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Clinical presentation and vascular imaging in giant cell arteritis of the femoropopliteal and tibioperoneal arteries. Analysis of four cases

2006; Elsevier BV; Volume: 44; Issue: 1 Linguagem: Inglês

10.1016/j.jvs.2006.02.054

1097-6809

Federico Tatò, Ulrich Hoffmann,

Peripheral Artery Disease Management

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 erythrocyte sedimentation rate and C-reactive protein level. Lower limb involvement affected preferentially the femoropopliteal, deep femoral, and tibioperoneal arteries. Hypoechogenic, concentric mural thickening suggestive of vasculitis was readily visible in all involved arterial segments by duplex ultrasound imaging, whereas angiography was rather unspecific. Typical changes for large-vessel vasculitis were also detectable by magnetic resonance imaging and fluorine-18-desoxyglucose positron 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. 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 erythrocyte sedimentation rate and C-reactive protein level. Lower limb involvement affected preferentially the femoropopliteal, deep femoral, and tibioperoneal arteries. Hypoechogenic, concentric mural thickening suggestive of vasculitis was readily visible in all involved arterial segments by duplex ultrasound imaging, whereas angiography was rather unspecific. Typical changes for large-vessel vasculitis were also detectable by magnetic resonance imaging and fluorine-18-desoxyglucose positron 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. Giant cell arteritis (GCA) is a chronic vasculitis of large- and medium-sized arteries that almost exclusively affects elderly patients. Involvement of the cranial arteries leads to the classic symptoms of headache, painful thickening of the temporal artery, jaw claudication, and visual loss.1Salvarani C. Cantini F. Boiardi L. Hunder G.G. Polymyalgia rheumatica and giant-cell arteritis.N Engl J Med. 2002; 347: 261-271Crossref PubMed Scopus (606) Google Scholar The most common extracranial manifestation of GCA is stenosis or occlusion of the subclavian and axillary artery, with loss of arm pulses and upper limb claudication.2Klein R.G. Hunder G.G. Stanson A.W. Sheps S.G. Large artery involvement in giant cell (temporal) arteritis.Ann Intern Med. 1975; 83: 806-812Crossref PubMed Scopus (420) Google Scholar Involvement of the lower limbs is considered rare in GCA. So far, only a few cases of GCA with involvement of the iliac or femoropopliteal arteries have been reported.3O'Brien P.K. Pudden A.J. Peripheral arterial insufficiency due to giant cell arteritis.Can J Surg. 1978; 21: 441-442PubMed Google Scholar, 4Lie J.T. Aortic and extracranial large vessel giant cell arteritis a review of 72 cases with histopathological documentation.Semin Arthritis Rheum. 1995; 24: 422-431Abstract Full Text PDF PubMed Scopus (207) Google Scholar, 5Dupuy R. Mercie P. Neau D. Longy-Boursier M. Conri C. Giant cell arteritis involving the lower limbs.Rev Rhum Engl Ed. 1997; 64: 500-503PubMed Google Scholar, 6Garcia Vasquez J.M. Carreira J.M. Seoane C. Vidal J.J. Superior and inferior limb ischemia in giant cell arteritis angiography follow-up.Clin Rheumatol. 1999; 18: 61-65Crossref PubMed Scopus (27) Google Scholar, 7Le Hello C. Levesque H. Jeanton M. Cailleux N. Galateau F. Peillon C. et al.Lower limb giant cell arteritis and temporal arteritis followup of 8 cases.J Rheumatol. 2001; 28: 1407-1412PubMed Google Scholar However, the true frequency of lower limb GCA may be underestimated if the involvement of this vascular region remains silent or if it is confused with arteriosclerotic vascular disease. Duplex ultrasound imaging,8Schmidt W.A. Blockmans D. Use of ultrasonography and positron emission tomography in the diagnosis and assessment of large-vessel vasculitis.Curr Opin Rheumatol. 2005; 17: 9-15Crossref PubMed Scopus (118) Google Scholar magnetic resonance imaging (MRI),9Choe Y.H. Han B.K. Koh E.M. Kim D.K. Do Y.S. Lee W.R. Takayasu's arteritis assessment of disease activity with contrast-enhanced MR imaging.AJR. 2000; 175: 505-511Crossref PubMed Scopus (145) Google Scholar, 10Narvaez J. Narvaez J.A. Nolla J.M. Sirvent E. Reina D. Valverde J. Giant cell arteritis and polymyalgia rheumatica usefulness of vascular magnetic resonance imaging studies in the diagnosis of aortitis.Rheumatol. 