Rheumatology Advance Access originally published online on November 18, 2006
Rheumatology 2007 46(4):672-677; doi:10.1093/rheumatology/kel376
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Repetitive 18-fluorodeoxyglucose positron emission tomography in isolated polymyalgia rheumatica: a prospective study in 35 patients
Department of General Internal Medicine and 1Department of Nuclear Medicine, University Hospital Gasthuisberg, Leuven, Belgium.
Correspondence to: D. Blockmans, MD, PhD, Department of General Internal Medicine, University Hospital Leuven, Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. E-mail: Daniel.Blockmans{at}uz.kuleuven.ac.be
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Abstract |
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Objective. To study fluorodeoxyglucose (FDG) deposition in different vascular beds and in the large joints of patients with isolated polymyalgia rheumatica (PMR), and to investigate whether there is a relation between FDG-positron emission tomography (PET) results and risk of relapse.
Methods. All consecutive patients with isolated PMR underwent a FDG–PET scan before treatment with steroids was started and—if logistics allowed—at 3 and 6 months. PET scans were scored at seven different vascular areas and a total vascular score (TVS) was calculated, ranging from 0 to 21. FDG uptake in the shoulders, the hips and the processi spinosi of the vertebrae was scored as 0 (no uptake), 1 (moderate uptake) or 2 (intense uptake).
Results. Thirty-five patients entered the study. At diagnosis, vascular FDG uptake was noted in 11 patients (31%), predominantly at the subclavian arteries. Mean TVS was low. FDG uptake in the shoulders was noted in 94% of patients, in the hips in 89% and in the processi spinosi of the vertebrae in 51%. The intensity of FDG uptake in the large vessels or in the shoulders, hips or processi spinosi did not correlate with the risk of relapse.
Conclusions. Only one in three patients has an (moderately) increased vascular FDG uptake, especially in the subclavian arteries. The vast majority has inflammation of shoulders and hips, and half of them have increased FDG-uptake at the processi spinosi. Results of FDG–PET scans in patients with PMR did not correlate with their risk of relapse.
KEY WORDS: Polymyalgia rheumatica, Positron emission tomography, Vasculitis, Giant cell arteritis
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Introduction |
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Polymyalgia rheumatica (PMR) is a clinical syndrome of proximal muscle pain and stiffness in patients over 50 yrs of age. PMR is diagnosed by the exclusion of other disorders that can cause similar complaints and by its rapid response to low-dose corticosteroids [1, 2]. PMR can occur as an isolated condition or concomitantly with giant cell arteritis (GCA): about 40% of patients with this type of large vessel vasculitis have PMR complaints [3].
The exact nature of PMR is not known: is it a form of vasculitis limited to the subclavian or axillary arteries, or is it a synovitis or perisynovitis of the shoulders and/or hips?
Previous studies from our group with fluorodeoxyglucose–positron emission tomography (FDG–PET) scans in patients with GCA and/or PMR suggested that PMR might have a vasculitic nature [4]. In a recent larger trial of patients with biopsy-proven GCA, combined PMR complaints correlated with increased FDG uptake in the shoulders, but not with FDG uptake in the subclavian or axillary arteries [5].
In the present study, we wanted to study FDG uptake in patients with isolated PMR, without signs of GCA on temporal artery biopsy.
