presentation in a series of 240 patients. Medicine (Baltimore). 2005 Sep;84(5):269-76.Parikh M, Miller NR, Lee AG, et al. Prevalence of a normal C-reactive protein with an elevated erythrocyte sedimentation rate in biopsy-proven giant cell arteritis. Ophthalmology. 2006 Oct;113(10):1842-5.Costello F, Zimmerman MB, Podhajsky PA, Hayreh SS. Role of thrombocytosis in diagnosis of giant cell arteritis and differentiation of arteritic from non-arteritic anterior ischemic optic neuropathy. Eur J Ophthalmol. 2004 May-Jun;14(3):245-57.

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The epidemiologic characteristics of giant cell arteritis (GCA) have been studied in large populations from the United States,1-4, United Kingdom,5, 6 Sweden,7-9 Denmark,10 Norway,11Israel12,13 and Saudi Arabia14 where incidences have been estimated mainly through retrospective study designs. These studies have demonstrated that GCA occurs more commonly in populations of Nordic descent,15 fluctuations in incidence with distinctive peaks were reported by some investigators;2,5,13,16-18 however this was not observed by others.16,19The epidemiologic characteristics of this disease have never been studied in Australasia. We present the first epidemiological study evaluating clinical and laboratory characteristics of biopsy proven GCA in the population of Otago, New Zealand; comparing the characteristics of the biopsy positive with the biopsy negative group and the annual incidence rate in Otago, New Zealand to internationally reported figures.Materials and Methods A retrospective analysis of the clinical presentation, management and postoperative course of 363 consecutive patients obtained from the surgical database at Dunedin Hospital, Otago, New Zealand between 1996-2005 was undertaken. All cases of suspected giant cell arteritis in the Otago region are referred to this centre for a temporal artery biopsy. Patients who underwent or were evaluated for a temporal artery biopsy (TAB) were included in the study, cases lacking sufficient medical information were excluded. Of a total of 369 cases, 6 cases had insufficient medical information and were excluded from this study. A total of 363 cases fulfilled the inclusion criteria. Variables documented from the medical records included demographic factors such as age and gender, and major symptoms and signs. An ophthalmic trainee or ophthalmologist evaluated all cases within 1 week of starting systemic steroids and temporal artery biopsies were conducted within 2 weeks of starting steroids. Inflammatory markers were requested for all cases at the time of referral. The decision to undertake a TAB was based on clinical criteria and raised inflammatory markers and / or platelet count. Trainees performed biopsies within 1 week of clinical assessment. A repeat biopsy was performed within 1 week in histologically negative cases if clinical features were judged to be sufficiently suggestive, inflammatory markers were raised inexplicably or the initial biopsy was shorter than 2 mm. An experienced pathologist examined all histological specimens. Temporal artery biopsies were processed and cut at 4-5 00b5m thickness from at least 3 levels. Hematoxylin and eosin stains slides were produced from each paraffin block. Cases with visual involvement were admitted to hospital and biopsy was performed within 24 hours and methylprednisone 1mg/kg/day was administered intravenously for 3 days. Follow-up within 1 week was arranged after the biopsy to ensure the improvement of symptoms, compliance with treatment and wound assessment. Major features assessed to determine the presence of GCA were giant cells in the intima and the media, lymphocytes and histiocytes in the media, reduplication/fragmentation of the internal elastic lamina and intimal thickening. Healed GCA was diagnosed in the presence of intimal fibrosis, media scarring with eccentric and segmented disruption of the internal elastic lamina or chronic media inflammation with neovascularisation. However, if one or more of