IntroductionLow-density lipoprotein cholesterol (LDL-C) has been reported to increase platelet activation. Reducing the level of LDL-C with statins induces important pleiotropic effects such as platelet inhibition. This association between platelet activity and statin therapy may be clinically important in reducing the risk of ischemic stroke. We investigated the effect of simvastatin therapy on platelet activation markers (platelet CD62P, sP-selectin, and platelet-derived microparticles (PDMPs)) in hyperlipidemic patients after ischemic stroke.Material and methodsThe study group consisted of 21 hyperlipidemic patients after ischemic stroke confirmed by CT, and 20 healthy subjects served as controls. We assessed the CD62P expression on resting and thrombin-activated blood platelets. CD62P and PDMPs were analyzed by the use of monoclonal antibodies anti-CD61 and anti-CD62 on a flow cytometer. The level of sP-selectin in serum was measured by the ELISA (enzyme-linked immunosorbent assay) method. All markers were re-analyzed after 6 months of treatment with simvastatin (20 mg/day).ResultsHyperlipidemic patients presented a significantly higher percentage of CD62+ platelets and higher reactivity to thrombin compared to control subjects. After simvastatin therapy hyperlipidemic patients showed a reduction of the percentage of resting CD62P(+) platelets (p = 0.005) and a reduction of expression and percentage of CD62P(+) platelets after activation by thrombin (median p < 0.05; percentage: p = 0.001). A decrease of sP-selectin levels (p = 0.001) and percentage of PDMPs (p < 0.05) in this group was also observed.ConclusionsHMG-CoA reductase inhibitor therapy in stroke patients with hyperlipidemia may be useful not only due to the lipid-lowering effect but also because of a significant role in reduction of platelet activation and reactivity.
THE p olym or ph on uclear n eutr op h ils (PMN) po s s e s s s ufficie n t p ote ntial to affect both im m un e r es p o ns e an d in flam m ation , h o w e ver it h as no t been yet de s cribed in th e co urs e of m ultip le s cler o s is (MS). IntroductionMultiple sclerosis (MS) is a dise as e in w hich multifoc al inflammation and damage of the blood -brain barrier and myelin sheath are salie nt pathologic features. Overw he lming evidenc e demons trates that MS is a pre dominantly T-c ell and monoc yte/mac rophageme diated autoimmune disorde r.1 ,2 Polymorphonuclear ne utrop hils (PMN) have not be en considere d as a ce ll population participating in it.3 PMN can how e ver ex pre ss immunore gulatory abilities, that has not be en ye t de sc ribe d in the c ourse of MS. Activated in vitro PMN produc e a numbe r of immune mediators including cytokines like IL-1b , IL-4, IL-6, IL-8, IL-10, IL-12, TNF, TGF-b 1. 4 ,5 There fore the re gulatory functions of these ce lls may be postulate d in the c ourse of MS. PMN in the pe ripheral blood (PB) of MS patients can be primed mainly by inflammatory cytokine s like IL-1, INF-g , or by TNF-a sec re te d by mononuclear ce lls. Hypothetically PMN priming or activation in PB of MS patients may dep end also on compleme nt (especially C5a) immunologic al c omplex es, or certain me tabolite s of the arachidonic ac id (LTB 4 , PAF).Priming re sults in the enhanced ex p re ssion on PMN of re cep tors for chemokines and other chemotactic pep tide s, 6 priming also enhance s the ex pre ssion of CD11b/CD18 molecules on PMN c ell surface 7,8 w hich re sults in the indire ct ac tivation of PMN.9,10 In the pre sente d pap er w e have suggeste d that PMN priming can be obse rved in MS patie nts p eriphe ral blood. Patients and methodsPatients (34 total; 19 w omen and 15 men, aged 22-56 years) w ere se lecte d w ith a clinic ally definitive diagnosis of MS 1 1 and w ith Kurtzke Ex panded Disability Status Scale 12 scores 5 or few er and categorized as having the re lapsing-re mitting MS (RR-MS) course for at least 5 years but curre ntly in re mission (REM) (n =13), as having either sec ondary CP-MS for at least 2 ye ars (n =13) or RR-MS and currently ex pe riencing clinical ex ace rbation (REL) of the disease (n = 12). Ex acerbations w ere defined as the appearance of new symptoms or significant w orsening of the old ones, attributabl e to MS, for at least 24 hours w ithout any fever.The control group c onsiste d of patients w ith other ne urologic al diseas es (OND) (14 total; nine w omen and five men, aged from 24 to 37 ye ars), including those w ith vasomotor headache (n = 8) and ischialgia (n = 6). Sample collectionThe studies w e re performed on PMN of the p eripheral venous blood, c ollec te d into heparin-containin g tubes (10 U/ml).0962-9351/98/050335-04 $9.00 © 1998 Carfax Publishing Ltd 335 Research PaperMediators of Inflammation, 7, 335-338 (1998) TNF labelling with fluorescein isothiocyanate (FITC)The synthesis and biological analysis of the TNF molecules w ere pe rfor...
