title: Faecal calprotectin: a biomarker of gastrointestinal disease in systemic sclerosis.
abstract: BACKGROUND
  Assessment of gastrointestinal (GI) involvement in systemic sclerosis (SSc) is difficult. Measurement of calprotectin in faeces is a valuable tool for the assessment of inflammatory bowel diseases. Calprotectin is an intracellular protein found in leucocytes and is a potent activator of the innate immune system.
  
  
  OBJECTIVE
  To determine whether faecal calprotectin (F-calprotectin) could serve as a biomarker of GI disease in SSc.
  
  
  METHODS
  In a cross-sectional study, F-calprotectin and plasma calprotectin were measured in patients with SSc using an enzyme-linked immunosorbent assay. F-calprotectin concentrations were evaluated in relation to cineradiography, medical records, laboratory measurements and patients' subjective GI symptoms.
  
  
  METHODS
  The study was conducted at a tertiary referral centre for SSc.
  
  
  METHODS
  The study comprised 81 consecutive patients with SSc.
  
  
  RESULTS
  A majority of the patients had pathological levels of F-calprotectin when compared to accepted clinical reference values for healthy adults. F-calprotectin did not correlate with calprotectin levels in plasma. F-calprotectin was associated with the following patient characteristics: pathological cineradiography, history of referral to another clinic because of GI disease, treatment of vitamin or mineral deficiency and use of proton pump inhibitors. We did not find any significant correlation between F-calprotectin and patient-reported GI symptoms.
  
  
  CONCLUSIONS
  Faecal calprotectin is increased in a majority of patients with SSc. It correlates with objective and clinically important features of GI disease, and faecal concentrations do not vary with plasma concentrations. We suggest that F-calprotectin is a promising objective non-invasive biomarker of GI involvement in SSc.
authors.affiliation: Section for Rheumatology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden. kristofer.andreasson@med.lu.se
authors.forename: K
authors.initials: K
authors.lastname: Andréasson
authors.forename: A
authors.initials: A
authors.lastname: Scheja
authors.forename: T
authors.initials: T
authors.lastname: Saxne
authors.forename: B
authors.initials: B
authors.lastname: Ohlsson
authors.forename: R
authors.initials: R
authors.lastname: Hesselstrand
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000032:analysis; D003430:Cross-Sectional Studies; D004334:Drug Administration Schedule; D005243:Feces / Q000737:chemistry*; D005260:Female; D005767:Gastrointestinal Diseases / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy / Q000209:etiology; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D039841:Leukocyte L1 Antigen Complex / Q000032:analysis* / Q000097:blood; D008297:Male; D008875:Middle Aged; D054328:Proton Pump Inhibitors / Q000008:administration & dosage; D012595:Scleroderma, Systemic / Q000097:blood / Q000150:complications*
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D039841:Leukocyte L1 Antigen Complex; D054328:Proton Pump Inhibitors