CASE REPORTS

Clinical presentation and vascular imaging in giantcell arteritis of the femoropopliteal andtibioperoneal arteries. Analysis of four casesFederico Tatò, MD, and Ulrich Hoffmann, MD, Munich, Germany

We present four patients with rapidly progressive claudication of the lower limbs due to extracranial giant cell arteritis.Additional findings suggestive of giant cell arteritis were involvement of the axillary or brachial arteries in two patients,symptoms of polymyalgia rheumatica or temporal arteritis in three, and all patients had severely elevated erythrocytesedimentation rate and C-reactive protein level. Lower limb involvement affected preferentially the femoropopliteal, deepfemoral, and tibioperoneal arteries. Hypoechogenic, concentric mural thickening suggestive of vasculitis was readilyvisible in all involved arterial segments by duplex ultrasound imaging, whereas angiography was rather unspecific. Typicalchanges for large-vessel vasculitis were also detectable by magnetic resonance imaging and fluorine-18-desoxyglucosepositron emission tomography. More widespread use of these vascular imaging techniques may show that giant cell

arteritis of the lower limbs is more frequent than previously assumed. (J Vasc Surg 2006;44:176-82.)

Giant cell arteritis (GCA) is a chronic vasculitis of large-and medium-sized arteries that almost exclusively affectselderly patients. Involvement of the cranial arteries leads tothe classic symptoms of headache, painful thickening of thetemporal artery, jaw claudication, and visual loss.1 Themost common extracranial manifestation of GCA is steno-sis or occlusion of the subclavian and axillary artery, withloss of arm pulses and upper limb claudication.2

Involvement of the lower limbs is considered rare inGCA. So far, only a few cases of GCA with involvement ofthe iliac or femoropopliteal arteries have been reported.3-7

However, the true frequency of lower limb GCA may beunderestimated if the involvement of this vascular regionremains silent or if it is confused with arteriosclerotic vas-cular disease.

Duplex ultrasound imaging,8 magnetic resonance im-aging (MRI),9,10 and fluorine-18-desoxyglucose positronemission tomography (18F-FDG-PET)11-13 have greatlyimproved the noninvasive diagnosis of large-vessel vasculi-tis. These methods allow the detection of arterial inflam-mation while still at an early stage, even in asymptomaticpatients. More widespread use of these imaging techniquesmay reveal that lower limb artery involvement in GCA ismore common than previously assumed.

From the Division of Vascular Medicine, Medizinische Poliklinik, Ludwig-Maximilians University.

Competition of interest: none.Reprint requests: Federico Tatò, MD, Division of Vascular Medicine,

Medizinische Poliklinik, Ludwig-Maximilians University, Pettenkofer-strasse 8a, D-80336 Munich, Germany (e-mail: federico.tato@med.uni-muenchen.de).

0741-5214/$32.00Copyright © 2006 by The Society for Vascular Surgery.

doi:10.1016/j.jvs.2006.02.054

176

We recently observed four patients with GCA involvingthe femoropopliteal and crural arteries who presented withtypical symptoms of lower limb ischemia mimicking arte-riosclerotic peripheral arterial disease. We present the keyclinical findings in this unusual cause of peripheral arterialdisease and discuss our experience with digital subtractionangiography, duplex sonography, MRI, and 18F-FDG-PET in the diagnostic work-up of these patients.

CASE REPORTS

The patients were two men and two women aged between 58and 73 years. The key clinical findings of the four patients aresummarized in Tables I and II. Claudication was preceded byseveral months of malaise and typical symptoms of polymyalgiarheumatica in patients 1, 2, and 4. Two patients complained oftemporal headache, and one had sudden blindness of the left eyedue to optic nerve ischemia 4 months before the onset of claudi-cation.

Temporal artery biopsy was performed on three patients, andthe specimen was positive for GCA in two. Patient 4, who did nothave a biopsy, had clinically normal temporal arteries and no signsof temporal arteritis in duplex sonography.

Before the onset of prednisone treatment, all patients had amarkedly elevated erythrocyte sedimentation rate (ESR) andplasma C-reactive protein (CRP). Three patients had mild, medi-cally controlled hypertension; patient 4 had quit smoking 5 yearsprior (25 pack-years). None of the patients was diabetic or hadhyperlipidemia.