2005; 44: 479-483Crossref PubMed Scopus (96) Google Scholar and fluorine-18-desoxyglucose positron emission tomography (18F-FDG-PET)11Turlakow A. Yeung H.W.D. Pui J. Macapinlac H. Liebovitz E. Rusch V. et al.Fludeoxyglucose positron emission tomography in the diagnosis of giant cell arteritis.Arch Intern Med. 2001; 161: 1003-1007Crossref PubMed Scopus (104) Google Scholar, 12Belhocine T. Blockmans D. Hustinx R. Vandevivere J. Mortelmans L. Imaging of large vessel vasculitis with 18FDG PET:illusion or reality? A critical review of the literature data.Eur J Nucl Med Mol Imaging. 2003; 30: 1305-1313Crossref PubMed Scopus (146) Google Scholar, 13Webb M. Chambers A. Al-Nahhas A. Mason J.C. Maudlin L. Rahman L. et al.The role of 18F-FDG PET in characterising disease activity in Takayasu arteritis.Eur J Nucl Med Mol Imaging. 2004; 31: 627-634Crossref PubMed Scopus (215) Google Scholar have greatly improved the noninvasive diagnosis of large-vessel vasculitis. These methods allow the detection of arterial inflammation while still at an early stage, even in asymptomatic patients. More widespread use of these imaging techniques may reveal that lower limb artery involvement in GCA is more common than previously assumed. We recently observed four patients with GCA involving the femoropopliteal and crural arteries who presented with typical symptoms of lower limb ischemia mimicking arteriosclerotic peripheral arterial disease. We present the key clinical findings in this unusual cause of peripheral arterial disease and discuss our experience with digital subtraction angiography, duplex sonography, MRI, and 18F-FDG-PET in the diagnostic work-up of these patients. The patients were two men and two women aged between 58 and 73 years. The key clinical findings of the four patients are summarized in Table I, Table II. Claudication was preceded by several months of malaise and typical symptoms of polymyalgia rheumatica in patients 1, 2, and 4. Two patients complained of temporal headache, and one had sudden blindness of the left eye due to optic nerve ischemia 4 months before the onset of claudication.Table ISymptoms at initial presentation, results of temporal biopsy, and laboratory tests for systemic inflammation in four patients with peripheral arterial disease due to giant cell arteritisPatient 1Patient 2Patient 3Patient 4Gender/age (years)Male/73Male/58Female/70Female/61Classic symptoms of giant cell arteritisPain in shoulders and neck, arthralgia, morning stiffness, temporal headache, fatigue, unilateral optic nerve ischemiaPain in shoulders and pelvic girdle, arthralgia, morning stiffness, weight loss, temporal headache, low-grade fever, fatigue, elevated liver enzymesNonePain in shoulders, neck and pelvic girdle, arthralgia, weight loss, fatigueTemporal biopsyPositivePositiveNot performedNegativeESR mm/h1028510884CRP mg/dL8.907.674.306.97ESR, Erythrocyte sedimentation rate; CRP, C-reactive protein. Open table in a new tab Table IIHemodynamic findings, traditional cardiovascular risk factors, distribution of peripheral arterial involvement, and performed vascular imaging in four patients with peripheral arterial disease due to giant cell arteritisPatient 1Patient 2Patient 3Patient 4Vascular symptomsBilateral calf claudication, rest pain in the right foot, ischemic lesion of the right halluxBilateral calf, foot and forearm claudication, interdigital lesions of both feetLeft-leading calf and foot claudicationLeft-leading foot claudicationAnkle pressures⁎Systolic pressures were measured in the posterior tibial and dorsalis pedis artery, the higher of the two values is shown. (right/left)40/105 mm Hg60/65 mm Hg180/90 mm Hg160/105 mm HgABI (right/left)0.25/0.66NR†ABI is not reported due to false-low brachial pressures in patients with upper limb involvement.NR†ABI is not reported due to false-low brachial pressures in patients with upper limb