these features were absent, healed arteritis or atherosclerosis was considered 20. Biopsy positive cases were placed on oral prednisone 1mg/kg/day immediately upon receiving the biopsy results. Statistical analysis was performed on the Statistical Package for the Social Sciences (SSPS) v16.0. The Exact method was used in calculating the confidence interval for the incidence of GCA. An independent-sample t-test was used to compare mean differences in clinical characteristics and laboratory findings between the GCA positive and negative groups. Annual age and gender specific incidence rates were calculated / 100,000 population aged 226550 years using the number of incident cases as the numerator and population estimates based on census counts as the denominator. Linear interpolation was used to estimate population size for intercensal years 21. Ninety five percent confidence intervals (95% CI) were computed for incidence rates. Results Patient demographicsThe population in Otago consists ethnically of Europeans (85.9%), M ori (7.1%), Pacific Islanders (1.8%), Asians (4.5%), Middle Eastern and African (0.7%). Over the 9 years of observation there was an estimated increase in total population numbers by 6265 (3.3%), an increase in the population age group 226550 years by 9484 (16.1%) and a decrease in the population <50 years by 3219 (2.4%). Temporal artery biopsies were performed on a total of 363 patients, of which 105 (29%) were males and 258 (71%) were females. The mean age of the population was 73.2 years (range 50-97 years, SD 9.3). The average follow up was 51.9 months (range 1-120, SD 24.9). A total of 70 (19%) patients with biopsy proven GCA (GCA+ve) were identified. The mean age at diagnosis was 72.8 years (range 57-91 years, SD 8.2). There were 52 (74%) females and 18 (26%) males giving a ratio of 2.9:1. The annual incidence of GCA/100,000 population aged 226550 years adjusted for gender and age is shown in Table 1, the mean annual incidence in the population 226550 years was 12.7/100,000 over the 9 years of observation. Table 1. Incidence of giant cell arteritis/100,000 population in the Otago region for the population age 226550 years. CI, confidence interval Variables Incidence /100,000 95% CI (P<0.5) All patients 12.7 11.7-14.3 Females 21.3 19.8-24.2 Males 8.8 8.3-10.2 Age 50-64 Age 65-74 Age 226575 21.0 144.3 342.7 20.9-21.5 143.2-146.4 340.2-347.3 The variation in annual incidence is shown in Figure 1. We observed a cyclic annual incidence with 2 peaks 5 years apart. Figure 1. Annual incidence of giant cell arteritis/100,000 population in the Otago region 1996-2005 for the population age 226550 years. The distribution is cyclic with a peak in 1998 and 2003 The incidence rates increased with age and there was a female: male ratio of 2.8:1. Seasonal variations were observed with more cases of GCA diagnosed in the spring 23 (32.8%) than the summer 17 (24.3%), autumn 16 (22.9%), and winter 14 (20%), however the difference between the seasons was not statistically significant (P<0.9). Among the biopsy positive cases 5 (1.4%) showed lesions consistent with healed giant cell arteritis. Unilateral biopsies were performed on 335 patients. These were positive in 67 cases (18.5%). In 28 cases bilateral sequential biopsies were performed of which 2/28 (7.2%) demonstrated active arteritic lesions and the other case was a lesion consistent with GCA. There were no reported postoperative complications from the procedure. A total of 293 (81%) patients were biopsy negative (GCA-ve). The mean age in this group was 73.4 years (range 50-97 years, SD 9.5). There were 88 (30%) males and 205 (70%) females. Discharge diagnoses included autoimmune conditions polymyalgia rheumatica, rheumatoid arthritis, systemic lupus erythematosus and other vasculitides in 54 (18.4%), optic neuropathies in 6 (2%), malignancies in 5 (1.7%), non-vasculitic cerebrovascular accident in 4 (1.4%), septicaemia in 3 (1.0%) and other diagnoses 15 (5.1%). No definite diagnosis was recorded in the medical notes of 206 (70%) cases. Clinical and laboratory differences between the biopsy positive and negative groupsThere was no difference in mean age between the GCA +ve and -ve groups (p<0.2) or gender (p<0.6). The major presenting symptoms and signs are summarised in Tables 2 and 3 respectively. Headache was the commonest symptom occurring in 198 (54.5%) patients. Fever was the commonest sign occurring in 38 (10.5%) of patients. In analysing the clinical difference in the GCA +ve and -ve groups, jaw claudication, anorexia and scalp tenderness were the most significant discriminating symptoms (Table 2). Table 2. Major symptoms in the study population Symptom GCA +ve cases GCA -ve cases Total cases (%) P value Headache PMR symptoms Jaw claudication Scalp tenderness Malaise Anorexia Weight loss Permanent visual loss Transient visual loss 47 (67.1%) 22 (31.4%) 17 (24.3%) 16 (22.9%) 12 (17.1) 10 (14.3%) 9 (12.9%) 10 (14.3%) 7 (10%) 156 (53.2%) 69 (23.5%) 17 (5.8%) 39 (13.3%) 39 (13.3%) 22 (7.5%) 30 (10.2%) 31 (10.6%) 24 (8.2%) 198 (54.5%) 91 (25%) 34 (9.4%) 55 (15.2%) 51 (14.1%) 32 (8.8%) 39 (10.7%) 41 (11.3%) 31 (8.5%) 0.1 0.1 0.0001 0.003 0.4 0.005 0.6 0.3 0.7 PMR=Polymyalgia rheumatica, GCA+ve= patients with giant cell arteritis, GCA-ve=patients without giant cell arteritis. The P value indicates the statistical significance of the difference in the prevalence of the symptom in the biopsy positive versus the biopsy negative population. Among the signs abnormalities of the superficial temporal arteries, a clinical diagnosis of arteritic anterior ischemic optic neuropathy (AAION) and raised inflammatory markers without suggestive clinical symptoms and signs were significant discriminators (Table 3). Table 3. Major signs in the study population Signs GCA +ve cases GCA -ve cases Total cases (%) P value Fever 9 (12.9%) 29 (9.9%) 38 (10.5%) 0.4 STA tenderness 9 (12.9%) 18 (6.1%) 27 (7.4%) 0.002 STA reduced pulse 6 (8.6%) 1 (0.3%) 7 (1.9%) 0.001 CVA 4 (5.7%) 11 (3.8%) 15 (4.1%) 0.3 Anemia 2 (2.9%) 4 (1.4%) 6 (1.7%) 0.2 Raised inflammatory markers without suggestive clinical symptoms and signs 1 (1.4%) 14 (4.8%) 15 (4.1%) 0.004 STA=superficial temporal artery, AAION=arteritic anterior ischemic optic neuropathy, CVA=cerebrovascular accident, GCA+ve= patients with giant cell arteritis, GCA-ve= patients without giant cell arteritis. The P value indicates the statistical significance of the difference in the prevalence of the sign in the biopsy positive versus the biopsy negative population. Table 4. The distribution of inflammatory markers in the study population ESR mm/hr GCA +ve cases GCA -ve cases 226420 21-70 71-120 121-170 2265171 3 (4.3%) 31 (44.3%) 30 (42.9%) 6 (8.6%) 3 (4.3%) 34 (11.6%) 160 (54.6%) 84 (28.7%) 14 (4.8%) 1 (0.3%) Total 70 293 CRP mg/dl 22645 6-50 51-95 96-140 2265141 3 (4.3%) 18 (25.7%) 31 (44.3%) 10 (14.3%) 8 (11.4%) 43 (14.7%) 64 (21.8%) 150 (51.2%)\r\n

Summary

Abstract

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

Hauser WA, Ferguson RH, Holley KE, Kurland LT. Temporal arteritis in Rochester, Minnesota, 1951 to 1967. Mayo Clin Proc. 1971 Sep;46(9):597-602.Salvarani C, Crowson CS, O'Fallon WM, et al. Reappraisal of the epidemiology of giant cell arteritis in Olmsted County, Minnesota, over a fifty-year period. Arthritis Rheum. 2004 Apr 15;51(2):264-8.Machado EB, Michet CJ, Ballard DJ, et al. Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota, 1950-1985. Arthritis Rheum. 1988 Jun;31(6):745-9.Smith CA, Fidler WJ, Pinals RS. The epidemiology of giant cell arteritis. Report of a ten-year study in Shelby County, Tennessee. Arthritis Rheum. 1983 Oct;26(10):1214-9.Smeeth L, Cook C, Hall AJ. Incidence of diagnosed polymyalgia rheumatica and temporal arteritis in the United Kingdom, 1990-2001. Ann Rheum Dis. 2006 Aug;65(8):1093-8.Jonasson F, Cullen JF, Elton RA. Temporal arteritis. A 14-year epidemiological, clinical and prognostic study. Scott Med J. 1979 Apr;24(2):111-7.Bengtsson BA, Malmvall BE. The epidemiology of giant cell arteritis including temporal arteritis and polymyalgia rheumatica. Incidences of different clinical presentations and eye complications. Arthritis Rheum. 