title: [Chronic inflammation and endothelial dysfunction: analysis of a cohort of patients with SLE and UCTD].
abstract: OBJECTIVE
  Cardiovascular complications, mainly caused by an accelerated atherosclerosis, are one of the leading causes of death and disability in patients with systemic autoimmune diseases. Endothelial dysfunction is considered the earliest and reversible step of atherogenesis. Aim of the present study is to investigate endothelial function (EF) in patients with systemic lupus erythematosus (SLE), undifferentiated connective tissue diseases (UCTD) and correlate the results with clinical and laboratory variables.
  
  
  METHODS
  EF was assessed on the peripheral microcirculation by the perfused forearm technique that can estimate both endothelium- dependent and endothelium- independent vasodilatation. The same evaluation has been repeated in two patients after the administration of 20 mg of 6-metilprednisolone.
  
  
  RESULTS
  Twenty-three female patients with SLE or UCTD, with a follow up of at least 1 year have been studied and compared with 8 healthy controls matched for epidemiological variables and traditional risk factors for cardiovascular disease. A significant reduction both in endothelium dependent than endothelium independent vasodilatation was observed in both patients groups compared with controls. In addition, UCTD patients demonstrated a significant reduction in the nitric oxide pathway compared with controls and SLE patients. Finally, steroid administration induced an improvement of vascular reactivity.
  
  
  CONCLUSIONS
  Despite the well documented side effects of chronic corticosteroid therapy, our data might suggest a role for antinflammatory and immunosuppressive therapy in the prevention of premature atherosclerosis in patients with systemic autoimmune diseases.
authors.affiliation: UO Reumatologia, Dipartimento di Medicina Interna, Università di Pisa, Italia.
authors.forename: C
authors.initials: C
authors.lastname: Tani
authors.forename: M
authors.initials: M
authors.lastname: Mosca
authors.forename: A
authors.initials: A
authors.lastname: d'Ascanio
authors.forename: D
authors.initials: D
authors.lastname: Versari
authors.forename: A
authors.initials: A
authors.lastname: Virdis
authors.forename: L
authors.initials: L
authors.lastname: Ghiadoni
authors.forename: S
authors.initials: S
authors.lastname: Taddei
authors.forename: A
authors.initials: A
authors.lastname: Salvetti
authors.forename: S
authors.initials: S
authors.lastname: Bombardieri
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000209:etiology / Q000517:prevention & control; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control; D015331:Cohort Studies; D003240:Connective Tissue Diseases / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D003627:Data Interpretation, Statistical; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D008775:Methylprednisolone / Q000008:administration & dosage / Q000627:therapeutic use*; D008833:Microcirculation; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D014664:Vasodilation / Q000502:physiology
chemical_list: D000893:Anti-Inflammatory Agents; D009569:Nitric Oxide; D008775:Methylprednisolone