Structural and functional parameters of myocardium were evaluated with 2D+ Doppler echocardiography in two similar age groups of MS patients: S1: 12 subjects in 3-4 Degrees EDSS (Expanded Disability Status Scale), S2: 12 subjects in 5-7 degrees EDSS. The control group comprised 12 healthy subjects temporarily (at least 1 month) immobilized due to lower limb fractures. Investigations were performed in the supine position and 3 min after tilting to the erect position. Symptoms of organic myocardial injury which might have caused its insufficiency were not observed in any subjects. All structural parameters evaluated by this method did not differ significantly in the examined groups. Symptoms suggesting myocardial insufficiency were found in patients from group S2. Statistically significant decrease of ejection fraction (EF) and cardiac output (CO) was observed in the supine position of S2 patients as compared to S1 and the controls. These symptoms intensified in the erect position in S2 patients and they were accompanied by the decreased values of stroke volume (SV). The fact that in the majority of patients orthostatic hypotonia was not observed and that those disorders were not compensated by significant intensification of heart rate suggest to us that besides disorders resulting from autonomic nervous system dysfunction they may have been caused by secondary myocardial injury in the course of MS.
Background: To investigate the relationship between hyperlipidemia and platelet activation markers – platelet and soluble P-selectin (sP-selectin), and platelet-derived microparticles (PDMPs) – in patients after ischemic stroke. Methods: 41 patients after ischemic stroke (>3 months) confirmed by CT were divided into 2 groups: with hyperlipidemia (HL, n = 21) and normolipidemia (NL, n = 20). Twenty healthy subjects served as controls. CD62P-positive platelets and PDMPs in whole blood were analyzed by the use of a flow cytometer and anti-CD61 and anti-CD62P monoclonal antibodies. Platelets were activated by thrombin (0.08 units). The level of sP-selectin in serum was measured by ELISA. Results: We observed a significantly higher CD62P expression and percentage of CD62P-positive resting and thrombin-activated platelets in the HL as compared to the NL group. The sP-selectin concentration was also significantly higher in HL than NL subjects (p < 0.05). Moreover, we observed a significantly higher percentage of PDMPs in patients after stroke (NL: p < 0.05; HL: p = 0.005) in comparison with the control group. Conclusions: Patients after stroke present symptoms of platelet hyperreactivity. HL in the patients may be a risk factor for vascular events due to the increase in platelet activation.
CD13 Ag and CD11a, CD11b, CD18 molecule expression on peripheral blood mononuclear cells (PBMC) were studied as these cells' adherent or transendothelial migration properties in three different multiple sclerosis (MS) patients groups (total 38): with clinically active MS (acute exacerbation of MS and primary chronic progressive MS (CP-MS)) and with MS remission. The control group consisted of patients, suffering from other non-inflammatory neurological diseases (OND). The results of our study suggest that CD11a/CD18 molecules expression on PB lymphocytes, although higher on these cells' surface in the course of MS as compared to OND, does not differentiate clinical forms of MS. CD11a molecule expression on monocytes did not differ significantly in all tested MS patient groups in comparison to OND. Although the expression of CD11b/CD18 molecules on monocytes' surface shows their activation in the course of MS, it does not differentiate them either. However, CD13 Ag of APN expression on PBMC surface may be an immunological marker of MS clinical form. CD13 Ag expression may also be a sensitive marker of these cells' transendothelial migration properties.
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