1981 Jul;24(7):899-904.Nordborg E, Bengtsson BA. Epidemiology of biopsy-proven giant cell arteritis (GCA). J Intern Med. 1990 Apr;227(4):233-6.Ostberg G. Temporal arteritis in a large necropsy series. Ann Rheum Dis. 1971 May;30(3):224-35.Boesen P, Sorensen SF. Giant cell arteritis, temporal arteritis, and polymyalgia rheumatica in a Danish county. A prospective investigation, 1982-1985. Arthritis Rheum. 1987 Mar;30(3):294-9.Haugeberg G, Paulsen PQ, Bie RB. Temporal arteritis in Vest Agder County in southern Norway: incidence and clinical findings. J Rheumatol. 2000 Nov;27(11):2624-7.Friedman G, Friedman B, Benbassat J. Epidemiology of temporal arteritis in Israel. Isr J Med Sci. 1982 Feb;18(2):241-4.Sonnenblick M, Nesher G, Friedlander Y, Rubinow A. Giant cell arteritis in Jerusalem: a 12-year epidemiological study. Br J Rheumatol. 1994 Oct;33(10):938-41.Chaudhry IA, Shamsi FA, Elzaridi E, et al. Epidemiology of giant-cell arteritis in an Arab population: a 22-year study. Br J Ophthalmol. 2007 Jun;91(6):715-8.Lane SE, Watts R, Scott DG. Epidemiology of systemic vasculitis. Curr Rheumatol Rep. 2005 Aug;7(4):270-5.Petursdottir V, Johansson H, Nordborg E, Nordborg C. The epidemiology of biopsy-positive giant cell arteritis: special reference to cyclic fluctuations. Rheumatology (Oxford). 1999 Dec;38(12):1208-12.Elling P, Olsson AT, Elling H. Synchronous variations of the incidence of temporal arteritis and polymyalgia rheumatica in different regions of Denmark; association with epidemics of Mycoplasma pneumoniae infection. J Rheumatol. 1996 Jan;23(1):112-9.Bas-Lando M, Breuer GS, Berkun Y, et al. The incidence of giant cell arteritis in Jerusalem over a 25-year period: annual and seasonal fluctuations. Clin Exp Rheumatol. 2007 Jan-Feb;25(1 Suppl 44):S15-7.Gonzalez-Gay MA, Garcia-Porrua C, Rivas MJ, et al. Epidemiology of biopsy proven giant cell arteritis in northwestern Spain: trend over an 18 year period. Ann Rheum Dis. 2001 Apr;60(4):367-71.Ray-Chaudhuri N, Kine DA, Tijani SO, et al. Effect of prior steroid treatment on temporal artery biopsy findings in giant cell arteritis. Br J Ophthalmol. 2002 May;86(5):530-2.Statistics NZ. Statistics New Zealand; 2006 Population Census Data. 2006. http://www.stats.govt.nz/census/default.htmSalvarani C, Gabriel SE, O'Fallon WM, Hunder GG. The incidence of giant cell arteritis in Olmsted County, Minnesota: apparent fluctuations in a cyclic pattern. Ann Intern Med. 1995 Aug 1;123(3):192-4.Elling P, Olsson AT, Elling H. Synchronous variations in the incidence of temporal arteritis and polymyalgia rheumatica in Danish counties. Association with epidemics of Mycoplasma pneumonia infection. Ugeskr Laeger. 1997 Jun 23;159(26):4123-8.Llorca J, Bringas-Bollada M, Amor-Dorado JC, et al. Lack of association between altitude and incidence of giant cell arteritis in Northwest Spain. Clin Exp Rheumatol. 2004 Mar-Apr;22(2):270.Gonzalez-Gay MA, Miranda-Filloy JA, Lopez-Diaz MJ, et al. Giant cell arteritis in northwestern Spain: a 25-year epidemiologic study. Medicine (Baltimore). 2007 Mar;86(2):61-8.Narvaez J, Clavaguera MT, Nolla-Sole JM, et al. Lack of association between infection and onset of polymyalgia rheumatica. J Rheumatol. 2000 Apr;27(4):953-7.Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA. 2002 Jan 2;287(1):92-101.Gonzalez-Gay MA, Barros S, Lopez-Diaz MJ, et al. Giant cell arteritis: disease patterns of clinical presentation in a series of 240 patients. Medicine (Baltimore). 2005 Sep;84(5):269-76.Parikh M, Miller NR, Lee AG, et al. Prevalence of a normal C-reactive protein with an elevated erythrocyte sedimentation rate in biopsy-proven giant cell arteritis. Ophthalmology. 2006 Oct;113(10):1842-5.Costello F, Zimmerman MB, Podhajsky PA, Hayreh SS. Role of thrombocytosis in diagnosis of giant cell arteritis and differentiation of arteritic from non-arteritic anterior ischemic optic neuropathy. Eur J Ophthalmol. 2004 May-Jun;14(3):245-57.

