LYMPHADENOPATHIES IN LONG-STANDING SYSTEMIC LUPUS ERYTHEMATOSUS AND THE ROLE OF MAINTENANCE THERAPY WITH RITUXIMAB.
- Ingrid Ruiz-Ordoñez, Colombia
Abstract
Background and Aims
Systemic Lupus Erythematosus (SLE) is a chronic multisystemic autoimmune inflammatory disease that may cause lymphadenopathies. The present study aimed to report the etiology of lymphadenopathies and the possible role of long-standing rituximab treatment on the expression of B cell-stimulating factors in lymph nodes.
Methods
This a retrospective cohort of 205 patients with SLE, of which 13 patients (6.3%) had lymphadenopathy. Immunohistochemistry was performed in 4 available cases of follicular hyperplasia to compare the expression of BAFF, BAFFR, and BCMA between patients who received Rituximab and those who did not.
Results
The etiology of 13 lymph nodes was as follows: follicular hyperplasia in 7 (53.85%) patients, Kikuchi's syndrome in 3 (23.08%), metastasis of papillary necrotizing lymphadenitis in 1 (7.69%), follicular B-cell lymphoma in 1 (7.69%) and tuberculosis in 1 (7.69%). Three patients presenting lymphadenopathies were in remission for several years and were receiving monotherapy with rituximab. Immunohistochemical study in one of these patients showed BAFF overexpression in the follicles and moderate expression of BAFF-R confined to the mantle zone (Figure 1). No significant differences were seen on the expression of BAFF, BAFF-R and BCMA when comparing with patients who did not received Rituximab.
Conclusions
The most common cause of lymphadenopathies in our series was follicular hyperplasia. Immunohistochemistry of one patient who received Rituximab showed overexpression of BAFF and moderate expression of BAFF-R. This finding could suggest that lymph node enlargement after CD20 depletion therapy may be mediated by compensatory expression of BAFF and its receptors.