SEX-HORMONES IN CHRONIC SYSTEMIC LUPUS-ERYTHEMATOSUS - CORRELATION WITH CLINICAL AND BIOLOGICAL PARAMETERS

Sex hormones may play a major role in the pathogenesis and course of s ystemic lupus erythematosus (SLE). Objective. - To evaluate the immuno regulatory effect of gonadal steroids in SLE and their mechanisms of a ction, and to establish a correlation with the clinical and biological activity. Design. - Cross-sectional study of a cohort with SLE. Setti ng. - Outpatient SLE clinic. Patients. - 27 patients with chronic SLE, 14 were fertile women, 8 postmenopausal women and 5 men. Measurement. - Serum gonadotropins (FSH, LH), prolactin (PRL), progesterone (PG), testosterone (T), estradiol (E2) and total urinary estrogens (UE) were studied in SLE patients and in 35 healthy controls of similar age and sex. Blood and urine samples of several days of the study cycle were obtained for hormonal assay. Results. - An increased LH activity was o bserved in all groups of patients. There were no changes in serum T le vels, but absence of steroid therapy increased their levels in fertile women. A decrease in E2 values in the fertile women was observed, but total UE was similar to those in controls. This suggests an alteratio n in intermediate estrogen metabolism. Men with SLE showed a higher le vels in PG and UE than controls. Also, in both groups of women on ster oid treatment, a decrease of PRL was observed compared to the controls . In the fertile women with luteal phase, there was a decrease in PG. In the fertile women with higher clinical activity in the midcycle pha se, and those with higher biological activity in the luteal phase, a d ecrease in serum E2 was seen. Conclusions. - Our results support the h ypothesis that there is an alteration of intermediate metabolism of th e estrogens and of the testosterone. As well, a lower production of PR L during steroid treatment, and a lower production of PG may be import ant contributing factors in immunomodulation of SLE. Mechanism for thi s action should be mediated through a stimulation of the gonadotropins as LH.