Arthritis & Rheumatism, Volume 60,
October 2009 Abstract Supplement
The 2009 ACR/ARHP Annual Scientific Meeting
Philadelphia October 16-21, 2009.
Rituximab in Cutaneous Lupus: Responsiveness Depends On Pattern of Skin Involvement
Vital1, Edward M., Dass1, Shouvik, Buch1, Maya H., Pease2, Colin T., Martin2, Michael F., Rawstron2, Andrew C., Goodfield2, Mark
Rituximab in SLE has been described in >200 published cases; positive responses were seen in all systems. However, cutaneous pathology in lupus is heterogeneous, including some lesions that occur in patients without autoantibodies. Responses to targeted B cell therapies therefore warrant more detailed assessment.
35 SLE patients were treated with 2 × rituximab 1000mg + methylprednisolone 100mg. Patients with skin involvement were reviewed in a combined rheumatology/dermatology clinic. B cells were monitored using highly sensitive flow cytometry.
14 patients had significant cutaneous disease. Antimalarials (5/14) or other immunosuppressants (7/14) were continued. The skin was the primary indication for treatment in 3 patients.
Non-cutaneous disease: 12 had significant (BILAG A/B) non-cutaneous disease including renal(2), cerebral(3), haematological(3) and arthritis(3). Responses were good with reduction of BILAG A/B to C/D in 11/12.
Discoid LE: 4 patients had discoid disease. None showed significant change after treatment.
Cutaneous vasculitis: 2 patients had cutaneous vasculitis with purpura; both responded completely.
Changing pattern of lupoid cutaneous disease: 1 patient with papulosquamous subacute LE responded well for 11 months then relapsed with the same rash. In 3 other patients, acute photoaggravated LE responded, but they then developed disseminated discoid LE. In these patients B cell depletion was incomplete, transient improvement occurred during depletion, and change in pattern of skin disease occurred during repopulation.
Developing non-lupoid cutaneous disease: 3 patients developed non lupoid rashes. 2 patients were treated for arthritis with initial good response. Following a second cycle of rituximab 1 developed Sweet's syndrome and 1 pemphigus erythematosus. 1 patient was treated for thrombocytopenia and cerebral vasculitis but developed psoriasis. These rashes occurred while B cell depleted. All were biopsy-proven.
Responsiveness of cutaneous lupus to rituximab is complex. Discoid lesions did not respond. Acute non-discoid LE and vasculitis in patients with active systemic disease initially improved along with other manifestations. However, some patients switched to a disseminated discoid pattern following B cell repopulation. This may be explained by expansion of a T cell population during B cell depletion that becomes activated during repopulation. Alternatively transient and incomplete B cell depletion may alter the pathological B cell repertoire. Some patients develop other cutaneous diseases, but the mechanism for this is unclear. The role of B cells may vary between different patterns of skin disease in SLE and rituximab may not be the most appropriate therapy for all patients. Careful monitoring of the skin is needed when using rituximab in SLE. These results may have implications for the design and interpretation of clinical trials of B cell therapies in SLE.
To cite this abstract, please use the following information:
Vital, Edward M., Dass, Shouvik, Buch, Maya H., Pease, Colin T., Martin, Michael F., Rawstron, Andrew C., et al; Rituximab in Cutaneous Lupus: Responsiveness Depends On Pattern of Skin Involvement [abstract]. Arthritis Rheum 2009;60 Suppl 10 :275