Pattern of extracranial artery involvement. Two patientshad involvement of both upper and lower limbs, and two patientsonly of the lower limbs (Table II). Upper limb involvementconsisted of occlusion of both axillary arteries in patient 3 and long,

high-grade stenosis of both axillary and brachial arteries in patient

JOURNAL OF VASCULAR SURGERYVolume 44, Number 1 Tatò and Hoffmann 177

2. Upper limb involvement was completely asymptomatic in pa-tient 3 and caused mild arm claudication in patient 2.

All patients complained of rapidly progressive, bilateral calf andfoot claudication. Measurements of ankle pressures and pulse volumerecordings showed compensated lower limb perfusion in patients 3and 4 (systolic ankle pressures �70 mm Hg and abnormal butpulsatile pulse volume recordings of the foot) and critical limb isch-emia in patients 1 and 2 (Table II). Patient 1 presented with nocturnalrest pain of the right foot and a small ischemic ulceration at the tip ofthe right hallux. Patient 2 complained of intermittent rest pain in bothfeet and had bilateral interdigital lesions.

The physical examination and the results of vascular imagingdemonstrated symmetrical involvement of the popliteal and crural

Table I. Symptoms at initial presentation, results of tempofour patients with peripheral arterial disease due to giant ce

Patient 1

Gender/age (years) Male/73 MaClassic symptoms of giant cellarteritis

Pain in shoulders andneck, arthralgia,morning stiffness,temporal headache,fatigue, unilateraloptic nerve ischemia

Paipastlfe

Temporal biopsy Positive PosESR mm/h 102 85CRP mg/dL 8.90 7.6

ESR, Erythrocyte sedimentation rate; CRP, C-reactive protein.

Table II. Hemodynamic findings, traditional cardiovasculand performed vascular imaging in four patients with perip

Patient 1

Vascular symptoms Bilateral calf claudication,rest pain in the right foot,ischemic lesion of theright hallux

Bilfib

Ankle pressures* (right/left) 40/105 mm Hg 60/ABI (right/left) 0.25/0.66 NRPVR of the foot (right/left) Flat/abnormal‡ FlaTraditional risk factors Hypertension No

Distribution of peripheralarterial involvement

Multiple stenoses of bothSFAs, PAs, and DFAs;occlusion of the righttibioperoneal trunk;multiple occlusions of theTPAs

MubsbaTsa

Imaging tests performed Duplex, DSA, MRI, PET Du

PVR, Pulse volume recording; ABI, ankle/brachial index; NR, not reporteTPA, tibioperoneal arteries; AA, axillary artery; BA, brachial artery; DSA, demission tomography.*Systolic pressures were measured in the posterior tibial and dorsalis pedis a†ABI is not reported due to false-low brachial pressures in patients with upp‡Indicates pathologic but pulsatile PVR.

arteries in all patients. The superficial femoral arteries were involved in

patients 1 and 3. Involvement of the deep femoral arteries wasdocumented in patients 1 and 2, who were evaluated by digitalsubtraction angiography. None of the patients had evidence of aorticor iliac artery involvement.

Vascular imaging. Digital subtraction angiography was per-formed on the two patients presenting with critical ischemia (patients1 and 2). Patient 1 had multiple stenoses of the superficial femoralarteries and occlusion of the right tibioperoneal trunk (Fig 1). Patient2 had long, smooth narrowing of both popliteal arteries (Fig 2). Bothpatients had multiple stenoses of the deep femoral arteries (Fig 1,A and 2, A) and extensive occlusions of the calf arteries (Fig 1, Cand 2, C).