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The epidemiologic characteristics of giant cell arteritis (GCA) have been studied in large populations from the United States,1-4, United Kingdom,5, 6 Sweden,7-9 Denmark,10 Norway,11Israel12,13 and Saudi Arabia14 where incidences have been estimated mainly through retrospective study designs. These studies have demonstrated that GCA occurs more commonly in populations of Nordic descent,15 fluctuations in incidence with distinctive peaks were reported by some investigators;2,5,13,16-18 however this was not observed by others.16,19The epidemiologic characteristics of this disease have never been studied in Australasia. We present the first epidemiological study evaluating clinical and laboratory characteristics of biopsy proven GCA in the population of Otago, New Zealand; comparing the characteristics of the biopsy positive with the biopsy negative group and the annual incidence rate in Otago, New Zealand to internationally reported figures.Materials and Methods A retrospective analysis of the clinical presentation, management and postoperative course of 363 consecutive patients obtained from the surgical database at Dunedin Hospital, Otago, New Zealand between 1996-2005 was undertaken. All cases of suspected giant cell arteritis in the Otago region are referred to this centre for a temporal artery biopsy. Patients who underwent or were evaluated for a temporal artery biopsy (TAB) were included in the study, cases lacking sufficient medical information were excluded. Of a total of 369 cases, 6 cases had insufficient medical information and were excluded from this study. A total of 363 cases fulfilled the inclusion criteria. Variables documented from the medical records included demographic factors such as age and gender, and major symptoms and signs. An ophthalmic trainee or ophthalmologist evaluated all cases within 1 week of starting systemic steroids and temporal artery biopsies were conducted within 2 weeks of starting steroids. Inflammatory markers were requested for all cases at the time of referral. The decision to undertake a TAB was based on clinical criteria and raised inflammatory markers and / or platelet count. Trainees performed biopsies within 1 week of clinical assessment. A repeat biopsy was performed within 1 week in histologically negative cases if clinical features were judged to be sufficiently suggestive, inflammatory markers were raised inexplicably or the initial biopsy was shorter than 2 mm. An experienced pathologist examined all histological specimens. Temporal artery biopsies were processed and cut at 4-5 00b5m thickness from at least 3 levels. Hematoxylin and eosin stains slides were produced from each paraffin block. Cases with visual involvement were admitted to hospital and biopsy was performed within 24 hours and methylprednisone 1mg/kg/day was administered intravenously for 3 days. Follow-up within 1 week was arranged after the biopsy to ensure the improvement of symptoms, compliance with treatment and wound assessment. Major features assessed to determine the presence of GCA were giant cells in the intima and the media, lymphocytes and histiocytes in the media, reduplication/fragmentation of the internal elastic lamina and intimal thickening. Healed GCA was diagnosed in the presence of intimal fibrosis, media scarring with eccentric and segmented disruption of the internal elastic lamina or chronic media inflammation with neovascularisation. However, if one or more of these features were absent, healed arteritis or atherosclerosis was considered 20. Biopsy positive cases were placed on oral prednisone 1mg/kg/day immediately upon receiving the biopsy results. Statistical analysis was performed on the Statistical Package for the Social Sciences (SSPS) v16.0. The Exact method was used in calculating the confidence interval for the incidence of GCA. An independent-sample t-test was used to compare mean differences in