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High white blood cell count in patients with giant cell arteritis predicts an increased risk of stenosis in upper extremity arteries
  1. M Both1,
  2. K Schulte1,
  3. F Moosig2,
  4. E Fritzer3,
  5. WL Gross2,
  6. M Heller1,
  7. J Biederer1
  1. 1Department of Diagnostic Radiology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany
  2. 2Department of Rheumatology and Clinical Immunology, Vasculitis Center, University Hospital Schleswig-Holstein, Campus Luebeck and Klinikum Bad Bramstedt, Luebeck, Germany
  3. 3Institute of Medical Informatics and Statistics, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany
  1. Correspondence to Dr med Marcus Both, Department of Diagnostic Radiology, University Hospital Schleswig-Holstein, Campus Kiel, Arnold-Heller-Strasse 3, 24105 Kiel, Germany; mboth{at}rad.uni-kiel.de

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Stenosis of the arteries of the upper extremities occurs in 13–29% of patients with giant cell arteritis (GCA).1,,3 Endovascular therapy has been reported to be successful, especially prior to extensive vessel obstruction.4 Until now, no predictive parameter is known for the early identification of persons at risk of ischaemic disease of the upper limbs. Therefore, we retrospectively analysed laboratory markers of inflammation in 105 patients (86 women, mean age 65.2 years) from a tertiary rheumatological care centre with a clinical diagnosis of GCA. Fulfilment of the American College of Rheumatology criteria was required, except for patients with typical stenosis of the arm arteries, older than 50 years of age at disease onset.5 6 Laboratory findings were obtained from the primary care physician or the medical centre consulted at disease onset, preceding anti-inflammatory therapy.

After a mean follow-up of 31 months (range 1–157 months), a magnetic resonance angiography (MRA) of the thorax, including the subclavian, axillary and brachial arteries, was performed in all patients. We found at least one stenosis of an arm artery in 40 patients (group A, positive temporal artery biopsy (pTAB): 45%), thoracic aortic aneurysm in 14 patients (group B, pTAB: 29%) and no extra-cranial involvement in 47 patients (group C, pTAB: 51%). Four patients had concomitant stenosis and aneurysm (median white blood cell (WBC) count 11 900/mm3) and were excluded.

The WBC count was significantly higher in group A compared with group C (median 11 600/mm3 vs 10 100/mm3, p=0.01, Mann–Whitney test) and group B (median 10 105/mm3) plus group C (p=0.02, figure 1). A WBC count >14 000/mm3 was measured in 25% of the cases with stenosis, but in only 8.2% of the other patients. In 5 of 6 patients, a WBC count >16 000/mm3 was associated with stenosis.

Figure 1

Box-and-whisker plots of the white blood cell (WBC) count (leucocytes) at the time of disease onset in patients with stenosis of the arteries of the upper extremities and those with unremarkable arm arteries during the course of disease as determined by magnetic resonance angiography; p=0.02.

Subsuming all patients with extra-cranial involvement (group A+B), leucocytes were still significantly higher (p=0.023) compared with group C. No further significant differences were found between all groups for the differential WBC, C reactive protein, erythrocyte sedimentation rate (ESR), thrombocytes and haemoglobin.

The degree of significance of the difference in WBC counts between groups A and B+C was similar whether polymyalgia rheumatica was present in A (p=0.025) or not (p=0.030).

Stenosis did not depend on disease duration as there were no significant differences in time between GCA onset and MRA in all groups (mean (months): A: 30; B: 33; C: 31). The mean long-term corticosteroid dose from diagnosis to MRA could be determined in 96 of 101 patients and was not significantly different between the groups (A: 16 mg/day, B: 13 mg/day, C: 14 mg/day).

Differences in the clinical presentation of patients with exclusively cranial GCA and those with arm artery manifestation were previously reported.3 6 In our patients, symptoms of arm artery stenosis (claudication, pulse differences or bruits) were found in 23 out of 40 cases. However, only limited data are available regarding the association between laboratory parameters and arm artery involvement. Lower ESRs have been described in patients with large artery vasculitis than in those with pure cranial GCA.1 2 6 By contrast, other studies, including ours, found no differences in ESR or C reactive protein between these groups.3 7 Gonzalez-Gay et al found no differences in patients with and without leucocytosis with regard to limb claudication at disease onset, but development of stenosis was not assessed during the disease course.8

Taken together, our data indicate that the risk of developing stenosis in the upper extremity arteries is increased in GCA patients with an initial high WBC count, especially in cases with leucocytosis of >16 000/mm3. As interventional treatment is most successful in limited lesions, these patients should be examined early with special attention to arm artery involvement.4 Further prospective studies in larger cohorts with GCA are warranted.

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Footnotes

  • Provenance and peer review Not commissioned; externally peer reviewed.

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