Relevance of platelet factor four (PF₄) plasma levels in multiple sclerosis

Abstract

In order to study the role of platelets in Multiple Sclerosis (MS) we assessed, in a group of patients during a quiescent phase of the disease, the plasma levels of beta-thromboglobulin (beta-TG) and platelet factor four (PF4) both in absence of treatment and during administration of aspirin (ASA) at the dose of 50 mg/daily. In the MS patients studied, the basal plasma levels of beta-TG and PF4 were significantly higher than in control subjects. The increase in the beta-TG plasma levels occurred independently of the age, sex and severity of the disease, whereas the modification in the PF4 plasma levels was significantly correlated with the severity of the disease. Administration to the patients of ASA, at the dose that does not affect prostacyclin production, determined a decrease of beta-TG in 77% of the patients. Mean PF4 plasma levels remained unchanged. These results suggest that PF4 in the plasma of MS patients may originate not only from the platelets but also from the mast cells following platelet aggregating factor (PAF) stimulation and immunocomplex formation.

Activities of enzymes that hydrolyze adenine nucleotides in platelets from rats experimentally demyelinated with ethidium bromide and treated with interferon-β

“…( a,b ) indicates a significant difference at P b 0.001 from columns not labeled with these letters. the surface membrane of the platelets (Chiang et al, 1982;Neu et al, 1982;Khan et al, 1985;Cananzi et al, 1987). In regard to this, alterations in the membrane of platelets (Remijin et al, 2002;Wagner and Burger, 2003;Keating et al, 2004) could be a decisive factor in changing the conformational state of the NTPDase molecule, which would explain the reduced activity observed in the present study in the period between seven and fifteen days.…”

“…Considering that alteration of platelet function has been observed in this condition (Millar et al, 1966;Neu et al, 1982;Khan et al, 1985;Cananzi et al, 1987), an experimental demyelination model was used in this study to evaluate possible changes in NTPDase and 5′-nucleotidase activity in platelets, as these are two important enzymes involved in the thromboregulation process (Kaczmarek et al, 1996;Gayle et al, 1998;Kawashima et al, 2000).…”

“…Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system of unknown etiology, characterized by various degrees of reactive astrogliosis, oligodendroglial loss and axonal pathology (Bjartmar et al, 2003;Reipert, 2004;Lassman, 2005). The medical literature has reported the occurrence of anomalous platelet behavior in this pathological condition (Millar et al, 1966;Neu et al, 1982;Khan et al, 1985;Cananzi et al, 1987). Platelets of MS patients exhibit a greater tendency to spontaneous aggregation and higher sensitivity to ADP induced aggregation (Neu et al, 1982).…”

“…Platelets of MS patients exhibit a greater tendency to spontaneous aggregation and higher sensitivity to ADP induced aggregation (Neu et al, 1982). Besides, thrombus development in the demyelinating plaques has suggested that platelets may play a role in the demyelination of white matter (Cananzi et al, 1987).…”

NTPDase and 5'‐nucleotidase activities in physiological and disease conditions: New perspectives for human health

“…Moreover, studies have reported that platelets are involved in thrombi development in the demyelinating plaques, suggesting that these cells may play a role in the demyelination of white matter [22]. Furthermore, platelets have been recognized for decades as key pathological components of the processes associated with vascular inflammation and thrombosis [5].…”