Sodium (18)F-sodium fluoride PET failed to predict responses to TNFα antagonist therapy in 31 patients with possible spondyloarthritis not meeting ASAS criteria.

OBJECTIVES

To determine whether (18)F-NaF positron-emission tomography (PET) contributes to the diagnosis of spondyloarthritis and whether observed uptakes predict the response to TNFα antagonist therapy.

METHODS

We studied patients who had suspected spondyloarthritis but did not meet ASAS criteria and who were referred for an assessment of eligibility for TNFα antagonist therapy. (18)F-NaF PET was offered instead of bone scintigraphy. TNFα antagonist therapy was given if the clinician's level of confidence in the diagnosis of spondyloarthritis based on (18)F-NaF PET findings was ≥50/100.

RESULTS

Thirty-one patients accepted to undergo (18)F-NaF PET. Their mean age was 39.9±11.7 years; 22% were HLA-B27-positive and none had evidence of sacroiliitis by magnetic resonance imaging. Of the 31 patients, 30 had abnormal (18)F-NaF PET findings. However, of the 312 high-uptake foci, only 123 (39.4%) matched sites of pain. TNFα antagonist therapy was given to 16 patients. The treated group and untreated group (n=15) were not significantly different for the mean number of high-uptake foci per patient (11.7±8.1 vs. 8.3±5.1, respectively) or for the proportion of patients with high uptake by the sacroiliac joints (13/16 [81%] vs. 8/15 [53%], respectively). In the treated group, 5 patients met ASAS response criteria after 3 months. These 5 patients were among the 9 treated patients who met Amor's modified criteria (arthritis instead of asymmetrical oligoarthritis). In the 5 responders, the (18)F-NaF uptake scores were nonsignificantly lower than in the 11 nonresponders (9.0±8.5 vs. 13.0±6.4, respectively). In the patients for whom the (18)F-NaF PET findings increased the level of confidence in the diagnosis of spondyloarthritis, this effect was short-lived.

DISCUSSION: The positive predictive value of (18)F-NaF PET for diagnosing spondyloarthritis or predicting a response to TNFα antagonist therapy seems very low. This finding is probably ascribable to poor specificity.