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Patients and methods
All consecutive patients admitted to the General Internal Medicine Department of our university hospital between May 2000 and July 2003 with a clinical diagnosis of isolated PMR underwent a FDG–PET scan before treatment with steroids was started. A unilateral temporal artery biopsy (2 cm or greater in length) to actively exclude GCA was ordered, except when patients formally refused. Isolated PMR was diagnosed if the following clinical symptoms were present: age > 50 yrs, bilateral aching or morning stiffness lasting
30 min, persisting for at least 1 month, and involving two of the following three areas: neck, shoulder or proximal regions of the arms, hips or proximal thighs, and exclusion of other diseases which could provoke these symptoms. Typical symptoms of GCA (visual disturbances, headache or jaw claudication) had to be absent and temporal artery biopsy had to be negative. Patients with positive temporal artery biopsies were included in another, similar trial, which was published elsewhere [5]. Patients fasted for at least 6 h before PET scanning. One hour before imaging, a weight-related dose of FDG was injected intravenously [dose (MBq) = Weight (kg) x 4 + 20]. Whole body images were obtained using a Siemens PET HRplus scanner with an axial field of view of 15.5 cm. PET scans were scored independently by two nuclear medicine specialists who were unaware of the treatment of the patient (before treatment, after 3 or 6 months). If their scores differed, they had to reach a consensus. PET scans were scored at seven different vascular regions (thoracic aorta, abdominal aorta, subclavian arteries, axillary arteries, carotid arteries, iliac arteries and femoral arteries) as negative (0) or positive, further scored semi-quantitatively as 1 (minimal but not negligible FDG uptake), 2 (clearly increased FDG uptake) or 3 (very marked FDG uptake). Hence, a ‘total vascular score’ (TVS) could be calculated ranging from 0 (no vascular FDG uptake in any of the seven vascular regions) to 21 (vascular FDG uptake scored 3 in all seven territories). Both subclavian, axillary, carotid, iliac and femoral arteries were counted as one vascular region; when the score differed from right to left artery, the highest score was taken for that vascular region. FDG uptake in the shoulder and hip regions and in the processi spinosi of the vertebrae was scored as 0 (no uptake), 1 (moderate uptake) or 2 (intense uptake).
PET scans were repeated—as far as logistical limitations allowed—at 3 and 6 months. A patient was said to relapse if (i) there was a recrudescence of compatible clinical symptoms (morning stiffness, proximal girdle pain) and an increase in inflammatory parameters (sedimentation rate >40 mm/h and/or C-reactive protein (CRP) >30 mg/l), or (ii) the reoccurrence of compatible clinical symptoms was not associated with increased inflammatory parameters but persisted over a 4-week period. An isolated increase in CRP or sedimentation rate without clinical symptoms was not considered a relapse. When patients relapsed, they ended the study.
Treatment for all patients consisted of 12 mg methylprednisolone/day as starting dose for 2 weeks, followed by 8 mg/day for 4 weeks, 6 mg/day for 6 weeks, 4 mg/day for 7 weeks, 2 mg/day for another 7 weeks and then stopped. Hence, the total therapy lasted 26 weeks. Patients were seen at each dose adjustment and every 3 months after the end of therapy for possible late relapses. All patients received calcium tablets and vitamin D for osteoporosis prevention. All female patients underwent a bone mineral content measurement, and when the T-score at the lumbar spine or the femoral neck was <2.5 SDs, biphosphonates were additionally prescribed. Follow-up was closed end of December 2004.
The protocol of the study was approved by the local Ethical Committee of the University Hospital Gasthuisberg, Leuven, Belgium and all patients gave informed consent, according to the Declaration of Helsinki.
Statistical analysis
All values are given as means and SD. All P-values were two-sided and considered significant if <0.05. Chi-square test was used to compare ordinal variables and Wilcoxon signed ranks test to compare continuous variables.
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Patients
Thirty-six patients (16 males, 20 females) entered the study. One patient was excluded later on since his condition turned out to be seronegative rheumatoid arthritis rather than PMR. In the remaining 35 patients (15 males, 20 females, mean age 68.5 ± 7.2 yrs, mean age of males 67.8 ± 6.5 yrs, mean age of females 69.0 ± 7.8 yrs), our clinical diagnosis of PMR was sustained throughout follow-up. Chuang [1] and Healey [2] criteria for PMR were met in 30 patients, the five remaining patients had a sedimentation rate <40 mm/h at diagnosis (19, 20, 30, 31 and 37 mm/h, respectively). Temporal artery biopsy was performed in 30 patients and was always negative. Mean sedimentation rate of the whole group at diagnosis was 70 ± 32 mm/h, mean CRP level was 79 ± 52 mg/l (normal <5 mg/l).
Vascular FDG uptake
At diagnosis, vascular FDG uptake was noted in 11 patients (31%): vascular uptake was slight or moderate in nine patients (TVS was one in six patients, two in two patients and three in one patient) and rather intense in two patients (TVS: seven). In 10 of these 11 patients, vascular uptake was seen in the subclavian arteries, in four patients there was also FDG uptake in the thoracic aorta, in two patients each the axillary arteries, the abdominal aorta and the iliac arteries took up FDG and in one patient each there was FDG uptake in the femoral and carotid arteries. Mean TVS of all 35 patients was 0.8 ± 1.7.
