Late-onset SLE in Latin Americans had a distinct disease expression compared to the younger-onset group. The disease seems to be mild with lower cumulative SLE criteria, reduced renal/mucocutaneous involvements, and less use of cyclophosphamide. Nevertheless, these patients have a higher risk of death and of ocular, pulmonary, and cardiovascular involvements.
Different immunological alterations may condition systemic lupus erythematosus (SLE) activity. However, it is not known whether alterations in the phenotype of circulating antigen-presenting cells (APCs) and in the response to CpG oligodeoxynucleotides (ODN-CpG) correlate with disease activity. APC expression of HLA-DR, costimulatory molecules, and TLR9 expression was determined in patients with SLE, other autoimmune diseases, and healthy controls. Monocyte and B cell response to synthetic ODN-CpG sequences was also evaluated. Monocytes from patients with moderate SLE activity had higher expression of CD40 and CD86. Decreased numbers of CD19+CD80+ and BDCA-3+CD40+ cells were found in patients with severe SLE activity. In patients with moderate SLE activity, non-adherent and enriched B cell response to ODN-CpG was similar to healthy controls. Adherent and enriched B cells from patients with severe SLE activity did not increase costimulatory molecule expression or cytokine production after ODN-CpG stimulation. APCs from patients with SLE, regardless of disease activity, displayed higher percentage of TLR9+ cells, as well as increased expression of TLR9, compared to healthy controls. Results suggest that the B cell response to ODN-CpG correlates with the SLE activity, independently of TLR9 expression, indicating that alterations in B cell response in severe activity SLE may be caused by events down-stream to TLR9.
The aims of this study were to describe the clinical features of patients with systemic lupus erythematosus (SLE) who developed cryptococcal infection and ascertain their outcomes when treated with glucocorticoids and immunosuppressive agents in conjunction with long-term maintenance antifungal therapy. Six cases of cryptococcal infection in SLE were reviewed retrospectively. The mean age at the time of infection was 26.3 (11.7) years. Three patients had active SLE and all were receiving glucocorticoids [median prednisone dose of 40 (21.2-60.0) mg/day] at the time of infection diagnosis. Concomitant cytotoxic agents were used in five patients. Meningitis was the most common clinical manifestation (n = 5) and cryptococcemia was found in three cases. The patient, who developed pulmonary cryptococcosis, died from respiratory distress syndrome. All patients received induction anti-fungal therapy with amphotericin B and the five surviving patients switched to oral fluconazole indefinitely as maintenance therapy and none of them has had relapses of cryptococcal infection to last medical evaluation. As SLE patients have intrinsic abnormalities of cell-mediated immunity and receive immunosuppressive therapy, indefinite maintenance therapy with fluconazole is recommended in SLE patients with cryptococcosis.
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