clinical characteristics and laboratory findings between the GCA positive and negative groups. Annual age and gender specific incidence rates were calculated / 100,000 population aged 226550 years using the number of incident cases as the numerator and population estimates based on census counts as the denominator. Linear interpolation was used to estimate population size for intercensal years 21. Ninety five percent confidence intervals (95% CI) were computed for incidence rates. Results Patient demographicsThe population in Otago consists ethnically of Europeans (85.9%), M ori (7.1%), Pacific Islanders (1.8%), Asians (4.5%), Middle Eastern and African (0.7%). Over the 9 years of observation there was an estimated increase in total population numbers by 6265 (3.3%), an increase in the population age group 226550 years by 9484 (16.1%) and a decrease in the population <50 years by 3219 (2.4%). Temporal artery biopsies were performed on a total of 363 patients, of which 105 (29%) were males and 258 (71%) were females. The mean age of the population was 73.2 years (range 50-97 years, SD 9.3). The average follow up was 51.9 months (range 1-120, SD 24.9). A total of 70 (19%) patients with biopsy proven GCA (GCA+ve) were identified. The mean age at diagnosis was 72.8 years (range 57-91 years, SD 8.2). There were 52 (74%) females and 18 (26%) males giving a ratio of 2.9:1. The annual incidence of GCA/100,000 population aged 226550 years adjusted for gender and age is shown in Table 1, the mean annual incidence in the population 226550 years was 12.7/100,000 over the 9 years of observation. Table 1. Incidence of giant cell arteritis/100,000 population in the Otago region for the population age 226550 years. CI, confidence interval Variables Incidence /100,000 95% CI (P<0.5) All patients 12.7 11.7-14.3 Females 21.3 19.8-24.2 Males 8.8 8.3-10.2 Age 50-64 Age 65-74 Age 226575 21.0 144.3 342.7 20.9-21.5 143.2-146.4 340.2-347.3 The variation in annual incidence is shown in Figure 1. We observed a cyclic annual incidence with 2 peaks 5 years apart. Figure 1. Annual incidence of giant cell arteritis/100,000 population in the Otago region 1996-2005 for the population age 226550 years. The distribution is cyclic with a peak in 1998 and 2003 The incidence rates increased with age and there was a female: male ratio of 2.8:1. Seasonal variations were observed with more cases of GCA diagnosed in the spring 23 (32.8%) than the summer 17 (24.3%), autumn 16 (22.9%), and winter 14 (20%), however the difference between the seasons was not statistically significant (P<0.9). Among the biopsy positive cases 5 (1.4%) showed lesions consistent with healed giant cell arteritis. Unilateral biopsies were performed on 335 patients. These were positive in 67 cases (18.5%). In 28 cases bilateral sequential biopsies were performed of which 2/28 (7.2%) demonstrated active arteritic lesions and the other case was a lesion consistent with GCA. There were no reported postoperative complications from the procedure. A total of 293 (81%) patients were biopsy negative (GCA-ve). The mean age in this group was 73.4 years (range 50-97 years, SD 9.5). There were 88 (30%) males and 205 (70%) females. Discharge diagnoses included autoimmune conditions polymyalgia rheumatica, rheumatoid arthritis, systemic lupus erythematosus and other vasculitides in 54 (18.4%), optic neuropathies in 6 (2%), malignancies in 5 (1.7%), non-vasculitic cerebrovascular accident in 4 (1.4%), septicaemia in 3 (1.0%) and other diagnoses 15 (5.1%). No definite diagnosis was recorded in the medical notes of 206 (70%) cases. Clinical and laboratory differences between the biopsy positive and negative groupsThere was no difference in mean age between the GCA +ve and -ve groups (p<0.2) or gender (p<0.6). The major presenting symptoms and signs are summarised in Tables 2 and 3 respectively. Headache was the commonest symptom occurring in 198 (54.5%) patients. Fever was the commonest