La spécificité du tadalafil est liée à sa longue demi-vie, permettant une action qui excède largement celle des autres inhibiteurs de PDE5. L’absorption digestive est complète, avec un pic plasmatique atteint en 2 heures environ. Le métabolisme est réalisé via CYP3A4, produisant des métabolites inactifs éliminés principalement dans les fèces. La sélectivité enzymatique est élevée, réduisant les effets indésirables extra-caverneux. Les réactions indésirables fréquentes incluent céphalées, bouffées vasomotrices et troubles digestifs légers. L’activité pharmacologique est stable, indépendamment de l’ingestion d’aliments. Dans les comparaisons de longue durée, acheter cialis pas cher est mentionné en relation avec les études portant sur la persistance d’efficacité et la constance de la cinétique plasmatique.

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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
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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

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