involvement.0.94/0.62PVR of the foot (right/left)Flat/abnormal‡Indicates pathologic but pulsatile PVR.Flat/flatNormal/abnormalNormal/abnormalTraditional risk factorsHypertensionNoneHypertensionHypertension, smokingDistribution of peripheral arterial involvementMultiple stenoses of both SFAs, PAs, and DFAs; occlusion of the right tibioperoneal trunk; multiple occlusions of the TPAsMultiple stenoses of both DFAs; long, smooth stenoses of both PAs; occlusions and stenoses of the TPAs; long, smooth stenoses of both AAs and BAsLong occlusion of the left SFA; circular wall thickening of the right SFA, of both PAs and of the TPAs; bilateral occlusion of both AasBilateral, circular wall thickening of PAs and TPAs with multiple high-grade stenoses of the crural arteriesImaging tests performedDuplex, DSA, MRI, PETDuplex, DSADuplex, PETDuplex, PETPVR, Pulse volume recording; ABI, ankle/brachial index; NR, not reported; SFA, superficial femoral artery; DFA, deep femoral artery; PA, popliteal artery; TPA, tibioperoneal arteries; AA, axillary artery; BA, brachial artery; DSA, digital subtraction angiography; MRI, magnetic resonance imaging; PET, positron emission tomography. Systolic pressures were measured in the posterior tibial and dorsalis pedis artery, the higher of the two values is shown.† ABI is not reported due to false-low brachial pressures in patients with upper limb involvement.‡ Indicates pathologic but pulsatile PVR. Open table in a new tab ESR, Erythrocyte sedimentation rate; CRP, C-reactive protein. PVR, Pulse volume recording; ABI, ankle/brachial index; NR, not reported; SFA, superficial femoral artery; DFA, deep femoral artery; PA, popliteal artery; TPA, tibioperoneal arteries; AA, axillary artery; BA, brachial artery; DSA, digital subtraction angiography; MRI, magnetic resonance imaging; PET, positron emission tomography. Temporal artery biopsy was performed on three patients, and the specimen was positive for GCA in two. Patient 4, who did not have a biopsy, had clinically normal temporal arteries and no signs of temporal arteritis in duplex sonography. Before the onset of prednisone treatment, all patients had a markedly elevated erythrocyte sedimentation rate (ESR) and plasma C-reactive protein (CRP). Three patients had mild, medically controlled hypertension; patient 4 had quit smoking 5 years prior (25 pack-years). None of the patients was diabetic or had hyperlipidemia. Two patients had involvement of both upper and lower limbs, and two patients only of the lower limbs (Table II). Upper limb involvement consisted of occlusion of both axillary arteries in patient 3 and long, high-grade stenosis of both axillary and brachial arteries in patient 2. Upper limb involvement was completely asymptomatic in patient 3 and caused mild arm claudication in patient 2. All patients complained of rapidly progressive, bilateral calf and foot claudication. Measurements of ankle pressures and pulse volume recordings showed compensated lower limb perfusion in patients 3 and 4 (systolic ankle pressures >70 mm Hg and abnormal but pulsatile pulse volume recordings of the foot) and critical limb ischemia in patients 1 and 2 (Table II). Patient 1 presented with nocturnal rest pain of the right foot and a small ischemic ulceration at the tip of the right hallux. Patient 2 complained of intermittent rest pain in both feet and had bilateral interdigital lesions. The physical examination and the results of vascular imaging demonstrated symmetrical involvement of the popliteal and crural arteries in all patients. The superficial femoral arteries were involved in patients 1 and 3. Involvement of the deep femoral arteries was documented in patients 1 and 2, who were evaluated by digital subtraction angiography. None of the patients had evidence of aortic or iliac artery involvement. Digital subtraction angiography was performed on the two patients presenting with critical ischemia (patients 1 and 2). Patient 1 had multiple stenoses of the superficial femoral arteries and occlusion of the right tibioperoneal trunk (Fig 1). Patient 2 had long, smooth narrowing of both popliteal arteries (Fig 