title: Cholesterol metabolism in cardiac sarcoidosis.
abstract: OBJECTIVE
  Patients with cardiac sarcoidosis (CS) suffer from myocardial inflammation, but atherosclerosis is not infrequent in these patients. However, the classical atherosclerotic risk factors, such as perturbed serum lipids and whole-body cholesterol metabolism, remain unravelled in CS.
  
  
  METHODS
  We assessed serum non-cholesterol sterols, biomarkers of whole-body cholesterol synthesis and cholesterol absorption efficiency, with gas-liquid chromatography in 39 patients with histologically verified CS and in an age-adjusted random population sample (n = 124).
  
  
  RESULTS
  CS was inactive or responding to treatment in all patients. Concentrations of serum, LDL, and HDL cholesterol and serum triglycerides were similar in CS patients and in control subjects. Cholesterol absorption markers were higher in CS patients than in controls (eg serum campesterol to cholesterol ratio in CS 246 ± 18 vs in controls 190 ± 8 10(2) x μmol/mmol of cholesterol, p = 0.001). Cholesterol synthesis markers were lower in CS patients than in controls (eg serum lathosterol to cholesterol ratio in CS 102 ± 8 vs in controls 195 ± 5 10(2) x μmol/mmol of cholesterol, p = 0.000). In CS patients, cholesterol absorption markers significantly correlated with plasma prohormone brain natriuretic peptide (proBNP), a marker of hemodynamic load.
  
  
  CONCLUSIONS
  High cholesterol absorption efficiency, which is suggested to be atherogenic, characterized the metabolic profile of cholesterol in CS patients. The association between cholesterol absorption efficiency and plasma proBNP concentration, which suggests a link between inflammation, cholesterol homeostasis, and hemodynamic load, warrants further studies in order to confirm this finding and to reveal the underlying mechanisms.
authors.affiliation: University of Helsinki and Helsinki University Central Hospital, Heart and Lung Center, Division of Cardiology, P.O. BOX 340, FI-00029 HUS, Helsinki, Finland. Electronic address: piia.simonen@hus.fi.
authors.forename: Piia
authors.initials: P
authors.lastname: Simonen
authors.affiliation: University of Helsinki and Helsinki University Central Hospital, Heart and Lung Center, Division of Cardiology, P.O. BOX 340, FI-00029 HUS, Helsinki, Finland. Electronic address: jukka.lehtonen@hus.fi.
authors.forename: Jukka
authors.initials: J
authors.lastname: Lehtonen
authors.affiliation: University of Helsinki and Helsinki University Central Hospital, Division of Internal Medicine, P.O. BOX 700, FI-00029 HUS, Helsinki, Finland. Electronic address: helena.gylling@hus.fi.
authors.forename: Helena
authors.initials: H
authors.lastname: Gylling
authors.affiliation: University of Helsinki and Helsinki University Central Hospital, Heart and Lung Center, Division of Cardiology, P.O. BOX 340, FI-00029 HUS, Helsinki, Finland. Electronic address: markku.kupari@hus.fi.
authors.forename: Markku
authors.initials: M
authors.lastname: Kupari
mesh_terms: D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000378:metabolism*; D015992:Body Mass Index; D009202:Cardiomyopathies / Q000378:metabolism; D016022:Case-Control Studies; D002784:Cholesterol / Q000031:analogs & derivatives* / Q000378:metabolism*; D008076:Cholesterol, HDL / Q000378:metabolism; D008078:Cholesterol, LDL / Q000378:metabolism; D004032:Diet; D015536:Down-Regulation; D005260:Female; D005387:Finland; D006331:Heart Diseases / Q000378:metabolism*; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D007249:Inflammation; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D010840:Phytosterols / Q000378:metabolism*; D012307:Risk Factors; D012507:Sarcoidosis / Q000378:metabolism*; D012855:Sitosterols / Q000378:metabolism
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008074:Lipoproteins; D010840:Phytosterols; D012855:Sitosterols; C021273:campesterol; C025473:gamma-sitosterol; C001521:lathosterol; D002784:Cholesterol
keywords: Atherosclerosis; Campesterol; Cholesterol absorption; Cholesterol synthesis; Inflammation; Lathosterol; Myocardial disease