sign occurring in 38 (10.5%) of patients. In analysing the clinical difference in the GCA +ve and -ve groups, jaw claudication, anorexia and scalp tenderness were the most significant discriminating symptoms (Table 2). Table 2. Major symptoms in the study population Symptom GCA +ve cases GCA -ve cases Total cases (%) P value Headache PMR symptoms Jaw claudication Scalp tenderness Malaise Anorexia Weight loss Permanent visual loss Transient visual loss 47 (67.1%) 22 (31.4%) 17 (24.3%) 16 (22.9%) 12 (17.1) 10 (14.3%) 9 (12.9%) 10 (14.3%) 7 (10%) 156 (53.2%) 69 (23.5%) 17 (5.8%) 39 (13.3%) 39 (13.3%) 22 (7.5%) 30 (10.2%) 31 (10.6%) 24 (8.2%) 198 (54.5%) 91 (25%) 34 (9.4%) 55 (15.2%) 51 (14.1%) 32 (8.8%) 39 (10.7%) 41 (11.3%) 31 (8.5%) 0.1 0.1 0.0001 0.003 0.4 0.005 0.6 0.3 0.7 PMR=Polymyalgia rheumatica, GCA+ve= patients with giant cell arteritis, GCA-ve=patients without giant cell arteritis. The P value indicates the statistical significance of the difference in the prevalence of the symptom in the biopsy positive versus the biopsy negative population. Among the signs abnormalities of the superficial temporal arteries, a clinical diagnosis of arteritic anterior ischemic optic neuropathy (AAION) and raised inflammatory markers without suggestive clinical symptoms and signs were significant discriminators (Table 3). Table 3. Major signs in the study population Signs GCA +ve cases GCA -ve cases Total cases (%) P value Fever 9 (12.9%) 29 (9.9%) 38 (10.5%) 0.4 STA tenderness 9 (12.9%) 18 (6.1%) 27 (7.4%) 0.002 STA reduced pulse 6 (8.6%) 1 (0.3%) 7 (1.9%) 0.001 CVA 4 (5.7%) 11 (3.8%) 15 (4.1%) 0.3 Anemia 2 (2.9%) 4 (1.4%) 6 (1.7%) 0.2 Raised inflammatory markers without suggestive clinical symptoms and signs 1 (1.4%) 14 (4.8%) 15 (4.1%) 0.004 STA=superficial temporal artery, AAION=arteritic anterior ischemic optic neuropathy, CVA=cerebrovascular accident, GCA+ve= patients with giant cell arteritis, GCA-ve= patients without giant cell arteritis. The P value indicates the statistical significance of the difference in the prevalence of the sign in the biopsy positive versus the biopsy negative population. Table 4. The distribution of inflammatory markers in the study population ESR mm/hr GCA +ve cases GCA -ve cases 226420 21-70 71-120 121-170 2265171 3 (4.3%) 31 (44.3%) 30 (42.9%) 6 (8.6%) 3 (4.3%) 34 (11.6%) 160 (54.6%) 84 (28.7%) 14 (4.8%) 1 (0.3%) Total 70 293 CRP mg/dl 22645 6-50 51-95 96-140 2265141 3 (4.3%) 18 (25.7%) 31 (44.3%) 10 (14.3%) 8 (11.4%) 43 (14.7%) 64 (21.8%) 150 (51.2%)\r\n

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Association with epidemics of Mycoplasma pneumonia infection. Ugeskr Laeger. 1997 Jun 23;159(26):4123-8.Llorca J, Bringas-Bollada M, Amor-Dorado JC, et al. Lack of association between altitude and incidence of giant cell arteritis in Northwest Spain. Clin Exp Rheumatol. 2004 Mar-Apr;22(2):270.Gonzalez-Gay MA, Miranda-Filloy JA, Lopez-Diaz MJ, et al. Giant cell arteritis in northwestern Spain: a 25-year epidemiologic study. Medicine (Baltimore). 2007 Mar;86(2):61-8.Narvaez J, Clavaguera MT, Nolla-Sole JM, et al. Lack of association between infection and onset of polymyalgia rheumatica. J Rheumatol. 2000 Apr;27(4):953-7.Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA. 2002 Jan 2;287(1):92-101.Gonzalez-Gay MA, Barros S, Lopez-Diaz MJ, et al. Giant cell arteritis: disease patterns of clinical presentation in a series of 240 patients. Medicine (Baltimore). 2005 Sep;84(5):269-76.Parikh M, Miller NR, Lee AG, et al. Prevalence of a normal C-reactive protein with an elevated erythrocyte sedimentation rate in biopsy-proven giant cell arteritis. Ophthalmology. 2006 Oct;113(10):1842-5.Costello F, Zimmerman MB, Podhajsky PA, Hayreh SS. Role of thrombocytosis in diagnosis of giant cell arteritis and differentiation of arteritic from non-arteritic anterior ischemic optic neuropathy. Eur J Ophthalmol. 2004 May-Jun;14(3):245-57.

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