At 3 months therapy, while patients were taking 6 mg methylprednisolone/day, the sedimentation rate had decreased to 14 ± 10 mm/h (n = 30) and CRP levels to 6.7 ± 7.6 mg/l (n = 33). FDG–PET scan was repeated in 22 patients, including 8 of the 11 patients with vascular FDG uptake at diagnosis. In these eight patients, vascular FDG uptake had disappeared in three (TVS went from 1 at diagnosis to 0 at 3 month in all the three patients), it remained unchanged in three patients (TVS twice 1 and once 2) and it decreased in two patients (TVS from 2 to 1 in one patient, from 7 to 1 in another patient). In 14 patients without vascular FDG uptake at diagnosis, TVS remained at zero in 13 patients and scored 1 in one patient. Mean TVS of these 22 patients decreased from 0.7 ± 1.5 at baseline to 0.3 ± 0.6 (P = 0.096) at 3 months.
At the end of therapy at 6 months, mean sedimentation rate was 18 ± 18 mm/h (n = 28) and CRP level was 9.3 ± 12.1 mg/l (n = 29). Nine patients underwent a third PET scan, including the four patients with vascular FDG uptake at 3 months. TVS had become negative in one patient, it had remained at 1 in another patient (who did a relapse at that moment) and in the two remaining patients, there was a slight increase in TVS from 1 to 2 and from 2 to 3, respectively. In five other patients in whom PET was done at 6 months, TVS was always scored zero. Mean TVS of these nine patients remained unchanged from 3 months (mean TVS 0.6 ± 0.7) to 6 months (mean TVS 0.7 ± 1.1).
The distribution of TVS at diagnosis, at 3 and at 6 months of therapy is given in Fig. 1.
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FDG uptake in the shoulders, hips and processi spinosi of the vertebrae
FDG uptake in these regions is shown in Fig. 2, at diagnosis (A), at 3 months (B) and at 6 months of therapy (C). At baseline, FDG uptake in the shoulders was present in all but two patients. Mean score for the shoulders decreased significantly from 1.7 ± 0.6 at diagnosis to 1.1 ± 0.5 at 3 months therapy (P = 0.001), which is due to a shift in the scoring system from 2 to 1; again only two patients had no FDG uptake in the shoulders after 3 months of steroid therapy. After 6 months of therapy, there is no further decrease in FDG uptake in the shoulders (mean score 1.1 ± 0.8). Mean score for the hips drops from 1.3 ± 0.7 at baseline to 0.7 ± 0.6 at 3 months (P < 0.0005), but again, there is no further decrease at 6 months (mean score 0.8 ± 0.8). Mean score for the processi spinosi goes from 0.6 ± 0.7 at diagnosis to 0.4 ± 0.6 (P = 0.021) at 3 months and to 0.3 ± 0.7 at the end of therapy. At diagnosis, FDG uptake was seen in the processi spinosi of the lumbar vertebrae in 15 patients, at the dorsal level in seven patients (of whom five had also an increased FDG uptake in the processi spinosi of the lumbar spine) and in the cervical spine in three patients (of whom two also at the lumbar level).
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Figure 3 shows an example of FDG–PET pictures at diagnosis (A) and at 3 months (B) of therapy.
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Relation between FDG–PET results and risk of relapse
All patients were followed-up until they relapsed, or until 31 December 2004 for those who remained relapse free. Two patients were lost to follow-up very early in the study. One patient did not come back to her control visit at 12 weeks as she was afraid of undergoing a second PET scan; a second patient could not come to the hospital any more since her husband had died. These two patients were further treated by their general practitioner. Nineteen patients (19/33 = 58%) had a relapse of their disease, a mean of 5.9 ± 1.9 months after the start of therapy. Two patients had their relapse already at 1.5 and 3 months of therapy, respectively, taking 6 mg and 4 mg methylprednisolone/day each. Their TVS at diagnosis was zero in both, as well as their TVS at the time of relapse. Fourteen patients remained without relapse, after a mean follow-up of 37.0 ± 11.4 months.
There was no relation between the height of the inflammatory parameters at diagnosis and the likelihood to relapse: baseline sedimentation rate was 79 ± 33 mm/h in those who relapsed, 63 ± 29 mm/h in those who did not (P = 0.23); CRP was 94 ± 51 mg/l in those who relapsed, 66 ± 50 mg/l in those who did not (P = 0.10).
