Offset

Ernesto Cairoli,*,**,*** Alfonso Cayota,***,**** María José Iriarte,*** age was 38.5 ± 15 years and duration of disease was We read with great interest the article written by 8.5 ± 10 years in the total of SLE patients included.
Ferreira et al1 recently published in your journal.
16 patients (53%) had non active disease (SLEDAI Considering the comments made in discussion by 1.0 ± 1) and 14 patients (47%) had active disease the authors, we highlight some differences obtai- (SLEDAI 13 ± 6). No significant differences of age, ned in our work. The objectives of the present study disease duration, percentage and total number of were to quantify the levels of circulating CD4+ T lymphocyte among the groups were detected. A de- cells in systemic lupus erythematosus (SLE) pa- crease in the concentrations of complement C3 and tients and further correlate their levels with the de- treatment with high doses of prednisone were gree of disease activity. A prospective study was found in SLE active group (Table I). The absolute performed in the Unit of Systemic Autoimmune Di- number of CD4+ T lymphocyte (cell/µl) and the sease, Hospital de Clínicas, School of Medicine, percentage in the non active and active SLE pa- Uruguay. Thirty consecutive (hospitalized and am- tients was 508 ± 153 and 471 ± 288 and 39.7 ± 8.5% bulatory) patients with SLE were included. All pa- and 36.5 ± 11.0% respectively. The active patients tients fulfilled four or more of the revised classifi- seemed to have lower mean levels of CD4+ T cells cation criteria for SLE of ACR.2 Disease activity was than inactive patients, however the difference was scored based on the SLE disease activity index (SLE- not statistically significant. No significant correla- DAI),3 with one group comprising patients with non tion between absolute cell numbers of CD4+ T cells active disease (SLEDAI < 5; n = 16) and another and SLEDAI score in the active SLE patients was de- group with active disease (SLEDAI ≥ 5; n = 14) with tected (Spearman r = -0.347). There were no oppor- or without immunosuppressive treatment. Peri- tunistic infections and only in 3 patients (with acti- pheral blood samples were drawn for simultaneous ve disease) bacterial infection was confirmed.
measurements of total white blood cells and CD4+ Lymphopenia correlates with disease flares that T cells (theses by flow cytometry). In all cases infor- may contribute to the development of susceptibi- med consent was obtained according to local lity to infections,4,5 however, CD4+ T cells abnorma- approved ethical rules. Comparison between the lities were not generalized to all SLE patients.6,7 different groups was performed using Mann-Whit- In the context of a retrospective study. the re- ney U test and correlations between absolute num- sults of Ferreira et al,1 could be influenced by the in- ber of CD4+ T cells and SLEDAI scores were asses- clusion of patients with severe immunosupression.
sed by nonparametric Spearman correlation. A In our case, the prospective inclusion of consecu- p< 0.05 was considered statistically significant.
tively patients could better reflect the status of 29 out of the 30 patients were female. The mean CD4+ T cell deficits in SLE. Although the samplesize is small, our series included only one male pa-tient, better reflecting the gender distribution *Unidad de Enfermedades Autoinmunes Sistémicas, Hospital deClínicas, Facultad de Medicina, Universidad de la República, observed in the SLE in this age range. We have not found significant differences between CD4+ T cell **Clínica Médica «C», Hospital de Clínicas, Facultad de Medicina, number and either non active or active SLE pa- Universidad de la República, Uruguay.
tients. This result, could be explained at least in ***Departamento Básico de Medicina, Hospital de Clínicas.
part, by changes induced by high doses of predni- Facultad de Medicina, Universidad de la República, Uruguay.
****Institut Pasteur, Montevideo, Uruguay.
sone in patients with active disease. Our results do Ó R G Ã O O F I C I A L D A S O C I E D A D E P O R T U G U E S A D E R E U M AT O L O G I A - A C TA R E U M P O R T. 2009;34:559-560 Table I. Clinical features of SLE patients
Total SLE
Non active SLE
Active SLE
not support the view that CD4+ T cell counts could References
constitute a marker of disease activity.
1. Ferrerira S, Vasconcelos J, Marinho A, et al. CD4 lymphocytopenia in systemic lupus erythematosus.
Correspondence to
Acta Reumatol Port 2009; 34:200 - 206.
2. Tan E, Cohen A, Fries J, et al. The 1982 revised criteria Unidad de Enfermedades Autoinmunes Sistémicas. for the classification of systemic lupus erythemato- Clínica Médica «C». Hospital de Clínicas. Avenida Italia sus. Arthritis Rheum 1982; 25:1271 - 1277.
s/n. piso 8. telefax: +5982 487 87 02.
3. Bombardier C, Gladman D, Urowitz M, et al. Deriva- tion of the SLEDAI: a disease activity index for lupuspatients. the Committee on Prognosis Studies in SLE.
Acknowledgments
This work was supported in part by “Programa para la In- 4. Duffy KN, Duffy CM, Gladman D. Infection and di- vestigación Biomédica” (PROINBIO) and Fundación Ma- sease activity in systemic lupus erythematosus: a re- nuel Pérez. Facultad de Medicina. Universidad de la Re- view of hospitalized patients. J Rheumatol 1991; 5. Iliopoulos A, Tsokos G, Immunopathogenesis and spectrum of infections in systemic lupus erythema-tosus. Semin Arthritis Rheum 1996; 25:318 - 336.
6. Via C, Tsokos G, Bermas B, et al. T cell-antigenpre- senting cell interactions in human systemic lupuserythematosus. J Immunol 1993; 151:3914 - 3922.
7. Wouters C, Diegenant C, Ceuppens J, et al. The circu- lating lymphocyte profiles in patients with discoidlupus erythematosus and systemic lupus erythema-tosus suggest a pathogenetic relationship. Br J Der-matol 2004; 150:693 - 700.
Ó R G Ã O O F I C I A L D A S O C I E D A D E P O R T U G U E S A D E R E U M AT O L O G I A - A C TA R E U M P O R T. 2009;34:559-560

Source: http://www.autoinmunes.hc.edu.uy/images/stories/circulating_cd4_t_cells_levels_in_active_and_non_active_systemic_lupus_erythematosus_patients.pdf