OBJECTIVE: To determine in patients with systemic lupus erythematosus (SLE) (1) the frequency of antiprolactin (anti-PRL) autoantibodies, and (2) the relationships among anti-PRL autoantibodies, serum prolactin (PRL) levels, and lupus activity. METHODS: In a cross sectional study 259 consecutive patients with SLE were tested for serum PRL levels and anti-PRL autoantibodies based on disease activity. RESULTS: The frequency of anti-PRL was 5% (13/259), and all SLE patients with anti-PRL had hyperprolactinemia. There was lupus activity in 110 patients (42.5%) and there was no significant difference in frequency of anti-PRL autoantibodies between patients with or without lupus activity (5.5 vs 4.7%; p = 0.99). Only a high level of serum PRL was associated with lupus activity independent from other studied variables (p = 0.024). There was a negative but nonsignificant correlation between the titers of anti-PRL autoantibody and SLEDAI (r(s) = -0.16, p = 0.59). Anti-PRL positive patients had higher levels of serum PRL than anti-PRL negative patients (33.2+/-13.8 vs 11.6+/-13.2 ng/ml; p = 0.0001) and a significantly different frequency of hyperprolactinemia (100 vs 11.4%; p = 0.00001). CONCLUSION: The presence of anti-PRL autoantibodies was associated with hyperprolactinemic status and high serum PRL levels; these data suggest that anti-PRL autoantibodies could be the cause of hyperprolactinemia in a subset of patients with SLE. An increase in serum PRL levels proved to be an important independent factor related to lupus activity, but there was no relationship between anti-PRL autoantibodies and lupus activity.
OBJECTIVE: To determine in patients with systemic lupus erythematosus (SLE) (1) the frequency of antiprolactin (anti-PRL) autoantibodies, and (2) the relationships among anti-PRL autoantibodies, serum prolactin (PRL) levels, and lupus activity. METHODS: In a cross sectional study 259 consecutive patients with SLE were tested for serum PRL levels and anti-PRL autoantibodies based on disease activity. RESULTS: The frequency of anti-PRL was 5% (13/259), and all SLEpatients with anti-PRL had hyperprolactinemia. There was lupus activity in 110 patients (42.5%) and there was no significant difference in frequency of anti-PRL autoantibodies between patients with or without lupus activity (5.5 vs 4.7%; p = 0.99). Only a high level of serum PRL was associated with lupus activity independent from other studied variables (p = 0.024). There was a negative but nonsignificant correlation between the titers of anti-PRL autoantibody and SLEDAI (r(s) = -0.16, p = 0.59). Anti-PRL positive patients had higher levels of serum PRL than anti-PRL negative patients (33.2+/-13.8 vs 11.6+/-13.2 ng/ml; p = 0.0001) and a significantly different frequency of hyperprolactinemia (100 vs 11.4%; p = 0.00001). CONCLUSION: The presence of anti-PRL autoantibodies was associated with hyperprolactinemic status and high serum PRL levels; these data suggest that anti-PRL autoantibodies could be the cause of hyperprolactinemia in a subset of patients with SLE. An increase in serum PRL levels proved to be an important independent factor related to lupus activity, but there was no relationship between anti-PRL autoantibodies and lupus activity.
Authors: Luis J Jara; Gabriela Medina; Miguel A Saavedra; Olga Vera-Lastra; Honorio Torres-Aguilar; Carmen Navarro; Monica Vazquez Del Mercado; Luis R Espinoza Journal: Immunol Res Date: 2017-04 Impact factor: 2.829
Authors: Luis J Jara; Gabriela Medina; Miguel A Saavedra; Olga Vera-Lastra; Carmen Navarro Journal: Clin Rev Allergy Immunol Date: 2011-02 Impact factor: 8.667