Duplex sonography was performed on all patients and

iopsy, and laboratory tests for systemic inflammation interitis

atient 2 Patient 3 Patient 4

Female/70 Female/61houlders andgirdle,lgia, morningss, weight loss,ral headache,ade fever,, elevated liveres

None Pain in shoulders, neckand pelvic girdle,arthralgia, weight loss,fatigue

Not performed Negative108 844.30 6.97

k factors, distribution of peripheral arterial involvement,l arterial disease due to giant cell arteritis

atient 2 Patient 3 Patient 4

calf, foot andm claudication,igital lesions ofeet

Left-leading calf andfoot claudication

Left-leading footclaudication

m Hg 180/90 mm Hg 160/105 mm HgNR† 0.94/0.62Normal/abnormal Normal/abnormalHypertension Hypertension,

smokingstenoses ofFAs; long,

h stenoses ofAs; occlusions

enoses of thelong, smoothes of both AAsAs

Long occlusion of theleft SFA; circular wallthickening of theright SFA, of bothPAs and of the TPAs;bilateral occlusion ofboth Aas

Bilateral, circularwall thickening ofPAs and TPAswith multiplehigh-gradestenoses of thecrural arteries

DSA Duplex, PET Duplex, PET

, superficial femoral artery; DFA, deep femoral artery; PA, popliteal artery;ubtraction angiography; MRI, magnetic resonance imaging; PET, positron

the higher of the two values is shown.b involvement.

ral bll ar

P

le/58n in selvicrthratiffneempoow-gratiguenzymitive

7

ar rishera

P

ateralorearnterdoth f65 m

†

t/flatne

ltipleoth Dmoototh Pnd stPAs;

tenosnd Bplex,

d; SFAigital s

rtery,er lim

showed a long, circular, hypoechogenic wall thickening of the

JOURNAL OF VASCULAR SURGERYJuly 2006178 Tatò and Hoffmann

Fig 1. Digital subtraction angiogram of the right leg of patient 1, a 73-year-old man presenting with criticallower-limb ischemia. A, Multiple stenoses of the deep femoral artery and irregularities of the superficial femoral artery.B, Multiple stenoses of the distal superficial femoral artery and the supragenual popliteal artery. C, Occlusion of the

tibioperoneal trunk and of the proximal calf arteries.

Fig 2. Digital subtraction angiography of both legs in patient 2, a 58-year-old man with critical ischemia of both feet.A, Multiple stenoses of both deep femoral arteries. B, Long, smooth narrowing of both popliteal arteries. C, Occlusion

of the posterior tibial and fibular arteries and multiple stenoses of the anterior tibial arteries.

JOURNAL OF VASCULAR SURGERYVolume 44, Number 1 Tatò and Hoffmann 179

involved arteries leading to varying degrees of stenosis. Duplexsonography was able to identify this characteristic finding notonly in the femoropopliteal region but also in the tibial andperoneal arteries (Fig 3). Patient 3 had a long occlusion of theleft superficial femoral artery. The occlusion was hypoecho-genic, with the circular wall thickening well visible around theoccluded lumen (Fig 4).

Contrast enhanced MRI of the right popliteal region wasperformed on patient 1. T1-weighted MRI of the right poplitealartery showed circular thickening and marked enhancement of thearterial wall (Fig 5).

Patients 1, 3, and 4 were evaluated by whole body 18F-FDG-PET and all showed markedly increased 18F-FDG uptake in theaffected femoropopliteal and crural arteries (Fig 6, A and B).Abnormal tracer uptake was limited to the femoropopliteal andcrural arteries in patients 1 and 4; the subclavian and axillaryarteries were also involved in patient 3. Involvement of the aorta oriliac arteries (Fig 6, C) was not evident in any patient.

Follow-up. Once the inflammatory nature of the vascular

Fig 3. Color-coded duplex sonography in patient 4, aand bilateral foot-claudication. Longitudinal (A) andhypoechogenic wall thickening.

Fig 4. Color-coded duplex sonography in patient 3, a 7Longitudinal (A) and enlarged cross-section (B) of thesurrounded by a halo of hypoechogenic wall thickening.

disease had been established, all patients were treated medically,

and no vascular intervention was performed. All patients receivedan initial prednisone dose of 1 mg/kg body weight. Tapering ofthe prednisone dose was performed according to the recommen-dations for GCA, guided by the clinical symptoms and laboratorysigns of systemic inflammation. Patients 1 and 2 were treated withintravenous prostaglandin E1 (Alprostadil, Schwarz Pharma AG,Monheim, Germany) for 3 weeks.

