Reactive follicular hyperplasia in the lymph node lesions from systemic lupus erythematosus patients: A clinicopathological and immunohistological study of 21 cases

To clarify the clinicopathological and immunohistological findings of react ive follicular hyperplasia in systemic lupus erythematosus (SLE) lymphadeno pathy, we examined 21 such cases, including four males and 17 females. Thre e main patterns could be delineated: pattern A, histological features of Ca stleman's disease (n = 6); pattern B, follicular hyperplasia with pronounce d arborizing vasculature in the paracortex resembling T-zone dysplasia with hyperplastic follicles (n = 6); and pattern C, follicular hyperplasia with out any other specific findings (n = 9). The patients who showed patterns A and B on histology were all female with a median age of 36 years, and pres ented with the lymphadenopathy within 4 months, some before a definitive di agnosis could be made. The group with pattern C included four males and fiv e females with an age ranging from 20 to 58 years (mean, 37 years). In seve n of them, the lymphadenopathy was noted 6 months or more after the therapy had been initiated. In a virological study, a small to moderate number of the lymphoid cells were positive for the Epstein-Barr virus-encoded small R NA in five of 10 cases examined. Human herpesvius 8 was not detected in the four cases examined by polymerase chain reaction and immunohistochemistry. The present study demonstrated that SLE lymphadenopathy showed histologica l variety and occasionally represented histopathological findings of multic entric Castleman's disease or findings similar to T-zone dysplasia with hyp erplastic follicles in the biopsied specimens. We emphasize that careful at tention to these morphological features, together with clinical and laborat ory examinations, should allow a firm diagnosis of SLE to be made, providin g information that is pertinent to the treatment of the disease. Moreover, disarray of the follicular dendritic cell (FDC) network, which could be eas ily detected by immunohistochemistry, was found in approximately 60% of our series. SLE lymphadenopathy should be listed as one of the diseases occasi onally associated with disarray of the FDC network, although its clinicopat hological significance remains unclear.