New Treatment Strategies in Large-vessel Vasculitis
New Treatment Strategies in Large-vessel Vasculitis
As in GCA, IL-6 is highly expressed within inflamed arteries in TAK, and serum IL-6 levels correlate with disease activity. During the early stages of the disease, IL-6 might be important in stimulating T cells and recruiting monocytes to the sites of inflammation. Later, IL-6 could be involved in angiogenesis and fibrosis.
Nishimoto et al. reported successful use of tocilizumab in a patient with refractory TAK in 2008. Since then, eight additional cases of TAK treated with tocilizumab have been reported. For these nine cases ( Table 2 ), IL-6R therapy was utilized for a mean period of 11 months (range 4–41 months). One case was treatment naive and received tocilizumab monotherapy, and eight patients were refractory to concomitant prednisone (mean dose 23 mg/day; range 5–40 mg/day) and other immunosuppressants (methotrexate, n = 5; azathioprine, n = 3; mycophenolate mofetil, n = 3; cyclophosphamiden = 2; cyclosporinen = 1; infliximab, n = 4; and adalimumabn = 1). All patients achieved disease control, and those on glucocorticoids were able to either discontinue or significantly taper prednisone after 3–6 months of tocilizumab therapy. Serial imaging in eight patients (MRA, n = 2; CT, n = 2; PET/CT, n = 4)showed improvement of vasculitic features in seven patients, evidenced by decreased vascular 18-fluordeoxyglucose uptake (n = 4), decreased vascular paramagnetic contrast enhancement (n = 2) or decreased aortic wall thickness (n = 1). One patient was shown to have a decrease in the thickness of the aortic wall following tocilizumab treatment, but progressive narrowing of the lumens of the renal, subclavian, and vertebral arteries was also observed. One patient relapsed after 8 months of treatment while still receiving tocilizumabat 8 mg/kg every 4 weeks. A second patient relapsed within 3 months of discontinuing treatment.
Anti-interleukin-6 Therapy (Tocilizumab) for Takayasu Arteritis
As in GCA, IL-6 is highly expressed within inflamed arteries in TAK, and serum IL-6 levels correlate with disease activity. During the early stages of the disease, IL-6 might be important in stimulating T cells and recruiting monocytes to the sites of inflammation. Later, IL-6 could be involved in angiogenesis and fibrosis.
Nishimoto et al. reported successful use of tocilizumab in a patient with refractory TAK in 2008. Since then, eight additional cases of TAK treated with tocilizumab have been reported. For these nine cases ( Table 2 ), IL-6R therapy was utilized for a mean period of 11 months (range 4–41 months). One case was treatment naive and received tocilizumab monotherapy, and eight patients were refractory to concomitant prednisone (mean dose 23 mg/day; range 5–40 mg/day) and other immunosuppressants (methotrexate, n = 5; azathioprine, n = 3; mycophenolate mofetil, n = 3; cyclophosphamiden = 2; cyclosporinen = 1; infliximab, n = 4; and adalimumabn = 1). All patients achieved disease control, and those on glucocorticoids were able to either discontinue or significantly taper prednisone after 3–6 months of tocilizumab therapy. Serial imaging in eight patients (MRA, n = 2; CT, n = 2; PET/CT, n = 4)showed improvement of vasculitic features in seven patients, evidenced by decreased vascular 18-fluordeoxyglucose uptake (n = 4), decreased vascular paramagnetic contrast enhancement (n = 2) or decreased aortic wall thickness (n = 1). One patient was shown to have a decrease in the thickness of the aortic wall following tocilizumab treatment, but progressive narrowing of the lumens of the renal, subclavian, and vertebral arteries was also observed. One patient relapsed after 8 months of treatment while still receiving tocilizumabat 8 mg/kg every 4 weeks. A second patient relapsed within 3 months of discontinuing treatment.
Source...