Risk factors for cranial ischemic complications in giant cell arteritis

被引:108
作者
Nesher, G
Berkun, Y
Mates, M
Baras, M
Nesher, R
Rubinow, A
Sonnenblick, M
机构
[1] Shaare Zedek Med Ctr, Dept Internal Med, IL-91031 Jerusalem, Israel
[2] Bikur Cholim Hosp, Jerusalem, Israel
[3] Hadassah Med Ctr, Sch Publ Hlth, IL-91120 Jerusalem, Israel
[4] Hebrew Univ Jerusalem, Hadassah Med Sch, IL-91010 Jerusalem, Israel
[5] Sapir Med Ctr, Kefar Sava, Israel
关键词
D O I
10.1097/01.md.0000119761.27564.c9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cranial ischemic complications (CICs) are among the presenting manifestations of giant cell arteritis (GCA). Yet patients with GCA may develop CICs at a later stage, despite steroid therapy. In the current report we delineate risk factors for CICs, both at presentation and during follow-up, and review the relevant literature. We reviewed charts of 175 patients with GCA. Follow-up data were available for 166 patients. CICs at presentation or developing within 2 weeks of GCA diagnosis were considered GCA related. CICs developing later were considered GCA related only when associated with other GCA-related manifestations or acute-phase reactions. Associations between CICs and other variables were tested by multivariate analysis. At presentation, 43 patients (24.6%) had CICs. Risk factors were transient cerebro-ophthalmic ischemic episodes (COIEs) (odds ratio [OR] 4.3) and male sex (OR 2.5), while the presence of systemic symptoms was "protective" (OR 0.3). During follow-up 8.4% of patients with GCA developed new CICs. Risk factors in these cases were previous CICs at presentation (OR 5.6) and transient COIEs developing during follow-up (OR 14.8). The use of low-dose aspirin was protective (OR 0.2). These data, together with data from the literature review, suggest that GCA patients with transient COIEs and without fever or other systemic symptoms are at increased risk of presenting with CICs. Risk factors for late-developing CICs were CICs at presentation and late-developing transient COIEs.
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页码:114 / 122
页数:9
相关论文
共 33 条
[11]  
2-P
[12]   Antiphospholipid antibodies and thrombophilic factors in giant cell arteritis [J].
Espinosa, G ;
Tàssies, D ;
Font, J ;
Muñoz-Rodríguez, FJ ;
Cervera, R ;
Ordinas, A ;
Reverter, JC ;
Ingelmo, M .
SEMINARS IN ARTHRITIS AND RHEUMATISM, 2001, 31 (01) :12-20
[13]  
ESPINOZA LR, 1991, AM J MED, V90, P474
[14]  
Font C, 1997, BRIT J RHEUMATOL, V36, P251
[15]   Visual manifestations of giant cell arteritis -: Trends and clinical spectrum in 161 patients [J].
González-Gay, MA ;
García-Porrúa, C ;
Llorca, J ;
Hajeer, AH ;
Brañas, F ;
Dababneh, A ;
González-Louzao, C ;
Rodriguez-Gil, E ;
Rodríguez-Ledo, P ;
Ollier, WER .
MEDICINE, 2000, 79 (05) :283-292
[16]  
González-Gay MA, 1998, ARTHRITIS RHEUM, V41, P1497, DOI 10.1002/1529-0131(199808)41:8<1497::AID-ART22>3.0.CO
[17]  
2-Z
[18]   Ocular manifestations of giant cell arteritis [J].
Hayreh, SS ;
Podhajsky, PA ;
Zimmerman, B .
AMERICAN JOURNAL OF OPHTHALMOLOGY, 1998, 125 (04) :509-520
[19]   Temporal arteritis - A cough, toothache, and tongue infarction [J].
Hellmann, DB .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2002, 287 (22) :2996-3000
[20]   Elevated production of interleukin-6 is associated with a lower incidence of disease-related ischemic events in patients with giant-cell arteritis -: Angiogenic activity of interleukin-6 as a potential protective mechanism [J].
Hernández-Rodríguez, J ;
Segarra, M ;
Vilardell, C ;
Sánchez, M ;
García-Martínez, A ;
Esteban, MJ ;
Grau, JM ;
Urbano-Márquez, A ;
Colomer, D ;
Kleinman, HK ;
Cid, MC .
CIRCULATION, 2003, 107 (19) :2428-2434