Patients who relapsed did not have more vascular FDG uptake at diagnosis, compared with those who did not (mean TVS 0.5 ± 0.9 vs 0.7 + 1.9, P = 0.81), nor at 3 months (mean TVS 0.4 ± 0.6 vs 0.2 ± 0.4, P = 0.69). At the end of the 6 months of therapy, seven patients who relapsed had a new PET scan. It did not show any vascular FDG uptake in five patients, while TVS was one and three, respectively, in the remaining patients. Two patients who did not relapse had a third PET scan: TVS was zero in one and two in the other.
Table 1 shows the mean scores for FDG uptake in the shoulders, the hips and the processi spinosi at the three time points (at diagnosis, at 3 months of therapy and at the end of therapy), for those who relapsed and for those who did not relapse. There was no difference in FDG uptake in the shoulders, hips or processi spinosi at diagnosis or at 3 months of therapy in the patients who relapsed vs those who did not. Two patients in fact had their relapse at 3 months of therapy. Their vascular score at that time was zero, FDG uptake in shoulders and hips was scored 1 and the processi spinosi did not take up FDG in neither patient.
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At the end of therapy, there was no further decrease in FDG uptake in the patients who relapsed compared with 3 months of therapy. This might be due to the fact that six of the seven patients who relapsed and underwent a third PET scan, had their relapse very shortly after that third PET scan: at 6 months (around the time of the PET scan, two patients), 7 months (1 month after the PET scan, two patients), 8 months (2 months later, one patient) and 9 months (3 months later, one patient). The number of patients who did not relapse and had a PET scan at 6 months was too small (n = 2) to reach statistical significance in terms of FDG uptake in the shoulders, hips or processi spinosi with the seven patients who relapsed and had a PET scan at 6 months.
A flow diagram, clarifying the conduct of the study, is given in Fig. 4.
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Discussion |
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Our results using FDG–PET confirm those of other radioisotopic studies, arthroscopic studies, ultrasonographic studies and magnetic resonance imaging that PMR is a manifestation of a synovitis of the proximal joints [6–10]. The distinction between perisynovitis and synovitis is, however, hard to make on a PET scan, due to the low resolution of the pictures. The vast majority of our patients with isolated PMR had increased FDG uptake in the shoulders and hips. In a former study by our group, we noted increased FDG uptake in the shoulders in 14/44 (32%) of the control patients, who were matched for age and inflammatory parameters with 25 GCA/PMR patients [4]. Five of these control patients were diagnosed as rheumatoid arthritis patients, one each as reactive arthritis and psoriatic arthritis. We can imagine that periarthritis scapulo-humeralis or chondrocalcinosis also may induce an increased FDG uptake in the shoulders. Therefore, FDG uptake in the shoulders or hips has a low specificity for PMR, but a high sensitivity.
Another advantage of performing FDG–PET scans in patients with PMR-like symptoms is the possible detection of underlying disorders responsible for these complaints. This was not the case in our patients, but it is reported in the literature [11].
What is new, and came to us as a surprise, is a clearly increased FDG uptake in the processi spinosi of the lumbar > dorsal > cervical vertebrae in half of our patients. This involvement may be responsible for the morning stiffness in the back in PMR patients.
Vascular involvement was noticed in 31% of patients at baseline, mostly a very mild one with vascular scores ranging from 1 to 3 (with a maximum of 21). Two patients (both with negative temporal artery biopsies) had a clearly more pronounced FDG uptake in their arteries, resulting in a TVS of seven each. Compared with our patients with GCA [5], vascular involvement is significantly less frequent and less intense in isolated PMR patients. Mean TVS at baseline of 35 GCA patients was 6.0 ± 6.2 [5], compared with 0.8 ± 1.7 in our 35 patients with isolated PMR. These results contrast with former work by our group [4, 12], in which a more intense vascular involvement in PMR was suspected. These former studies however were on fever PMR patients (12 and 5 patients, respectively), and it is possible that some of the patients who were considered isolated PMR suffered in fact from large vessel vasculitis not affecting the temporal arteries, a condition not well-known at that time [13].