Patient 1 showed complete resolution of right-sided rest painand healing of the ulceration of the right hallux 4 weeks afterinitiation of treatment. Patient 2 has been observed for 19 months.After the interdigital lesions were healed, he experienced progres-sive improvement in pain-free walking distance. At his last exami-nation, ankle pressures had improved to 85/75 mm Hg (right/left), pulse volume recordings of the feet were pulsatile, and theself-reported pain-free walking distance was 1000 meters. Patients3 and 4 were treated with walking exercise. Patient 3 reported anincrease in pain-free walking distance from 50 meters at initialpresentation to 300 meters after 12 months follow-up. At her lastvisit, systolic ankle pressures had risen to 170/120 mm Hg (right/

ar-old woman presenting with polymyalgia rheumatica-section (B) of the peroneal artery show concentric,

r-old woman presenting with bilateral calf-claudication.superficial femoral artery show occlusion of the lumen

61-yecross

0-yealeft

left). Patient 4 was observed by our rheumatology department and

JOURNAL OF VASCULAR SURGERYJuly 2006180 Tatò and Hoffmann

reported an unlimited walking distance after 3 months of treat-ment. Hemodynamic measurements were not repeated.

DISCUSSION

Although the cranial arteries are the typical localizationof GCA, this vasculitis may involve any large- or medium-sized artery. Involvement of extracranial arteries has been

Fig 5. Contrast-enhanced, T1-weighted MRI of the right popli-teal region of patient 1, a 73-year-old man presenting with criticallower limb ischemia shows concentric thickening and markedenhancement of the popliteal artery wall (arrow).

Fig 6. Fluorine-18-desoxyglucose positron emission tocritical lower limb ischemia. Lateral (A) and frontal (B)

vascular tracer uptake. C, Head and trunk of the same patient

estimated to occur in 10% to 15% of patients with GCA.The aorta and the upper limb arteries (particularly thesubclavian and axillary artery) are the most common local-ization of extracranial GCA. Loss of upper limb pulses is awell-established symptom of GCA,1,2 and an increasedincidence of aortic aneurysms and dissections is considereda serious late complication of this disease.14,15

Involvement of the lower limb arteries has been re-ported in up to 18% of patients with extracranial GCA.4

However, there have been only few reports of patients withGCA in whom lower limb claudication was the leadingclinical problem,3-7 and GCA is usually not considered aclinically relevant cause of lower limb ischemia.

We report the cases of four patients who recently pre-sented to our institution for claudication or critical isch-emia of the lower limbs and who were found to have GCAof the femoropopliteal and crural arteries. Based on thisexperience, we believe that symptomatic GCA of the lowerlimb arteries may be a more common clinical problem thanpreviously assumed. We have reviewed the symptoms, thephysical findings, and the results of vascular imaging studiesof these four patients to identify the characteristic clinicalfeatures of lower limb GCA.

Lower limb involvement was associated with other,more typical manifestations of GCA in most of our patients.Only one patient presented with calf claudication as theonly symptom. One patient had classic temporal arteritiswith unilateral loss of vision, three patients complained offatigue, myalgia, and arthralgia, and two patients had oligo-or asymptomatic involvement of the axillary and brachialarteries evident on physical examination. Systemic symp-

raphy in patient 1, a 73-year-old man presenting withof the popliteal and tibioperoneal arteries show marked

mogviews

without significant tracer uptake in the central arteries.

JOURNAL OF VASCULAR SURGERYVolume 44, Number 1 Tatò and Hoffmann 181

toms, polymyalgia rheumatica, classic symptoms of tempo-ral arteritis, or signs of upper limb involvement may there-fore provide the first clinical indication of GCA in patientspresenting with rapidly progressive lower limb ischemia.

Markedly elevated ESR and CRP are a hallmark for thediagnosis of GCA.1 ESR and CRP were severely elevated inall our patients, thus supporting the usefulness of labora-tory tests for systemic inflammation in patients with clau-dication and suspected large-vessel vasculitis.

A temporal artery biopsy specimen positive for GCA isgenerally considered diagnostic proof. Extracranial arteriesare not readily accessible for biopsy. However, histologicproof of temporal arteritis may also be obtained in patientspresenting only with symptoms of extracranial involve-ment. In the largest series of histologically documentedextracranial GCA, the rate of positive temporal artery bi-opsy specimens was 25%.4 Two of three temporal arterybiopsy specimens were positive in our patients. This findingconfirms that temporal artery biopsy is worthwhile in pa-tients with suspected extracranial GCA.

