Androgen and Prolactin (Prl) Levels in Systemic Sclerosis (SSc)

U.O.C. Reumatologia--Cattedra di Reumatologia, Catholic University, Rome, Italy.
Annals of the New York Academy of Sciences (Impact Factor: 4.38). 07/2006; 1069(1):257-62. DOI: 10.1196/annals.1351.023
Source: PubMed


Testosterone (T), sex hormone-binding globulin, (SHBG), dehydroepiandrosterone sulfate (DHEAS), and prolactin (Prl) serum levels were measured by electrochemiluminescense immunoassay (ECLIA) in 39 patients with systemic sclerosis (SSc) and compared with serum hormonal levels in control subjects matched for sex and reproductive status. A possible relationship with disease duration and disease severity was examined. Our data show an altered androgen and prolactin (Prl) status in SSc patients, in most cases related to disease duration and disease severity score. We can hypothesize that hormonal dysregulation is a consequence of the chronicity of the disease. The altered hormonal status could result in relative immunological hyperactivity contributing to enhance tissue damage and disease severity.

20 Reads
  • Source
    • "The association of breast cancer with SSc may be attributed to the potential role of sex hormones in disease development of SSc and breast cancer. Increased levels of prolactin and low dehydroepiandrosterone in patients with SSc [42,43] and breast cancer [44] lend further support to this association. It is also noteworthy that the heterogeneity of SSc may preclude a definitive conclusion regarding the association of SSc and cancer. "
    [Show abstract] [Hide abstract]
    ABSTRACT: We assessed the profile and frequency of malignancy subtypes in a large single centre UK cohort for patients with scleroderma (systemic sclerosis; SSc). We evaluated the cancer risk among SSc patients with different antibody reactivities and explored the temporal association of cancer with the duration between onset of SSc and cancer diagnosis. A retrospective study of a well-characterised cohort of SSc cases attending a large tertiary referral centre was undertaken with clinical data collected through our clinical database and review of patient records. We evaluated development of all cancers in this cohort and comparison was assessed with the SSc cohort without cancer. The effect of demographics and clinical details including antibody reactivities were explored to find associations for development of cancer in SSc. Among 2177 patients with SSc, 7.1% of patients had a history of cancer. 26% were positive for anti-centromere antibodies (ACA), 18.2% were positive for anti-Scl70 antibodies and 26.6% were positive for anti-RNA polymerase III antibody (RNAP). The major malignancy subtypes were breast cancer (42.2%), haematological (12.3%), gastrointestinal (11.0%) and gynaecological cancers (11.0%). The frequency of cancers among patients with RNAP (14.2%) was significantly increased than those with anti-Scl70 (6.3%) and ACA (6.8%) (p < 0.0001 and p < 0.001 respectively). Among the patients, who were diagnosed with cancer within 36 months of the clinical onset of SSc, there were more patients with RNAP (55.3%) than other autoantibody specificities (ACA 23.5%; p < 0.008 and anti-Scl70 antibodies 13.6%, p < 0.002 respectively). Breast cancers were temporally associated with onset of SSc among patients with anti-RNAP and SSc patients with anti-RNAP had two-fold increased hazard ratio for cancers compared to patients with ACA (p < 0.0001). Our study confirmed independently, in the largest population examined to date, that there is an association with cancer among SSc patients with anti-RNAP antibodies in close temporal relationship to onset of SSc, which supports the paraneoplastic phenomenon in this subset of SSc cases. An index of suspicion should be cautiously maintained in these cases and investigations for underlying malignancy should be considered where clinically appropriate.
    Arthritis research & therapy 02/2014; 16(1):R53. DOI:10.1186/ar4486 · 3.75 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The enhanced immunoreactivity in females is a double-edged sword that provides better protection against infections, but may lead to enhanced autoreactivity and thereby contribute to the induction of autoimmunity. Autoimmune diseases demonstrate a gender bias and represent the fifth leading cause of death by disease among females of reproductive age. Clinical and murine experimental studies indicate that the gender bias in autoimmunity may be influenced by sex hormones, predominantly displayed in the development and exacerbations of the prototypical autoimmune disease lupus. The associations between sex hormones and other autoimmune diseases are less clear. Our review on the impact of gender via sex hormones and sex related genes in the pathogenesis of several autoimmune diseases suggests that a better understanding of the underlying mechanisms behind the sexual dimorphism of the immune system may lead to the development of novel therapeutic approaches to autoimmunity.
    Autoimmunity Reviews 07/2007; 6(6):366-72. DOI:10.1016/j.autrev.2006.10.001 · 7.93 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: More than 50 different neurological pathologies have a confirmed or suspected autoimmune etiology affecting an estimated number of 75 million people worldwide. Autoantibodies are a useful diagnostic marker for most autoimmune diseases even though their pathological role is not evident, and several tests for their detection are commercially available. However, for autoimmune diseases involving the nervous system, lack of clear information on the identity of antineural antibody targets and the presence of many rare diseases have hampered the development of specific diagnostic assays. This review focuses on the actual knowledge on confirmed and suspected autoimmune diseases that target the CNS and the diagnostic relevance of corresponding antineural autoantibodies.
    Expert Review of Clinical Immunology 11/2007; 3(6):949-73. DOI:10.1586/1744666X.3.6.949 · 2.48 Impact Factor
Show more