Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: A possible role in glucocorticoid deficiency

Maurizio Averna, Grazia Ida Altieri, Tania Tomaselli, Luisa Spadaro, Roberto Scicali, Giuseppe Fede, Graziella Privitera, Francesco Purrello, Salvatore Piro, Davide Noto, Francesca Fayer

Risultato della ricerca: Article

8 Citazioni (Scopus)

Abstract

Backgrounds and aims: 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. Conclusion. 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.
Lingua originaleEnglish
pagine (da-a)347-354
Numero di pagine8
RivistaScandinavian Journal of Gastroenterology
Volume50
Stato di pubblicazionePublished - 2015

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Adrenal Insufficiency
Apolipoproteins
HDL Lipoproteins
Glucocorticoids
Apolipoprotein A-I
HDL Cholesterol
Triglycerides
Lipoproteins
Hydrocortisone
Electrophoresis
Liver Diseases
Healthy Volunteers
Fibrosis
Multivariate Analysis
Gels
Cholesterol

All Science Journal Classification (ASJC) codes

  • Gastroenterology

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Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: A possible role in glucocorticoid deficiency. / Averna, Maurizio; Altieri, Grazia Ida; Tomaselli, Tania; Spadaro, Luisa; Scicali, Roberto; Fede, Giuseppe; Privitera, Graziella; Purrello, Francesco; Piro, Salvatore; Noto, Davide; Fayer, Francesca.

In: Scandinavian Journal of Gastroenterology, Vol. 50, 2015, pag. 347-354.

Risultato della ricerca: Article

Averna, M, Altieri, GI, Tomaselli, T, Spadaro, L, Scicali, R, Fede, G, Privitera, G, Purrello, F, Piro, S, Noto, D & Fayer, F 2015, 'Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: A possible role in glucocorticoid deficiency', Scandinavian Journal of Gastroenterology, vol. 50, pagg. 347-354.
Averna M, Altieri GI, Tomaselli T, Spadaro L, Scicali R, Fede G e altri. Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: A possible role in glucocorticoid deficiency. Scandinavian Journal of Gastroenterology. 2015;50:347-354.
Averna, Maurizio ; Altieri, Grazia Ida ; Tomaselli, Tania ; Spadaro, Luisa ; Scicali, Roberto ; Fede, Giuseppe ; Privitera, Graziella ; Purrello, Francesco ; Piro, Salvatore ; Noto, Davide ; Fayer, Francesca. / Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: A possible role in glucocorticoid deficiency. In: Scandinavian Journal of Gastroenterology. 2015 ; Vol. 50. pagg. 347-354.
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title = "Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: A possible role in glucocorticoid deficiency",
abstract = "Backgrounds and aims: 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. Conclusion. 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.",
keywords = "Adrenal insufficiency, Apolipoprotein AI, Cirrhosis, Gastroenterology, HDL cholesterol",
author = "Maurizio Averna and Altieri, {Grazia Ida} and Tania Tomaselli and Luisa Spadaro and Roberto Scicali and Giuseppe Fede and Graziella Privitera and Francesco Purrello and Salvatore Piro and Davide Noto and Francesca Fayer",
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pages = "347--354",
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TY - JOUR

T1 - Apolipoprotein AI and HDL are reduced in stable cirrhotic patients with adrenal insufficiency: A possible role in glucocorticoid deficiency

AU - Averna, Maurizio

AU - Altieri, Grazia Ida

AU - Tomaselli, Tania

AU - Spadaro, Luisa

AU - Scicali, Roberto

AU - Fede, Giuseppe

AU - Privitera, Graziella

AU - Purrello, Francesco

AU - Piro, Salvatore

AU - Noto, Davide

AU - Fayer, Francesca

PY - 2015

Y1 - 2015

N2 - Backgrounds and aims: 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. Conclusion. 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.

AB - Backgrounds and aims: 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. Conclusion. 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.

KW - Adrenal insufficiency

KW - Apolipoprotein AI

KW - Cirrhosis

KW - Gastroenterology

KW - HDL cholesterol

UR - http://hdl.handle.net/10447/127420

UR - http://www.tandf.co.uk/journals/titles/00365521.asp

M3 - Article

VL - 50

SP - 347

EP - 354

JO - Scandinavian Journal of Gastroenterology

JF - Scandinavian Journal of Gastroenterology

SN - 0036-5521

ER -

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