2). Both patients had multiple stenoses of the deep femoral arteries (Fig 1, A and 2, A) and extensive occlusions of the calf arteries (Fig 1, C and 2, C).Fig 2Digital 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.View Large Image Figure ViewerDownload (PPT) Duplex sonography was performed on all patients and showed a long, circular, hypoechogenic wall thickening of the involved arteries leading to varying degrees of stenosis. Duplex sonography was able to identify this characteristic finding not only in the femoropopliteal region but also in the tibial and peroneal arteries (Fig 3). Patient 3 had a long occlusion of the left superficial femoral artery. The occlusion was hypoechogenic, with the circular wall thickening well visible around the occluded lumen (Fig 4).Fig 4Color-coded duplex sonography in patient 3, a 70-year-old woman presenting with bilateral calf-claudication. Longitudinal (A) and enlarged cross-section (B) of the left superficial femoral artery show occlusion of the lumen surrounded by a halo of hypoechogenic wall thickening.View Large Image Figure ViewerDownload (PPT) Contrast enhanced MRI of the right popliteal region was performed on patient 1. T1-weighted MRI of the right popliteal artery showed circular thickening and marked enhancement of the arterial 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 the affected femoropopliteal and crural arteries (Fig 6, A and B). Abnormal tracer uptake was limited to the femoropopliteal and crural arteries in patients 1 and 4; the subclavian and axillary arteries were also involved in patient 3. Involvement of the aorta or iliac arteries (Fig 6, C) was not evident in any patient. Once the inflammatory nature of the vascular disease had been established, all patients were treated medically, and no vascular intervention was performed. All patients received an initial prednisone dose of 1 mg/kg body weight. Tapering of the prednisone dose was performed according to the recommendations for GCA, guided by the clinical symptoms and laboratory signs of systemic inflammation. Patients 1 and 2 were treated with intravenous prostaglandin E1 (Alprostadil, Schwarz Pharma AG, Monheim, Germany) for 3 weeks. Patient 1 showed complete resolution of right-sided rest pain and healing of the ulceration of the right hallux 4 weeks after initiation of treatment. Patient 2 has been observed for 19 months. After the interdigital lesions were healed, he experienced progressive improvement in pain-free walking distance. At his last examination, ankle pressures had improved to 85/75 mm Hg (right/left), pulse volume recordings of the feet were pulsatile, and the self-reported pain-free walking distance was 1000 meters. Patients 3 and 4 were treated with walking exercise. Patient 3 reported an increase in pain-free walking distance from 50 meters at initial presentation to 300 meters after 12 months follow-up. At her last visit, systolic ankle pressures had risen to 170/120 mm Hg (right/left). Patient 4 was observed by our rheumatology department and reported an unlimited walking distance after 3 months of treatment. Hemodynamic measurements were not repeated. Although the cranial arteries are the typical localization of GCA, this vasculitis may involve any large- or medium-sized artery. Involvement of extracranial arteries has been estimated to occur in 10% to 15% of patients with GCA. The aorta and the upper limb arteries (particularly the subclavian and axillary artery) are the most common localization of extracranial GCA. Loss of upper limb pulses is a well-established symptom of GCA,1Salvarani C. Cantini F. Boiardi L. Hunder G.G. Polymyalgia rheumatica and giant-cell arteritis.N Engl J Med. 2002; 347: 261-271Crossref PubMed Scopus (606) Google Scholar, 2Klein R.G. Hunder G.G. Stanson A.W. Sheps S.G. Large artery involvement in giant cell (temporal) arteritis.Ann Intern Med. 1975; 83: 806-812Crossref PubMed Scopus (420) Google Scholar and an increased incidence of aortic aneurysms and dissections is considered a serious late complication of this disease.14Evans J.M. O'Fallon W.M. Hunder G.G. Increased incidence of aortic aneurysm and dissection in giant cell (temporal) arteritis a population-based study.Ann Intern Med. 1995; 122: 502-507Crossref PubMed Scopus (482) Google Scholar, 15Bongartz T. Matteson E.L. Large-vessel involvement in giant cell arteritis.Curr Opin Rheumatol. 