Our results confirm the close relationship between GCA and PMR: 37% of the 35 GCA patients had PMR complaints (which correlated with increased FDG uptake in the shoulders) [5], while 31% of the patients with isolated PMR, presented here (in whom GCA was actively excluded by a negative temporal artery biopsy in all but five patients), had an increased FDG uptake in the larger arteries, especially the subclavian arteries. The results of the present study, with a rather low incidence and intensity of vascular FDG uptake, contrast with those of Moosig et al. [14] who reported an increased tracer uptake of the aorta or its proximal branches in 12 of their 13 PMR patients. However, three of their patients had biopsy-proven GCA, one patient had a normal temporal artery biopsy, and in the other 9 patients temporal artery biopsy was not performed, owing to very low pre-test probability [14]. In our study, 30 out of the 35 patients agreed to undergo temporal artery biopsy, which was always normal. We judged it unnecessary to let our patients undergo a bilateral artery biopsy since this improves the diagnostic yield in only 3%, whereas in 97% of patients the two biopsy specimen share the same finding [15]. Five of our 35 patients did not fulfil Chung or Healey criteria for PMR, since their sedimentation rate at diagnosis did not reach 40 mm/h; however, their clinical picture was typical of PMR. Therefore, we decided to include these five patients in our analysis, since some studies have reported that 7–20% of patients with PMR have a normal sedimentation rate at the time of diagnosis [16].
Weyand et al. [17, 18] found very similar levels of messenger RNA for inflammatory cytokines in temporal artery biopsies of patients with GCA and in patients with isolated PMR, clearly different from patients without these diseases. Interferon-
, however, is only produced in GCA and not in PMR, which suggests that this cytokine may be crucial for the development of frank vasculitis. Cantini et al. [3] reported that 42 of their 92 (46%) patients with biopsy-proven GCA observed over a 5-yr period had PMR. PMR developed before GCA in eight patients, simultaneously in 21 and after the diagnosis of GCA in 13. Conversely, they found that 12 of 76 (16%) consecutive patients with PMR had histological evidence of GCA, but only one (1.3%) of these patients did not have any clinical manifestation of GCA. Therefore, these authors suggest to perform temporal artery biopsies only in PMR patients with cranial symptoms and/or signs [3].
As could be expected, repetitive PET scintigraphy after 3 months of steroid treatment resulted in a decrease of TVS and a lower intensity of FDG uptake in shoulders, hips and processi spinosi. At 3 months all but two patients who relapsed around that time were asymptomatic and laboratory parameters of inflammation had significantly decreased. These lower FDG uptakes under treatment confirm older observations that FDG uptake diminishes under steroid therapy [12]. This decrease of FDG uptake probably reflects a lower disease activity, but sedimentation rate and CRP levels, which are much cheaper to perform, reflect the same. So this does not justify a repeat PET scan. What might have justified repeat PET scans would have been the finding that patients with higher vascular or articular FDG uptake were more prone to relapse, but this could not be concluded from the present study. In comparison with patients without relapse, patients who relapse have similar TVS, similar FDG uptake in the large joints and the processi spinosi, at baseline and at 3 months of therapy. PET scans at 6 months of therapy are hard to interpret, since at that time point, steroids were stopped and many patients relapsed around that time, reflected in a higher sedimentation rate and CRP level at 6 than at 3 months. Only two patients who had a repeat PET scan at 6 months did not relapse. Therefore, the number of patients without relapse was too low to reach statistical significance.
We decided to treat our patients with a relatively small starting dose (methylprednisolone 12 mg/day), with a relatively fast taper and cessation of steroid treatment at 6 months. By doing so, we had a relapse rate of 54%, but likewise, 40% of patients had stable remissions after a mean follow-up of 37.0 ± 10.9 months.
In conclusion, this study using FDG–PET scintigraphies in patients with isolated PMR has confirmed that PMR is mainly a (peri)synovitis of the larger joints, including the processi spinosi of the vertebrae. Vascular involvement is seen in about 30% of patients, but much less intense than what is found in GCA. Vascular and articular FDG uptake decreases during treatment with steroids, but FDG–PET results at the time of diagnosis and during steroid treatment do not predict which patients are at risk for later relapses. Therefore, we do not think that repetitive FDG–PET scans offer any advantage over the traditional follow-up of PMR patients, based on clinical evaluation and periodic determination of sedimentation rate and/or CRP levels. FDG–PET has a role in the diagnosis but not in prognostication or follow-up of PMR.
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The authors want to express their great gratitude to Mrs Helga Ceunen and Marina Lejeune, study nurses, for their valuable help in collecting the data.
The authors have declared no conflicts of interest.
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