Skip Navigation LinksHome > October 2013 - Volume 47 - Issue 9 > CD4+ T-Cell Function and the Risk for Developing Spontaneous...
Journal of Clinical Gastroenterology:
doi: 10.1097/MCG.0b013e3182854969

CD4+ T-Cell Function and the Risk for Developing Spontaneous Bacterial Peritonitis in Patients With Cirrhosis

Confer, Bradley D. DO*; Lopez, Rocio MS, MPH; Zein, Nizar N. MD*

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Background/Goals: Spontaneous bacterial peritonitis (SBP) is common in cirrhotic patients and has high associated mortality. SBP is preventable with antibiotic prophylaxis. The aim of this study was to identify patients at high risk to develop SBP based on their peripheral blood CD4+ T-cell function.

Methods: Fifty-seven patients with cirrhosis and ascites were followed for the development of SBP. All patients had CD4+ assay performed through phytohemagglutinin stimulation of peripheral blood, which was quantified by measuring adenosine triphosphate (ATP) release by luciferin/luciferase assay. A receiver operating characteristic curve was used to evaluate the CD4+ assay as a predictor of SBP. A time to SBP or death analysis was performed and Kaplan-Meier plots were used to assess the association between CD4+ ATP concentration and hazard of SBP or mortality.

Results: The median follow-up time was 7.3 (4.8, 13) months. Patients who developed a first episode of SBP had a lower median CD4+ ATP concentration compared to patients without SBP (120 vs. 239 ng/mL; P<0.001). The best independent predictor of SBP was peripheral CD4+ function and an ATP level of ≤201 ng/mL provides 83% sensitivity and 71% specificity for future prediction of SBP. Patients with ATP concentration ≤201 ng/mL had a 4.7 times greater hazard of developing SBP than those with ATP level >201 ng/mL (P<0.001). Patients with SBP had 7.9 times higher hazard of mortality then those without SBP (P=0.008).

Conclusion: The risk of developing SBP was significantly increased in patients with cirrhosis and ascites who had depressed CD4+ T-cell function.

© 2013 by Lippincott Williams & Wilkins


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