2006; 18: 10-17Crossref PubMed Scopus (136) Google Scholar Involvement of the lower limb arteries has been reported in up to 18% of patients with extracranial GCA.4Lie J.T. Aortic and extracranial large vessel giant cell arteritis a review of 72 cases with histopathological documentation.Semin Arthritis Rheum. 1995; 24: 422-431Abstract Full Text PDF PubMed Scopus (207) Google Scholar However, there have been only few reports of patients with GCA in whom lower limb claudication was the leading clinical problem,3O'Brien P.K. Pudden A.J. Peripheral arterial insufficiency due to giant cell arteritis.Can J Surg. 1978; 21: 441-442PubMed Google Scholar, 4Lie J.T. Aortic and extracranial large vessel giant cell arteritis a review of 72 cases with histopathological documentation.Semin Arthritis Rheum. 1995; 24: 422-431Abstract Full Text PDF PubMed Scopus (207) Google Scholar, 5Dupuy R. Mercie P. Neau D. Longy-Boursier M. Conri C. Giant cell arteritis involving the lower limbs.Rev Rhum Engl Ed. 1997; 64: 500-503PubMed Google Scholar, 6Garcia Vasquez J.M. Carreira J.M. Seoane C. Vidal J.J. Superior and inferior limb ischemia in giant cell arteritis angiography follow-up.Clin Rheumatol. 1999; 18: 61-65Crossref PubMed Scopus (27) Google Scholar, 7Le Hello C. Levesque H. Jeanton M. Cailleux N. Galateau F. Peillon C. et al.Lower limb giant cell arteritis and temporal arteritis followup of 8 cases.J Rheumatol. 2001; 28: 1407-1412PubMed Google Scholar and GCA is usually not considered a clinically relevant cause of lower limb ischemia. We report the cases of four patients who recently presented to our institution for claudication or critical ischemia of the lower limbs and who were found to have GCA of the femoropopliteal and crural arteries. Based on this experience, we believe that symptomatic GCA of the lower limb arteries may be a more common clinical problem than previously assumed. We have reviewed the symptoms, the physical findings, and the results of vascular imaging studies of these four patients to identify the characteristic clinical features 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 the only symptom. One patient had classic temporal arteritis with unilateral loss of vision, three patients complained of fatigue, myalgia, and arthralgia, and two patients had oligo- or asymptomatic involvement of the axillary and brachial arteries evident on physical examination. Systemic symptoms, polymyalgia rheumatica, classic symptoms of temporal arteritis, or signs of upper limb involvement may therefore provide the first clinical indication of GCA in patients presenting with rapidly progressive lower limb ischemia. Markedly elevated ESR and CRP are a hallmark for the diagnosis of GCA.1Salvarani C. Cantini F. Boiardi L. Hunder G.G. Polymyalgia rheumatica and giant-cell arteritis.N Engl J Med. 2002; 347: 261-271Crossref PubMed Scopus (606) Google Scholar ESR and CRP were severely elevated in all our patients, thus supporting the usefulness of laboratory tests for systemic inflammation in patients with claudication and suspected large-vessel vasculitis. A temporal artery biopsy specimen positive for GCA is generally considered diagnostic proof. Extracranial arteries are not readily accessible for biopsy. However, histologic proof of temporal arteritis may also be obtained in patients presenting only with symptoms of extracranial involvement. In the largest series of histologically documented extracranial GCA, the rate of positive temporal artery biopsy specimens was 25%.4Lie J.T. Aortic and extracranial large vessel giant cell arteritis a review of 72 cases with histopathological documentation.Semin Arthritis Rheum. 