Division of Angiology, Department of Internal Medicine, 1Division of Nuclear Medicine and Endocrinology, Department of Internal Medicine and 2Division of Nuclear Medicine, Department of Radiology, University Hospital Graz, Austria
Correspondence to:
M. Brodmann, Division of Angiology, Department of Internal Medicine, Karl Franzens University Graz, Auenbruggerplatz 15, A-8036 Graz, Austria. E-mail: marianne.brodmann{at}kfunigraz.ac.at
SIR, The diagnosis of giant cell arteritis and polymyalgia rheumatica remains a challenge, especially in patients presenting with non-specific symptoms [1]. Angiography and magnetic resonance angiography are standard diagnostic procedures. They may show non-specific lesions that cannot be differentiated from lesions of arteriosclerotic origin [2], and they cannot fully evaluate the extent of disease. Histological examinations are positive in only 70% of patients who also present with temporal artery involvement. All the other diagnostic tools involving clinical symptoms and laboratory parameters are also non-specific. Colour-coded duplex sonography with the typical findings of hypoechogenic intimal wall thickening seems to be one of the best diagnostic tools for this disease entity, although it is limited by the impossibility of scanning all the vascular regions that could potentially be affected, e.g. the thoracic vessels and aorta [3]. 2-18F-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (F18-FDG-PET) has shown promise in the diagnosis of vasculitic disorders [4, 5].
In a 6 month period, we saw seven patients (six females and one male) with a mean age of 71.9 yr (range 6178 yr) for whom colour-coded duplex sonography strongly suggested a diagnosis of giant cell arteritis, which was confirmed by F18-FDG-PET. One of them had undergone subclavian bypass surgery on her left upper extremity three times, twice for bypass graft reocclusion, accompanied by severe shoulder pain and deteriorating general condition. Two further patients presented with sudden onset of severe headache and three with severe pain in the neck and shoulders and worsened general condition. An extensive examination had ruled out other systemic disease, e.g. malignancy. The final patient presented with typical upper extremity claudication accompanied by malaise.
All patients showed differing extents of hypoechogenic hyperplasia of the neointima of the supra-aortic vessels. The two patients presenting with clinical signs of temporal arteritis showed additional involvement of the temporal arteries. Thickening of the neointima was also found in the iliac arteries and the abdominal aorta in two patients.
As indicators of disease activity, the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level were used. They were highly elevated at the time of diagnosis. All patients received prednisolone, starting with a high loading dose (2 mg/kg body weight per day), which led to rapid improvement of clinical symptoms. The patients were monitored by duplex sonography and clinical chemistry (ESR and CRP) at 1, 3 and 6 months, and by F18-FDG-PET 3 months after diagnosis. Two patients so far have had follow-up evaluations by both F18-FDG-PET and duplex sonography.
F18-FDG-PET confirmed the findings of duplex sonography as to the extent of intimal hyperplasia in the affected vessels, except in the patients with temporal artery involvement. In these patients there was no FDG uptake in the temporal vessels, in contrast to the other affected supra-aortic vessels. All but one patient showed FDG uptake in the ascending part of the aorta and the thoracic aorta.
In the two patients who had follow-up evaluations by both F18-FDG-PET and duplex sonography, along with the clinical improvement the inflammatory parameters normalized and the thickening of the neointima of the affected vessels was significantly reduced (from 0.27 to 0.14 cm). In these two patients, the follow-up F18-FDG-PET also showed significantly reduced FDG uptake in the affected vessels (Fig. 1A and B).
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When giant cell arteritis also affects the temporal arteries, a biopsy may easily be taken, but it is positive in only 70% of patients at best. Laboratory parameters are not specific. Colour-coded duplex sonography is the only diagnostic procedure so far that shows typical findings in the affected vessels, i.e. hypoechogenic neointimal thickening [3]. But some regions of interest cannot be scanned, so that the extent of disease cannot be determined with precision. With F18-FDG-PET, the whole body can be scanned on a single occasion and all the vascular regions are visible on one image. This is the first major advantage of this diagnostic procedure.
The second is the pathophysiological basis of the procedure itself, which involves increased accumulation of fluorine-18-fluorodesoxyglucose by inflammatory cells and granulation tissue [5]. When the acute inflammatory process improves, FDG uptake should be diminished, at least in the affected vessels. This was confirmed in the two patients for whom we have a follow-up F18-FDG-PET. Nevertheless, this pathophysiological basis can cause some false-positive results, as FDG uptake can occur in atherosclerotic lesions with an accumulation of inflammatory cells. Usually these images are less clearly positive and the distribution is different.
F18-FDG-PET not only seems to be a useful tool in the diagnosis of giant cell arteritis itself, but it also seems to be helpful in the evaluation of the extent and activity of the disease.
References