title: Intravenous immunoglobulin increases plasma viscosity without parallel rise in blood pressure.
abstract: OBJECTIVE
  Intravenous immunoglobulin (IVIg) is a commonly used therapy for autoimmune disease, but may cause chronic hypertension and thrombosis. We determined whether: (i) IVIg systematically affects blood pressure in the short term; (ii) acute changes in plasma viscosity because of IVIg correlate with blood pressure effects; (iii) effects of IVIg on acute blood pressure are related to baseline blood pressure or hypertension status and (iv) IVIg influences plasma markers of inflammation, anticardiolipin antibodies and homocysteine as additional putative prothrombotic risk factors.
  
  
  METHODS
  Twenty adults with autoimmune neurological disease who received a course of IVIg were evaluated immediately before and after each infusion, on every day of the course. Blood pressure, pulse and the following haematological parameters were determined: plasma viscosity, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), haematocrit, fibrinogen, interleukin-6 (IL-6), homocysteine and anticardiolipin positivity.
  
  
  RESULTS
  Intravenous immunoglobulin caused both acute and cumulative rises in plasma viscosity across a treatment course, but no concordant changes in blood pressure. There was also no correlation between individual blood pressure changes and viscosity, baseline blood pressure or hypertension status. Levels of IL-6 rose across the course of therapy, but the acute-phase reactants CRP and fibrinogen did not. One patient developed anticardiolipin antibodies during therapy.
  
  
  CONCLUSIONS
  Individual courses of IVIg do not systematically raise blood pressure. Where IVIg is found to cause hypertension, this does not appear to be due to a direct effect of IVIg on plasma viscosity.
authors.affiliation: Imperial College Cerebrovascular Research Unit, Imperial College London, Charing Cross Campus, London, UK. p.bentley@imperial.ac.uk
authors.forename: P
authors.initials: P
authors.lastname: Bentley
authors.forename: M
authors.initials: M
authors.lastname: Rosso
authors.forename: A
authors.initials: A
authors.lastname: Sadnicka
authors.forename: S
authors.initials: S
authors.lastname: Israeli-Korn
authors.forename: M
authors.initials: M
authors.lastname: Laffan
authors.forename: P
authors.initials: P
authors.lastname: Sharma
mesh_terms: D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000032:analysis; D020274:Autoimmune Diseases of the Nervous System / Q000097:blood / Q000276:immunology / Q000628:therapy*; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D001809:Blood Viscosity; D015331:Cohort Studies; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000209:etiology; D016756:Immunoglobulins, Intravenous / Q000009:adverse effects* / Q000627:therapeutic use; D015850:Interleukin-6 / Q000097:blood; D008131:London / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013927:Thrombosis / Q000453:epidemiology / Q000209:etiology; D055815:Young Adult
chemical_list: D017153:Antibodies, Anticardiolipin; D015415:Biomarkers; C508600:IL6 protein, human; D016756:Immunoglobulins, Intravenous; D015850:Interleukin-6; D006710:Homocysteine