1995; 24: 422-431Abstract Full Text PDF PubMed Scopus (207) Google Scholar Two of three temporal artery biopsy specimens were positive in our patients. This finding confirms that temporal artery biopsy is worthwhile in patients with suspected extracranial GCA. Abnormal findings on duplex sonography of the temporal artery may facilitate the selection of the biopsy site and increase the likelihood of a positive biopsy result. In a recent meta-analysis, ultrasonography of the temporal artery achieved moderate sensitivity (69%) but good specificity (82%) for the diagnosis of temporal arteritis compared with temporal biopsy.16Karassa F.B. Matsagas M.I. Schmidt W.A. Ioannidis J.P.A. Meta-analysis test performance of ultrasonography for giant-cell arteritis.Ann Intern Med. 2005; 142: 359-369Crossref PubMed Scopus (276) Google Scholar Patients presenting with symptoms of lower limb ischemia are frequently evaluated by digital subtraction angiography. We performed a digital subtraction angiography on patients 1 and 2, who presented with critical lower limb ischemia. Patient 2 had long, smooth narrowing of the popliteal arteries and multiple "beaded" stenoses of the deep femoral arteries (Fig 2, B), which would be unusual for arteriosclerotic vascular disease. Several of our angiographic findings closely resemble arteriosclerosis, however. The femoropopliteal obstructions shown in Fig 1, B and the extensive occlusions of tibial and peroneal arteries present in both patients (Figs 1, C and 2, C) are indistinguishable from advanced arteriosclerosis and resemble diabetic peripheral arterial disease. Long, smooth, or beaded appearance of arterial stenoses is believed to be suggestive of vasculitis on angiography.17Stanson A.W. Klein R.G. Hunder G.G. Extracranial angiographic findings in giant cell (temporal) arteritis.Am J Roengenol. 1976; 127: 957-963Crossref PubMed Scopus (43) Google Scholar These findings are not specific, however. Beaded stenoses are also typical of fibromuscular dysplasia,18Slovut D.P. Olin J.W. Fibromuscular dysplasia.N Engl J Med. 2004; 350: 1862-1871Crossref PubMed Scopus (617) Google Scholar and long, smooth arterial narrowing may be seen in other noninflammatory conditions such as postinterventional myointimal hyperplasia, ergotism, or after dissection. The distinction between vasculitis and other nonarteriosclerotic vascular disorders should, therefore, include patient history, distribution of the disease, laboratory tests for inflammation, and assessment of arterial wall morphology by other imaging techniques. Our data suggest that the angiographic diagnosis of large vessel vasculitis is particularly unreliable in the femoropopliteal and tibioperoneal arteries, where the angiographic appearance of inflammatory arterial lesions may be very similar to arteriosclerotic vascular disease. Suspicion of the presence of a nonarteriosclerotic, inflammatory vascular disease was initially triggered in our patients by the results of duplex sonography. Large-vessel vasculitis leads to long, circular, hypoechogenic thickening of the arterial wall, which may be accompanied by a perivascular, hypoechogenic halo.8Schmidt W.A. Blockmans D. Use of ultrasonography and positron emission tomography in the diagnosis and assessment of large-vessel vasculitis.Curr Opin Rheumatol. 2005; 17: 9-15Crossref PubMed Scopus (118) Google Scholar The sensitivity and specificity of duplex ultrasound imaging for the detection of extracranial large-vessel vasculitis has not been studied systematically. Published reports on sonographic findings in extracranial GCA and Takayasu's arteritis,8Schmidt W.A. Blockmans D. Use of ultrasonography and positron emission tomography in the diagnosis and assessment of large-vessel vasculitis.Curr Opin Rheumatol. 