Format

Send to

Choose Destination
J Clin Apher. 2016 Aug;31(4):388-92. doi: 10.1002/jca.21413. Epub 2015 Jun 30.

Lipoprotein apheresis reduces circulating galectin-3 in humans.

Author information

1
Amitabha Medical Clinic and Healing Center, Santa Rosa, California.
2
University of Kansas Medical Center, Atherosclerosis and Lipid-Apheresis Center, Kansas City, Kansas.
3
Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas.

Abstract

BACKGROUND:

Plasma galectin-3 (Gal-3) is elevated in, and drives, diverse systemic inflammatory disorders, including cancer, cardiovascular diseases, and diabetes. Circulating Gal-3 promotes tumorigenesis and metastasis, as well as fibrotic remodeling, and is a promising therapeutic target. Apheresis has proven utility in reducing circulating disease-promoting substances, exemplified by the success of lipoprotein apheresis (LA) in abrogating cardiovascular disease progression in drug-refractory hypercholesterolemia patients. We compared the clinical utility of two FDA-approved LA systems in reducing plasma Gal-3 in humans.

METHODS:

Plasma Gal-3 levels were assessed by ELISA in blinded samples drawn pre- and post-apheresis from hypercholesterolemia patients (n = 10/group) undergoing therapeutic LA using either a heparin-induced extracorporeal LDL precipitation (HELP) or dextran sulfate-adsorption (DSA) system.

RESULTS:

Mean baseline plasma Gal-3 concentrations (±SD) were 14.3 ± 5.1 (range 6.6-22.8) and 14.5 ± 2.8 (range 10.6-19.8) ng/mL in the HELP and DSA groups, respectively. Post-apheresis Gal-3 levels were respectively reduced by 19.4% and 22.7% in the HELP (P = 0.0094) and DSA (P = 0.0027) systems (paired t-tests); the difference between devices was insignificant (P = 0.5288; Mann-Whitney). Post-treatment Gal-3 levels were 11.3 ± 3.7 (HELP; range 4.5-16.3) and 11.3 ± 3.8 (DSA; range 7.5-20.7) ng/mL.

CONCLUSIONS:

Circulating Gal-3 levels showed a statistically significant decrease in humans undergoing therapeutic LA. Although absolute Gal-3 reduction was ≈19-23%, this effect, combined with reducing atherogenic LDL and other inflammation mediators (e.g., CRP, fibrinogen, Lp-PLA2 ), may enhance apheresis clinical benefits. Applying new Gal-3-specific extraction technologies to apheresis may be advantageous in treating diverse pathologies that are promoted by elevated plasma Gal-3. J. Clin. Apheresis 31:388-392, 2016. © 2015 Wiley Periodicals, Inc.

KEYWORDS:

apheresis; biomarker; cancer; galectin; heart disease; inflammation

PMID:
26126949
DOI:
10.1002/jca.21413
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center