Abnormal findings on duplex sonography of the tem-poral artery may facilitate the selection of the biopsy siteand increase the likelihood of a positive biopsy result. In arecent meta-analysis, ultrasonography of the temporal ar-tery achieved moderate sensitivity (69%) but good specific-ity (82%) for the diagnosis of temporal arteritis comparedwith temporal biopsy.16

Patients presenting with symptoms of lower limb isch-emia are frequently evaluated by digital subtraction angiog-raphy. We performed a digital subtraction angiography onpatients 1 and 2, who presented with critical lower limbischemia. Patient 2 had long, smooth narrowing of thepopliteal arteries and multiple “beaded” stenoses of thedeep femoral arteries (Fig 2, B), which would be unusualfor arteriosclerotic vascular disease. Several of our angio-graphic findings closely resemble arteriosclerosis, however.The femoropopliteal obstructions shown in Fig 1, B andthe extensive occlusions of tibial and peroneal arteriespresent in both patients (Figs 1, C and 2, C) are indistin-guishable from advanced arteriosclerosis and resemble dia-betic peripheral arterial disease.

Long, smooth, or beaded appearance of arterial steno-ses is believed to be suggestive of vasculitis on angiogra-phy.17 These findings are not specific, however. Beadedstenoses are also typical of fibromuscular dysplasia,18 andlong, smooth arterial narrowing may be seen in othernoninflammatory conditions such as postinterventionalmyointimal hyperplasia, ergotism, or after dissection. Thedistinction between vasculitis and other nonarterioscleroticvascular disorders should, therefore, include patient his-tory, distribution of the disease, laboratory tests for inflam-mation, and assessment of arterial wall morphology byother imaging techniques. Our data suggest that the angio-graphic diagnosis of large vessel vasculitis is particularlyunreliable in the femoropopliteal and tibioperoneal arter-ies, where the angiographic appearance of inflammatoryarterial lesions may be very similar to arteriosclerotic vascu-

lar disease.

Suspicion of the presence of a nonarteriosclerotic, in-flammatory vascular disease was initially triggered in ourpatients by the results of duplex sonography. Large-vesselvasculitis leads to long, circular, hypoechogenic thickeningof the arterial wall, which may be accompanied by a perivas-cular, hypoechogenic halo.8

The sensitivity and specificity of duplex ultrasoundimaging for the detection of extracranial large-vessel vascu-litis has not been studied systematically. Published reportson sonographic findings in extracranial GCA and Takaya-su’s arteritis,8 as well as our own experience with thesepatients, suggest that smooth, circular, hypoechogenic wallthickening of long arterial segments is virtually pathogno-monic for large-vessel vasculitis. We have observed a similarsonographic appearance only in myointimal hyperplasiaafter balloon angioplasty, a condition easily distinguishablefrom vasculitis by patient history and lack of systemicinflammation. All of our patients had these typical sono-graphic changes in the involved vascular segments. Thehypoechogenic wall thickening was visible in the stenosedand in the occluded arterial segments (Fig 4) and was easilydetectable even in the distal tibial and peroneal arteries (Fig 3).

Lacking histologic proof of vasculitis from the periph-eral arteries, we cannot totally exclude the coincidence ofGCA and lower limb arteriosclerosis in our patients. How-ever, based on the typical sonographic appearance of theaffected arteries, the absence of generalized arteriosclerosis,and the sudden onset of claudication simultaneously withthe systemic symptoms of GCA, we consider arterioscle-rotic peripheral arterial disease highly unlikely.

We performed contrast-enhanced MRI of the poplitealregion on patient 1 and were able to detect marked thick-ening and inflammatory enhancement in the wall of theright popliteal artery (Fig 5). MRI has been shown to havehigh sensitivity and specificity for the detection of thecircular wall thickening in large-vessel vasculitis.9,10 Moststudies have focused on the aorta and its major branches,however, and only very limited data are available on theperformance of MRI in the femoropopliteal or even tibio-peroneal region.