2005; 17: 9-15Crossref PubMed Scopus (118) Google Scholar as well as our own experience with these patients, suggest that smooth, circular, hypoechogenic wall thickening of long arterial segments is virtually pathognomonic for large-vessel vasculitis. We have observed a similar sonographic appearance only in myointimal hyperplasia after balloon angioplasty, a condition easily distinguishable from vasculitis by patient history and lack of systemic inflammation. All of our patients had these typical sonographic changes in the involved vascular segments. The hypoechogenic wall thickening was visible in the stenosed and in the occluded arterial segments (Fig 4) and was easily detectable even in the distal tibial and peroneal arteries (Fig 3). Lacking histologic proof of vasculitis from the peripheral arteries, we cannot totally exclude the coincidence of GCA and lower limb arteriosclerosis in our patients. However, based on the typical sonographic appearance of the affected arteries, the absence of generalized arteriosclerosis, and the sudden onset of claudication simultaneously with the systemic symptoms of GCA, we consider arteriosclerotic peripheral arterial disease highly unlikely. We performed contrast-enhanced MRI of the popliteal region on patient 1 and were able to detect marked thickening and inflammatory enhancement in the wall of the right popliteal artery (Fig 5). MRI has been shown to have high sensitivity and specificity for the detection of the circular wall thickening in large-vessel vasculitis.9Choe Y.H. Han B.K. Koh E.M. Kim D.K. Do Y.S. Lee W.R. Takayasu's arteritis assessment of disease activity with contrast-enhanced MR imaging.AJR. 2000; 175: 505-511Crossref PubMed Scopus (145) Google Scholar, 10Narvaez J. Narvaez J.A. Nolla J.M. Sirvent E. Reina D. Valverde J. Giant cell arteritis and polymyalgia rheumatica usefulness of vascular magnetic resonance imaging studies in the diagnosis of aortitis.Rheumatol. 2005; 44: 479-483Crossref PubMed Scopus (96) Google Scholar Most studies have focused on the aorta and its major branches, however, and only very limited data are available on the performance of MRI in the femoropopliteal or even tibioperoneal region. Presently, we believe that MRI is particularly valuable for the evaluation of central vascular regions not readily accessible for high-resolution ultrasonography. A disadvantage of ultrasonography is the persistence of mural thickening during treatment and the resulting lack of correlation between sonographic findings and disease activity.8Schmidt W.A. Blockmans D. Use of ultrasonography and positron emission tomography in the diagnosis and assessment of large-vessel vasculitis.Curr Opin Rheumatol. 2005; 17: 9-15Crossref PubMed Scopus (118) Google Scholar The degree of contrast enhancement detected by MRI may prove superior to sonographic measurements of wall thickness for the follow-up of disease activity.9Choe Y.H. Han B.K. Koh E.M. Kim D.K. Do Y.S. Lee W.R. Takayasu's arteritis assessment of disease activity with contrast-enhanced MR imaging.AJR. 2000; 175: 505-511Crossref PubMed Scopus (145) Google Scholar, 10Narvaez J. Narvaez J.A. Nolla J.M. Sirvent E. Reina D. Valverde J. Giant cell arteritis and polymyalgia rheumatica usefulness of vascular magnetic resonance imaging studies in the diagnosis of aortitis.Rheumatol. 2005; 44: 479-483Crossref PubMed Scopus (96) Google Scholar Recently, 18F-FDG-PET has been introduced in the evaluation of GCA and Takayasu's arteritis with very promising results. This method allows the direct assessment of vascular inflammation on a whole-body scale, and the level of vascular FDG uptake was shown to correlate well with changes in inflammatory activity during treatment.11Turlakow A. Yeung H.W.D. Pui J. Macapinlac H. Liebovitz E. Rusch V. et al.Fludeoxyglucose positron emission tomography in the diagnosis of giant cell arteritis.Arch Intern Med. 2001; 161: 1003-1007Crossref PubMed Scopus (104) Google Scholar, 12Belhocine T. Blockmans D. Hustinx R. Vandevivere J. Mortelmans L. Imaging of large vessel vasculitis with 18FDG PET:illusion or reality? A critical review of the literature data.Eur J Nucl Med Mol Imaging. 2003; 30: 1305-1313Crossref PubMed Scopus (146) Google Scholar, 13Webb M. Chambers A. Al-Nahhas A. Mason J.C. Maudlin L. Rahman L. et al.The role of 18F-FDG PET in characterising disease activity in Takayasu arteritis.Eur J Nucl Med Mol Imaging. 2004; 31: 627-634Crossref PubMed Scopus (215) Google Scholar, 19Meller J. Strutz F. Scheel A. Sahlmann C.O. Lehmann K. Conrad M. et al.Early diagnosis and follow-up of aortitis with 18F-FDG PET and MRI.Eur J Nucl Med Mol Imaging. 