Influence of continuous high-volume hemofiltration on IRAK-4 protein expression in severe acute pancreatitis.
- Author:
Chun-Mu MIAO
1
;
Guang-Quan ZHANG
;
Zuo-Jin LIU
;
Jian-Ping GONG
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Blotting, Western; Female; Hemodiafiltration; methods; Humans; Interleukin-1 Receptor-Associated Kinases; blood; genetics; metabolism; Male; Middle Aged; Pancreatitis, Acute Necrotizing; blood; pathology; therapy; RNA, Messenger; genetics; metabolism; Reverse Transcriptase Polymerase Chain Reaction; Tumor Necrosis Factor-alpha; blood
- From: Journal of Southern Medical University 2008;28(6):948-951
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the influence of continuous high-volume hemofiltration (CHVHF) on interleukin 1 receptor-associated kinase-4 (IRAK-4) and tumor necrosis factor-alpha (TNF-alpha) levels in patients with severe acute pancreatitis (SAP).
METHODSForty-one patients with SAP were randomly divided into two groups to receive treatment with CHVHF plus conventional therapy (21 patients) and conventional therapy only (20 patients). Venous blood samples were taken before and 12, 24, and 72 h after the treatment for evaluation of APACHE II scores. The mRNA and protein levels of IRAK-4 in the monocytes were determined by real-time PCR and Western blotting, respectively, and serum TNF-alpha levels was detected using enzyme-linked immunosorbent assay (ELISA).
RESULTSAmong the 21 patients receiving CHVHF, 18 survived and 3 died, and in the conventional therapy group, death occurred in 5 cases. In the surviving patients of CHVHF group, the APACHE II scores, IRAK-4 mRNA and protein levels and TNF-alpha levels were all significantly lowered after the treatment, and these indices were also significantly lower than those in the conventional group after treatment (P<0.05).
CONCLUSIONCHVHF is effective in reducing monocyte IRAK-4 levels and serum TNF-alpha level in SPA patients, and thus alleviates the symptoms and improves the prognosis of SAP, possibly by reducing the level of the activators that induce monocyte activation via the Toll-like receptor.