title: Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: a possible role in glucocorticoid deficiency.
abstract: OBJECTIVE
  Adrenal insufficiency (AI) has been reported in patients with stable cirrhosis. A lack of substrates has been suggested as a possible contributing pathogenic mechanism leading to glucocorticoid deficiency in these subjects. To better explore this hypothesis, we studied lipoproteins in cirrhotics with and without AI.
  
  
  METHODS
  A total of 81 cirrhotic patients and 30 normal volunteers were enrolled. The severity of liver disease was graded by Child-Pugh score. Total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG), and apolipoprotein AI (Apo-AI) levels were evaluated. HDL subfractions were measured by gradient gel electrophoresis. Adrenal function was assessed by the Low-Dose Short Synacthen Test.
  
  
  RESULTS
  Cirrhotic patients showed a significant reduction of TC, HDL, LDL, TG, and Apo-AI levels compared with controls. HDL3 was significantly lower, while HDL2 was higher, in cirrhotics compared with the controls. AI was observed in 26 patients. TC, TG, HDL, and Apo-AI were significantly reduced in cirrhotics with AI compared with those with normal adrenal function. HDL2 and HDL3 did not differ between these two groups. Delta cortisol was related to TC (r = 0.30, p < 0.01), TG (r = 0.22, p = 0.05), and Apo-AI (r = 0.37, p < 0.001). Multivariate analysis revealed that Apo-AI and HDL were independently associated with AI.
  
  
  CONCLUSIONS
  Our study shows that TC, TG, HDL, and Apo-AI are reduced in cirrhotics with AI. In particular, because both HDL and Apo-AI play a primary role in providing substrates for steroidogenesis to adrenal cells, this deficiency may contribute to the pathogenesis of AI in these patients.
authors.affiliation: Department of Clinical and Molecular Biomedicine, Garibaldi Hospital, University of Catania , Catania , Italy.
authors.forename: Luisa
authors.initials: L
authors.lastname: Spadaro
authors.forename: Davide
authors.initials: D
authors.lastname: Noto
authors.forename: Graziella
authors.initials: G
authors.lastname: Privitera
authors.forename: Tania
authors.initials: T
authors.lastname: Tomaselli
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Fede
authors.forename: Roberto
authors.initials: R
authors.lastname: Scicali
authors.forename: Salvatore
authors.initials: S
authors.lastname: Piro
authors.forename: Francesca
authors.initials: F
authors.lastname: Fayer
authors.forename: Ida
authors.initials: I
authors.lastname: Altieri
authors.forename: Maurizio
authors.initials: M
authors.lastname: Averna
authors.forename: Francesco
authors.initials: F
authors.lastname: Purrello
mesh_terms: D000309:Adrenal Insufficiency / Q000097:blood*; D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood*; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood*; D015331:Cohort Studies; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008103:Liver Cirrhosis / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides; D006854:Hydrocortisone
keywords: HDL cholesterol; adrenal insufficiency; apolipoprotein AI; cirrhosis