2003; : 730-736Crossref PubMed Scopus (341) Google Scholar A high aortal FDG-uptake was shown to have a sensitivity of 92% and a specificity of 100% for the diagnosis of Takayasu's arteritis.13Webb M. Chambers A. Al-Nahhas A. Mason J.C. Maudlin L. Rahman L. et al.The role of 18F-FDG PET in characterising disease activity in Takayasu arteritis.Eur J Nucl Med Mol Imaging. 2004; 31: 627-634Crossref PubMed Scopus (215) Google Scholar Vascular FDG uptake in the large thoracic arteries has been reported in 14 (56%) of 25 patients with GCA compared with 2% of control subjects.20Blockmans D. Stroobants S. Maes A. Mortelmans L. Positron emission tomography in giant cell arteritis and polymyalgia rheumatica evidence for inflammation of the aortic arch.Am J Med. 2000; 108: 246-249Abstract Full Text Full Text PDF PubMed Scopus (300) Google Scholar The same study reports vascular uptake in the arteries of the legs in 64% of GCA patients and in 23% of controls. This finding suggests an unexpectedly high frequency of lower limb involvement in GCA, but also a lower specificity of vascular FDG uptake in the arteries of the legs. Arterial inflammation due to arteriosclerosis is believed to be the cause of vascular FDG uptake seen in elderly subjects.21Yun M. Yeh D. Arujo L.I. Jang S. Newberg A. Alavi A. F-18 FDG uptake in the large arteries. A new observation.Clin Nucl Med. 2001; 26: 314-319Crossref PubMed Scopus (220) Google Scholar Most investigators agree that FDG uptake due to arteriosclerosis is usually mild, whereas a high level of uptake is suggestive of vasculitis. A cut-off level for distinguishing between vasculitis and arteriosclerosis has not been defined, however. Presently, 18F-FDG-PET appears to be most valuable for the early diagnosis of large-vessel vasculitis in young patients with unspecific symptoms. In elderly patients with GCA, the results of 18F-FDG-PET need to be interpreted carefully together with the clinical findings and the results of other vascular imaging tests. Under these conditions, 18F-FDG-PET provides a unique opportunity to study the distribution of extracranial vascular inflammation in GCA patients. Moreover, 18F-FDG-PET may prove to be a very valuable technique for the follow-up of inflammatory activity during treatment of large-vessel vasculitis.19Meller J. Strutz F. Scheel A. Sahlmann C.O. Lehmann K. Conrad M. et al.Early diagnosis and follow-up of aortitis with 18F-FDG PET and MRI.Eur J Nucl Med Mol Imaging. 2003; : 730-736Crossref PubMed Scopus (341) Google Scholar The results of 18F-FDG-PET in our patients confirm a high degree of tracer uptake in the arterial segments clinically and sonographically affected by vasculitis. Severe vascular FDG uptake was limited to the popliteal and crural arteries in patients 1 (Fig 6) and 4 and also included the axillary arteries in patient 3. To our knowledge, this is the first report of calf artery GCA detected by 18F-FDG-PET, thus indicating a high sensitivity of this technique even in peripheral, medium-sized arteries. It is remarkable that none of our patients had evidence of aortic or iliac artery involvement. This finding suggests that if GCA affects the lower limbs, the disease involves preferentially the crural, femoropopliteal, and deep femoral arteries. In contrast, large-vessel vasculitis involving the aorta and iliac arteries may represent a different clinical entity more closely related to Takayasu's arteritis. In the future, more widespread use of 18F-FDG-PET may help to assess the true frequency and pattern of extracranial involvement in GCA. The mainstay of treatment of GCA is immunosuppression with prednisone. Previous reports indicate that invasive vascular reconstructions can be avoided in most GCA patients with peripheral artery involvement.7Le Hello C. Levesque H. Jeanton M. Cailleux N. Galateau F. Peillon C. et al.Lower limb giant cell arteritis and temporal arteritis followup of 8 cases.J Rheumatol. 2001; 28: 1407-1412PubMed Google Scholar Our follow-up data suggest that even patients with advanced lower limb ischemia due to GCA can improve substantially with adequate immunosuppressive treatment and medical management of peripheral arterial disease.