BACKGROUND: Recent studies suggest that platelet activation plays an important role in the pathophysiology of inflammatory bowel disease. In this study, we evaluated the effects of leukocytapheresis (LCAP) on platelet functions in patients with ulcerative colitis (UC). METHODS: Thirteen patients with active UC (five women and eight men) were treated with LCAP therapy. Platelet-rich plasma (PRP) was prepared, and platelet aggregation in response to agonist solution (epinephrine, collagen, and ADP) was measured with a platelet aggregometer. Platelet-derived microparticle (PDMP) plasma levels were determined by enzyme-linked immunosorbent assay. RESULTS: Nine patients responded to LCAP therapy, but no clinical responses were observed in four patients. The aggregation response to 0.1 microg/ml epinephrine was enhanced in all patients. In all responders, enhanced epinephrine aggregation was normalized after the LCAP session. However, in the four nonresponders, enhanced epinephrine aggregation was maintained after the LCAP session. In responders, the mean maximum aggregation induced by 0.1 microg/ml epinephrine was 76.8 +/- 5.0% before and 15.4 +/- 3.8% after LCAP, respectively (P < 0.05). Increased aggregation responses to both 0.2 microg/ml collagen and 1.0 microM ADP were observed, and LCAP also normalized these enhanced responses. LCAP significantly reduced circulating PDMP levels (56.8 +/- 28.3 U/ml before and 46.3 +/- 30.4 U/ml after LCAP, P < 0.05). CONCLUSIONS: LCAP reduced enhanced platelet aggregation responses in active UC patients. Because platelets play an important role in inflammatory and immune responses, therapeutic effects of LCAP may be partially mediated by reduction of increased platelet aggregation activities.
BACKGROUND: Recent studies suggest that platelet activation plays an important role in the pathophysiology of inflammatory bowel disease. In this study, we evaluated the effects of leukocytapheresis (LCAP) on platelet functions in patients with ulcerative colitis (UC). METHODS: Thirteen patients with active UC (five women and eight men) were treated with LCAP therapy. Platelet-rich plasma (PRP) was prepared, and platelet aggregation in response to agonist solution (epinephrine, collagen, and ADP) was measured with a platelet aggregometer. Platelet-derived microparticle (PDMP) plasma levels were determined by enzyme-linked immunosorbent assay. RESULTS: Nine patients responded to LCAP therapy, but no clinical responses were observed in four patients. The aggregation response to 0.1 microg/ml epinephrine was enhanced in all patients. In all responders, enhanced epinephrine aggregation was normalized after the LCAP session. However, in the four nonresponders, enhanced epinephrine aggregation was maintained after the LCAP session. In responders, the mean maximum aggregation induced by 0.1 microg/ml epinephrine was 76.8 +/- 5.0% before and 15.4 +/- 3.8% after LCAP, respectively (P < 0.05). Increased aggregation responses to both 0.2 microg/ml collagen and 1.0 microM ADP were observed, and LCAP also normalized these enhanced responses. LCAP significantly reduced circulating PDMP levels (56.8 +/- 28.3 U/ml before and 46.3 +/- 30.4 U/ml after LCAP, P < 0.05). CONCLUSIONS: LCAP reduced enhanced platelet aggregation responses in active UC patients. Because platelets play an important role in inflammatory and immune responses, therapeutic effects of LCAP may be partially mediated by reduction of increased platelet aggregation activities.
Authors: T Hidaka; K Suzuki; M Kawakami; M Okada; K Kataharada; T Shinohara; M Takamizawa-Matsumoto; F Ohsuzu Journal: J Clin Apher Date: 2001 Impact factor: 2.821
Authors: W Miehsler; W Reinisch; E Valic; W Osterode; W Tillinger; T Feichtenschlager; J Grisar; K Machold; S Scholz; H Vogelsang; G Novacek Journal: Gut Date: 2004-04 Impact factor: 23.059