Presently, we believe that MRI is particularly valuablefor the evaluation of central vascular regions not readilyaccessible for high-resolution ultrasonography. A disadvan-tage of ultrasonography is the persistence of mural thicken-ing during treatment and the resulting lack of correlationbetween sonographic findings and disease activity.8 Thedegree of contrast enhancement detected by MRI mayprove superior to sonographic measurements of wall thick-ness for the follow-up of disease activity.9,10

Recently, 18F-FDG-PET has been introduced in theevaluation of GCA and Takayasu’s arteritis with very prom-ising results. This method allows the direct assessment ofvascular inflammation on a whole-body scale, and the levelof vascular FDG uptake was shown to correlate well withchanges in inflammatory activity during treatment.11-13,19

A high aortal FDG-uptake was shown to have a sensitivityof 92% and a specificity of 100% for the diagnosis of

Takayasu’s arteritis.13 Vascular FDG uptake in the large

JOURNAL OF VASCULAR SURGERYJuly 2006182 Tatò and Hoffmann

thoracic arteries has been reported in 14 (56%) of 25patients with GCA compared with 2% of control subjects.20

The same study reports vascular uptake in the arteries of thelegs in 64% of GCA patients and in 23% of controls. Thisfinding suggests an unexpectedly high frequency of lowerlimb involvement in GCA, but also a lower specificity ofvascular FDG uptake in the arteries of the legs.

Arterial inflammation due to arteriosclerosis is believedto be the cause of vascular FDG uptake seen in elderlysubjects.21 Most investigators agree that FDG uptake dueto arteriosclerosis is usually mild, whereas a high level ofuptake is suggestive of vasculitis. A cut-off level for distin-guishing between vasculitis and arteriosclerosis has notbeen defined, however.

Presently, 18F-FDG-PET appears to be most valuablefor the early diagnosis of large-vessel vasculitis in youngpatients with unspecific symptoms. In elderly patients withGCA, the results of 18F-FDG-PET need to be interpretedcarefully together with the clinical findings and the resultsof other vascular imaging tests. Under these conditions,18F-FDG-PET provides a unique opportunity to study thedistribution of extracranial vascular inflammation in GCApatients. Moreover, 18F-FDG-PET may prove to be a veryvaluable technique for the follow-up of inflammatory activ-ity during treatment of large-vessel vasculitis.19

The results of 18F-FDG-PET in our patients confirm ahigh degree of tracer uptake in the arterial segments clinicallyand sonographically affected by vasculitis. Severe vascularFDG uptake was limited to the popliteal and crural arteries inpatients 1 (Fig 6) and 4 and also included the axillary arteriesin patient 3. To our knowledge, this is the first report of calfartery GCA detected by 18F-FDG-PET, thus indicating a highsensitivity of this technique even in peripheral, medium-sizedarteries.

It is remarkable that none of our patients had evidence ofaortic or iliac artery involvement. This finding suggests that ifGCA affects the lower limbs, the disease involves preferentiallythe crural, femoropopliteal, and deep femoral arteries. Incontrast, large-vessel vasculitis involving the aorta and iliacarteries may represent a different clinical entity more closelyrelated to Takayasu’s arteritis. In the future, more widespreaduse of 18F-FDG-PET may help to assess the true frequencyand pattern of extracranial involvement in GCA.

The mainstay of treatment of GCA is immunosuppressionwith prednisone. Previous reports indicate that invasive vascu-lar reconstructions can be avoided in most GCA patients withperipheral artery involvement.7 Our follow-up data suggestthat even patients with advanced lower limb ischemia due toGCA can improve substantially with adequate immunosup-pressive treatment and medical management of peripheralarterial disease.

AUTHOR CONTRIBUTIONS

Conception and design: FT, UHAnalysis and interpretation : FT, UHData collection: FT, UHWriting the article: FT, UH

Critical revision of the article: FT, UH

Final approval of the article: FT, UHStatistical analysis: Not applicableObtained funding: Not applicableOverall responsibility: FT

REFERENCES

1. Salvarani C, Cantini F, Boiardi L, Hunder GG. Polymyalgia rheumaticaand giant-cell arteritis. N Engl J Med 2002;347:261-71.

