title: Prolactin's role in the pathogenesis of the antiphospholipid syndrome.
abstract: Increased levels of serum prolactin have been reported in patients with various autoimmune diseases and have been associated with lupus disease activity. Currently, there is a lack of data regarding hyperprolactinaemia in patients with the antiphospholipid syndrome. Hence, this study was carried out in order to evaluate the prevalence and clinical significance of hyperprolactinaemia in antiphospholipid syndrome. A total of 172 European patients with antiphospholipid syndrome and 100 geographically and sex-matched healthy controls were included in the study; none had obvious causes of hyperprolactinaemia. All patients underwent clinical assessment for disease manifestations, in addition to laboratory assessment for serum prolactin, antiphospholipid antibodies and some other biomarkers of autoimmune diseases. The tests were performed utilizing the LIAISON® Analyzer (DiaSorin, Sallugia Italy). Hyperprolactinaemia was detected in 21/172 patients with antiphospholipid syndrome and 0/100 controls (p < 0.001). This significant difference was present in both genders and was obvious even after subgrouping the patients into primary and secondary antiphospholipid syndrome. When clinical features were compared, hyperprolactinaemia was associated with reproductive failure, including early and late pregnancy loss (p < 0.05), as well as intrauterine growth retardation (p < 0.05). Hyperprolactinaemia was negatively related to arthralgias, venous thrombosis, pulmonary microthrombosis, pulmonary hypertension in both primary antiphospholipid syndrome and antiphospholipid syndrome secondary to other diseases, and to neurological manifestations in primary antiphospholipid syndrome (p<0.05). The data indirectly imply that prolactin may play a role in the pathogenesis of antiphospholipid syndrome, especially antiphospholipid syndrome-related reproductive failure.
authors.affiliation: Department of Rheumatology, University Clinical Center Ljubljana, Ljubljana, Slovenia.
authors.forename: S
authors.initials: S
authors.lastname: Praprotnik
authors.forename: N
authors.initials: N
authors.lastname: Agmon-Levin
authors.forename: B S
authors.initials: BS
authors.lastname: Porat-Katz
authors.forename: M
authors.initials: M
authors.lastname: Blank
authors.forename: P L
authors.initials: PL
authors.lastname: Meroni
authors.forename: R
authors.initials: R
authors.lastname: Cervera
authors.forename: W
authors.initials: W
authors.lastname: Miesbach
authors.forename: L
authors.initials: L
authors.lastname: Stojanovich
authors.forename: M
authors.initials: M
authors.lastname: Szyper-Kravitz
authors.forename: B
authors.initials: B
authors.lastname: Rozman
authors.forename: M
authors.initials: M
authors.lastname: Tomsic
authors.forename: Y
authors.initials: Y
authors.lastname: Shoenfeld
mesh_terms: D000022:Abortion, Spontaneous / Q000453:epidemiology / Q000209:etiology; D000328:Adult; D017152:Antibodies, Antiphospholipid / Q000097:blood*; D016736:Antiphospholipid Syndrome / Q000209:etiology / Q000503:physiopathology*; D016022:Case-Control Studies; D005060:Europe; D005260:Female; D005317:Fetal Growth Retardation / Q000453:epidemiology / Q000209:etiology; D006801:Humans; D006966:Hyperprolactinemia / Q000453:epidemiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011247:Pregnancy; D011388:Prolactin / Q000097:blood*
chemical_list: D017152:Antibodies, Antiphospholipid; D011388:Prolactin