Rheumatology 2004; 43: 679
Rheumatology Vol. 43 No. 5 (c) British Society for Rheumatology 2004; all rights reserved
Letter to the Editor |
Fluorodeoxyglucose positron emission tomography for the diagnosis of giant cell arteritis
Internal Medicine and 1Rheumatology Unit, San Camillo Hospital, Rome and 2Department of Experimental Medicine, University of L’Aquila, L’Aquila, Italy
Correspondence to: G. Famularo, Department of Internal Medicine, San Camillo Hospital, Circonvallazione Gianicolense, 00152, Rome, Italy. E-mail: gfamularo{at}scamilloforlanini.rm.it
SIR, Brodmann et al. [1] report interesting results with the use of 2-18F-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (F18-FDG-PET) for the diagnosis of giant cell arteritis. However, we argue that the practical application of F18-FDG-PET may have important limitations in the clinical setting. The method indeed failed to disclose the involvement of the temporal arteries in the only two patients with clinical signs of temporal arteritis and the discrepancy in both cases with the finding on duplex sonography of hypoechogenic hyperplasia of the neointima is also disappointing.
One simple explanation could be that the temporal arteries were not involved by the vasculitis and the clinical signs consistent with a diagnosis of temporal arteritis were not correctly interpreted. An alternative and more appealing hypothesis is that those patients no longer had an active inflammation of the artery, with thickening and outgrowth of the intima being the morphological hallmarks of the disease process rather than a transmural inflammation. This should not be surprising if we consider that F18-FDG-PET has high sensitivity for the detection of the metabolic changes associated with inflammation in the arterial wall [2]. It is worth noting that the finding of intimal hyperplasia with a modest, or even absent, inflammatory infiltrate is not by itself in contrast with the diagnosis of giant cell arteritis [3, 4]. Some patients have only a small-vessel vasculitis surrounding an otherwise normal temporal artery [5] and, in other cases, thickening of the intima, which is a non-specific response of arterial vessels to injury, could be the only histological abnormality [3, 4]. We have no information about the histology of temporal arteries in those two patients with negative findings on F18-FDG-PET but, if our postulate is correct, the study by Brodmann et al. seems to suggest that F18-FDG-PET might be inaccurate for the detection of the clinically most important subgroup of patients with giant cell arteritis, i.e. those with a lumen-occlusive disease who are at especially high risk for vascular insufficiency and tissue ischaemia. It is known that giant cell arteritis does not necessarily result in luminal stenosis and may proceed without compromising blood flow [6]. However, when the response pattern of the arterial wall to injury is switched towards an unbalanced production of platelet-derived and vascular endothelial growth factors, proliferation of myofibroblasts and deposition of extracellular matrix become central events early in the course of the disease and exuberant intimal hyperplasia rapidly ensues leading to luminal stenosis [6]. Under these circumstances, severe ischaemic complications such as jaw claudication, headache or visual loss are often an early manifestation of the disease, and this could be substantially independent of the presence of an inflammatory infiltrate in the arterial wall.
In our opinion, recognizing giant cell arteritis remains a clinical skill. If the clinical picture is consistent with the diagnosis and a syndrome of systemic inflammation is present, conventional X-ray angiography and digital subtraction angiography remain the imaging procedures of choice to assess vessel anatomy and luminal status. An appropriately performed biopsy of the temporal artery, with the surgeon asked to obtain a fairly long specimen as the pathological findings may be patchy, stands as the benchmark test to confirm the diagnosis. For an imaging procedure to be valuable in clinical practice, it should be able to add diagnostic or prognostic information to available methods at a reasonable cost and help to guide patient management. This has not yet been definitely shown for F18-FDG-PET. Using sophisticated technologies carries the risk of providing results that are potentially misleading for clinicians.
The authors have declared no conflicts of interest.
References
- Brodmann M, Passath A, Aigner R et al. F18-PDG-PET as a helpful tool in the diagnosis of giant cell arteritis. Rheumatology 2003;42:1264–6.
[Free Full Text] - Turlakow A, Yeung HW, Pui J et al. Fludeoxyglucose positron emission tomography in the diagnosis of giant cell arteritis. Arch Intern Med 2001;161:1003–7.
[Abstract/Free Full Text] - Salvarani C, Cantini F, Boiardi L, Hunder GG. Polymyalgia rheumatica and giant-cell arteritis. N Engl J Med 2002;347:261–71.
[Free Full Text] - Weyand CM, Goronzy JJ. Giant-cell arteritis and polymyalgia rheumatica. Ann Intern Med 2003;139:505–15.
[Abstract/Free Full Text] - Esteban M-J, Font C, Hernandez-Rodriguez J et al. Small-vessel vasculitis surrounding a spared temporal artery: clinical and pathological findings in a series of twenty-eight patients. Arthritis Rheum 2001;44:1387–95.[CrossRef][Web of Science][Medline]
- Weyand CM, Goronzy JJ. Medium- and large-vessel vasculitis. N Engl J Med 2003;349:160–9.
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