In the axial form of PsA, the HLA-B27:05:02 allele is associated with symmetrical sacroiliitis, and the HLA-B:08:01–HLA-C:07:01 haplotype is associated with asymmetric sacroiliac involvement.5
Putting all of this information together, Dr. Helliwell posited that two phenotypes of axial inflammatory arthritis exist: the classical phenotype and the alternative phenotype. Dr. Helliwell further opined that the majority of patients with axial spondyloarthritis will tend to demonstrate the classical phenotype of disease, but the majority of patients with axial involvement in PsA will demonstrate the alternative phenotype. He explained that such distinctions are essential for clinicians to make because this helps with proper classification of disease and selection of appropriate treatment for patients. (Editor’s note: For more on this topic, see “Axial Disease in Psoriatic Arthritis.”)
Axial disease has not been assessed in most randomized clinical trials of PsA, & thus it has been challenging to create evidence-based recommendations for this manifestation.
Treatments
When treatment options are considered, it is important to note that axial disease has not been assessed in most randomized clinical trials of PsA, and thus it has been challenging to create evidence-based recommendations for this manifestation.
Several reasons exist for the absence of clinical trials of axial disease in PsA. These reasons include lack of a validated definition of axial involvement in PsA, lack of a validated outcome measure for the assessment of treatment, the fact that a minority of patients in PsA clinical trials have axial involvement, leading to underpowered assessment of this domain, and the cost and time associated with the serial radiographs and magnetic resonance imaging studies that would be needed to comprehensively assess disease.
Dr. Helliwell did cite a phase 3b study from Baraliakos et al. that evaluated the effect of secukinumab in patients with PsA and axial manifestations. In this double-blind, placebo-controlled, multi-center trial, nearly 500 patients were randomized to receive 300 mg of secukinumab, 150 mg of secukinumab or placebo weekly for four weeks and then every four weeks thereafter for 52 weeks. Patients receiving the 300 mg and 150 mg doses of secukinumab showed significantly improved Assessment of SpondyloArthritis International Society 20 (ASA20) responses at week 12 compared with patients receiving placebo.6
Because secukinumab is an inhibitor of interleukin (IL) 17A and this interleukin is closely linked to the actions of IL-23, it is reasonable to ask if IL-23 inhibition would also be effective in treating axial involvement in PsA. However, Dr. Helliwell noted that studies on IL-23 inhibition have demonstrated less successful results, perhaps because it has been shown that cells in the spine are capable of producing IL-17 without IL-23. He did indicate, however, that more studies on IL-23 and Il-12 inhibition may be warranted to see if groups of patients could benefit from such treatments.