2. Klein RG, Hunder GG, Stanson AW, Sheps SG. Large artery involve-ment in giant cell (temporal) arteritis. Ann Intern Med 1975;83:806-12.

3. O’Brien PK, Pudden AJ. Peripheral arterial insufficiency due to giantcell arteritis. Can J Surg 1978;21:441-2.

4. Lie JT. Aortic and extracranial large vessel giant cell arteritis: a review of72 cases with histopathological documentation. Semin Arthritis Rheum1995;24:422-31.

5. Dupuy R, Mercie P, Neau D, Longy-Boursier M, Conri C. Giant cellarteritis involving the lower limbs. Rev Rhum Engl Ed 1997;64:500-3.

6. Garcia Vasquez JM, Carreira JM, Seoane C, Vidal JJ. Superior andinferior limb ischemia in giant cell arteritis: angiography follow-up. ClinRheumatol 1999;18:61-5.

7. Le Hello C, Levesque H, Jeanton M, Cailleux N, Galateau F, Peillon C,et al. Lower limb giant cell arteritis and temporal arteritis: followup of 8cases. J Rheumatol 2001;28:1407-12.

8. Schmidt WA, Blockmans D. Use of ultrasonography and positronemission tomography in the diagnosis and assessment of large-vesselvasculitis. Curr Opin Rheumatol 2005;17:9-15.

9. Choe YH, Han BK, Koh EM, Kim DK, Do YS, Lee WR. Takayasu’sarteritis: assessment of disease activity with contrast-enhanced MRimaging. AJR 2000;175:505-11.

10. Narvaez J, Narvaez JA, Nolla JM, Sirvent E, Reina D, Valverde J. Giantcell arteritis and polymyalgia rheumatica: usefulness of vascular mag-netic resonance imaging studies in the diagnosis of aortitis. Rheumatol2005;44:479-83.

11. Turlakow A, Yeung HWD, Pui J, Macapinlac H, Liebovitz E, Rusch V,et al. Fludeoxyglucose positron emission tomography in the diagnosisof giant cell arteritis. Arch Intern Med 2001;161:1003-7.

12. Belhocine T, Blockmans D, Hustinx R, Vandevivere J, Mortelmans L.Imaging of large vessel vasculitis with 18FDG PET: illusion or reality? Acritical review of the literature data. Eur J Nucl Med Mol Imaging2003;30:1305-13.

13. Webb M, Chambers A, Al-Nahhas A, Mason JC, Maudlin L, Rahman L,et al. The role of 18F-FDG PET in characterising disease activity inTakayasu arteritis. Eur J Nucl Med Mol Imaging 2004;31:627-34.

14. Evans JM, O’Fallon WM, Hunder GG. Increased incidence of aorticaneurysm and dissection in giant cell (temporal) arteritis: a population-based study. Ann Intern Med 1995;122:502-7.

15. Bongartz T, Matteson EL. Large-vessel involvement in giant cell arteri-tis. Curr Opin Rheumatol 2006;18:10-17.

16. Karassa FB, Matsagas MI, Schmidt WA, Ioannidis JPA. Meta-analysis:test performance of ultrasonography for giant-cell arteritis. Ann InternMed 2005;142:359-369.

17. Stanson AW, Klein RG, Hunder GG. Extracranial angiographic find-ings in giant cell (temporal) arteritis. Am J Roengenol 1976;127:957-63.

18. Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med 2004;350:1862-71.

19. Meller J, Strutz F, Scheel A, Sahlmann CO, Lehmann K, Conrad M, etal. Early diagnosis and follow-up of aortitis with 18F-FDG PET andMRI. Eur J Nucl Med Mol Imaging 2003;730-736.

20. Blockmans D, Stroobants S, Maes A, Mortelmans L. Positron emissiontomography in giant cell arteritis and polymyalgia rheumatica: evidencefor inflammation of the aortic arch. Am J Med 2000;108:246-249.

21. Yun M, Yeh D, Arujo LI, Jang S, Newberg A, Alavi A. F-18 FDG uptakein the large arteries. A new observation. Clin Nucl Med 2001;26:314-319.

Submitted Dec 26, 2005; accepted Feb 6, 2006.