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

Abstract

To clarify the clinicopathological and immunohistological findings of reactive follicular hyperplasia in systemic lupus erythematosus (SLE) lymphadenopathy, we examined 21 such cases, including four males and 17 females. Three main patterns could be delineated: pattern A, histological features of Castleman's disease (n = 6); pattern B, follicular hyperplasia with pronounced arborizing vasculature in the paracortex resembling T-zone dysplasia with hyperplastic follicles (n = 6); and pattern C, follicular hyperplasia without 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 presented with the lymphadenopathy within 4 months, some before a definitive diagnosis could be made. The group with pattern C included four males and five females with an age ranging from 20 to 58 years (mean, 37 years). In seven 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 RNA 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 histological variety and occasionally represented histopathological findings of multicentric Castleman's disease or findings similar to T-zone dysplasia with hyperplastic follicles in the biopsied specimens. We emphasize that careful attention to these morphological features, together with clinical and laboratory examinations, should allow a firm diagnosis of SLE to be made, providing information that is pertinent to the treatment of the disease. Moreover, disarray of the follicular dendritic cell (FDC) network, which could be easily detected by immunohistochemistry, was found in approximately 60% of our series. SLE lymphadenopathy should be listed as one of the diseases occasionally associated with disarray of the FDC network, although its clinicopathological significance remains unclear.

International, evidence-based consensus diagnostic criteria for HHV-8–negative/idiopathic multicentric Castleman disease

“…For instance, nearly all enlarged lymph nodes from patients with RA and 15% to 30% of SLE display MCD-like histopathology. [39][40][41][42] Therefore, disorders that can mimic iMCD should be excluded before a diagnosis of iMCD is accepted. The diagnostic evaluation required to exclude other diseases should be based on the clinical presentation, and may require additional biopsies, serologic or microbiology studies as indicated, and careful clinical correlation.…”

HHV-8-negative, idiopathic multicentric Castleman disease: novel insights into biology, pathogenesis, and therapy

“…9,10,12 Of note, these histopathological features are nonspecific, reactive to hypercytokinemia from any source in the body, and can be found in several infectious, rheumatologic, and neoplastic diseases (Table 1). 3,[22][23][24] Thus, iMCD lymph nodes should not be considered tumors. The plasmablastic variant is only found in HHV-8-associated MCD and will not be discussed.…”

Mitochondrial hyperpolarization: a checkpoint of T-cell life, death and autoimmunity

“…Swollen lymph nodes of patients with SLE harbor increased numbers of necrotic T cells and dendritic cells (DCs) [49]. Necrotic, but not apoptotic, cell death generates inflammatory signals that are necessary for the activation and maturation of DCs, which are the most potent antigen-presenting cells [50][51][52].…”