Potential conflict of interest: Nothing to report.
Liver Failure/Cirrhosis/Portal Hypertension
Relative adrenal insufficiency in decompensated cirrhosis: Relationship to short-term risk of severe sepsis, hepatorenal syndrome, and death
Article first published online: 7 AUG 2013
© 2013 by the American Association for the Study of Liver Diseases
Volume 58, Issue 5, pages 1757–1765, November 2013
How to Cite
Acevedo, J., Fernández, J., Prado, V., Silva, A., Castro, M., Pavesi, M., Roca, D., Jimenez, W., Ginès, P. and Arroyo, V. (2013), Relative adrenal insufficiency in decompensated cirrhosis: Relationship to short-term risk of severe sepsis, hepatorenal syndrome, and death. Hepatology, 58: 1757–1765. doi: 10.1002/hep.26535
Supported by FIS PI10/01373; Juan Acevedo was supported by a grant from Instituto de Salud Carlos III (CM08/00129) and Hospital Clinic. CIBEREHD is funded by the Instituto de Salud Carlos III.
- Issue published online: 30 OCT 2013
- Article first published online: 7 AUG 2013
- Accepted manuscript online: 31 MAY 2013 08:39AM EST
- Manuscript Accepted: 15 MAY 2013
- Manuscript Revised: 9 MAY 2013
- Manuscript Received: 19 FEB 2013
The prevalence of relative adrenal insufficiency (RAI) in critically ill cirrhosis patients with severe sepsis is over 60% and associated features include poor liver function, renal failure, refractory shock, and high mortality. RAI may also develop in noncritically ill cirrhosis patients but its relationship to the clinical course has not yet been assessed. The current study was performed in 143 noncritically ill cirrhosis patients admitted for acute decompensation. Within 24 hours after hospitalization adrenal function, plasma renin activity, plasma noradrenaline and vasopressin concentration, and serum levels of nitric oxide, interleukin-6 and tumor necrosis factor alpha were determined. RAI was defined as a serum total cortisol increase <9 μg/dL after 250 μg of intravenous corticotropin from basal values <35 μg/dL. Patients were followed for 3 months. RAI was detected in 26% of patients (n = 37). At baseline, patients with RAI presented with lower mean arterial pressure (76 ± 12 versus 83 ± 14 mmHg, P = 0.009) and serum sodium (131 ± 7 versus 135 ± 5 mEq/L, P = 0.007) and higher blood urea nitrogen (32 ± 24 versus 24 ± 15 mg/dl, P = 0.06), plasma renin activity (7.1 ± 9.9 versus 3.4 ± 5.6 ng/mL*h, P = 0.03), and noradrenaline concentration (544 ± 334 versus 402 ± 316 pg/mL, P = 0.02). During follow-up, patients with RAI exhibited a higher probability of infection (41% versus 21%, P = 0.008), severe sepsis (27% versus 9%, P = 0.003), type-1 hepatorenal syndrome (HRS) (16% versus 3%, P = 0.002), and death (22% versus 7%, P = 0.01). Conclusion: RAI is frequent in noncritically ill patients with acute decompensation of cirrhosis. As compared with those with normal adrenal function, patients with RAI have greater impairment of circulatory and renal function, higher probability of severe sepsis and type-1 HRS, and higher short-term mortality. (Hepatology 2013;58:1757–1765)